i 

“HISTOPATHOLOGICAL STUDY OF MYOMETRIAL

LESIONS OF

CORPUS UTERI – TWO YEAR STUDY”

By

DR ANITA. B. SAJJANAR

Dissertation Submitted to the

Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka

In Partial Fulfillment Of the requirements for the degree of

DOCTOR OF MEDICINE in Specialty of

PATHOLOGY

Under the Guidance of

Dr. SUREKHA. S. PATIL, MD, Associate Professor.

ASSOCIATE PROFESSOR

DEPARTMENT OF PATHOLOGY

AL-AMEEN MEDICAL COLLEGE, BIJAPUR

KARNATAKA

2008 – 2011

ii 

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

KARNATAKA, BANGALORE

DECLARATION BY THE CANDIDATE

I here by declare that this dissertation/ thesis entitled

“HISTOPATHOLOGICAL STUDY OF MYOMETRIAL LESIONS OF

CORPUS UTERI – TWO YEAR STUDY” is a bonafide and genuine research work

carried out by me under the guidance of Dr. SUREKHA. S. PATIL, MD, Associate

Professor.

Date:

Place: BIJAPUR DR ANITA. B. SAJJANAR

iii 

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

KARNATAKA, BANGALORE

CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled “HISTOPATHOLOGICAL

STUDY OF MYOMETRIAL LESIONS OF CORPUS UTERI – TWO YEAR

STUDY” is a bonafide research work done by Dr. ANITA. B. SAJJANAR in partial

fulfillment of the requirement for the degree of DOCTOR OF MEDICINE in

PATHOLOGY.

Date:

Place : BIJAPUR Dr. SUREKHA. S. PATILM.D(Pathology)

Associate Professor

iv 

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

KARNATAKA, BANGALORE

CERTIFICATE BY THE CO – GUIDE

This is to certify that the dissertation entitled “HISTOPATHOLOGICAL

STUDY OF MYOMETRIAL LESIONS OF CORPUS UTERI – TWO YEAR

STUDY” is a bonafide research work done by Dr.ANITA. B. SAJJANAR in partial

fulfillment of the requirement for the degree of DOCTOR OF MEDICINE in

PATHOLOGY.

Date: Dr.VIDYA A. THOBBI M.S.

Place : BIJAPUR (Obs & Gynaecology) Professor & HOD Dept. of obs & gynaecology

v 

ENDORSEMENT BY THE HOD, PRINCIPAL / HEAD OF THE

INSTITUTE

This is to certify that the dissertation entitled “HISTOPATHOLOGICAL

STUDY OF MYOMETRIAL LESIONS OF CORPUS UTERI –TWO YEAR

STUDY” is a bonafide research work done by Dr ANITA. B. SAJJANAR under the

guidance of Dr. SUREKHA. S. PATIL, Associate Professor, Department of

Pathology.

Seal and Signature of the HOD Signature of the Principal

Dr.A.M.PATIL M.D Dr. B.S. Patil. MD General Medicine Professor and HOD Principal & Dean Department of Pathology Al – Ameen Medical College, Al – Ameen Medical College, Bijapur Bijapur  

 

vi 

COPYRIGHT

DECLARATION BY THE CANDIDATE

I hereby declare that the Rajiv Gandhi University of Health Science,

Karnataka Shall have the rights to preserve, use and disseminate this dissertation /

thesis in print or electronic format for academic / research purpose.

 

Date : Signature of the Candidate

Place : Bijapur

Dr Anita. B. Sajjanar

© RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA

 

vii 

ACKNOWLEDGEMENT

I sincerely thank Dr.Surekha .S.Patil, M.D. Associate Professor, Department

of Pathology Al Ameen Medical College, BijapUR whose valuable guidance, constant

help and support facilitated me toaccomplish this dissertation.

I sincerely thank Dr.Vidya. A.Thobbi, M.S Professor& Head, Department of

Obstetrics & Gynaecology Al Ameen Medical College, Bijapur whose Valuable co-

guidance, constant help and support facilitated me to accomplish this dissertation

I am highly grateful to Dr. A. M. Patil M.D., Professor & Head, Department of

Pathology, Al Ameen Medical College Bijapur for his overall guidance and help

during the course of my study.

I acknowledge my sincere and heartfelt thanks to Dr .B. B. Sajjanar, M.D.,

D.C.P., Professor for his valuable guidance and knowledge imparted to me during my

work.

I wish to express my sincere gratitude to Dr. Harish. Mane, M.D Associate

Professor, Dr. V. D. Daffle, M.D., Associate Professor, Dr. Saeed. Yendigeri M.D,

Assistant Professor, Dr. Mohd. Arifullah. K M.D, Assistant Professor, Dr. Nasheen. 

Fathima M.D, Assistant Professor for their encouragement and suggestions.

I am also thankful to District Surgeon and his colleagues for providing

materials and support.

My heartful thanks to my postgraduate colleagues, technical staff, and non

teaching staff, Department of Pathology Al Ameen Medical College, Bijapur, for their

support and cooperation.

I express my sincere gratitude to my family for their continuous support and

encouragement throughout the course.

viii 

It has been my good fortune to have enjoyed the affection and loyalty of my

husband Dr.Vijay. G. Bidkar and my in laws for their help and unconditional support

throughout the course.

Lastly, I thank to all those who helped me directly or indirectly in preparing

dissertation work.

Date:

Place: Dr. Anita. B. Sajjanar

 

ix 

LIST OF ABBREVIATIONS USED

CT ,………………………….Computed Tomography

D & C,……………………….Dilatation and curettage

DUB,……………………….. Dysfunctional uterine bleeding

GnRH,………………………Gonadotrophin releasing hormone

H&E,……………………….. Hemotoxylin and Eosin

HPF ,……………………….. High power field

IHC,………………………… Immunohistochemistry

IVL,………………………… Intravenous leiomyomatosus

MAL,………………………. Mitotically active leiomyoma

MF,…………………………. Mitotic figures

SOD,……………………….. Superoxide dismutase

STUMP,……………………. Smooth muscle tumors of uncertain malignant potential

USG,……………………….. Ultrasonography

UTROSCTs,…………………Uterine tumors resembling ovarian sex cord tumors

WDPV,………………………White discharge per vagina

WHO,………………….…… World Health Organization

 

Viii 

 

x 

ABSTRACT

Introduction: The uterus is subject to a variety of disorders, the most common of

which result from smooth muscle tumors .Leiomyomata (uterine fibroids) are the

most common tumours of the female pelvis. The normal myometrium of leiomyomas

containing uteri expresses higher levels of estrogen receptors a fact related to

pathogenesis. The leiomyosarcoma, is the malignant counterpart of the leiomyoma

and is the most common pure sarcoma of the uterus. Adenomyosis is the most

common tumor like condition involving the myometrium. Clinical diagnosis of

adenomyosis is difficult, because of the non-specific nature of symptoms.

Furthermore, leiomyomas are frequently associated with adenomyosis, hindering the

differential diagnosis.

Aims: The aim of the present study is to study the incidence of various types of

myometrial lesion in and around Bijapur, from hysterectomy specimens and

myomectomy specimens (if available), to study the histopathological features of the

myometrial lesions, and to study the pattern of occurrence of different myometrial

lesion in relation to age, parity and mode of presentation.

Methods: The present two year prospective study in the Department of Pathology

from June2008 to June 2010 done at Al Ameen Medical College, Bijapur. It includes

517 hysterectomy specimens, which were studied grossly and microscopically to

document the various myometrial lesions. Hysterectomy specimens were processed

and stained with routine H&E on paraffin sections.

Results: In the present study, leiomyomas were most common benign neoplastic

lesions, most of the patients harbouring leiomyomas were multiparous. Most of the

patients with fibroids were in their 3rd decade. Adenomyosis was the common tumor

xi 

like condition encountered in majority of the patients. Menorrhagia, dysmenorrhea

were the most commonest clinical symptoms both in leiomyoma and adenomyosis.

Leiomyosarcoma,rare tumor diagnosed in single specimen.

Summary & Conclusion: Leiomyomas and adenomyosis are the most common

findings in the hysterectomy specimens. In the present study myometrial lesions of

uterine corpus constituted (53.38%) of the total in which leiomyoma constituted

(55.79%) of the total. Adenomyosis encountered in (18.84%) of uteri. However,

malignant tumors were diagnosed in only 1 specimen (0.39%) out of 517 specimens

studied

Key Words: Leiomyomas; Adenomyosis; Leiomyosarcoma

 

 

 

 

 

 

 

xii 

LIST OF CONTENTS

Table No Title Page No

1 Introduction 1

2 Objectives 4

3 Review of Literature 5

4 Methodology 68

5 Results 70

6 Discussion 97

7 Summary & Conclusion 116

8 Bibliography 118

9 Annexures 134

 

xiii 

LIST OF TABLES

Table No

Title Page No

1 Age distribution in myometrial lesions 71

2 Clinical Diagnosis 72

3 Clinical Features 73

4 Morphology of the Uterus 74

5 Cut section 75

6 Histopathological lesion 76

7 Location and number of leiomyoma 78

8 Histological types of leiomyomas 79

9 Degenerative changes in leiomyoma 80

10 Variants of leiomyoma 82

11 Endometrial changes in leiomyomatous Uterus 83

12 Comparative percentage of leiomyomas in various Studies 98

13 Distribution noted by various authors in leiomyomas according to age in various studies

99

14 Parity distribution noted by various authors in leiomyoma 100

15 Comparative of statement of various symptoms with other studies

101

16 Comparative percentage of abnormal uterine bleeding in various studies

102

17 Comparison of location of leiomyomas in various studies 103

18 Comparative percentage of degenerative changes in various Studies

104

19 Comparative percentage of hyaline change in leiomyomas noted by various studies

105

20 Comparative percentage of incidence of calcification in different studies

106

21 Comparative percentage of endometrial changes in leiomyoma

109

22 Comparative percentage of leiomyosarcoma in various studies 110

23 Comparative percentage of adenomyosis in various studies 112

24 Comparison of distribution of adenomyosis in different age

groups

113

25 Association of leiomyoma with adenomyosis in different studies

115

xiv 

LIST OF FIGURES

Table No

Title Page No

1 Embryology 5

2 Normal anatomy 8

3 Gross structure of uterus 9

4 Normal proliferative endometrium in the menstrual cycle 13

5 Early secretory endometrium 13

6 Myometrium 14

7 Cut section of uterus showing submucosal leiomyomas 85

8 Cut section of uterus showing intramural leiomyoma 85

9 Gross section of uterus showing subserosal leiomyoma 86

10 Cut section of uterus showing subserosal leiomyoma 86

11 Gross section of uterus showing multiple leiomyomas 87

12 Cut section of uterus showing multiple leiomyomas 87

13 Gross section of bulky uterus 88

14 Cut section of uterus showing calcification 88

15 Cut section of uterus showing subserosal mucoid

degeneration

89

16 Gross section of the adenomyosis 89

17 Microphotograph of classical leiomyoma 90

18 Photomicrograph of leiomyoma with foci of myxoid change 90

19 Photomicrograph showing cellular leiomyoma 91

20 Photomicrograph showing of cellular leiomyoma High power

view

91

21 Photomicrograph of epitheloid leiomyoma 92

22 Photomicrograph of schwannoma like leiomyoma 92

23 Photomicrograph of symplastic leiomyoma 93

24 Photomicrograph of Leiomyoma showing mitotically active

leiomyoma

93

25 Photomicrograph of Leiomyoma showing diffuse hyaline 94

xv 

change

26 Photomicrograph showing Medial Monckebergs calcification 94

27 Photomicrograph of Adenomyosis 95

28 Gross section of uterus showing leiomyosarcoma 95

29 Photomicrograph of leiomyosarcoma, low power view 96

30 Photomicrograph of leiomyosarcoma High power view 96

 

1

INTRODUCTION

The uterus is subject to a variety of disorders, the most common of which

result from endocrine imbalances, complications of pregnancy, and neoplastic

proliferation. Together with the lesions that affect the cervix (causing abnormal pap

smears), the lesions of the corpus of the uterus and the endometrium (causing

abnormal vaginal bleeding) account for most patients visit to gynaecologic clinic.

The uterus has two major components: the myometrium and the endometrium.

The myometrium is composed of tightly interwoven bundles of smooth muscle that

form the wall of the uterus. The internal cavity of the uterus is lined by the

endometrium composed of glands embedded in a cellular stroma.

The endometrium lies under influence of hormones, denuded monthly of its

endometrial mucosa and transiently inhabited by fetus.1

Leiomyomata (uterine fibroids) are the most common tumours of the female

pelvis. Presentation of most cases of fibroids is usually straightforward making

diagnosis and management easy. However, when they undergo various kinds of

pathologic changes, they pose both diagnostic and management difficulties2

Leiomyomas of the uterus are extremely common neoplasms.The overall

incidence is between 4% and 11% but rises to nearly 40% in women over the age of

50 years. The normal myometrium of leiomyomas containing uteri expresses higher

levels of estrogen receptors a fact related to pathogenesis.

Leiomyomas are much more common in black women, in whom they have

tendency to be very numerous. Clinically apparent lesions are more common in

nulliparous, postmenopausal women. Rarely associated with polycythemia, which

regresses when tumor is excised, it may interfere with pregnancy or block ureters if

large. Estrogen responsive; may regress after menopause or castration, enlarge during

2

pregnant, difficult to diagnose from D & C, since it resembles superficial

myometrium.3

The importance of Leiomyomas lies in the symptoms they cause, the chief

being menstrual irregularities especially menorrhagia.4

Adenomyosis is infrequently diagnosed and its symptomatology is not clearly

understood. In spite of long cognizance and many publications, there is still a

widespread disagreement as to its incidence, theories of origin, symptomatology and

associated pathology.5.

Clinical diagnosis of adenomyosis is difficult, because of non specific nature

of symptoms. Furthermore, leiomyomas are frequently associated with adenomyosis

hindering the differential diagnosis6. Adenomyosis has been difficult to diagnose

without the surgical pathology of a hysterectomy specimen7.

The difficulty of predicting the biologic behavior of uterine smooth muscle

tumors has been recognized for many years. While the vast majority of these

neoplasms will follow an entirely benign course, a small but significant minority will

have aggressively exemplified by metastatic disease or recurrence8.

Uterine sarcomas comprise less than 5% of all primary uterine neoplasms.

The majority of these tumors are either leiomyosarcomas or mixed mesoderm

sarcomas; both carry a more ominous prognosis than adenocarcinoma of the uterus.

Patients with leiomyosarcomas often have advanced disease at the time of initial

diagnosis and many subsequently recur with distant metastasis.9

Despite the performance of a preoperative endometrial biopsy or dilatation and

curettage in patients with abnormal uterine bleeding and irregular uterine enlargement

because of leiomyosarcoma the diagnosis is not reliably established preoperatively10.

3

Thus in assuming a benign cause, surgical therapy might be delayed11.

However, diagnostic microscopic criteria must be carefully employed so that patients

with cellular or bizarre leiomyomas are not subjected to the potentially hazardous

therapy required for leiomyosarcomas12.

Histopathology assumes a paramount importance in the documentation of

myometrial lesions, tumors and their grading accurately. The present study will be an

effort to explore elucidate and document the lesions affecting the uterine musculature

(myometrial lesions).

4

AIMS & OBJECTIVES OF THE STUDY

In the present prospective study is an effort to analyze in detail, the various features of

uterine myometrial lesions:

1. To study the incidence of various types of myometrial lesion in and around

Bijapur, from hysterectomy specimens and myomectomy specimens (if

available)

2. To study the histopathological features of the myometrial lesions.

3. To study the pattern of occurrence of different myometrial lesions in relation

to age, parity and mode of presentation.

5

REVIEW OF LITERATURE

EMBRYOLOGY AND NORMAL ANATOMY:

Embryology: Figure 1

The adult uterus is mesodermal in origin. The corpus uteri arises as a result of

the fusion of the caudal portions of the mullerian ducts, which themselves arise as

invaginations of coelomic epithelium. From the beginning of its formation, the lumen

of this canal is lined by a columnar epithelium, from which the endometrial glands

later proliferate13.

The embryology of the female genital tract is relevant to both anomalies in

this region and the histogenesis of various tumors. The primordial germ cells rise in

the wall of the yolk sac by the fourth week of gestation; by the fifth or sixth week,

they migrate into the urogenital ridge. The mesodermal epithelium of the urogenital

ridge then proliferates, eventually to produce the epithelium and stroma of the gonad.

6

The dividing germ cells of endodermal origin are incorporated into these proliferating

epithelial cells form the ovary14.

A second component of female genital development is the mullerian duct. At

about the sixth week, invagination and subsequent fusion of the coelomic lining

epithelium form the lateral mullerian (or paramesonephric) duct. Mullerian ducts

progressively grow caudally to enter the pelvis, where they swing medially to fuse

with the urogenital sinus at the mullerian tubercle. Further caudal growth brings these

fused ducts into contact with the urogenital sinus, formed when the cloaca is

subdivided by the urorectal septum.

The urogenital sinus eventually becomes the vestibule of the external

genitalia. Normally, the unfused portions mature into the fallopain tubes, the fused

caudal portion developing into the uterus and upper vagina and the urogenital sinus

forming the lower vagina and vestibule.

Consequently, the entire lining of the uterus and tubes as well as the ovarian

surface is ultimately derived from coelomic epithelium (mesothelium).

This close embryologic relationship between the mesothelium and mullerian

system may be reflected in adult life in the form of benign (endometriosis) and

malignant (endometrioid and serous neoplasia) lesions, which may arise in both the

surface mesothelium of the ovaries and the peritoneal surfaces.

The epithelium of the vagina, cervix, and urinary tract is formed by induction

of basal cells from the underlying stroma, which undergo squamous and urothelial

differentiation15. A portion of these cells remains uncommitted, forming the reserve

7

cells of the cervix. The latter are capable of both squamous and columnar cell

differentiation16.

Many of the events in the formation of the internal and external genitalia and

their epithelial coverings result from reciprocal epithelial-stromal signaling, leading to

mesenchymal remodeling and changes in epithelial cell fate17.

8

NORMAL ANATOMY

Figure 2

The uterus is a hollow, thick-walled and muscular organ, normally situated in

the lesser pelvis between the urinary bladder and rectum. Into its upper part open the

uterine tubes, one on each side; below, it continues into the vagina.

In the adult nulliparous state it is pear shaped, though somewhat flattened

anteroposteriorly, and its long axis tilted superiorly for uterus lies behind the bladder

and (unless the bladder in full) bent forward above it. It is situated inferior to the

sigmoid colon and in front of the rectum, and completely below the pelvic inlet. In

size, the adult non-pregnant uterus is about 7.5 cm long, 5 cm in breadth at its widest

and nearly 2.5 cm thick; it weighs 30-40 gm18.

9

GROSS STRUCTURE OF THE UTERUS

Figure 3

 

DIVISIONS OF THE UTERUS

The uterus is divisible into two main regions, the body of the uterus (corpus

uteri) forming its upper two-thirds, and a narrower, more cylindrical cervix (cervix

uteri), demarcated by a slight constriction. The rounded upper part of the corpus

above the entry-points of the uterine tubes is the fundus (this is, of course, the highest

part but the deepest when approached via the cervix).

The lumen of the corpus is flat anteroposteriorly, but that of the cervix is

round in section and quite narrow, its upper end communicating with the corpus by an

aperture, the internal os, and its lower end opening into the vagina by an external os18

Uterine body (corpus uteri)

The pear-shaped uterine body gradually narrows from the fundus down to the

internal os. Its anterior (vesical) surface, apposed to the urinary bladder, is flattened

and covered by peritoneum, reflected on to the bladder as the uterovesical fold, level

10

with the internal os. The posterior (intestinal) surface of the uterus is convex

transversely. The dome-like fundus is covered by peritoneum continuous with that of

neighbouring surfaces. The lateral margins of the body is convex, and on each side

their peritoneum is reflected laterally to form the broad ligament, extending as a flat

sheet to the pelvic wall near its upper end, the body receives a uterine tube on either

side, the point of fusion of each being a uterine cornu; below the cornu, and slightly in

front is attached the round ligament and postero-inferior to it the ligament of the

ovary, both running in the broad ligament, a round ligament and stretching from the

lateral uterine margin to the lateral pelvic wall18.

Uterine cavity:

In length, it measures about 6 cm from external os to wall of the fundus.

The lumen is small in comparison with its thick wall; in the uterine body is very flat

anteroposteriorly, being a mere transverse slit in saggital or transverse section, with

the anterior and posterior wall almost in contact18.

Cervix (cervix uteri)

This part of the uterus is about 2.5 cm long in the adult non-pregnant state; it

is narrower and more cylindrical than the corpus, and is widest at its midlevel; it is

also less mobile than the body of the uterus, so that their axes are seldom in line. The

external end of the cervix bulges into the anterior wall of the vagina, which divides it

into supravaginal and vaginal regions18.

MICROSTRUCTURE OF THE UTERUS

The uterine wall is composed of three major layers, from internal to outside;

endometrium (mucosa), myometrium (smooth muscle coat) and perimetrium (serosa).

Of these the myometrium is by far the largest component18.

11

Myometrium

This fibromuscular layer forms most of uterine wall. In nulliparae it is dense,

firm greyish and (in the fixed state) cuts almost like cartilage. It is about 1.3 cm thick

at the uterine midlevel and fundus but thin at the tubal orifices. It is composed largely

of smooth muscle fasciculi mingled with loose connective tissue, blood vessels,

lymphatic vessels and nerves. The body of the uterus is often described as having four

more or less distinct layers:

The most internal layer (stratum submucosum) is composed mostly of

longitudinal and some oblique smooth muscle; where the lumen of the uterine

tubes pass through the uterine wall this layer forms circular, sphincter like

muscle coats which have been suggested to have a sphincteric action although

radio-opaque tracers pass readily from the uterus into the tubes.

External to the submucosal layer is the stratum vasculare, a zone rich in blood

vessels as well as longitudinal muscle.

Next is a layer of predominantly circular muscular, the stratum supravasculare.

Finally a thin longitudinal layer, the stratum subserosum, lies adjacent to the

perimetrium or adjacent connective tissue18.

Perimetrium (serosa)

This is composed of peritoneum (mesothelium overlying a connective tissue

lamina propria) posteriorly covering the uterine body and supravaginal cervix, but

anteriorly only the body. Over the most inferior quarter of the uterine length the

peritoneum is separated posteriorly from the underlying uterus by loose cellular tissue

and large veins. Beneath the peritoneum is a subserous layer of loose fibrous tissue18.

12

Blood Supply:

The blood supply of the uterus is derived from the uterine artery, a branch of

anterior division of the internal iliac artery. This uterine artery on each side divides

near the uterus into an ascending branch that joins with the vaginal arteries. The

arteries freely anastomose in the infundibulopelvic and cardinal ligaments and send

branches at regular intervals into the myometrium. These branches penetrate the

myometrium at right angles, divided and supply the myometrium and penetrate to the

endometrium. In the endomyometrial region, the vessels divide into horizontal and

vertical branches. The horizontal branches supply the basal endometrium (basalis)

while the vertical branches supply the more superficial endometrium of the

functionalis. The vertical vessels during the luteal phase of the cycle becomes the

spiral arterioles. The coiling of the spiral arteriole during the menstrual cycle comes

under the influence of ovarian steroid hormones and prostaglandins18.

Venous and lymphatic vessels closely follow the course of the arteries.

Lymphatic drainage is to the pelvic and para-aortic lymphnodes. The autonomicnerve

supply comes directly from the ovarian and hypogastric plexuses; sympathetic

preganglionic fibres proceed from the twelfth thoracic and first lumbar spinal

segments while parasympathetic preganglionic axons issue in the second to fourth

ventral sacral spinal roots18.

13

HISTOLOGY:  

Figure 4 Normal proliferative endometrium in the menstrual cycle.

Figure 5 Early secretory endometrium

 

 

 

14

Figure 6 Myometrium:

 

The myometrium is the thickest layer of the uterine wall. It is composed of

three indistinctly defined layers of smooth muscles. The central muscle layer,

containing numerous large blood vessels and lymphatics called as stratum vasculare.

It is thickest part and has smooth muscle bundles oriented in a circular or spiral

pattern. The smooth muscle bundles in the inner and outer layers are predominantly

oriented in parallel to the long axis of the uterus18.

The smooth muscle cells are of uniform size contain abundant, eosinophilic

fibrillar cytoplasm. The nuclei are elongated with blunt or tapered ends and have

finely dispersed chromatin. Mitotic figures are rare19, 20.

15

Endometrium:

The endometrium undergoes marked cyclical changes that constitute the

menstrual cycle. The menstrual cycle is divided into proliferative, secretory and

menstrual phase. The cyclic changes in the endometrium take place under the

influence of oestrogen and progesterone hormones produced by the ovary1.

Proliferative phase which is under the influence of oestrogen, is characterized

by extremely rapid growth of both glands and stroma. The glands are round, tubular

lined by regular pseudo stratified columnar epithelium. The stroma is dense and

compact1.

Secretory changes appears after ovulation and shows dilated large tortuous

glands lined by secretory epithelium. Stroma is loose, oedematous, decidual changes

and spiral arterioles appear at the end of the secretory phase. These changes are

accompanied by the presence of neutrophils and occasional lymphocytes. Finally

followed by menstrual phase1

16

PATHOLOGY OF MYOMETRIAL LESIONS:

Incidence and Etiology:

Uterine leiomyomas are the most common pelvic neoplasm of gynaecologic

origin, as well as the most frequently occurring tumor of the uterus. They are benign

and account for the single largest indication for hysterectomy.21.

These tumors are most frequently seen clinically between the ages of 30 and

45,although they may start developing in the early twenties22.

The tumors are most common between the ages of 35 and 45, half of the cases

being found in patients in this decade of life. Thirty percent are found in patients

between the ages of 30 and 40. The tumors are very rare indeed before the age of 20,

but are found not infrequently in women of postmenopausal age, in patients between

the ages of 40 and 50. The distribution is as follows; Virgins – 10%, nulliparae –

30%, uniparae – 20% and multiparae – 40%. Women with high parity is far less likely

to develop myomata than a woman who has never been pregnant at all. The statistics

show that 60% of myomata arise in women who have either never been pregnant or

have had only one child23.

The course of fibromyoma is undetermined. Many factors have been

considered on theoretical grounds; but practical support is lacking. Heredity is

sometimes considered to be a factor – fibroids run in families24.

Etiology:

The origin of myomas is not clear. Bonney believed that the tumors arise

before the age of 30 and it grows and becomes clinically obvious any time after that25.

17

Recent evidences has strengthened the view that estrogens and estrogen

receptors play a major role in the pathogenesis of leiomyomas26

Although estrogen, growth hormones and possibly human placental lactogen

have been implicated in the growth of the myomas, the evidence in support of

estrogen dependance for their growth is impressive27:

Myomas are rarely found before puberty, and they generally ceases to grow

after menopause.

New myomas rarely appear after menopause.

The association of fibroids in women with hyperestrogenism is evidenced by

endometrial hyperplasia, dysfunctional metropathic bleeding and endometrial

carcinoma.

Myomas are known to increase in size during pregnancy and with oral

contraceptives.

Progesterone inhibits the growth of myomas.

GnRH also causes shrinkage of the tumor26.

 Human uterine smooth muscle and leiomyoma cells differ in their rapid 17beta-

estradiol signaling: implications for proliferation29

Leiomyomas are rare prior to the menarche, common in reproductive life and

a tendency to regress after the menopause or castration suggests that the tumors are

dependent on estrogen hormones. Myer attributes the shrinkage of fibromyomas

following natural or induced menopause as possibly due to decrease blood supply to

the tumors and its association with emotional hyperplasia has been suggested as

evidence of estrogenic influence. The experiments to grow fibroids by injecting

estrogen in animals by Nelson and Lipschutz were not convincing. However,

18

Goodman attempted to control the growth of fibromyoma in patients by the use of

steroid hormones22,25,28.

Regulation of Leiomyoma Growth:

The regulation of leiomyoma growth by steroid hormones including estrogen,

progesterone and several peptide growth factors have been observed.

It is predominantly an estrogen dependent tumor. Estrogen and progesterone is

incriminated as the cause.

Estrogen dependency is evidenced by:

1) Growth potentiality is limited during childbearing age group

2) Increased growth during pregnancy

3) They do not occur before menarche

4) Following menopause, there is cessation of growth and there is no growth at

all.

5) It seems to contain more estrogen receptors than the adjacent myometrium.

6) Frequent association of an ovulation.

On the whole, the rate of growth is slow and it takes about 3-5years to be

sufficiently felt per abdomen.27

LEIOMYOMA:

Leiomyoma are most common uterine neoplasms of smooth muscles, which

occurs in women of reproductive age group30

Kusum D Jashnani et al reported six cases. Uterine leiomyomas have spectrum

of histology and growth patterns following various degenerative changes. This often

causes diagnostic difficulty. It is essential to recognize and differentiate conventional

19

leiomyomas from various other alarming variants as some of these are fraught with

diagnostic difficulty histologically when located extra uterine and can lead to overt

management.31

Achari K et al studied endometrial and ovarian changes in 76 cases of

fibromyomas. From the analysis of statistical data, they concluded that conditions

recognized as evidence of hyperestrinism are definitely and closely associated with

fibromyoma. The commonest endometrial change was endometrial hyperplasia with

multiple or single follicular cysts of ovary32.

Fechner RE studied 4 cases of leiomyoma with synthetic progestin therapy

which showed enlarged hyperchromatic nucleus with large nucleolus and occasionally

multinucleated giant cells resulting in atypical leiomyoma features and they pointed

out these areas of atypia were focal and should not be considered as sarcoma arising

in a leiomyoma of a leiomyosarcoma33.

Rosario P studied 237 cases of fibromyoma and concluded that myomas

commonly found in the reproductive age group in women who have high incidence of

follicular cysts of the ovary, hyperplasia of endometrium, anovulatory cycles and

clinically with a dysfunctional type of bleeding and sterility34.

Persaud V et al studied 298 patients with uterine leiomyomas and revealed that

there is no significant relationship between the presenting symptoms and degenerative

changes in the tumors. Degeneration was demonstrated in 65% of specimens, of

which hyaline degeneration occurred most frequently, accounting for 63%,

sarcomatous change occurred in two tumors, giving an incidence of 0.37%35.

20

Silverberg SS while analyzing reproducibility of the mitotic count in the

histological diagnosis of smooth muscle tumors of the uterus concluded that, a

quantitative estimation of mitotic activity is helpful as one of the diagnostic

andprognostic criteria in the assessment of uterine and smooth muscle tumors, but that

it could not be used as the sole criteria for distinguishing benign from malignant

tumors36.

Mukkerjee Sood M et al reported a case of leiomyoma of uterus with ascites.

They concluded that enormous size and peritoneal irritation by its parasitic attachment

could be responsible for ascites, which regressed after the removal of the tumor37.

Fisher ER et al described myofibroblastic nature of the flexiform tumor of the

uterus by light and electron microscopic study showing characteristics of both smooth

muscle cells and fibroblasts, which allowed for their identification was

myofibroblast38.

Benign metastasizing leiomyomas refers to a type of lesion characterised by

leiomyomatous alterations without any indication of malignancy. It presents as either

a singular nodule or multiple nodules of proliferating smooth muscle cells and is

generally found in the lungs of women who have undergone a hysterectomy39.

Nogales FF et al gave an update and report of 7 cases of uterine intravascular

leiomyomatosis, finding of which suggested intravascular leiomyomatosis originated

from a pre-existing leiomyoma, as all lesions were associated with typical mural

tumors and both the primary tumor and the intravascular extensions were

histologically identical40.

21

Immunohistological and ultrastructural study of clear cell variant of uterine

epitheloid leiomyoma was done by Hyde HE et al showed the presence of cell

markers like actin, vimentin, desmin, muscle specific antigens in tumor cells

indicating a smooth muscle origin41.

Moune Lai et al reported a case of diffuse uterine leiomyomatosis with

hemorrhage in a patient who was on hormonal therapy for primary infertility. They

observed that intraabdominal hemorrhage in this case of diffuse leiomyomatosis was

due to norethindrone oleate treatment given after the cessation of clomiphene

therapy42.

Shimokama T et al reported a rare case of leiomyoma with granular change

and compared the histological and immuno-cytochemical nature of this tumor with

granular cell schwannoma. They opined that marked granular change in leiomyoma is

attributed to degenerative change43.

Colgan PJ in his study observed that the most striking microscopic feature

after GnRH treatment for leiomyomas of uterus is coagulative necrosis. These

extensive areas within the leiomyoma are known to be surrounded by a rim of

inflammatory cells44.

Exaconstos C and Rosati P while studying 12708 pregnant patients who

underwent ultrasound scan showed 492 uterine myomas, 88% of cases had single

myomas and rest 12% with multiple myomas. They observed significant increase in

the incidence of threatened abortions, threatened preterm delivery, abruption placenta

and pelvic pain45.

22

Mulvany et al in a clinicopathological study of 22 cases of intravenous

leiomyoma, concluded that good prognosis resulted partially from surgical resection

at early tumor stage and from benign biological nature of intravenous leiomyoma

even when metastasis was present46.

Mulvany NJ et al described clinical and pathological features of four cases of

the rare entity of diffuse leiomyomatosis of the uterus and established the benign

nature of these tumors by a follow-up period from 6 months to 12 years47.

Oliva E et al conducted comparative morphological and immunohistochemical

analysis of 33 highly cellular leiomyomas and 6 endometrial stromal nodules. In their

study, fascicular growth pattern, vessels of large calibre with thick muscular walls,

merging with the adjacent myometrium, the presence of cleft like spaces and absence

of foamy histiocytes and immunoreactivity for desmin favoured the diagnosis of

highly cellular leiomyomas over endometrial stromal nodules48.

In addition, cultured cells from leiomyomas have a significantly higher

response to estrogen than do matched cultures of myometrial cells from the same

patient, particularly if the tissue is taken for culture in proliferative phase49.

Sreenam et al studied the histopathological findings in 107 uterine leiomyomas

following treatment with leuprolide acetate and compared with 126controls. In their

study there was no significant histological change between the two groups50.

Cotyledonoid dissecting leiomyoma of the uterus is a recently described rare

variant of benign uterine leiomyoma a case report presented with menorrhagia and

abdominal pain. Microscopy revealed a benign smooth muscle proliferation in the

myometrium that extended beyond the uterus and into the broad ligament. The lesion

23

appeared to be dissecting the myometrial fibres and showed areas of oedema,

hyalinisation and perinodular hydropic change. It is important to recognize this benign

and unusual appearing variant of leiomyoma in order to prevent inappropriate

treatment. Locally relapsed and metastatic uterine leiomyomas.51

According to WHO definition “A leiomyoma with giant cells with or without

mitotic activity is bizzare leiomyoma”. Dowens KA and Hart WR conducted a

comprehensive pathological study of 24 cases with long-term followup firmly

established the benign behavior of bizzare leiomyoma52.

Steinmetz O et al and Suginami H et al reported the uterine leiomyomatosis

extending into the heart and they opined that intravenous leiomyomatosis commonly

involves extension of the intravascular element beyond the confines of the

leiomyoma, 80% spreading outside the uterus into the pelvic veins and occasionally

along the inferior vena cava into the chambers of the heart53,54.

Subramanian N et al reported a case of leiomyoblastoma of uterus in a 40 year

old parous women with metastasis in the lung and liver, which was confirmed

immunocytochemically for desmin and vimentin55.

Symplastic or atypical leiomyomas and lipoleiomyoma are 2 very rare

morphological variants and common site is intramural.56

In one study by Stjernquist M on treatment of uterine fibroids with GnRH

analogues prior to hysterectomy, showed that during treatment both uterus and the

leiomyoma decrease in size, but most of latter return to their original size once the

treatment is stopped or within a year even if treatment is continued57.

24

A study of cell proliferation indices (Ki 67 and proliferating cell nuclear

antigen) by Greenspan DL et al suggested that the reduction in size of leiomyomas

treated by GnRH agonists is due to a reduction in the number of cycle cells, secondary

to reduced levels of estrogen and progesterone receptor58.

Latorga JBM noted a massive lymphocytic infiltration and thickening of blood

vessel walls with narrowing of the lumen, in patients treated by GnRH analogues for

uterine leiomyoma59.

A rare case of a large degenerated parasitic leiomyoma in the peritoneal cavity

deriving its blood supply from the omentum and attached to a normal looking uterus

by a narrow avascular stalk. Ultrasound, x-ray and physical examination did not help

with the diagnosis. It was at laparatomy that the diagnosis was made and later

confirmed by histological examination.2

The epidemiologic data from 285 sister pairs diagnosed with uterine

leiomyomata to identify risk factors in a racially diverse population of women with a

family history of Uterine leiomyomas, and to evaluate their contribution to disease

severity and age at diagnosis60

Quade BJ et al on disseminated peritoneal leiomyomatosis, observed clonality

by X-chromosome inactivation using polymerase chain reaction has shown that in

each of the four patient studied, the same parental X-chromosome was non-randomly

inactivated in all the peritoneal tumors, indicating all of the tumors were clonally

related61.

25

Nearly all the cases with disseminated peritoneal leiomyomatosis runs a

benign course, undergoing spontaneous regression. Nevertheless, six cases

ofmalignancy have developed in diffuse peritoneal leiomyomatosis62.

In a clinicopathological study on 1422 patients suffering from smooth muscle

tumors, by use of both conventional histology (HE and Giemsa) and

immunohistochemistry, a revealed that more than 95% of the smooth muscle tumors

were leiomyomas63.

Associated Lesions:

Leiomyoma and leiomyosarcoma can be accurately separated by evaluating

extent of tumor, degree of atypia of the stromal cells, multinucleated giant cells,

vascular invasion and mitotic rate, while stressing importance of mitotic activity, thus

concluded that tumors with less than 5 mitosis/ 10 HPF were benign and those with

higher mitotic counts were malignant. However, behavior of smooth muscle tumors

with mitotic counts between 4-9/ 10 HPF was less certain64.

Kurman RJ and Noris HJ studied 26 cases of atypical smooth muscle tumors

of the uterus like leiomyoblastoma, epitheloid leiomyomas, clear cell leiomyoma and

flexiform tumor-let and, they proposed that neoplasms having 5 or more mitotic

figures per 10 HPFs be termed as epithelioid leiomyosarcomas and those with less

than 5 mitotic figures/ 10 HPFs as epithelioid leiomyomas65.

Mark AS et al described differential diagnosis of adenomyosis and leiomyoma

with MR imaging technique in 21 patients. They correlated MR imaging findings with

histological diagnosis in which all adenomyosis (8) and majority of leiomyoma (10)

were correctly diagnosed, while small leomyomas and microscopic foci of

adenomyosis were not demonstrated with this technique66.

26

A study of 46 cases of smooth muscle neoplasms of the uterus other than

ordinary leiomyomas was done by Evans et al in 1988. 37 cases were diagnosed as

leiomyosarcoma on the basis of mitosis of >5/10 HPFs in the most active areas of the

tumor. They considered tumor size was the most prognostic factor when compared to

other morphological factors. Rest of them were leiomyoma variants, which were

tumor free on follow67.

Bell SW et al in there retrospective study of 213 cases of uterine smooth

muscle neoplasm, developed a classification system based on mitotic index,

cytological atypia, type of coagulative tumor cell necrosis, infiltrative margins and

intravascular growth68. Based on their criteria, it is a leiomyoma if there is no necrosis

with or without mild cellular atypia and it is a leiomyosarcoma if there is coagulated

tumor cell necrosis with moderate to severe atypia regardless of mitotic counts13.

Parker, Fu and Berek reviewed 1332 cases operated for symptomatic uterine

leiomyomas or rapidly growing leiomyomas to determine the incidence of uterine

sarcoma among patients operated for uterine leiomyomas. Extremely low and rapid

growth does not substitute the concept of increased risk of sarcomas in these

women69.

Pathology of Leiomyomas:

These are the most common benign uterine neoplasms of smooth muscles

encountered in gynaecological practice. They occur in 20-40% of women of

reproductive age group70.

Grossly leiomyomas are well circumscribed, discrete, grey white tumor. They are

solid round to spherical on shape firm in consistency and varying in size from barely

visible nodules to large tumors that fill the pelvis. They are white to tan in color and

27

have a whorled cut surface20. Leiomyomas arise anywhere within the myometrium.

Intramural distribution being the most common (75%), next submucosal (15%) and

least are suberosal (10%). The gross appearances are often altered by infarction,

hemorrhage, necrosis and other degenerative changes25.

Microscopically leiomyomas consists of anastomosing and whorled fascicles of

fusiform to spindle shaped cells of a relatively uniform size. These cells contains

abundant, eosinophilic and fibrillar cytoplasm. The nuclei are elongated, with bent or

tapered ends and have finely dispersed chromatin with small inconspicuous nucleoli.

Mitotic figures are rare (1-4/10 HPF).

Ultrastructurally leiomyomas have abundant myofilaments, prominent, pinocytic

vesicles, a well defined basement membrane and a prominent extracellular

collagenous matrix. The cells within the leiomyomas are different from those of

normal myometrium in their increased nuclear size, more numerous mitochondria and

increased amount of free ribosomes19,20.

Cytogenetics:

Most leiomyomas have normal karyotypes, but approximately 40% have a

simple chromosomal abnormality. Several cytogenetic subgroups have been

recognized: a balanced translocation between chromosomes 12 and 14 (i.e., t (12;14)

(q14–q15;q23–q24)), partial deletions of the long arm of chromosome 7 (i.e., del (7)

(q22–q32)), trisomy 12, and rearrangements of 6p, 3q, and 10q. The rearrangements

of 12q14 and 6p involving the HMGIC and HMGIY genes, respectively, which are

also implicated in a variety of other benign neoplasms. Both genes encode closely

related DNA-binding factors that regulate chromatin structure1.

28

Activating transcription factor 3 gene expression suggests that tissue stress plays a

role in leiomyoma development 71 Estrogen receptor β gene polymorphisms and

susceptibility to uterine fibroids72

IHC MARKERS :

Positive stains: Desmin, H-caldesmon, occasional focal CD10.

Negative stains: Keratin (usually), EMA (usually)3

Degenerative Changes:

1. Atrophy: As result of diminished vascularity due to the natural or artificial

enopause, there is a striking shrinkage in the size of the tumor, which becomes

firmer and more fibrotic. A similar change occurs in leiomyomas after

delivery25,26.

2. Hyaline degeneration: The hyaline change is most common degenerative

change seen in leiomyomas. It is due to deficient blood supply and is seen

frequently in the centre of the growths. When a large area is affected, the

centre frequently undergoes liquefaction and irregular cavities are seen.

Hyaline change is best identified microscopically. The outline of the muscle

cell becomes indefinite and the cell cytoplasm merges with structurelessintra

cellular matrix, which stains uniformly with eosin22,25,26.

3. Hyaline necrosis: Hyalinization can result in tumor cell necrosis (it is called

as hyaline necrosis). Grossly such lesions are yellow in appearance

microscopically hyaline is present around the necrotic areas along with

thickened hyalinized blood vessels19.

4. Cystic degeneration: Cystic degeneration represents late stage of hyaline

degeneration when hyaline material undergoes liquefaction, the tumor

29

becomes soft and on cut section shows irregular space filled with clear fluid

and sometimes filled with cloudy reddish brown fluid when infected. On

histological examination, the wall of the cystic area is composed or hyalinized

leiomyoma, which is devoid or epithelial lining19,25,26.

5. Fatty degeneration: A yellow fat tumor may be due to deposition of fat in a

fibroid or may be lipoma. Fatty change in a fibroid is rare should be of

sufficient degree to provide a greasy surface. The characteristic whorled

pattern is obliterated and the affected tissue is homogenous yellow and soft. It

is believed that it is due to metaplasia in leiomyomas19.

6. Red degeneration: This complication of uterine myoma develops most

frequently during pregnancy or with contraceptive medication. It is

characterized by pain abdomen, vomiting, fever. The tumor itself assumes a

peculiar purple-red color and develops fishy odour. The tumor if correctly

examined reveals thrombosis of some of the large vessels of the capsule and

small blood vessels in the substance of the tumor. The discoloration is

possibly caused by diffusion of blood pigments from the thrombosed vessels.

Histologically these lesions show central area of hemorrhagic necrosis,

peripheral inflammation granulation tissue like response and frequent mitotic

areas22,25,74.

7. Myxoid and mucinous degeneration: It is characterized by focal areas

showing cysts filled with mucoid material. Microscopically, myxoid changes

is characterized by a fibrillar matrix containing scattered cells with elongated

nuclei and tiny wisps of cytoplasm. In lesions having mucinous degeneration

muscle fibers are separated by pools of basophilic material19,70.

30

8. Telangiectasis: It is a rare entity showing cystic space filled with blood in

leiomyomas. They are merely distended blood vessels at the tumor

possiblydue to mechanical obstruction of blood flow24.

9. Calcification: It is seen in elderly women with long standing myomas. It is

assumed that fatty degeneration may occur first subsequently the fatty acids

are changed first into soaps and finally by interaction with carbonates and

phosphates of the blood into calcium phosphate and carbonate. In contrast to

hyaline change which commences in the centre calcification occurs at the

periphery of the growth where the blood supply is more abundant calcification

grossly appears as white, gritty, streak along the sides of the blood vessels19, 24,

25, 26, 70.

10. Lymphangiectasis: This may occur in a leiomyomas due to distension of

lymphatics. The cystic spaces are lined by endothelium24.

11. Oedema: It is rarely seen in leiomyomas, other than during pregnancy or

following torsion. The fluid which escapes when a fibroid is bisected is

usually derived from liquefaction of hyaline material24.

12. Pyomyoma or leiomyoma with acute inflammation: and abscess formation

may occur secondary to bacterial infection. Microscopically a dense acute

inflammatory cell infiltrate, consisting mainly of neutrophils is present75.

13. Necrosis: Necrosis in a fibroid may result from degenerative changes.

Whenever blood supply of a fibroid is suddenly arrested, as after torsion of its

pedicle, necrosis occurs. As blood supply of leiomyoma is deficient in the

centre, necrosis usually commences in these areas24.

31

Variants of Leiomyoma:

There are several histopathological variants of leiomyoma, that deserves

special consideration. These includes cellular leiomyoma, bizzarre leiomyoma,

hemorrhagic cellular leiomyoma, mitotically active leiomyoma, benign metastasizing

leiomyoma, intravenous leiomyoma and others20.

1. Cellular Leiomyoma: Leiomyomas are those unusually cellular but

otherwise typical devoid of nuclear atypia, mitotic rate of four or fewer per 10

high power field(MF|\10HPF)are refered to as cellular leiomyomas.

Grossly they may resemble typical leiomyomas but sometimes have a more

fleshy, tan-brown sectioned surface. Hemorrhage, necrosis, slightly infiltrative

borders, or combinations thereof, are present in a minority of cases.

Microscopically composed of dense cellularity, devoid of nuclear atypia, a

mitotic rate of 4 or fewer mitotic figures per 10 high power fields19,70,75.

2. Epitheloid Smooth Muscle Tumors: The clinical presentation of Epitheloid

smooth muscle tumors does not differ significantly from that of typical

leiomyoma. The cells are usually arranged in a clustered or cord like fashion

and contain rounded nuclei with fine chromatin and a single nucleolus75.

Grossly, epitheloid leiomyomas do not differ from other leiomyomas, being

yellowish or greenish, often with the areas of hemorrhage and necrosis. They

tend to be softer and well circumscribed. They occur in any part of the uterus

and are mostly solitary75.

IHC MARKER: Positive stains: Keratin, Desmin, Smooth muscle actin3

32

Microscopically, three sub-types of epitheloid leiomyomas have been

described. They are:

a) Leiomyoblastoma

b) Clear cell leiomyoma

c) Plexiform tumor29, 70.

a) Leiomyoblastoma: It is a tumor that occurs commonly in the walls of the

stomach than in the uterus. Histologically, it is composed of rounded cells

with eosinophilic cytoplasm and a fairly slight degree of cytoplasmic

vacuolation70, 76.

IHC MARKER: Positive stains: Desmin4

b) Clear cell leiomyomas: This tumor is composed of clear cells. These

tumor cells may contain glycogen and rarely lipids. These cells have usually

centrally placed round or angulated nucleus and sometimes it may be

eccentrically placed, resulting in a signet ring appearance. Nuclear

pleomorphism is mild to moderate and rarely it may have bizarre appearance.

The mitotic figures are generally less than three mitotic figures/ 10 HPF, but

several clinically malignant tumors i.e., epitheloid leiomyosarcomas have

mitosis more than 5 mitotic figure/ 10 HPF75.

c) Plexiform Tumors: It is similarly composed of round cells but with

marked hyalinization of the stroma resulting in cords and trabeculae of the

stroma resulting in cords and trabeculae of the tumor cells in these lesions, the

cells are somewhat smaller and darker than the other epitheloid leiomyomas.

Multiple, microscopic foci of cells are sometimes called as Plexiform

tumorlets. All reported plexiform tumors behave in a benign fashion19, 70, 75.

33

3. Symplastic or Bizarre leiomyomas: This tumor is characterized by the

presence of a few or numerous giant cells. Grossly, these tumors are identified

to those described for cellular leiomyomas70,75.

Microscopically, these leiomyomas contain bizarre tumor cells having

multilobulated or multinucleated, densely stained hyper-chromatic level.

These tumors lack significant mitotic activity. These tumors have been

variously referred to as “symplastic”, “atypical” or “bizarre” leiomyomas. The

bizarre nuclei may contain cytoplasmic pseudoinclusions. They often show

degenerative changes with the symplastic cells predominantly at the edge of

the degenerative areas70,75.

4. Leiomyoma with increased Mitotic Figures: It is a leiomyoma with mitosis

up to 5/10 HPFs lacking cytological atypia and have a benign course. The term

“mitotically active leiomyoma (MAL)” or leiomyoma with increased mitotic

figures have been suggested to such tumors. MAL almost invariably occurs in

women of reproductive age and are typically associated with the secretory

phase of the menstrual cycle, pregnancy or the use of exogenous hormones

and there may be a history of rapid growth of the leiomyomaleading to clinical

suspicion of a sarcoma19,75.

Grossly they are soft, fleshy and cystic. In some cases visible areas of

hemorrhage may be present.

Microscopically they have features of usual leiomyomas with increase mitotic

index i.e., 5-20 MF/ 10 HPF. They have pushing borders and compress the

adjacent myometrium but they rarely infiltrate the adjacent

myometrium14,19,70,75.

34

5. 5.Apoplectic Leiomyoma (Hemorrhage Cellular Leiomyoma): Occur in the

leiomyomas of women who are pregnant or using oral ontraceptives75.Grossly

these leiomyomas show extensive hemorrhage with cyst formation75.

Microscopically these lesions appear as circumscribed, densely cellular

proliferations of oval and spindle shaped smooth muscle cells that have areas

of central hemorrhage and edema. The cells lack malignant features, but

mitotic activity should not exceed four mitotic figures/ 10 HPF in the most

reactive areas of neoplasm. Vascular alterations, including intimal myxoid

change and fibrosis, medial hypertrophy, fibrinoid necrosis and thrombosis

may be encountered within the leiomyomas or the surrounding myometrium75.

6. Myxoid Leiomyomas: Grossly they are well circumscribed and are

composed of homogenous, soft, gray, jelly like material75. Microscopically

the neoplastic cells are often stellate in shape and are widely separated by the

extracellular material.Myxoid stroma is produced by the myxoid degeneration

of collagen surrounding the nodules of smooth muscles.

7. Hydropic Leiomyomas: Grossly, marked degrees of hydropic degeneration

may result in cystic degeneration, occasionally large myometrial cysts

represent leiomyomas with total or subtotal cystic degeneration75.

Microscopically, hydropic degeneration is typically accompanied by variable

amounts of hyalinization (Hyaline degeneration) within the leiomyoma. In

some hydropic leiomyomas, sparsely cellular hydropic connective tissue

subdivides part or all of the leiomyomas into numerous, small typically

nonhydropic leiomyomatus nodules resulting in a false impression that

nodules are lying within vascular spaces75.

35

8. Leiomyoma with tubules or glands: Tubules or glands are found in an

otherwise characteristic leiomyoma, these are neoplasm. Most uterine

mesenchymal neoplasm with such structures are endometrial stromal

neoplasm or adenosarcomas. Tubular differentiation in a leiomyoma has no

prognostic importance. These tubules are lined by uniform cuboidal cells that

had the ultrastructural features of mesothelial cells19.

9. Lipoleiomyoma: Both lipoma and lipoleiomyoma may arise from either the

uterine cervix or the uterine corpus. They are found in adults at any age19. It

is belived that this tumor and the even rarer lipoma result from adipose

metaplasia in leiomyomas14,19.

Grossly, the lesions are circumscribed, gray white and firm with some yellow

soft areas, which are often greasy on cut section. The color and consistency

depends on the amount of adipose tissue present within the neoplasm.

Microscopically, the fat cells are usually mature, arranged in aggregates

mixed with smooth muscle cells and fibrous connective tissue, but occasional

lipoblasts can be found, particularly in lesions in which fat necrosis is

present14,19.

10. Schwannoma like Leiomyoma: Schwannoma probably do not occur in the

uterus Ultrastructural studies of a few neoplasms resembling them have

demonstrated smooth muscle differentiation19. Morphologically a

schwannoma like leiomyoma is composed of cells with elongated nuclei

arranged in palisades similar to schwannoma. Hyaline is often present and

prominent19.

36

11. Leiomyoma with Benign Heterologous Elements: Leiomyomas can show

osseous or chondroid metaplasia or skeletal muscle differentiation, but it is

rare19,75

Leiomyomas with Unusual Growth Patterns:

Diffuse Leiomyomatosis: Grossly, it is characterized by symmetric uterine

enlargement due to the presence of leiomyomatous nodules within the

myometrium. These are small with infiltrative margins, clinical presentation is

similar to typical uterine leiomyomas19,47,75.

Microscopically nodules are composed of benign typically cellular,

mitotically inactive smooth muscle cells. Perivascular condensation has been

observed, the term leiomyomatosis has been applied to this process19.

Leiomyoma with Vascular Invasion: Microscopic intrusion of benign

smooth muscle cells into the vessels within the confines of a leiomyomas has

not been associated with aggressive behavior or extension of tumor outside the

uterus19. The vascular invasion is not visible grossly is an incidental

microscopic finding and the intrusion must occur within the confines of the

leiomyoma. The constituent smooth muscle cells must be morphologically

benign and without atypia19.

Intravascular Leiomyomatosis: It is an uncommon neoplasm characterized

by nodular mass of histopathologically benign projections of smooth muscle

growing within uterine veins. The intravascular growth takes the form of

worm like projections that may extend a variable distance outside the confines

of a myometrial leiomyoma and sometimes into extrauterine veins. The

clinical presentation is usually similar to that of typical uterine leiomyoma,

37

although these patients have presented with manifestations relative to cardiac

involvement14.

Grossly, the uterus is enlarged and bosselated with thickening of the

myometrium. Intravenous leiomyomatosis presents as coiled or nodular well

demarcated masses in the myometrium with convoluted, often mobile, worm

like extensions into the uterine veins14.

Extensions to the venacava occurs in more than 10% of cases. Within or in

continuity with dilated veins sharp demarcation separates these neoplasms

from the surrounding myometrium14.

Microscopic appearance is cytologically benign, smooth muscle cells, that are

present within veins and endothelium lined spaces. The most common

microscopic appearance is that of normal appearing smooth muscle cells

arranged in whorled pattern typical of a leiomyoma but, is present in an

abnormal location14. The diagnosis of IVL requires the presence of

histologically benign smooth muscle with multiple intravascular profusion14.

IHC MARKER: Positive stains: ER, PR

Molecular: Breakpoint at 12q, similar to t(12;14) in uterine leiomyomas.3

Benign Metastasizing Leiomyoma: Benign metastasizing leiomyoma is an

exceedingly rare disorder characterized by the presence of single or multiple

pulmonary nodules composed of benign appearing mitotically inactive smooth

muscle in women who have had typical uterine leiomyomas. Spread to the

retroperitoneal, mediastinal lymphnodes and other sites such as bone and soft

tissue has been reported less often, with or without associated pulmonary

38

involvement. In almost all instances, the patient has a history of prior

myomectomy or subtotal or total hysterectomy19, 75.

IHC MARKER: Positive stains: Estrogen receptor3

Peritoneal Leiomyomas (Parasitic Leiomyoma): Uterine leiomyomas

arising near the serosa of the uterus, particularly those with a pedicle, on rare

occasions are said to take up a blood supply from a nearby contiguous organ

and detach themselves from the uterus. Usual reported sites are broad

ligament, the pelvic peritoneum, the cul-de-sac and the omentum19.

Disseminated Peritoneal Leiomyomatosis: It is a rare condition in which

multiple small, nodular deposits of histologically benign smooth muscle and

fibrous tissue are found in the superficial subperitoneal tissues including the

surface of uterus, tubes, ovaries, omentum, serosal surface of small and large

intestine, liver, gall bladder, etc. The process involves the abdominal and

pelvic peritoneum as well as the mesentry. There is a strong association with

hormonal stimulus; most of the patients have been pregnant or had hormone

producing tumors of ovary or hormone administration70.

Grossly, These nodules are almost always less than 2 cms although there are

reports of nodules up to 10 cms19.

Microscopically The nodules consists of uniform, spindle shaped cells with

eosinophilic cytoplasm and parallel longitudinal intracytoplasmic fibrils

typical of smooth muscle. The cellularity within each nodule is variable.

Collagen, decidual cells, fibroblasts and smooth muscle cells may be admixed

together in the same nodule. Zones of hemorrhage may be present. Mitotic

figures are generally infrequent, and nuclear atypia and pleomorphism are

39

minimal or absent. The stroma of the nodule is scanty and contains small

blood vessels. Electron microscopic observations have confirmed that most

nodules are composed of smooth muscle and decidual cells, but some are

mixtures of deciduas and fibroblasts or myofibroblasts14,19,20,70,75.

40

SMOOTH MUSCLE TUMORS OF UNCERTAIN MALIGNANT

POTENTIAL - REVIEW OF LITERATURE

Historical Aspects:

Clement PB summarized recent advances in the pathology of uterine corpus.

He studied the diagnostic problems in uterine smooth muscle tumors using minimum

pathological criteria. Uterine smooth muscle tumors that are unclassified by current

criteria as benign or malignant have been referred to as smooth muscle tumors of

uncertain malignant potential (STUMP): although to date there is a uniform definition

of these tumors77.

Peters et al reviewed “smooth muscle tumors of uncertain malignant potential,

which were classified earlier by Hendrickson and Kempson. In these tumors with

aggressive clinical course, they observed mild to moderate cellular atypia with 5-10

mitosis/ HPF78.

Jeffers MD, Richmond and Macaulay, opined from their study that DNA

ploidy, age, grade of atypia are independently associated with outcome of smooth

muscle tumors and measurement of DNA ploidy may be useful in identification of

cases with an adverse prognosis79.

Pathology:

Uterine smooth muscle tumors are unclassifiable by current criteria as

unequivocally benign or malignant have been referred to as “smooth muscle tumors of

uncertain malignant potential (STUMP)”. These tumors have not been studied in

sufficient numbers to allow prediction of their behavior based on their morphological

features. Although there is as yet no uniform microscopic definition of STUMP, the

criteria used by Kempson and Hendrickson include the presence of (1) cytologic

41

atypia and 2 to 4 MF/ 10 HPF; (2) more than 15 MF/ 10 HPF in the absence of

hypercellularity and cytologic atypia; and (3) mitoses less than those of above in the

presence of abnormal mitotic figures or necrotic tumor cells75.

Malignant Tumor – Leiomyosarcoma:

History:

Sarcomas of the uterus are the most lethal tumors encountered by the

gynaecologist80. The initial description of a sarcoma dates back to 3000 BC, when a

soft, fleshly intra abdominal tumor was described by Smith Papyrus. In 1804,

Abernathy described the clinical and anatomical characteristics of a group of diseases,

which are now recognized as sarcomas81. Their existence has been recognized since

1860, when the first case was presented to the Berlin Obstetrical Society by Meyer

and the pathology was described by Virchow80. The leiomyosarcoma a rare lesion,

being encountered not more than once or twice a year in most university hospital and

probably even less frequently in most community hospitals82.

Incidence and Etiology:

Epidemiologically, risk factors for uterine sarcomas are virtually unexplored,

largely because of the rarity of this tumor75. Leiomyosarcoma account for

approximately 25-45% of uterine sarcomas. The estimated yearly incidence is 0.67/

1,00,000 women aged > 20 years, representing 1.3% of all uterine malignancies. The

incidence ratio between leiomyomas and leiomyosarcoma has been estimated to be

800:183.

The usual age range for leiomyosarcoma is from 30 to 80 years but the modal

age is in the 40-60 years range. The parity does not appear to play a role in this group

of sarcomas. A higher incidence and a poorer prognosis are reported in black women.

42

A history of previous irradiation has been related to the development of uterine

sarcomas80.

Harlow et al observed 60% increased risk leiomyosarcoma among blacks

compared with whites. Early onset of menses (before age 13 years) was associated

with an increased risk of leiomyosarcomas84. Leiomyosarcoma usually arise denovo.

In large series of studies, origin of leiomyosarcoma could not be documented in a

leiomyoma; whereas Hart and Billman have documented a single case that apparently

arose in leiomyoma. Similarly, William et al convinced that sarcoma may arise in a

primary existing leiomyoma64,85.

The diagnosis of leiomyosarcoma of uterus remains a problem as there is lack

of uniformly accepted diagnostic criteria. Taylor HB and Norris HJ analyzed 63

highly cellular uterine tumors previously diagnosed as leiomyosarcomas. They

observed that number of mitotic figures in the most active areas within a tumor

proved to be a reliable basis for separating leiomyomas from leiomyosarcomas86.

Aaro LA et al analyzed clinical and pathological features of 177 cases of

uterine sarcomas, and found that mitotic activity was the most significant factor in

grading these lesions87.

Hart WR and Billman JK histologically reviewed 28 uterine neoplasms

originally diagnosed as leiomyosarcomas. They emphasized to select the most active

areas of tumor for counting mitotic figures, together with hypercellularity and nuclear

atypism for the diagnosis of leiomyosarcoma12.

43

Reports of two cases of myxoid leiomyosarcoma showing high mitotic counts

concluded that the role of myxoid stroma in influencing the prognosis in

leiomyosarcoma is uncertain88.

Bessemer J et al presented 3 cases of epitheloid leiomyosarcoma and

concluded that fundamental differences in biologic behavior of this subset of uterine

smooth muscle tumors cannot be discerned89.

Sieinski W, described a unique association of uterine malignant giant cells

tumor with leiomyosarcoma and concluded that malignant giant cell tumor and

leiomyosarcoma were coexistent neoplasms and were derived probably from different

progenitor cells90.

Seidmann JD et al reported the presence of epitheloid component within

uterine leiomyosarcoma in a 70 year old woman simulating metastatic carcinoma

using DNA flow cytometry91.

Tinkler SD, Cowie VJ et al, observed that the stage of the disease at initial

examination is an important prognostic indicator and concluded that uterine sarcomas

are more aggressive than there epithelial counterparts92.

Angeles Rovirosa MD et al reviewed 60 patients diagnosed with uterine

sarcoma retrospectively. Vascular and lymphatic space invasion was a relevant

prognostic factor in their study, with an impact on survival and distant metastasis free

survival in early stages. Myometrial invasion >50% had an impact on local relapse93.

PATHOLOGY OF LEIOMYOSARCOMA:

It is the malignant counterpart of leiomyoma and is the most common pure

sarcoma of uterus70.

44

Patients usually present with abnormal vaginal bleeding, pain or both and

usually have an enlarged uterus on pelvic examination. In rare patients, the presenting

manifestations of the tumor have been related to tumor rupture, hemoperitoneum and

extrauterine metastasis. One case of uterine leiomyosarcoma was associated with

fever, eosinophilia and alkaline phosphatase production. Cytological evaluation and

examination of curetting are unrewarding in patients with leiomyosarcoma, except in

those with tumors that are submucosal or protrude into the endometrial cavity.

Occasionally patients with high staged disease have had an elevated serum levels of

CA-125 at presentation.

This marker may also be useful in detecting recurrent tumor. Rare patients

with leiomyosarcoma have had prior pelvic irradiation75.

IHC MARKERS: Positive stains: Actin, Myosin, Desmin, H- caldesmon Keratin

(epithelioid tumors), p53, Focal CD10 Negative stains:CD443

Gross Features:

Leiomyosarcomas are typically large solitary masses with diameter varying up

to 10 cm. Approximately 2/3rd (50-65%) of leiomyosarcomas are intramural, 1/5th

(20-25%) submucosal and 1/10th (15-16%) subserosal. They are almost always well

circumscirbed than leiomyomas and cannot be shelled out from the adjacent

myometrium75.

Most of leiomyosarcomas are soft, fleshy and often with the areas of

hemorrhage and necrosis without the whorled appearance characteristic of

leiomyoma. Uncommonly, it may arise in cervix. Although leiomyosarcomas are

frequently associated with benign leiomyomas in the same uterus, convincing

45

examples of leiomyosarcoma arising in a leiomyoma or leiomyoma variant are very

rare75.

Microscopic Features:

These neoplasms are densely cellular, have increased mitotic activity and are

cytologically atypical and pleomorphic. The degree of cytological atypia,

pleomorphism and mitotic activity (at least 5, but usually more than 10/ 10 HPF)

varies greatly from case to case. Spindle cells arranged in bundles intersecting at

various angles are the hallmark of leiomyosarcoma. Individual cells appear fusiform

and have abundant eosinophilic cytoplasm, which has a fibrillar appearance when

stained with phosphotungstic acid hemotoxylin (PTAH) stain.

In some areas the tumors cells appear rounded or irregular and pleomorphic.

The nuclei of these cells are blunt and the cells possess copious eosinophilic

cytoplasm. Cytoplasmic intranuclear inclusions, which are actually invaginations of

cytoplasm into the nucleus are common. The presence of intranuclear inclusions,

however, is a poor predictor of malignancy. They are frequently present in

leiomyosarcoma. But are also present in 50% of bizzare leiomyomas. Atypical mitotic

figures are frequent multinucleate giant cells (present in 1/4th of cases) and rarely

osteoclastic giant cells can be seen in leiomyosarcoma14,75.

Prognosis:

Prognostic factors associated with an unfavourable outcome include high

mitotic rate, high histopathologic grade, infiltrating tumor border, postmenopausal

status, large uterine size and extrauterine extension. Vascular invasion is an indicator

of an extremely poor prognosis. The frequency of vascular invasion varies from 10 to

46

67 percent. Less than 25 percent of women with leiomyosarcoma with vascular

invasion survives with this disease14.

Factors that do not appear to be prognostic significance include the size of uterus, the

presence or absence of atypical mitotic figures, the presence of symplastic giant cells,

and the presence or absence of nuclear inclusions14.

Xanthomatous Variant: Devancy and Tavassali (1991) described the

xanthomatous variant of leiomyosarcoma. Grossly it appears focally or

diffusely yellow75.

Microscopic examination reveals large cells with abundant cytoplasm

containing lipid vacuoles and multiple or multilobulated nuclei. Sometimes

disposed in a wreath like arrangement. The xanthomatous cells grow in solid

sheets or were intimately admixed with the spindle smooth muscle cells.

Mitotic figures were numerous (>10 MF/ 10 HPF) in both xanthomatous and

spindle cell areas75.

Myxoid Leiomyosarcoma: It is a rare variant of uterine leiomyosarcoma75.

Grossly, these tumors are usually found within the myometrium (less

commonly). The tumors size varies from 5 to 16 cm in diameter and typically

exhibit a strikingly gelatinous cut surface and an apparently well

circumscribed border75.

Microscopically these tumors typically infiltrate the myometrium in irregular

tongues and in some cases, myometrial veins. Most or all of the tumor is

characterized by an abundant paucicellular myxoid matrix that is weakly

basophilic or eosinophilic, weakly positive with the periodic acid-schiff (PAS)

47

and mucicarmine methods and strongly positive with alcian blue and colloidal

iron staining. Most of the material that stains with colloidal iron is not

removed by hyaluronidase pre-treatment75.

IHC MARKERS: Positive stains: High MIB-1 index although may have low

mitotic count

Epitheloid Leiomyosarcoma: It is described under epitheloid leiomyomas.

Epitheloid leiomyosarcoma considered if the mitotic figures are five or more

than five per 10 HPF19.

Epitheloid leiomyosarcoma is considered if:

a) Mitotic index less than 5 per 10 HPF, any degree of atypia and no coagulative

necrosis.

b) Any mitotic index and any degree of cytological atypia with coagulative

necrosis19.

This histological entity should be differentiated from benign leiomyoblastoma,

clear cell type and plexiform leiomyomas19,75.

OTHER TUMORS OF THE MYOMETRIUM

Extraovarian Brenner tumors are extremely rare. Arhelger RB and Bocian JJ

described a small tumor with histological features of Brenner tumor within the wall of

the uterus94.

Clement PB and Scully RE did a clinicopathological analysis of 14 uterine

tumors having unusual epithelial like differentiation resembling ovarian sex cord

tumors most often to granulosa cell tumor95.

48

Vascular neoplasms of the uterus are rare. Ghosh RN and Ghosh P described

hemangiopericytoma of the uterus in a 60 years old women96.

Quinonez GE et al described a case of angiosarcoma of the uterus. They

confirmed the diagnosis using light microscopy (by reticulin stain) and

ultrastructurally demonstrated Weibel-palade bodies in the tumor cells97.

A case report of metastatic carcinoma in uterine leiomyoma from an occult

primary site was published by Lanjewar DN and Shetty CR in 199698.

The significantly thickened myometrium was due to marked expansion of the

interstitial compartment of the myometrium, in which non-neoplastic smooth muscle

fascicles were widely separated by abundant extracellular mucin producing a striking

myxoid appearance (“myxoidosis”). These histologic findings are akin to the pattern

of dermal mucin deposition seen in lupus erythematosus. The lesion in each case

diffusely involved the entire myometrium73

Pathology:

Adenomatoid Tumor: Golden and Ash proposed the term adenomatoid

tumor20. The incidence in the uterus if reported to be less than that in the tube.

These are generally small and discrete and are almost invariably discovered

incidentally. These are benign neoplasms, which show mesothelial

differentiation, thus justifying the designation, adenomatoid mesothelioma19.

Grossly they range from microscopic findings up to 2 cms in maximum

diameter. Adenomatoid mesotheliomas are usually identified as leiomyomas.

The nodules appear more yellowish than the usual leiomyoma and very often

it is situated subserosally in the uteri cornu. Small cystic spaces may be

visible.

49

Microscopically, it shows three patterns – plexiform, tubular and canalicular,

all consisting of numerous spaces of varying sizes and shapes separated by

bands of connective tissues. The spaces are lined by a single layer of low

cuboidal or flattened cells with eosinophilic cytoplasm and oval nuclei. The

tumor is surrounded by the smooth muscle of the myometrium but is not

demarcated from it12,19,70,75.

Hemangiopericytoma: Vascular tumors occur relatively more frequently in

skin and it is rare for such neoplasms to occur in the uterus. Of the 2 cardinal

types of such vascular tumors that may possibly occur in the uterus, namely –

hemangioendothelioma and hemangiopericytoma the latter is relatively more

frequent, it is derived from the pericytes of Zimmermann96.

Grossly, these tumors look greyish white or yellow and not pink or red inspite

of the innumerable capillaries. The capillaries are either noncanalized or

blocked to pressure of multiple pericytes outside the wall of the capillaries96.

Microscopically, hemangiopericytoma is distinguished from the endothelioma

by the fact that in the former condition there is complete absence of any

multiplication of cells inside the wall of the vessels. The histopathological

study is usually aided by taking resort to reticulum, silver or masson’s

stain40,96.

The cells are more spindle shaped and fibroblastic with more intervening

collagen. The vascular spaces have more irregularity in the caliber of the

lumen and there is more variable thickness of the vessel wall with extensive

myxoid change40,96.

50

Uterine Tumors resembling Ovarian Sex Cord Tumors: “Uterine tumors

resembling ovarian sex cord tumors (UTROSCTs,1976)” was applied to a

heterogeneous group of rare uterine neoplasms characteried by pure or

predominant histologic patterns that closely resemble those of ovarian sex

cord tumors (granulosa cell tumors and sertoli cell tumors)99.

On gross examination, UTROSCTs are generally solid, round well

circumscribed myometrial masses that range from 3 to 10 cm in diameter,

occasional tumors are predominantly subserosal, the submucosal or

intramural, but are occasionally subserosal, the submucosal and subserosal

tumors may be polypoid. Rare tumors are located predominantly within the

endometrium. The cut surfaces are often yellow, but occasionally grey to tan,

and are soft, fleshy and homogenous without the whorled pattern of a

leiomyoma77.

Histologic examination usually reveals a well-circumscribed border with the

adjacent myometrium. Less commonly the tumor infiltrates the myometrium

either focally or diffusely. In such cases, invasion of lymphatics, blood vessels

or both has been encountered. The tumor cells typically form solid or hollow

tubules, cords and trabeculae often disposed in a plexiform arrangement, and

solid nests. The neoplastic cells vary from small, round and regular with

scanty cytoplasm to large with abundant eosinophilic, clear or foamy

cytoplasm that if often lipid rich. The nuclei are generally small and regular

with little pleomorphism and indistinct nucleoli. Nuclear grooves are rare or

absent and mitotic figures are typically sparse77.

51

Although most UTROSCTs had a benign clinical course, after hysterectomy,

occasional tumors have reconsidered or metastasized in two such cases77.

Myometrial hypertrophy: The absence of pathology in an enlarged but

otherwise normal uterus indicates hypertrophy of the myometrium. The size

and weight of the normal uterus varies with the age and parity of the patient.

In women of reproductive age, the range of normal uterine weight varies from

46 to 137 gm. There is documentation of normal uteri in parous women

weighing as much as 243 gm. Thus, in the presence of histologically normal

endometrium and myometrium, a uterus weighing more than 250 gm is

abnormal20.

Lymphoma and Leukemia: Rarely lymphoma and leukemia presents initially

in the uterus. Leukemia involving the uterus is much less common than

lymphoma. Today, immunohistochemistry allows easy resolution of this

problem19.

Neoplasms Metastatic to the Uterus: Extrauterine neoplasms may present

for the first time as uterine metastases. They are lobular carcinoma of breast,

carcinomas from the ovary, large bowel, stomach and increasingly the lung.

Malignant melanoma also often spreads to the uterus. The possibility of

metastasis also arises when special variant of endometrial carcinomas are

encountered19.

52

TUMOR LIKE CONDITION – ADENOMYOSIS:

History:

Adenomyosis in the past has been frequently spoken of as adenomyoma but

the suffix “oma” has reference to a tumor and the adenomyosis is not a tumor in the

proper sense of the word, anymore than is endometriosis. The term “adenomyoma”

should be limited to actual circumscribed tumors made up ofendometrium and muscle

tissue. Hence, the term adenomyosis is used commonly100.

Adenomyosis was first described by Rotansky as “cystosarcoma adenoid

uterinum”, Von Recklinghausen published on “Adenomyomata and cystadenomata of

the uterus and suggested that it arose in Wolffian remnants. Cullen was able to show,

this down growth or extension of endometrium into the myometrium and later he

classified into two histological types, adenomyoma and diffuse adenomyoma101, then

he published an excellent and very detailed review of 54 cases seen and proposed the

term “adenomyoma uteri diffusum benignum” for what is known today as

adenomyosis. Cullen was also the first to clearly identify adenomyosis as a symptom

producing disease. Abnormal uterine bleeding, acquired dysmenorrhea and changes in

uterine size have been recognized as classic symptoms of adenomyosis102,103. Later

Frankl, observed that the lesions were particularly frequent in rudimentary uterine

horns and used the term adenomyosis uteri101. Since then a large amount of literature

has been contributed on the disease by Robert Meyer, Sampson, Halban, Jeffcote,

Novak and Ludwig Emge103.

Etiology and Incidence of Adenomyosis:

The histological frequency of adenomyosis varies from 5-70%6. The

pathogenesis of this disease is unknown. Many theories have been proposed24. It has

been suggested that the uterine trauma of child birth leads to the breakdown of normal

53

myometrial endometrial border. Followed by reactive hyperplasia of the basalis

endometrium which leads to an invasion of the myometrium and subsequent

adenomyosis. Adenomyosis can be produced in pregnant rabbit by forcibly curetting

one horn and tube while allowing the pregnancy to continue in the opposite horn. In

this model, high levels of estrogen or progesterone and prolactin appears to be the

necessary factors for the development of adenomyosis. Salpingitis isthmica nodusa

resembles adenomyosis pathologically and infrequently accompanied by chronic

inflammati on of the surrounding tubal epithelium. Adenomyosis develops in a similar

fashion, following chronic postpartum endometritis, which damages the myometrial

endometrial border resulting in reactive hypoplasia of endometrium and invasion of

myometrium102. Adenomyosis is nine times more prominent in whites than in black

women in most reported series, the peak incidence is between 41-50 years and most

of cases of adenomyosis in young women are of mild degree and discovered

incidentally. 20% of adenomyotic cases were found in post menopausal women, these

adenomyotic foci usually demonstrate an atropic pattern consistent with their

hyperestrogenic state102.

Adenomyosis is relatively common condition, which is characterized by

presence of endometrial glands and stroma within the myometrium. It is observed

frequently in elderly women. More than a third of the hysterectomy specimen from

women aged 40 years and above reveals the presence of adenomyosis irrespective of

the indications for hysterectomy. Molitor JJ studied 281 cases of adenomyosis in

surgical removed uteri. He observed that, in 71% of these patients the symptoms were

due to or contributed by adenomyomas with major symptoms as menorrhagia (177

cases), metrorrhagia (110 cases), pain (74 cases) and dysmenorrhea (60 cases). He

also mentioned associated pathology in cases of adenomyosis103.

54

Bird CC et al, while studying 200 consecutive uteri observed adenomyosis in

61.5% of cases. They observed that menorrhagia increases in frequency as the degree

of uterine involvement increases. While dysmenorrhea increases as the depth of

penetration and involvement increases. They found an increase in size and weight of

the uterus in 80% of their cases in all parity groups and also described grading of

adenomyosis104.

Greenwood SM (1976) while analysing the relation of adenomyosis uteri to

co-existent endometrial carcinoma and endometrial hypoplasia, concluded that

statistical analysis showed no association between these conditions105.

Kilkku P et al (1984) conducted a prospective comparative survey in 212

patients about non-specific symptoms related to adenomyosis. They concluded that

patients undergoing a hysterectomy for non-malignant conditions had many

symptoms, but none of which seemed specific to adenomyosis106.

Hayata T and Kawashima Y (1987) in their clinicopathological study of 8

cases of uterine body cancers associated with uterine adenomyosis suggested a

common stimulus such as estrogen in both endometrial carcinoma and uterine

adenomyosis107.

Sakamoto in his clinicopathological study suggested that subserosal

adenomyosis may develop as a variant of pelvic endometrosis108.

Mori T et al described animal model of uterine adenomyosis using prolactin as

a potent inducer of adenomyosis in mice. They strongly suggested that prolactin is a

trigger in the genesis of adenomyosis and that estrogen and progesterone facilitate the

development of the lesion as promoters109.

55

Hayata T, conducted ultrastructural study of glandular epithelium in

adenomyosis in comparison with those of proliferative endometrium and well

differentiated endometrial cancer. The results revealed that morphologically the

adenomyotic glandular epithelium is somewhat less differentiated than proliferations

endometrium and that its cytoplasmic organelles have some similarities with those of

endometrial cancer110.

Fedele L et al conducted transvaginal ultrasonography in the differential

diagnosis of adenomyoma versus leiomyoma. They concluded that transvaginal

ultrasonography is an effective, non-invasive and relatively inexpensive, procedure

for the preoperative diagnosis of adenomyoma versus leiomyoma111.

Endometriosis is associated with immunologic abnormalities and high titres of

auto-antibodies have often been detected in serum obtained from the patients,

suggesting that an autoimmune process is involved in endometriosis112.

Fedele et al, while evaluating the diagnostic capability of transvaginal

ultrasonography in detecting diffuse adenomyosis, concluded that transvaginal

ultrasonography seems to represents a real advance in the preoperative diagnosis of

diffuse adenomyosis113.

McCausland AM described hysteroscopic myometrial biopsy and its use in

diagnosing and treating adenomyosis7.

Tamoxifen citrate is a non-steroidal agent that has demonstrated estrogen agonists and

antagonists properties. The rapid growth of leiomyoma was due to estrogen agonists

properties of tamoxifen or ovarian stimulation resulting in excessive endogenous

estrogen production114.

56

Various studies have noted an excellent prognosis in endometrial carcinoma

confined to the foci of adenomyosis115.

Ota Hirotaka and Igarashi S in their immunohistochemical analysis revealed

significantly increased expression of HLA-DR antigen in glandular cell in ectopic

endometria, concluded that immune systems is activated in endometriosis or

adenomyosis116.

Vgwumodu AH reported a case of adenomyosis and adenomyomatous

endometrial polyp induced by tamoxifen, which was used for the treatment of breast

cancer117.

Several studies have shown that oxygen free radicals participate in the

pathogenesis of various disease. Similarly free radicals may play a role in the

pathogenesis of adenomyosis, the same as they do in other inflammatory process118.

Progesterone partially related to the growth of adenomyosis. Thus

progesterone probably enhances aromatase activity and contributes the estrogen

biosynthesis in adenomyotic lesions119.

Goldblum et al suggested that low grade endometrial stromal sarcoma should

be included in differential diagnosis of adenomyosis with sparse gland after reviewing

7 post menopausal women aged from 51 to 81 years120.

Carter JE, Kong II (1994) in their study opined that there may be a possible

relationship between adenomyosis and previous tubal ligation121.

Ascher SM et al in his study on twenty women with clinically suspected

adenomyoisis opined that magnetic resonance (MR) imaging is significantly better

(p<0.02) than transvaginal sonography in the diagnosis of adenomyosis122.

57

Vercellin P et al in their suggested that parity may be associated with an

increased frequency of adenomyosis123.

Ota H (1999) in his study on SODs expression in endometrial tissue observed

that the expression of both SODs in endometriosis and adenomyosis was persistently

higher than the control levels throughout the menstrual cycle. He suggested that

superoxide plays a key role in infertility in endometriosis and adenomyosis124.

Propst AM et al (2001) in his study concluded that up regulation of basic

fibroblast growth factor (BFGF) receptor/ ligand system and increased cellular

proliferation in adenomyosis may contribute to the pathogenesis of abnormal uterine

bleeding associated with adenomyosis125.

Dueholm M et al (2001) in their study observed that magnetic resonance

imaging (MRI) was superior to transvaginal sonography (TVS) for the diagnosis of

adenomyosis. Magnetic resonance imaging had higher specificity than TVS, but their

sensitivities were in line126.

Kunz G et al (2005) in his study on 160 women with and 67 women without

endometriosis, concluded that with a prevalence of up to 90% uterine adenomyosis is

significantly associated with pelvic endometriosis and constitutes an important factor

of sterility in endometriosis presumably by impairing uterine sperm transport127.

PATHOLOGY OF ADENOMYOSIS:

Adenomyosis refers to the presence of endometrial glands and stroma deep

within the myometrium102.

58

Grossly adenomyosis may involve uterus in either diffuse or local fashion. The

posterior wall is most commonly affected. The uterus harbouring adenomyosis may

be of normal size if the condition is mild. In most cases that have clinical

implications, however the uterus is enlarged, either by an increase in bulk that may

affect only one way or by more or less focal involvement, which results in intramural

masses. In its most extreme form, adenomyosis will result in a grossly enlarged and

globular uterus. The increase in the size of a uterus containing adenomyosis is due to

the hypertrophy of the smooth muscle that accompanies the invading endometrium,

very little of the increase in bulk is due to the volume of the endometrial tissue itself.

Superficial adenomyosis is the superficial penetration of endometrial glands and

stroma into the myometrium and tend to resemble the non-functioning basalis

endometrium. Deep adenomyosis clearly within the myometrium produce dramatic

gross and microscopic abnormalities19,70.

Cut surface of the affected uterus has a prominent trabeculated pattern and the

hypertrophic swirls of smooth muscle separate the dull grey foci of endometrium.

Cystic spaces are seen in a minority of cases and occasionally blood is present in the

cavities of these cysts19,70.

The histological features of adenomyosis are well known. The infiltrating

islands of endometrium consists of both glands and stroma and the glandular tissue is

usually inactive and of basal endometrial pattern. The histologic criterion used in the

study for the diagnosis of adenomyosis is the identification of endometrial gland and

stroma at least one low power field below the basal layer of endometrial gland and is

surrounded by myometrium19,70

59

Most pathologist will not make a diagnosis of adenomyosis unless glandular

extension below the endometrial myometrial interphase (EMI) is greater than 2.5 mm,

whereas adenomyosis sub-basalis can be decide as minimally invasive adenomyosis

extending less than 2 mm beneath the basal endomyometrial6,100.

The latter approach as a particular significant in the post-menopausal and

gravid uterus because peri adenomyotic muscular hypertrophy in this type of uterus is

basically absent6,100.

Microscopically, the diagnosis of adenomyosis depends on the thresholds used by the

individual pathologist, some of which are very liberal indeed6,100.

Adenomyosis is graded according to the depth of penetration and the degree of

involvement. Depth of penetration is graded as below6:

Grade-I: Adenomyosis sub-basalis (identification of adenomyosis within one

low power field below the basal endometrium but with no further penetration).

Grade-II: Adenomyosis penetration to mid myometrium.

Grade-III: Adenomyosis penetration beyond mid myometrium.

Degree of involvement is graded as follows:

Mild: Few endometrial glands (1-3) per low power field

Moderate: Several endometrial glands (4-9) per low power field and

Marked: Many endometrial glands (10 or more) per low power field6, 128.

Associated Pathology:

About 60-80% of adenomyotic uteri has another pathologic process in the uterus102.

60

Adenomyosis and uterine malformation: Adenomyosis was observed in a

small number of specimens of congenital malformation of the uterus of

different types. Franks (1912) considered that there was an interrelationship

between the two conditions but Lockyer (1918) in recording some examples

did not support him24.

Adenomyosis and Tuberculosis: In such cases direct invasion of

adenomyosis by tuberculous arising in the tube or endometrium or by

hematogenous spread from extragenital foci may occur, this may give rise to

cassation and abscess formation24.

Adenomyosis and Neoplasm: The appearance of leiomyoma and

adenomyosis in the same uterus is not uncommon. Most often small intramural

fibroids quite separate from an area of diffuse adenomyosis may be seen.

Alternatively leiomyoma particularly those in the submucous location may

show permeation of their substance by areas of endometrium24.

Adenomyosis and Carcinoma: Malignant change in adenomyosis is rare but

has been recorded (Kumar and Anderson, 1958). Marcus (1961) also found an

association with endometrial hyperplastic and both he and Giammalvo and

Kaplan (1958) found adenomyosis associated with endometrial carcinoma.

There is no evidence that adenomyoma allows a facile route for extension of

endometrial carcinoma, since the degree of adenomyosis and extent of

penetration of the carcinoma did not appear to be related. Carcinoma of the

endometrium may coexist with either benign or malignant adenomyosis but

occasionally carcinoma appears to arise primarily in the ectopic endometrial

epithelium. Carcinoma in situ as also been reported in adenomyosis129,130.

61

Two patterns are described, the association between adenomyosis and surface

endometrial carcinoma and primary carcinomatous change, developing in the aberrant

endometrium within the myometrium130.

Colman and Rosenthal outlined three basic criteria that must be satisfied to

diagnose carcinoma developing exclusively with areas of adenomyosis129,130.

These criteria are:

1. Absence of carcinoma in the surface endometrium and elsewhere in the pelvis.

2. The carcinoma must arise from the epithelium of areas of adenomyosis and

not be invasive from another site.

3. Endometrial stromal cells must surround the aberrant glands in which

malignant change is noted to suggest the diagnosis of carcinoma arising in

adenomyosis129.

Mittal and Barwick (1993) found excellent prognosis in patients with

endometrial carcinoma involving adenomyosis without myometrial invasion.

Adenocarcinoma involving adenomyosis were characterized by prognosis proceeding

estrogen use, low histological growth and excellent prognosis115.

Adenomyosis and External Endometriosis: Association of adenomyosis and

external endometriosis is recognized. But its incidence varies in the literature.

Stromal Endometriosis: Uncommon lesions of the uterus which is relatively

rare. Sometimes being confused with other lesions and being described as a

form of sarcoma. It is called by various names as endometrium interstitiale,

62

endolymphatic stromal myosis stromatous endometriosis and stromatoid mural

sarcoma22,24.

Grossly the uterus is usually slightly enlarged and globular on sectioning the

fresh unfixed uterus, the myometrium is thickened and the myometrial surface

shows multiple small rounded yellow or creamy yellow nodules measuring

few mm in diameter giving the surface an appearance of a “Well Worn

Turkish Towel”. The nodules protrude slightly from the surface and if grasped

with forceps they stretch like a rubber band or sometimes can be pulled out of

the myometrium22,24.

Histologically, it consists of sheets of densely stained cells resembling

endometrial stroma are seen. These clusters are seen irregularly distributed in

the myometrium or there may be continuity between these areas and the basal

zone of the endometrium22,24. Adenomyosis with sparse gland is a rare

histological variant which should be differentiated from low grade endometrial

stromal sarcoma120.

Subserosal Adenomyosis: This is a histological variant where scattered

fragmented lesion of endometriotic tissue, including glands and stroma found

adjacent to serosa. These findings were subclinical, incidental and uterus was

not enlarged in this type of adenomyosis108.

Clinical Features of Adenomyosis:

These women are usually parous around the age of 40 years and usually

present within menorrhagia, dysmenorrhea, premenstrual staining, pelvic discomfort,

backache, dysparenia and other symptoms of adenomyosis. On clinical examination,

there is symmetrical enlargement of the uterus if the adenomyosis is diffuse. It may be

63

fluctuant (more marked premenstrual), globular and associated with tenderness. If

adenomyosis is localized, the enlargement is asymmetrical and resembles

myoma25,70,102,128

64

PATHOLOGY OF SMOOTH MUSCLE LESIONS

CLASSIFICATION OF MYOMETRIAL LESIONS:

(Clement and Young75, Hendrickson MR and Kempson RL19 and smooth JS and

Zaloudek C20).

Benign-Leiomyoma:

Variants:

Cellular

With bizarre nuclei (symplastic)

Mitotically active

Apoplectic haemorrhagic

Myxoid

Hydropic

With benign heterologus elements (Striated muscle, cartilage)

Schwannoma-like (Neurilemmoma – like)

Epitheloid

Malignant- Leiomyosarcoma:

Myxoid

Epitheloid

Smooth muscle tumors of uncertain malignant potential

65

Diffuse leiomyomatosis.

Leiomyoma with vascular invasion.

Intravenous leiomyomatosis

Benign metastasizing leiomyoma

Peritoneal leiomyoma

Diffuse peritoneal leiomyomatosis

Miscellaneous conditions:

Myometrial hypertrophy

Adenomatoid tumor

Haemangiopericytoma

Sex cord like tumors

Lymphoma and leukaemia

Metastatic neoplasms

Others

Tumor like condition

Adenomyosis (endometriosis interna)

WHO Histological Classification of Tumors of the Uterine Corpus131

Mesenchymal Tumors:

Endometrial stromal and related tumors

Endometrial stromal sarcoma,low grade

66

Endometrial stromal nodule

Undifferentiated endometrial sarcoma

Smooth muscle tumors

Leiomyosarcoma

Epithelioid variant

Myxoid variant

Smooth muscle tumor of uncertain malignant potential Leiomyoma, not otherwise

specified

Histological variants

Cellular variant

Epithelioid variant

Mitotically active variant

Hemorrhagic cell variant

Myxoid

Atypical variant

Lipoleiomyoma variant

Growth pattern variants

Diffuse leiomyomatosis

Dissecting leiomyoma

67

Intravenous leiomyomatosis

Metastasizing leiomyoma

Miscellaneous mesenchymal tumors

Mixed endometrial stromal and smooth muscle tumor

Perivascular epithelioid cell tumor

Adenomatoid tumor

Other malignant mesenchymal tumors

Other benign mesenchymal tumors

68

METHODOLOGY

This study consists of 517 hysterectomies cases were collected over a period

of 2 years from June 2008 to June 2010 (2 years prospective study). The material was

obtained from the patients admitted to Al Ameen Medical College And District

Hospital, Bijapur.

Brief essential clinical history and findings were recorded from the patients

case papers. Following the receipt of surgical specimens in 10% formalin at the

department of Pathology, a detailed gross examination including size, shape,

consistency and external surface were recorded. Additional cuts were made depending

on the size of the specimen and cut section morphology were recorded.

Then the specimens were allowed to fix in 10% formalin for 24-48 hours.

Multiple parallel sections through each half, about 1 cm apart were made and each

surface were carefully examined. In a leiomyomatous uteri, a detailed gross

morphology of myomas were noted, which included number, location, size, sessile,

pedenculated and secondary changes like hemorrhage, necrosis and calcification.

The tissue bits from representative area were taken for histopathological

examination and paraffin blocks were prepared. The number of blocks prepared

depended upon the size and morphology of tumors. Multiple sections of 5 microns

thickness were cut and routinely stained with haematoxylin and eosin stain. Detailed

micro-anatomic features were studied and recorded.

In this study, microscopically adenomyosis was diagnosed by the presence of

endometrial glands and stroma at least one low power field below the basal layer of

the endometrium.

Leiomyoma and leiomyosarcoma were distinguished based on the number of

mitosis/ 10 HPFs. When mitosis less than 5/10 HPFs, it was diagnosed as leiomyoma

69

and when mitosis were more than 10/10 HPFs associated with other malignant

features, it was diagnosed as leiomyosarcoma.

Finally associated microscopic lesions in the endometrium, cervix, fallopian

tubes and ovaries were studied wherever they were present.

70

OBSERVATION

Hysterectomy is the commonest surgical operative procedure encountered in

the Gynaecological practice. This is a two year prospective study from June 2008 to

June 2010 done at Al Ameen medical college, Bijapur. Histopathological study on

myometrial lesions of the uterus was undertaken in the Department of Pathology, Al

Ameen medical college and district hospital, Bijapur.

During this 2 years study period, 2226 specimens were received for

histopathological examination in the department, 517 were hysterectomy specimens

which constituted (23.22%) of the total surgical specimens. The study includes

histopathological proved 276 cases with myometrial lesions which constituted

(53.38%) of the total ysterectomy specimens

Age:

Patients who underwent hysterectomy with myometrial lesions were between

2nd and 7th decade of life. Youngest was 22 years old and oldest was 65 years old.

Majority of the patients were between 31-40 years accounting for (46.00%), followed

by (24.63%) cases between 41-50 years age, (20.28% ) cases were between 21-30

years, (9.05% )cases between 51-60 years,( 0.36%) of cases between 61-70 years.

71

Table 1 AGE DISTRIBUTION IN MYOMETRIAL LESIONS

Age No. of patients Percentage

21-30 56 20.28

31-40 127 46.00

41-50 68 24.63

51-60 25 9.05

61-70 1 0.36

Total 276 100

Clinical Diagnosis:

The commonest clinical diagnosis in the present study was prolapse in 86

patients (30.79%) followed by dysfunctional uterine bleeding in 76 patients (27.53%).

Fibroids in 60 patients (21.73%), PID in 53 patients (19.20%) and only 1 case each of

adenomyosis & leiomyosarcoma.

72

Table-2: Clinical Diagnosis

Clinical Diagnosis

No. of patients Percentage

Prolapse 85 30.79 DUB 76 27.53

Fibroid 60 21.73 PID 53 19.20

Adenomyosis 01 0.39 Leiomyosarcoma 01 0.39

Total 276 100  

Clinical Features:

In this study, menorrhagia was the commonest presenting symptom seen in 99

patients (36.00%), followed by dysmenorrhea in 49 patients (18.00%), in white

discharge per vagina 33 patients (12.00%) and mass per vagina in 53patients

(19.00%) other main clinical features observed were pain abdomen and mass per

abdomen, etc.

73

Table 3 Clinical Features

Clinical features No. of patients Percentage

Menorrhagia 99 36.00

Dysmenorrhea 49 18.00

White discharge per vagina

(WDPV)

33 12.00

Mass per vagina 53 19.00

Mass per abdomen 18 6.00

Pain in abdomen 18 6.00

Polymenorrhagia 3 1.00

Postmenopausal bleeding 3 1.00

Total 276 100.00

Parity:

Of 276 patients studied, 274 patients (99.27%) were parous and only 2 patients

(0.72%) were nullipara. Parity of the patients ranged from 1-8.

Morphology of the Uterus:

Of the 276 myometrial specimen studied, 170 (60.00%) were normal size,

65(23.00%) were slightly enlarged, 19 (7.00%) were bulky and 22 (8.00%) were

atrophic.

74

Table 4 Morphology of the Uterus

Uterine size No. of patients Percentage

Normal 170 62

Slightly bulky 65 23

Bulky 19 7

Atrophied 22 8

Total 276 100

Cut Section:

Among 276 uteri studied, the grey white whorled appearance was the

commonest finding seen in 118(42.84%), well defined coarse trabecular appearance,

was seen in 84 (30.43%) specimens. Coarse trabecular and grey white whorled

appearance was seen in 17 (6.15%) cases. However in 56, the cut section morphology

was unremarkable constituting (20.28%).

Myometrial invasion by tumors was seen in only hysterectomy specimens,

which were in the form of areas of hemorrhage, necrosis and with grey white to grey

brown areas suggestive of malignancy (0.39%).

75

Table 5 Cut section

Morphology of cut section No. of patients Percentage

Well defined grey white

whorled pattern 118 42.84

Coarse trabecular

appearance 84 30.43

Coarse trabecular &

whorled pattern 17 6.15

Myometrial lesion with

malignant features 1 0.39

Unremarkable 56 20.28

Total 276 100

Histopathology:

Histologically non-neoplastic lesions in the form of adenomyosis was seen in

52 uteri (18.84%).In neoplastic lesions, pure leiomyoma was diagnosed in 154

specimens (55.79%),whereas other 67 leiomyomas were associated with adenomyosis

(24.27%).Malignant lesions was encountered in 1 specimens, which was single case

of Leiomyosarcoma (0.39%).

76

Table 6 Histopathological lesion

Histopathological lesion No. of patients Percentage

Adenomyosis 52 18.84

Benign leiomyoma 154 55.79

Leiomyomas with

adenomyosis

67 24.29

Leiomyosarcoma 1 0.39

Monckeberg’s sclerosis 2 0.72

Total 276 100

 Leiomyomas

Age in Years:

Age of the patients with leiomyoma ranged from 21 to 70 years. Majority of

the patients (46.92%) were in the 3rd decade, followed by 4th decade (24.63%)

Parity:

In this study, majority of leiomyomas were diagnosed in multiparous women.

Of 154 patients with leiomyomas, 152 (98.74%) were parous, which includes 26 cases

of uniparous patients and only 2 were nulliparous (1.26%).

77

Symptoms of Leiomyoma:

Menorrhagia was the commonest symptom constituting (41.50%), followed by

dysmenorrhea (13.21%), mass per abdomen (10.06%), pain abdomen in 9.44%.

Location and number of leiomyoma

Number of leiomyomas observed in the present study varied from 1 to 6. Out

of 154 cases of leiomyomas, 80 were intramural in location, of which 62 were single

and 18 were multiple. 44 were sub-serosal in location, 31 cases were single and 13

were multiple in location. Rest 30 were sub mucosal which were single. Of 154

number of leiomyomas, 12(79.87%) were single and 31(20.12%) were multiple.

78

Table 7 Location and number of leiomyoma

Location of leiomyoma

Single location

Multiple location

Total no. of leiomyomas

Percentage

Intramural 62 18 80 52.00

Subserosal 31 13 44 29.00

Submucosal 30 - 30 19.00

Total 123 (79.87%) 31

(20.12%)

154 100%

 Size of Leiomyomas:

Sub-serosal leiomyomas varied from few mm to 16X14X12 cm in size.

Intramural leiomyomas varied from few mm to 10 cm in diameter. Sub-mucosal

leiomyomas varied from few mm to 5 cm in diameter.

Histological features of Leiomyoma:

In this study 107 cases (69.48%) showed features of leiomyoma consisting of

anastomosing and whorled fascicles of fusiform cells of a relatively uniform size.

These cells contain abundant eosinophilic and fibrillar cytoplasm with elongated

nuclei having finely dispersed chromatin with occasional nucleoli and with rare

mitotic figures. Associated secondary changes were seen in 47(30.51%) cases.

79

TABLE 8 Histological types of leiomyomas

Histological type of

leiomyoma

No. of patients Percentage

Typical leiomyoma 107 69.48

Secondary changes 47 30.51

Total 154 100

 

 

 

Degenerative Changes in Leiomyoma:

Degenerative changes were observed in 47 leiomyomas (30.51%). Among

these 30 leiomyomas showed (64.00%), hyaline change, which constituted the most

common degenerative change in the study observed in the study.

80

Table 9 Degenerative changes in leiomyoma

Degenerative changes No. of patients Percentage

Hyaline 30 64

Cystic 5 10.63

Mucoid 4 08.51

Calcification 1 2.12

Fatty changes 1 2.12

Hemorrhage 1 2.12

Leiomyoma with infarction 0 0

Leiomyoma with infection 1 2.12

Myxoid 2 4.25

Necrosis 2 4.25

Total 47 100

 Variants of Leiomyoma:

There were 6 types of variants of leiomyoma in the present study of the total

154 leiomyomas, which included following types of variants, cellular, epitheloid,

schwannoma like leiomyoma, myxoid, mitotically active & symplastic leiomyoma.

81

Cellular leiomyoma showed clinical features of excessive uterine bleeding and

dysmenorrhea. The histology revealed cells which were regular, elongated and

fusiform with scanty eosinophilic cytoplasm with few mitotic figures.

Epitheloid leiomyoma presented with menorrhagia and mass per abdomen. The

histology showed predominantly epitheloid type of cells. The cells were round to

polyhedral. Majority of these cells were having clear cytoplasm and few had

acidophilic cytoplasm.

Symplastic leiomyoma presented with menorrhagia and mass per abdomen.

Microscopically the tumor was cellular, showed pleomorphic cells bordered by

spindle cells. These cells had enlarged hyperchromatic nuclei with occasional mitosis.

Myxoid variant microscopically showed stellate shaped cells widely separated by

extracellular material. Myxoid stroma is produced by myxoid degeneration of

collagen surrounding the nodules of smooth muscle.

Mitotically active variant microscopically showed usual leiomyoma with increased

mitotic index i.e. 5-20 MF/10HPF. They have pushing border compressing adjacent

myometrium.

Schwannoma like leiomyoma variant microscopically composed of cells with

elongated nuclei arranged in palisades similar to schwannoma. Hyaline is often

present and prominent.

82

Table 10 Variants of leiomyoma

Variants of leiomyoma No. of patients Percentage

Cellular 81 52.60

Epitheloid 35 23.00

Schwannoma like Leiomyoma

11 8.40

Myxoid 09 5.00

Mitotically active 09 5.00

Symplastic 09 5.00

Total 154 100

Endometrial Changes in Leiomyomatous Uterus:

Out of 276 cases, leiomyoma was diagnosed in 154 hysterectomy specimen. In

the present study, the major associated endometrial change was proliferative

endometrium observed in 228 cases (72.15%), followed by secretory changes in 55

cases (17.42%).

83

Table 11: Endometrial Changes in Leiomyomatous Uterus

Types of endometrium No. of cases Percentage

Proliferative 74 48.23

Secretory 47 30.54

CGH 28 18.34

Atrophic 5 03.24

Total 154 100

CGH- cystoglandular hyperplasia

Associated pathology in leiomyomas:

Adenomyosis was found in 52 cases (18.84%) followed by 2 cases of

Monkeberg’s sclerosis (0.72%).

Primary Malignant Tumor:

In the present study, only one case of primary malignant tumor of

myometrium was diagnosed as leiomyosarcoma (0.39%).

Leiomyosarcoma:

Leiomyosarcoma was diagnosed in 40 years old woman. This patient

presented with abnormal uterine bleeding and mass per abdomen.

84

Grossly:

Uterus was bulky measuring 10x7x4.5 cms in size. One cut section

myometrium showed areas of hemorrhage and necrosis.

Microscopically showed pleomorphic oval to spindle shaped cells with

hyperchromatic nuclei and showed mitotic figures of 10-12/ HPF with cellular atypia.

Also seen are few giant cells with areas of hemorrhage and necrosis.

85

Figure-7: Cut section of uterus showing Submucosal leiomyomas

Figure-8: Cut section of uterus showing Intramural leiomyoma

86

Figure-9: Gross section of uterus showing Subserosal leiomyoma

Figure-10: Cut section of uterus showing Subserosal leiomyoma

87

Figure-11 Gross section of uterus showing Subserosal multiple leiomyomas

Figure-12 Cut section of uterus showing Multiple leiomyomas with whorl pattern

88

Figure-13: Gross section of Bulky uterus

Figure 14: Cut section of uterus showing Calcification of Intramural leiomyoma

89

Figure-15 Cut section of uterus showing Mucoid degeneration of Subserosal

leiomyoma

Figure-16: Gross section of the adenomyosis showing coarse trabecular

Appearance of Adenomyosis

90

Figure-17: Photomicrograph of classical leiomyoma showing bundles of

Smooth muscles running in different directions (H&E X60)

Figure-18: Photomicrograph of Leiomyoma with foci of myxoid change (low

power view)

91

Figure-19: Photomicrograph showing cellular leiomyoma (low power view)

Figure-20: Photomicrograph showing cellular leiomyoma (High power view)

92

Figure-21: Photomicrograph of epitheloid leiomyoma showing tumor cells with

clear cytoplasm and few cells with pink cytoplasm (High power view)

Figure-22: Photomicrograph of Schwannoma like leiomyoma

93

Figure-23: Photomicrograph of Symplastic leiomyoma showing pleomorphic

cells bordered by spindle shaped cells and was admixed with multinucleated

giant cells with mitosis.

Figure24: Photomicrograph of Leiomyoma showing mitotically active leiomyoma

94

 Figure-25: Photomicrograph of Leiomyoma showing diffuse hyaline change

 

Figure-26: Photomicrograph showing medial Monckebergs calcification in the

myometrial blood vessel wall (High power view)

95

Figure-27: Photomicrograph of Adenomyosis showing endometrial glands and

stroma within the myometrium (low power view)

Figure-28 Cut section of uterus showing leiomyosarcoma with areas of

hemorrhage and necrosis

96

Figure-29: Photomicrograph of leiomyosarcoma showing cellular areas with

cellular and nuclear atypia (low power view)

 

Figure-30: High power view of leiomyosarcoma showing bizarre cells having

hyperchromatic nuclei, abnormal mitotic figure and multinucleated giant cells

(High power view)

 

97

DISCUSSION

In this two years study includes histopathological proved 276 cases with

myometrial lesions which constituted (53.38%) of the total 517 hysterectomy

specimens studied. Highest numbers of patients included in this study were between

31-40 years (46.00%) and least number of cases were above 60 years of age (0.36%).

The average age being 43.50.

The most common preoperative diagnosis for all hysterectomy was Prolapse

(30.79%), followed by DUB (27.53%). Menorrhagia was the commonest clinical

symptom seen in (36.00%) of patients, followed by dysmenorrhea in 18.00% of cases.

Most of the patients were parous (99.27%) and only 2 patients were nulliparous

(0.72%).

In the present study, histologically myometrial lesions were classified into

non-neoplastic (19.56%) and neoplastic lesions (80.47%). Leiomyomas were the

commonest benign neoplastic lesions diagnosed in ( 55.79%) of the cases. Only 1

case of malignant neoplasm was encountered of which was leiomyosarcoma (0.39%).

Neoplastic Lesions of Myometrium:

Leiomyomas are benign neoplasms commonly encountered in Gynaecological

practice 24,30,34. In the present study neoplastic lesions constituted (80.47%) of the

total number of specimen studied. Leiomyoma was the commonest finding (154

cases) constituting 55.79% of the total neoplastic lesions. Only one case of

leiomyosarcoma was encountered constituting 0.39% of the total 276 specimens.

Leiomyoma:

In the present study, all the benign tumors are encountered in the uterus were

leiomyomas (55.79%). Percentage of leiomyomas (55.79%) in the present study is

98

comparable with the study of Tiltman70 (1980, 56%), Cramer and Patel19 (1990, 77%)

and Bazot M et al127 (2001, 47.5%) noted highest incidence of leiomyomas.

Table-12: Comparative Percentage of Leiomyomas in Various Studies

Authors Year Percentage

Tiltman 1980 56

Cramer and Patel 1990 77

Bazot M et al 2001 47.5

Present study 2010 55.79

Leiomyomas are usually found in reproductive age group19,20,70,75 In the

present study, the highest incidence (46.00%) was observed between 31-40 years.

This finding correlates well with the observations made by Reddy & Malathy30 (1963;

50%) and Rosario Pinto studies34.

99

Table-13: Distribution noted by various authors in leiomyomas according to age

in various studies

Age Reddy & Malathy(1963)

Rosario Pinto(1968)

Present study(2010)

10-20 2.80 - -

21-30 21.50 13.92 20.28

31-40 50.00 44.77 46.00

41-50 23.60 41.31 24.00

51 -60 2.10 0 09.05

61-70 0 0 0.36

 Parity:

Leiomyomas are believed to be common in nulliparous or relatively infertile

women23,74. But in the present study, most were multiparous (99.27%) and (0.72%)

were nulliparous. Chhabra and Jaiswal74 (1996, 82%), Achari and Khanan32 (1965,

87%) and Rosario Pinto34 (1968, 76.8%) in their studies also noted highest incidence

of leiomyomas in multiparous women and lowest incidence in nulliparous women.

100

Table-14: Parity distribution noted by various authors in leiomyoma

Parity

Parity Reddy & Malathy (1963)

Achari & Khanan (1965)

Rosario Pinto (1968)

Chhabra & Jaiswal (1996)

Present study (2010)

Nulliparous 38.1 2.50 23.2 5 0.72

Uniparous 15.4 10.50 - 13 -

2 or more 46.5 87.00 76.8 82 99.27

Clinical Features:

The clinical features of leiomyomas are variable, the vast majority being

symptomless especially when small the symptomatology. The symptoms and severity

usually depends on size, position and the number of leiomyomas present. In the

present study, highest number of patients with leiomyoma presented with

menorrhagia (36%) followed by dysmenorrhea (18.00%).

Menorrhagia was the commonest clinical symptom noted by Rosario Pinto34

(1968, 37.9%), whereas it is only about (16%) in Bhaskar Reddy and Malathy30.White

discharge per vagina in the present study (12%) correlates with the Reddy and

Malathy study30.

101

Table-15: Comparative of Statement of various symptoms with other studies

Symptoms

Symptoms Reddy Malathy (1963)

Rosario Pinto (1968)

Present study (2010)

Menorrhagia 16 37.9 36

Metorrhagia 43 32.9 0

Polymenorrhagia 0 1.2 1

Scanty periods 0 0.8 0

Post menopausal bleeding 0 2.4 1

Dysmenorrhea 0 4.2 18

Mass per abdomen 27 17.7 6

Pain abdomen 25 19.4 6

White discharge per vagina 9.5 0 12

Mass per vagina 0 0 19

Backache 0 0 0

Sterility 29.8 22.3 0

Fever 0 1.2 0

Postcoital bleeding 0 0.4 0

Pressure over the abdomen - 22.3 -

 

In the present study, abnormal uterine bleeding in the form of menorrhagia,

metorrhagia and polymenorrhagia was found in (37%) of cases, which is comparable

to the study conducted by Chhabra & Jaiswal74 (1996).

102

Table-16: Comparative Percentage of Abnormal Uterine Bleeding in various

Studies

Authors Year Percentage

Reddy & Malathy 1963 59

Rosario Pinto 1968 72.17

Chhabra & Jaiswal 1996 48.79

Present study 2010 37

Location of Leiomyoma:

In the present study, highest numbers of leiomyomas were intramural

Constituting (52%), followed by subserosal (29%), whereas the submucosal

leiomyoma constituted (19%). According to Chhabra and Ohwri32 reported intramural

leiomyomas as the commonest type observed in these studies which is comparable to

the present study. The location of subserosal leiomyomas in the present study (29%)

correlates with the Chhabra, Ohwri32 (22.5%). Similarly the distribution of

submucosal leiomyoma in the present study (19%) is comparable to Chhabra and

Ohwri32 (20%) studies.

103

Table-17: Comparison of location of Leiomyomas in various studies Location

Location Reddy & Malathy (1963)

Rosario Pinto (1968)

Shaw (1971)

Chhabra & Ohwri (1993)

Present study (2010)

Intramural 28 73.5 75 47.5 52

Subserosal 35 0.8 15 22.5 29

submucosal 37 25.7 10 20 19

In the present study, the number of leiomyomas in a uterus varied from 1-8,

whereas Rosario Pinto34 (1968) noted a maximum number up to 14.

Histological Features:

In the present study, secondary changes were observed in the (30.51%) of

leiomyomas. Persaud and Arjoon35 (1970) reported secondary changes in (65%) of the

leiomyomas and Reddy and Malathy30 (1963) observed some form of secondary

changes present in all leiomyomas (154 cases)30,34,35,69.

104

Table-18: Showing Comparative Percentage of Degenerative Changes in Various

Studies

Authors Year Percentage

Reddy & Malathy 1963 100

Rosario Pinto 1968 12.2

Persaud & Arjoon 1970 65

Present study 2010 30.51

In the present study, various types of degenerative changes were observed.

Hyaline degenerative was the commonest secondary change which was seen in 30

leiomyomas and thus constituted (64%). Norris & Zaloudek20 (1981, 60%) and

Persaud and Arjoon35 (1963), noted higher incidence of hyaline change, which is

comparable with the present study.

105

Table-19: Comparative Percentage of Hyaline Change in Leiomyomas noted by

various studies

Authors Year Percentage

Reddy & Malathy 1963 100

Persaud & Arjoon 1970 63

Norris & Zaloudek 1981 60

Rosario Pinto 1968 08

Present study 2010 64

The low incidence of calcification was observed (2.12%) in the present study, which

correlates well with Reddy and Malathy30

106

Table-20: Comparative Percentage of Incidence of Calcification in Different

Studies

Author Year Percentage

Reddy and Malathy 1963 2.50

Persuad & Arjoon 1970 7

Norris and Zaloudek 1981 10

Present study 2010 2.12

 

Sarcomatous change in the leiomyomas is rare35. In the present study, no case

of sarcomatous change was observed. The study of Corscaden and Singh (1958)

indicates the true incidence of sarcoma developing in leiomyomas was not more than

(0.13%) and probably as low as (0.33%)35.

Variants of Leiomyoma:

Several histopathological variants of leiomyomas have been described in the

literature, 6 variants encountered in the present study constituting cellular, epitheloid,

symplastic, mitotically active, myxoid & schwannoma like leiomyomas.

107

Cellular leiomyoma –The histological features of dense cellularity of cellular

leiomyoma in the present study were similar to the features mentioned by various

authors19,20,70,75. The clinical features, size, location and microscopic features were

similar to the study made by various authors.

Epitheloid Leiomyoma: epitheloid leiomyoma with classical microscopic features

with predominant clear cells and few cells with eosinophilic cytoplasm with mitosis

1-2/ 10 HPF. Similar features were described by various authors19,65,70,75.

Symplastic Leiomyoma: showed histologically pleomorphic cells bordered by

spindle shaped cells and was admixed with multinucleated giant cells with mitosis 1-

2/ 10 HPF. Similar features were described by various authors19,20,70,75.

Myxoid variant: microscopically showed stellate shaped cells widely separated by

extracellular material. Myxoid stroma is produced by myxoid degeneration of

collagen surrounding the nodules of smooth muscle. Similar features were described

by various authors19,65, 70,75.

Mitotically active variant: microscopically showed usual leiomyoma with increased

mitotic index i.e. 5-20 MF/10HPF. They have pushing border compressing adjacent

myometrium. Similar features were described by various authors19, 65, 70, 75.

Schwannoma like leiomyoma variant: microscopically composed of cells with

elongated nuclei arranged in palisades similar to schwannoma. Similar features were

described by various authors19,65,70,75.

Endometrial changes associated with leiomyomas :Majority of leiomyomatous

uteri in the present study showed proliferative endometrium (48.23%) an observation

108

comparable to the study of Rosario Pinto34 (1968, 51.1%) who also found highest

incidence of proliferative endometrium.

Achari & Khanan32 (1965) noted highest incidence of endometrial hyperplasia

(50%) in their study of 76 cases.

In the present study, secretory endometrium was seen in 30.54% of cases.

Incidence of atrophic endometrium in the present study is 3.24% which is comparable

to Achari &Khanan32 (1965, 2.6%).

109

Table-21: Comparative Percentage of Endometrial Changes in Leiomyoma in

Different Studies

Endometrial changes

Achari & Khanan (1965)

Rosario Pinto (1968)

Present study (2010)

Proliferative 34.2 51.1 48.23

Secretory 13.2 17.5 30.54

CGH 50 20.4 18.34

Atrophy 2.6 11 3.24

Leiomyosarcoma:

In the present study, only a single case of leiomyosarcoma was diagnosed

Constituting (0.39%) of the total number of specimen studied. Low incidence was

also noted in other studies11,25,63.

110

Table-22: Comparative Percentage of Leiomyosarcoma in various studies

Author Year Percentage

Christopherson et al 1972 0.67

Liebsohn et al 1990 0.69

Wald Mann J et al 2003 <1

Present study 2010 0.39

In the present study, leiomyosarcoma was diagnosed in 55 years old female,

who presented with abnormal vaginal bleeding, pain abdomen. The tumor was grey

white growth located intramural, with areas of hemorrhage and necrosis.

Microscopically, it consisted of atypical oval to spindle shaped cells with

hyperchromatic nuclei and good number of multinucleated giant cells with mitosis 10-

12/ HPF.

Tylor and Norris86 (1966) in their study of 39 cases of leiomyosarcoma,

described similar gross features and microscopic features and majority of the tumors

were intramural in location.

111

Hart & Billmen12 (1978), Cavanagh et al80 (1980 ) in their studies have

described similar clinical features and morphology of leiomyosarcoma.

In the present study, myometrium was unremarkable in 56 uteri (20.28%).

However, 2 uteri over the age of 50 years, showed Monckeberg’s sclerosis involving

medium sized arteries of the myometrium which constituted (0.72%)

Adenomyosis:

Adenomyosis was the commonest associated pathology observed in the

present study with an incidence of ( 18.84%), which is comparable to the study

conducted by Carter JE, Kong I I121 (23%)

112

Table-23: Comparative Percentage of Adenomyosis in Various Studies

Author Year Percentage

Rosario Pinto 1968 11.3

Carter JE, Kong I I 1994 23

Bazot M et al 2001 33

Present study 2010 18.84

The occurrence of adenomyosis in the present study correlates with the study

of Vavilis D et al132 (1997, 19.5%) The frequency of adenomyosis reported in the

literatures ranges widely from (5-70%)102. Although many reasons for this marked

variations have been advanced no really satisfactory answer has been found.

The degree of care with which the pathologic specimens is studied, the

selection criteria for the myometrial specimens, and the varying histologic criteria for

the diagnosis of adenomyosis contribute to the disparity in estimates102. Thus

pathologists awareness of this condition, the number and site of myometrial samples

analyzed, and the histological criteria used may all have an influence on the diagnosis

of adenomyosis132.

113

As endometriosis has always been defined as “the enigmatic disease” so also

adenomyosis has its label “the elusive disease”. This epitomizes the scanty reliability

of a preoperative clinical diagnosis of adenomyosis120. In this study, pre-operative

clinical diagnosis of adenomyosis was done in only 62 cases (3.98%).

Age: The peak incidence of adenomyosis is in 4th and 5th decades of life102. In the

present study, also the peak age incidence of adenomyosis was in fourth and fifth

decades (66.5%). Weed129 (1963, 71.4%) and Molitor103 (1971, 76.2%) studies also

noted similar findings.

Table-24: Comparison of Distribution of Adenomyosis in Different Age Groups

Author Year Age 30-50 Years %

Youngest % Oldest % Average age %

Weed 1963 71.40 24 71 --

Molitor 1971 76.20 27 85 --

Bird 1972 70.80 26 77 46

Present study

2010 66.5 26 -- --

Parity:

Adenomyosis typically affects multiparous patients102. In the present study, all

the patients were multiparous. Similarly, Bird et al128, Molitor103 and Paolo

Vercillini123 also noted higher incidence of adenomyosis in multiparous women.

Clinical Symptoms:

The symptoms classically associated with adenomyosis is excessive uterine

bleeding accompanied by worsening dysmenorrhea in a multipara in late reproductive

age with a diffusely enlarged uterus that is soft and tender on palpation. However,

adenomyosis may be entirely asymptomatic but it is still extremely difficult to make a

114

precise estimate of the percentage of women with adenomyosis and adenomyosis

without disturbances128,132.In the present study, (42.45%) of patients with

adenomyosis had menorrhagia and (29.24%) had dysmenorrhea.

In the present study, menorrhagia was seen in (42.45%). Similarly, Fraser

(1990, 51.0%), Bird (1972, 51.2%) and Loffer (1989, 54.1%) also noted higher

incidence of menorrhagia7,128 Percentage of patients of adenomyosis with

dysmenorrhea (29.24%) in the present study correlates with Bird128 (1972, 28.3%) and

Molitor103 (1971, 21.3%).

Uterine Size:

In the present study, adenomyotic uterine size was normal in (59.92%) of

cases, slightly enlarged or bulky in (35.84%) of cases and was atrophic in

(4.24%).Molitor103 (1971) estimated only( 25% ) of the uteri showed significant or

detectable uterine enlargement due to adenomyosis. Bird et al128 (1972) noted only

(19.5% ) of the uteri were normal size.

In the present study, the uterus was of normal size in ( 59.92%) or just bulky

in ( 35.84%) cases. The increased uterine size was due to associated fibroids.

Assuming the validity of Langlois103 (1970) data, an enlarged uterus by itself is

certainly not an invariable or even very frequent result of adenomyosis. This study

shows that adenomyosis is not always associated with clinically demonstrable uterine

enlargement unless they are associated with fibroids.

Association of Adenomyosis with Leiomyoma:

Leiomyoma was observed in ( 24.29% )of adenomyotic uteri. The association

of leiomyoma in the present study (24.29%) correlates with the observation made by

Loffer102 (1989, 16%) and comparatively less with other studies.

115

Table-25: Association of Leiomyoma with Adenomyosis in Different Studies

Author Year Leiomyoma (%)

Molitor 1971 38.40

Bird et al 1972 53.00

Loffer 1989 16.00

McCausland 1992 55.00

Present study 2010 24.29

In the present study, the findings do not support the notion that adenomyosis is

more frequently related to particular clinical conditions and suggest that parity may be

associated with an increased frequency of Adenomyosis7,102,123.

Associated pelvic diseases with adenomyosis like leiomyoma suggests

dysfunctional problem and tend to indicate probably hyperestrogenism as a common

denominator102,123.

116

SUMMARY AND CONCLUSION

In this 2 years study from June 2008 to June 2010, total 517 hysterectomy

specimens were studied, of which constituted 276 myometrial lesions received in the

Department of Pathology, Al Ameen Medical College, Bijapur.

o The patients were between 2nd and 7th decades of life. The youngest was 22

year old and oldest was 65 years old.

o The commonest clinical diagnosis for hysterectomy was Prolapse 30.79%

followed by Dysfunctional uterine bleeding 27.53% and Fibroids 21.73%.

o Adenomyosis was the commonest tumor like condition encountered in 18.84%

of uteri. Majority of the patients with adenomyosis were in 4th decade

43.86%, all the cases of adenomyosis were parous.

o Menorrhagia and dysmenorrhea were the commonest clinical features obtained

in 36% and 18% of patients respectively.

o Fibroids with adenomyosis were the commonest associated pathology seen in

24.29%.

o Neoplastic lesions of the uterine corpus constituted 80.47% of the total

specimen studied in which leiomyoma constituted 55.79% of the total.

o Majority of the patients with leiomyoma were in the 3rd decade constituting

46.92%. Most patients with leiomyoma were multiparous – 99.27% and only 2

cases were nulliparous – 0.72%.

o Menorrhagia and dysmenorrhea were the commonest clinical features

observed in 36% and 18% of patients respectively.

117

o Grossly most leiomyomas were intramural 52% followed by subserosal 29%

and least were submucosal leiomyomas 19%. The number of leiomyomas in a

uterus varied up to 6.

o Of the total 154 leiomyomas, degenerative changes were observed in 30.51%

of leiomyomas. Hyaline change was the commonest – 64%.

o 6 Variants of leiomyoma which included cellular, symplastic, myxoid,

schwannoma like, mitotically active and epitheloid leiomyoma.

o Proliferative endometrium (48.23%) was the commonest endometrial change

associated with leiomyomas.

o Malignant neoplasms of the uteri were comparatively less common. They

constituted 0.39% of the total specimens studied (276) cases.

o Only one case of leiomyosarcoma was encountered in the present study

constituting 0.39% of the total specimens studied.

o Myometrium was unremarkable in 56 cases (20.28%). Monckeberg’s sclerosis

was observed in 2 uteri over the age of 50 years, which constituted 0.72%.

118

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134

ANNEXURE-I

GYNAECOLOGICAL CASE SHEET

Name :

Age :

Occupation :

Religion :

Address:

Chief Complaints :

H/o present illness :

Obstetric history :

• Gravida :

• Parity :

• Living :

• Abortion :

• Menstrual history :

• Menarche :

• LMP :

• Past menstrual cycles : Regular/ Irregular

• Present menstrual cycles : Regular/ Irregular

• Age at menopause :

Past illness :

Family history :

Personal history :

• Diet :

• Appetite :

• Weight :

135

• Bowels :

• Micturition :

• Addictions :

Vital data :

• Pulse rate :

• Blood pressure :

• Respiratory rate :

• Temperature :

General examination :

• Anaemia :

• Thyroid :

• Breasts :

• Edema feet :

Systemic Examination :

• Cardiovascular system :

• Respiratory system :

• Liver, Spleen, Kidneys :

Abdominal examination:

• Inspection:

• Palpation:

• Percussion:

• Auscultation:

Per speculum examination:

Per vaginal examination:

Bimanual examination:

Per rectal examination:

Investigations:

136

Hematological Biochemical

Hb : RBC

TC: Blood urea

DLC: Serum creatinine

BT: Urine albumin

CT : Sugar

Blood Grouping: Microscopy

HIV : Urine pregnancy test

HbsAg:

VDRL :

Radiological:

• Chest X-ray:

• Ultrasound abdomen:

• Transvaginal ultrasonography:

Histological:

• Macroscopy

• Microscopy

• Special stains

Histopathological diagnosis

137

ANNEXURE-II

TECHNIQUE OF STAINING THE SECTIONS:

Haematoxylin & Eosin (H&E) Stain:

1. The deparaffinized slides were immersed in 1st Xylene bath for 3 minutes

2. Transferred to 2nd Xylene bath for 2-3 minutes

3. Immersed in the 1st bath of absolute alcohol for 3 minutes

4. Immersed in a bath of 95% ethyl alcohol for 1-2 minutes

5. Rinsed in running water for 1 minute and then briefly in distilled water.

6. Stained with Harris haematoxylin for 5-10 minutes and rinsed in tap water.

7. Differentiated in 1% acid alcohol by dipping 3-4 times and washed in tap

water briefly.

8. Bluing was done with ammonia water until sections appeared blue.

9. Rinsed in tap water for 10-20 minutes.

10. Stained with acidified 1% aqueous eosin for 15 seconds to 2 minutes

11. Washed in running tap water for 30 seconds to 2 minutes to differentiate eosin stain.

12. Dehydrated by passing through three baths of absolute alcohol with agitation.

13. Passed through two baths of Xylene for 15-20 seconds in each, mounted in DPX.

RESULTS:

Nuclei, RNA, Rich Cytoplasm, Calcium --------Blue

Muscle, Fibrin, Keratin -------Bright red

Collagen --------Pink

RBCs --------Orange/Red

138

VAN GIESON STAINING METHOD

1) Bring the section to water.

2) Rinse in distill water.

3) Stain with Weigerts haematoxylin (freshly prepared) for 40 minutes or (3ml Weigerts + 3ml iron solution) equal parts.

4) Celestin blue for 5 minutes rinse in water and stain with Mayer’s heamalum 5 minutes.

5) Wash in tap water.

6) 1% Acid Alcohol 3 to 5dips.

7) Van geison stain 3 minutes.

8) Rinse in distill water.

9) Dehydrate, clear and mount.

RESULTS

Nuclei ----Black

Collagen -----Red

Other tissue -----Yellow

139

MASSON’S TRICHROME STAINING METHOD

1) Bring the section to water.

2) Celestin blue -8 minutes, heamalum- 8 minutes.

3) Acid alcohol 3 to 5 dips.

4) Running water - 5 minutes.

5) 1% Acid fuchsin- 5 minutes.

6) Rinse in distill water.

7) 1% aqueous phosphomolybdic acid -5 minutes.

8) 1% methyl blue or 1% light green -2minutes.

9) Rinse in 1% acetic acid-30 seconds.

10) Dehydrate, clear and mount.

RESULTS

Nuclei ----Blue or Black

Muscle,RBCs, Cytoplasm ----Red

Collagen,Cartilage ----Blue or Green

140

141

142

143

144

145

146

147

148

ETHICAL COMMITTEE

AL-AMEEN MEDICAL COLLEGE, BIJAPUR. 

 

The following study entitled “HISTOPATHOLOGICAL STUDY OF

MYOMETRIAL LESIONS OF CORPUS UTERI – TWO YEAR STUDY”

(PROSPECTIVE STUDY) by DR. ANITA B. SAJJANAR, P.G. STUDENT in

Pathology belonging to 2008 batch has been cleared from ethical committee of this

institution for the purpose of dissertation work.

 

 

 

 

CHAIRMAN ETHICAL COMMITTEE AL-AMEEN MEDICAL COLLEGE,

BIJAPUR.

Sl. No Name Biopsy no Age Hospital IP/OP

No Parity Chief Complaints Clinicl diagnosis Gross Cut section morphology Histopatholgical diagnosis

1 Gangawa S/263/08 52 AMCH 7337 Multi WDPV PID Bulky Single,Intramural,Whorl pattern Leiomyoma with adenomyosis2 Heenabai S/277/08 30 AMCH 7333 Uni Pain abdomen Fibroid uterus Bulky Multiple,intramural, Whorl pattern Cellular leiomyoma with hyaline change3 Gouravva S/289/08 45 AMCH 8109 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis4 Laxmi S/290/08 50 AMCH 7824 Multi Mass per vagina UV Prolapse Slight Bulky Single,Subserosal,Whorl pattern Cellular leiomyoma with hyaline change5 Paravva S/474/08 45 AMCH 4914 Multi Menrrhagia UV Prolapse Bulky Coarse trabecular Adenomyosis6 Annapurna S/608/08 25 DHB 7147 Uni WDPV PID Slight Bulky Single,intramural ,Whorl pattern Cellular leiomyoma with hyaline change7 Ratnavva S/613/08 35 DHB 7245 Multi Menorrhagia UV Prolapse Bulky Coarse trabecular Adenomyosis8 Jayamma S/614/08 52 AMCH 12868 Multi Menorrhagia Fibroid uterus Slight Bulky Single, submucosal,Whorl pattern Epitheloid leiomyoma9 Rajashree S/627/08 40 DHB 7174 Uni WDPV PID Bulky Coarse trabecular Adenomyosis

10 Vimlabai S/686/08 40 AMCH 16031 Multi Dysmenorrhea DUB Slight Bulky Unremarkable Epitheloid leiomyoma11 Shantabai S/711/08 45 AMCH 1223 Multi Menorrhagia DUB Bulky Single,intramural ,Whorl pattern Cellular Leiomyoma12 Pramilabai S/712/08 40 AMCH 16428 Uni Menorrhagia UV Prolapse Bulky Multiple subserosal,Whorl pattern Epitheloid leiomyoma13 Champa S/713/08 40 DHB 8960 Uni Dysmenorrhea DUB Slight Bulky Single,intramural ,Whorl pattern Epitheloid leiomyoma14 Kamalabai S/03/09 35 DHB 9533 Uni WDPV Chronic PID Slight Bulky Single,subserosal,Whorl pattern Epitheloid leiomyoma15 Sushila S/08/09 44 AMCH 18029 Multi Menorrhagia Adenomyosis Slight Bulky Coarse trabecular Adenomyosis16 Nirmala S/30/09 45 AMCH 123 Multi Dysmenorrhea Fibroid uterus Slight Bulky Single,intramural ,Whorl pattern Epitheloid leiomyoma17 Geeta S/47/09 40 DHB 330 Multi WDPV Chronic PID Slight Bulky Coarse trabecular Adenomyosis18 Meena S/48/09 30 DHB 431 Uni WDPV PID Slight Bulky Coarse trabecular Adenomyosis19 Rukmini S/57/09 35 AMCH 1156 Uni WDPV PID Slight Bulky Coarse trabecular Adenomyosis20 Prema S/61/09 35 DHB 7245 Multi Menorrhagia Fibroid uterus Bulky Coarse trabecular Adenomyosis21 Suvarna S/58/09 50 AMCH 770 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis22 Rashmi S/60/09 32 AMCH 1371 Uni WDPV PID Slight Bulky Single,intramural ,Whorl pattern Cellular leiomyoma with hyaline change23 Rajani S/97/09 50 DHB 1165 Multi Mass per vagina UV Prolapse Bulky Unremarkable Epitheloid leiomyoma24 Kamala S/106/09 30 DHB 1420 Uni Pain abdomen Fibroid uterus Slight Bulky Single,intramural ,Whorl pattern Leiomyoma with adenomyosis25 Manjula S/109/09 46 AMCH 1530 Multi Dysmenorrhea DUB Bulky Multiple, subserosal, Whorl pattern Cellular leiomyoma with hyaline change26 Asha S/112/09 52 AMCH 1260 Multi WDPV PID Bulky Coarse trabecular Adenomyosis27 Sasamma S/114/09 40 AMCH 40 Multi WDPV PID Slight Bulky Coarse trabecular Adenomyosis28 Renuka S/141/09 30 DHB 1797 Uni Pain abdomen PID Slight Bulky Single,subserosal,Whorl pattern Epitheloid leiomyoma29MumtazbegaumS/143/09 30 DHB 4074 Uni Menorrhagia UV Prolapse Slight Bulky Single,subserosal,Whorl pattern Cellular leiomyoma with hyaline change30 Shabnam S/150/09 40 AMCH 2247 Multi WDPV PID Slight Bulky Unremarkable Epitheloid leiomyoma31 Heena S/151/09 33 AMCH 3342 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Adenomyosis32 Shantabai S/156/09 50 AMCH 2247 Multi WDPV PID Slight Bulky Unremarkable Leiomyoma with adenomyosis33 Seemabai S/162/09 56 AMCH 2576 Multi Dysmenorrhea PID Normal Unremarkable Leiomyoma with adenomyosis34 Zubeda S/168/09 46 AMCH 26982 Multi WDPV UV Prolapse Slight Bulky Single,subserosal,Whorl pattern Cellular Leiomyoma35 Somubai S/227/09 45 DHB 3675 Multi Menorrhagia Fibroid uterus Normal Single,subserosal,Whorl pattern Epitheloid leiomyoma

36 Shiamma S/239/09 50 DHB 3887 Multi Pain abdomen UV Prolapse Slight Bulky Coarse trabecular Adenomyosis37 Rama S/242/09 35 AMCH 3734 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Adenomyosis38 Zakiya S/250/09 57 AMCH 3836 Multi WDPV PID Bulky Single,subserosal,Whorl pattern Cellular Leiomyoma39 Ashabai S/267/09 60 DHB 3941 Multi Dysmenorrhea DUB Atropied Single,subserosal,Whorl pattern Leiomyoma with adenomyosis40 Fakirrava S/280/09 31 DHB 3322 Uni Menorrhagia PID Slight Bulky Single,intramural ,Whorl pattern Leiomyoma with adenomyosis41 Ameenbee S/286/09 27 AMCH 3411 Multi Menorrhagia UV Prolapse Normal Coarse trabecular Adenomyosis42 Gangabai S/290/09 46 DHB 3522 Multi Menorrhagia Fibroid uterus Bulky Multiple,subserosal,Whorl pattern Epitheloid leiomyoma43 Gouramma S/292/09 54 AMCH 745 Multi Pain abdomen Fibroid uterus Bulky Multiple,subserosal,Whorl pattern Cellular Leiomyoma44 Herabai S/302/09 43 DHB 5673 Multi WDPV Fibroid uterus Slight Bulky Single,submucosal,Whorl pattern Epitheloid leiomyoma45 Razabhi S/378/09 40 DHB 4223 Uni Dysmenorrhea DUB Slight Bulky Unremarkable Leiomyoma with adenomyosis46 Gayatri S/410/09 35 AMCH 6920 Uni Pain abdomen UV Prolapse normal Adenomyosis Adenomyosis47 Mallika S/476/09 45 AMCH 7730 Multi Dysmenorrhea DUB Atropied Multiple,intramural ,Whorl pattern Leiomyoma with adenomyosis47 Kasturibai S/497/09 55 AMCH 7568 Multi Pain abdomen UV Prolapse Slight Bulky Single,intramural Adenomyosis48 Shobha S/504/09 50 AMCH 8060 Multi Dysmenorrhea DUB Slight Bulky Single,intramural Adenomyosis49 Zahera S/521/09 65 AMCH 42002 Multi Dysmenorrhea DUB Bulky Multiple,subserosal,Whorl pattern Symplastic leiomyoma 50 Gangubai S/549/09 35 AMCH 2778 Uni Menorrhagia Fibroid uterus Slight Bulky Single,intramural,Whorl pattern Leiomyoma with adenomyosis51 Mahadevi S/564/09 38 AMCH 5167 Multi Dysmenorrhea DUB Atropied Single,intramural,Whorl pattern Cellular Leiomyoma52 Radhabai S/580/09 50 AMCH 8447 Multi Dysmenorrhea DUB Slight Bulky Unremarkable Epitheloid leiomyoma53 Revakka S/606/09 35 AMCH 5307 Uni Dysmenorrhea DUB Normal Unremarkable Epitheloid leiomyoma54 Anjana S/609/09 40 AMCH 40169 Uni Pain abdomen UV Prolapse Slight Bulky Single,subserosal,Whorl pattern Cellular leiomyoma with hyaline change55 Saleema S/633/09 35 AMCH 9682 Uni Pain abdomen UV Prolapse Normal Single,intramural,Whorl pattern Epitheloid leiomyoma56 Mudukibai S/643/09 45 AMCH 9798 Multi Menorrhagia DUB Normal Unremarkable Leiomyoma with adenomyosis57 Rahabai S/690/09 35 AMCH 6637 Uni Mass per vagina UV Prolapse Slight Bulky Single,intramural,Whorl pattern Leiomyoma with adenomyosis58 Kasturibai S/713/09 35 DHB 6774 Multi Pain abdomen PID Bulky Multiple,subserosal,Whorl pattern Cellular leiomyoma with hyaline change59 Sureka S/730/09 35 DHB 6468 Uni Pain abdomen UV Prolapse Normal Unremarkable Cellular Leiomyoma60 Shivleela S/731/09 47 DHB 6493 Multi Pain abdomen UV Prolapse Atropied Unremarkable Leiomyoma with adenomyosis61 Fathima S/740/09 35 DHB 7416 Uni Dysmenorrohea PID Normal Single,submucosal,Whorl pattern Cellular Leiomyoma62 Shabana S/741/09 30 DHB 7351 Uni Pain abdomen UV Prolapse Normal Single,intramural,Whorl pattern Cellular Leiomyoma63 Zarina S/750/09 35 DHB 7381 Uni WDPV Fibroid uterus Slight Bulky Single,subserosal,Whorl pattern Cellular Leiomyoma64 Sheena S/752/09 35 AMCH 7377 Uni Mass per vagina UV Prolapse Slight Bulky Single,subserosal,Whorl pattern Leiomyoma with adenomyosis65 Chandrabai S/755/09 40 DHB 12977 Multi Mass per vagina UV Prolapse Normal Single,intramural,Whorl pattern Cellular Leiomyoma66 Sheefa S/781/09 55 AMCH 7863 Multi Mass per vagina UV Prolapse Bulky Multiple,subserosal,Whorl pattern Cellular Leiomyoma with infection67 Shain S/782/09 24 DHB 7833 Nulli Dysmenorrhea Fibroid uterus Bulky Multiple,subserosal,Whorl pattern Cellular Leiomyoma68 Fameeda S/783/09 26 DHB 13990 Uni Dysmenorrhea PID Normal Single,intramural,Whorl pattern Leiomyoma with adenomyosis69 Rajeshwari S/789/09 40 DHB 8069 Uni Pain abdomen UV Prolapse Slight Bulky Unremarkable Leiomyoma with adenomyosis70 Mallava S/790/09 45 DHB 7900 Multi WDPV PID Slight Bulky Multiple,intramural,Whorl pattern Epitheloid leiomyoma

71 Rahabi S/791/09 35 AMCH 12114 Multi Mass per vagina UV Prolapse Slight Bulky Single,subserosal,Whorl pattern Leiomyoma with adenomyosis72 Kasturibai S/793/09 35 AMCH 6637 Multi Pain abdomen UV Prolapse Slight Bulky Single,intramural,Whorl pattern Leiomyoma with adenomyosis73 Vanmala S/794/09 35 DHB 6774 Multi Pain abdomen UV Prolapse Normal Single,subserosal,Whorl pattern Cellular leiomyoma with hyaline change74 Saraswati S/795/09 37 DHB 6678 Multi WDPV PID Normal Single,subserosal,Whorl pattern Symplastic leiomyoma 75 Kamala S/800/09 35 DHB 6693 Uni Dysmenorrhea PID Slight Bulky Unremarkable Epitheloid leiomyoma76 Shaila S/801/09 30 DHB 9416 Uni Pain abdomen UV Prolapse Normal Unremarkable Leiomyoma with adenomyosis77 Rathna S/802/09 35 DHB 7351 Multi WDPV Fibroid uterus Normal Unremarkable Cellular leiomyoma with hyaline change78 Meerabai S/805/09 35 DHB 7381 Uni Mass per vagina UV Prolapse Slight Bulky Multiple,subserosal,Whorl pattern Leiomyoma with adenomyosis79 Ammabai S/806/09 40 DHB 7377 Multi Mass per vagina UV Prolapse Normal Single,subserosal,Whorl pattern Cellular Leiomyoma80 Shantabai S/809/09 55 AMCH 12977 Uni Mass per vagina UV Prolapse Slight Bulky Multiple,intramural,Whorl pattern Epitheloid leiomyoma81 Chandibai S/810/09 24 DHB 7863 Uni Dysmenorrhea DUB Atropied Single,intramural,Whorl pattern Cellular Leiomyoma82 Kavita S/812/09 26 DHB 7833 Uni Dysmenorrhea DUB Normal Coarse trabecular Adenomyosis83 Hemmavva S/814/09 40 AMCH 13990 Multi WDPV PID Slight Bulky Unremarkable Leiomyoma with adenomyosis84 Nagamma S/819/09 45 DHB 8069 Uni WDPV PID Slight Bulky Single,submucosal,Whorl pattern Symplastic leiomyoma 85 Mallawa S/821/09 35 AMCH 7900 Multi Dysmenorrhea PID Slight Bulky Multiple,intramural,Whorl pattern Cellular Leiomyoma86 Zubeda S/822/09 33 AMCH 14757 Multi Menorrhagia UV Prolapse Atropied Single,intramural,Whorl pattern Epitheloid leiomyoma87 Ayesha S/826/09 36 AMCH 8501 Multi WDPV PID Atropied Single,intramural,Whorl pattern Cellular leiomyoma with hyaline change88 Kamalabai S/827/09 27 AMCH 837 Uni WDPV PID Atropied Unremarkable Leiomyoma with adenomyosis89 Yellawa S/829/09 30 DHB 14761 Uni Mass per vagina UV Prolapse Atropied Multiple,intramural,Whorl pattern Symplastic leiomyoma 90 Sunanda S/831/09 30 AMCH 15338 Uni Mass per vagina UV Prolapse Normal Single,intramural,Whorl pattern Leiomyoma with adenomyosis91 Keshubai S/834/09 45 AMCH 8368 Multi menorrhagia Fibroid uterus Slight Bulky Single,intramural,Whorl pattern Cellular Leiomyoma with cystic change92 Yasmin S/837/09 28 AMCH 8799 Uni Dysmenorrhea PID Slight Bulky Unremarkable Leiomyoma with adenomyosis93 Gouravva S/840/09 45 DHB 8995 Multi menorrhagia PID Normal Multiple,intramural,Whorl pattern Cellular leiomyoma with hyaline change94 Dilshad S/844/09 40 AMCH 16486 Multi Dysmenorrhea DUB Normal Single,intramural,Whorl pattern Leiomyoma with adenomyosis95 Satwa S/845/09 34 DHB 15712 Multi Menorrhagia Fibroid uterus Normal Single,subserosal,Whorl pattern Leiomyoma with adenomyosis96 Gangabai S/858/09 52 AMCH 9479 Multi Menorrhagia UV Prolapse Slight Bulky Single,intramural,Whorl pattern Epitheloid leiomyoma97 Mahadevi S/863/09 48 DHB 16778 Multi WDPV PID Normal Unremarkable Symplastic leiomyoma 98 Parvati S/883/09 30 DHB 17654 Uni WDPV PID Slight Bulky Unremarkable Leiomyoma with adenomyosis98 Malamma S/884/09 22 DHB 9733 Uni Dysmenorrhea DUB Slight Bulky Single,intramural,Whorl pattern Leiomyoma with schwannoma like change99 Sarlabai S/892/09 48 AMCH 97109 Multi Menorrhagia DUB Slight Bulky Single,subserosal,Whorl pattern Leiomyoma with adenomyosis100 Vasanti S/895/09 30 AMCH 18817 Uni WDPV PID Normal Single,submucosal,Whorl pattern Leiomyoma with adenomyosis101 Mahadevi S/902/09 22 DHB 10901 Uni Mass per vagina UV Prolapse Normal Single,intramural,Whorl pattern Cellular Leiomyoma102 Mallawa S/907/09 40 AMCH 11053 Multi Menorrhagia DUB Slight Bulky Unremarkable Leiomyoma with adenomyosis103 SushiIa S/914/09 43 DHB 19193 Multi Menorrhagia UV Prolapse Normal Single,intramural,Whorl pattern Epitheloid leiomyoma104 Mehboobi S/920/09 35 AMCH 11234 Multi WDPV PID Slight Bulky Multiple,intramural,Whorl pattern Symplastic leiomyoma 105 Neelamma S/923/09 40 DHB 11232 Uni Menorrhagia DUB Slight Bulky Multiple,intramural,Whorl pattern Cellular leiomyoma with hyaline change

106 Lata S/927/09 50 AMCH 11275 Multi WDPV Fibroid uterus Slight Bulky Single,intramural,Calcification Cellular Leiomyoma with calcification107 Asha S/945/09 30 AMCH 11407 Uni Menorrhagia DUB Normal Unremarkable Leiomyoma with schwannoma like change108 Mahadevi S/946/09 40 DHB 11455 Multi Menorrhagia Fibroid uterus Slight Bulky Multiple,subserosal,Whorl pattern Epitheloid leiomyoma109 Gangabai S/947/09 45 DHB 20577 Multi Mass per vagina UV Prolapse Slight Bulky Multiple,intramural,Whorl pattern Cellular leiomyoma with hyaline change110MumtazbegaumS/965/09 48 AMCH 11754 Multi menorrhagia DUB Atropied Single,intramural,Whorl pattern Symplastic leiomyoma 111 Jayashree S/04/10 30 AMCH 21723 Uni WDPV PID Slight Bulky Single,intramural,Whorl pattern Cellular leiomyoma with hyaline change112 Saibai S/08/10 22 AMCH 197 Uni Dysmenorrhea Fibroid uterus Normal Unremarkable Leiomyoma with adenomyosis113 Shashikala S/11/10 55 DHB 12167 Multi Menorrhagia UV Prolapse Slight Bulky Unremarkable Cellular leiomyoma with hyaline change113 Savitri S/70/10 41 AMCH 6 Multi Menorrhagia UV Prolapse Slight Bulky Multiple,intramural,Whorl pattern Cellular Leiomyoma114 Parvatri S/109/10 32 AMCH 266 Multi Menorrhagia PID Slight Bulky Single,subserosal,Whorl pattern Leiomyoma with adenomyosis

115 Goddamma S/124/10 45 DHB 322 Multi Mass per vagina Fibroid uterus Normal Multiple,subserosal,mucoid degeneration Epitheloid leiomyoma with mucoid change

116 Gangubai S/200/10 35 AMCH 2778 Uni Mass per vagina UV Prolapse Slight Bulky Single,intramural,Whorl pattern Cellular Leiomyoma117 Mahadevi S/290/10 38 AMCH 5167 Multi Dysmenorrhea DUB Atropied Single,intramural,Whorl pattern Cellular Leiomyoma118 Radhabai S/292/10 50 AMCH 8447 Multi Menorrhagia DUB Slight Bulky Coarse trabecular Adenomyosis119 Revakka S/313/10 35 AMCH 5307 Uni Menorrhagia DUB Atropied Coarse trabecular Adenomyosis120 Ranjana S/315/10 40 AMCH 40169 Uni Menorrhagia PID Slight Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis121 Saleema S/335/10 35 AMCH 9682 Uni Menorrhagia PID Normal Single,intramural,Whorl pattern Symplastic leiomyoma 122 Mudukibai S/343/10 45 AMCH 9798 Multi Menorrhagia DUB Normal Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis123 Rahabai S/390/10 35 AMCH 6637 Uni Mass per vagina UV Prolapse Slight Bulky Multiple,intramural,Whorl pattern Cellular leiomyoma with mucoid change124 Kasturibai S/413/10 35 DHB 6774 Multi Dysmenorrhea PID Atropied Unremarkable Cellular leiomyoma with hyaline change125 Kamala S/430/10 35 DHB 6468 Uni Menorrhagia PID Bulky Coarse trabecular Adenomyosis126 Shaila S/431/10 47 DHB 6493 Multi Mass per vagina UV Prolapse Normal Unremarkable Leiomyoma with adenomyosis127 Hanmavva S/440/10 35 DHB 7416 Uni Dysmenorrhea PID Atropied Coarse trabecular Adenomyosis128 Yamunavva S/741/10 30 DHB 7351 Uni Mass per vagina UV Prolapse Normal Single,intramural,Whorl pattern Cellular Leiomyoma129 Kasumibai S/450/10 35 DHB 7381 Uni WDPV Fibroid uterus Slight Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis130 Anandabai S/452/10 35 AMCH 7377 Uni Mass per vagina UV Prolapse Slight Bulky Multiple,subserosal,Whorl pattern Epitheloid leiomyoma131 Chandibai S/455/10 40 DHB 12977 Multi Mass per vagina UV Prolapse Normal Single,intramural,Whorl pattern Cellular leiomyoma with hyaline change132 Shafa S/481/10 55 AMCH 7863 Multi Mass per vagina UV Prolapse Atropied Unremarkable Leiomyoma with adenomyosis133 Kavita S/482/10 24 DHB 7833 Uni Mass per vagina UV Prolapse Atropied Single,subserosal,Whorl pattern Leiomyoma with adenomyosis134 Hameeda S/483/10 26 DHB 13990 Uni Dysmenorrhea PID Normal Single,intramural,Whorl pattern Cellular Leiomyoma135 Ningamma S/489/10 40 DHB 8069 Uni Menorrhagia PID Slight Bulky Coarse trabecular Mitotically active leiomyoma136 Mallawa S/490/10 45 DHB 7900 Multi WDPV PID Slight Bulky Multiple,intramural,Whorl pattern Cellular leiomyoma with hyaline change137 Rahabi S/509/10 35 AMCH 12114 Multi Mass per vagina UV Prolapse Slight Bulky Multiple,subserosal,Whorl pattern Leiomyoma with adenomyosis137 Kasturibai S/512/10 35 AMCH 6637 Multi Mass per vagina UV Prolapse Normal Single,intramural,Whorl pattern Cellular Leiomyoma138 Varmala S/513/10 35 DHB 6774 Multi Dysmenorrhea PID Atropied Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis139 Saraswati S/530/10 37 DHB 6678 Multi WDPV PID Normal Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis

140 Kamala S/531/10 35 DHB 6693 Uni Dysmenorrhea PID Slight Bulky Coarse trabecular Symplastic leiomyoma 141 Manjula S/549/10 46 AMCH 1530 Multi Mass per abdomen Fibroid uterus Bulky Unremarkable Epitheloid leiomyoma with cystic change142 Asha s/562/10 52 AMCH 1260 Multi WDPV PID Bulky Coarse trabecular Adenomyosis143 Sasamma S/584/10 40 AMCH 1440 Multi Menorrhagia Leiomyosarcoma Bulky soft,fleshy,areas of necrosis,haemrhge Leiomyosarcoma144 Renuka S/594/10 30 DHB 1797 Uni Dysmenorrhea PID Slight Bulky Coarse trabecular Cellular Leiomyoma145MumtazbegaumS/598/10 30 DHB 4074 Uni Dysmenorrhea DUB Slight Bulky Unremarkable Leiomyoma with adenomyosis146 Shabnam S/600/10 40 AMCH 2247 Multi WDPV PID Slight Bulky Single,submucosal,Whorl pattern Leiomyoma with adenomyosis147 Heena S/602/10 33 AMCH 3342 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Adenomyosis148 Shantabai S/603/10 50 AMCH 2247 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis149 Seemabai S/608/10 56 AMCH 2576 Multi Dysmenorrhea PID Normal Coarse trabecular Adenomyosis150 Zubeda S/610/10 46 AMCH 26982 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis151 Somubai S/613/10 45 DHB 3675 Multi Menorrhagia Fibroid uterus Normal Unremarkable Leiomyoma with adenomyosis152 Shiamma S/614/10 50 DHB 3887 Multi Dysmenorrhea PID Slight Bulky Coarse trabecular Adenomyosis153 Rama S/621/10 35 AMCH 3734 Uni Menorrhagia UV Prolapse Slight Bulky Coarse trabecular Adenomyosis154 Zakiya S/623/10 57 AMCH 3836 Multi stmenobleed prolap PID Bulky Single,subserosal,Whorl pattern Leiomyoma with adenomyosis155 Ashabai S/627/10 60 DHB 3941 Multi Mass per abdomen Fibroid uterus Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis156 Fakirrava S/630/10 31 DHB 3322 Uni Menorrhagia PID Slight Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis157 Ameenbee S/635/10 27 AMCH 3411 Nulli Menorrhagia DUB Normal Coarse trabecular Adenomyosis158 Gangabai S/642/10 46 DHB 3522 Multi Mass per abdomen Fibroid uterus Slight Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis159 Gouramma S/657/10 54 AMCH 745 Multi Mass per vagina UV Prolapse Bulky Unremarkable Epitheloid leiomyoma160 Herabai S/679/10 43 DHB 5673 Multi Dysmenorrhea PID Slight Bulky Coarse trabecular Adenomyosis161 Razabhi S/680/10 40 DHB 4223 Uni Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis162 Heenabi S/686/10 30 AMCH 7333 Uni Mass per abdomen Fibroid uterus Bulky Multiple,intramural, Whorl pattern Cellular leiomyoma with mucoid change163 Gouravva S/689/10 45 AMCH 8109 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis164 Laxmi S/690/10 50 AMCH 7824 Multi Mass per vagina UV Prolapse Slight Bulky Unremarkable Leiomyoma with adenomyosis165 Paravva S/694/10 45 AMCH 4914 Multi Mass per vagina UV Prolapse Bulky Coarse trabecular Adenomyosis166 Annapurna S/698/10 25 DHB 7147 Uni Dysmenorrhea DUB Slight Bulky Single,intramural,Whorl pattern Cellular leiomyoma with hyaline change167 Ratnavva S/700/10 35 DHB 7245 Multi Menorrhagia Fibroid uterus Bulky Coarse trabecular Cellular Leiomyoma168 Jayama S/704/10 52 AMCH 12868 Multi Menorrhagia Fibroid uterus Slight Bulky Unremarkable Leiomyoma with adenomyosis169 Rajashree S/707/10 40 DHB 7174 Uni Dysmenorrhea DUB Bulky Coarse trabecular Epitheloid leiomyoma170 Vimlabai S/709/10 40 AMCH 16031 Multi Menorrhagia UV Prolapse Slight Bulky Single, submucosal,Whorl pattern Leiomyoma with adenomyosis171 Shantabai S/711/10 45 AMCH 1223 Multi Mass per vagina UV Prolapse Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis172 Pramilabai S/712/10 40 AMCH 16428 Uni Menorrhagia Fibroid uterus Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis173 Champa S/713/10 40 DHB 8960 Uni Dysmenorrhea DUB Slight Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis174 Kamalabai S/723/10 35 DHB 9533 Uni Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Cellular leiomyoma with hyaline change175 Sushila S/728/10 44 AMCH 18029 Multi Menorrhagia Fibroid uterus Slight Bulky Single,intramural,Whorl pattern Cellular Leiomyoma

176 Nirmala S/730/10 45 AMCH 1345 Multi Mass per abdomen Fibroid uterus Slight Bulky Single,intramural,Whorl pattern Cellular leiomyoma with hyaline change177 Geeta S/747/10 40 DHB 330 Multi Polymenorrhagia PID Slight Bulky Coarse trabecular Adenomyosis178 Meena S/758/10 30 DHB 431 Uni Dysmenorrhea DUB Slight Bulky Coarse trabecular Adenomyosis179 Rukmini S/797/10 35 AMCH 1156 Uni Postmenobleed DUB Slight Bulky Coarse trabecular Adenomyosis180 Prema S/806/10 35 DHB 7245 Multi Menorrhagia Fibroid uterus Bulky Coarse trabecular Adenomyosis181 Suvarna S/858/10 50 AMCH 770 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis182 Rashmi S/860/10 32 AMCH 1371 Uni Menorrhagia Fibroid uterus Slight Bulky Multiple,intramural ,Whorl pattern Epitheloid leiomyoma183 Rajani S/877/10 50 DHB 1165 Multi Mass per vagina UV Prolapse Bulky Coarse trabecular Adenomyosis184 Ramala S/886/10 30 DHB 1420 Uni Dysmenorrhea Fibroid uterus Slight Bulky Single,intramural,Whorl pattern Cellular leiomyoma with hyaline change185 Vasanti S/895/10 30 AMCH 18817 Uni Mass per vagina UV Prolapse Bulky Unremarkable Cellular Leiomyoma186 Mahadevi S/902/10 22 DHB 10901 Uni Dysmenorrhea Fibroid uterus Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis187 Mallawa S/907/10 40 AMCH 11053 Multi Menorrhagia DUB Slight Bulky Unremarkable Epitheloid leiomyoma188 Sujata S/914/10 43 DHB 19193 Multi Menorrhagia Fibroid uterus Bulky Single,intramural,Whorl pattern Cellular Leiomyoma189 Mehboobi S/920/10 35 AMCH 11234 Multi Menorrhagia DUB Slight Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis190 Neelamma S/923/10 40 DHB 11232 Uni Mass per vagina UV Prolapse Slight Bulky Single,intramural,Whorl pattern Symplastic leiomyoma with cystic change191 Lata S/935/10 50 AMCH 11275 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis192 Asha S/945/10 30 AMCH 11407 Uni Menorrhagia DUB Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis193 Mahadevi S/946/10 40 DHB 11455 Multi Mass per abdomen Fibroid uterus Slight Bulky Coarse trabecular Leiomyoma with schwannoma like change194 Gangabai S/947/10 45 DHB 20577 Multi Dysmenorrhea Fibroid uterus Slight Bulky Unremarkable Cellular Leiomyoma195MumtazbegaumS/965/10 48 AMCH 11754 Multi Menorrhagia DUB Normal Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis196 Jayashree S/977/10 30 AMCH 21723 Uni Mass per vagina UV Prolapse Bulky Single,intramural,Whorl pattern Leiomyoma with myxoid change197 Seetabai S/985/10 22 AMCH 197 Uni Menorrhagia Fibroid uterus Bulky Coarse trabecular Adenomyosis198 Shashikala S/989/10 55 DHB 12167 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis199 Savitri S/990/10 41 AMCH 12676 Multi Mass per vagina UV Prolapse Slight Bulky Unremarkable Leiomyoma with myxoid change200 Parvatri S/996/10 32 AMCH 266 Multi Menorrhagia DUB Slight Bulky Multiple,intramural,Whorl pattern Cellular leiomyoma with hyaline change201 Goddamma S/1001/10 45 DHB 322 Multi Mass per vagina UV Prolapse Normal Coarse trabecular Adenomyosis202 Gangubai S/1002/10 35 AMCH 2778 Uni Mass per abdomen Fibroid uterus Slight Bulky Unremarkable Leiomyoma with myxoid change203 Mahadevi S/1003/10 38 AMCH 5167 Multi Dysmenorrhea DUB Normal Single,intramural,Whorl pattern Cellular Leiomyoma204 Radhabai S/1008/10 50 AMCH 8447 Multi Dysmenorrhea DUB Slight Bulky Unremarkable Cellular Leiomyoma205 Revakka S/1013/10 35 AMCH 5307 Uni Menorrhagia DUB Normal Coarse trabecular Leiomyoma with myxoid change206 Sanjana S/1015/10 40 AMCH 40169 Uni Menorrhagia PID Slight Bulky Coarse trabecular and Whorl pattern Leiomyoma with adenomyosis207 Saleema S/1035/10 35 AMCH 9682 Uni Menorrhagia UV Prolapse Normal Unremarkable Cellular Leiomyoma208 Mudukibai S/1043/10 45 AMCH 9798 Multi Menorrhagia DUB Normal Unremarkable Epitheloid leiomyoma209 Rahabai S/1048/10 35 AMCH 6637 Uni Mass per vagina UV Prolapse Slight Bulky Multiple,intramural,Whorl pattern Cellular Leiomyoma210 Kasturibai S/1054/10 35 DHB 6774 Multi Menorrhagia DUB Bulky Unremarkable Cellular Leiomyoma211 Kamala S/1057/10 35 DHB 6468 Uni Mass per vagina UV Prolapse Normal Single,submucosal,Whorl pattern Leiomyoma with adenomyosis

212 Shaila S/1061/10 47 DHB 6493 Multi Menorrhagia DUB Normal Coarse trabecular Adenomyosis213 Hanmavva S/1065/10 35 DHB 7416 Uni Dysmenorrohea DUB Normal Unremarkable Cellular Leiomyoma with cystic change214 Yamunavva S/1069/10 30 DHB 7351 Uni Menorrhagia Fibroid uterus Normal Unremarkable Cellular leiomyoma with hyaline change215 Rasumibai S/1077/10 35 DHB 7381 Uni Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Leiomyoma with schwannoma like change216 Anandabai S/1084/10 35 AMCH 7377 Uni Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis217 Chandibai S/1087/10 40 DHB 12977 Multi Mass per vagina UV Prolapse Normal Unremarkable Leiomyoma with adenomyosis218 Sheefa S/1089/10 55 AMCH 7863 Multi Mass per vagina UV Prolapse Bulky Coarse trabecular Mitotically active leiomyoma219 Kavita S/1093/10 24 DHB 7833 Nulli Mass in abdomen Fibroid uterus Bulky Coarse trabecular Adenomyosis220 Hameeda S/1095/10 26 DHB 13990 Uni Dysmenorrhea DUB Normal Single,intramural,Whorl pattern Leiomyoma with myxoid change221 Nagamma S/1097/10 40 DHB 8069 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Cellular Leiomyoma222 Mallava S/1099/10 45 DHB 7900 Multi Mass per abdomen Fibroid uterus Slight Bulky Coarse trabecular Adenomyosis223 Rahila S/1100/10 35 AMCH 12114 Multi Mass per vagina UV Prolapse Slight Bulky Single,subserosal,Whorl pattern Leiomyoma with adenomyosis224 Kasturibai S/1112/10 35 AMCH 6637 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Leiomyoma with myxoid change225 Varmala S/1113/10 35 DHB 6774 Multi Menorrhagia DUB Bulky Coarse trabecular Adenomyosis226 Saraswati S/1123/10 37 DHB 6678 Multi Menorrhagia DUB Bulky Coarse trabecular Epitheloid leiomyoma227 Kamala S/1131/10 35 DHB 6693 Uni Dysmenorrhea DUB Slight Bulky Single,submucosal,Whorl pattern Leiomyoma with adenomyosis228 Manjula S/1139/10 46 AMCH 1530 Multi Mass per abdomen Fibroid uterus Bulky Coarse trabecular Cellular leiomyoma with hyaline change229 Asha S/1142/10 52 AMCH 1260 Multi Menorrhagia DUB Bulky Coarse trabecular Adenomyosis230 Sasamma S/1158/10 40 AMCH 1140 Multi Polymenorrhagia DUB Slight Bulky Coarse trabecular Adenomyosis231 Renuka S/1161/10 30 DHB 1797 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Symplastic leiomyoma 232MumtazbegaumS/1163/10 30 DHB 4074 Uni Polymenorrhagia DUB Slight Bulky Unremarkable Monckebergs sclerosis in leiomyoma233 Shabnam S/1170/10 40 AMCH 2247 Multi Menorrhagia DUB Slight Bulky Unremarkable Cellular Leiomyoma234 Heena S/1172/10 33 AMCH 3342 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Adenomyosis235 Shantabai S/1178/10 50 AMCH 2247 Multi Dysmenorrhea DUB Slight Bulky Coarse trabecular Cellular Leiomyoma with cystic change236 Seemabai S/1186/10 56 AMCH 2576 Multi Postmeno bleed Fibroid uterus Normal Unremarkable Epitheloid leiomyoma237 Zubeda S/1188/10 46 AMCH 26982 Multi Menorrhagia Fibroid uterus Slight Bulky Single,subserosal,Whorl pattern Leiomyoma with adenomyosis238 Jamuna S/1193/10 35 DHB 7351 Multi Mass per abdomen Fibroid uterus Bulky Unremarkable Leiomyoma with myxoid change239 Ratnamma S/1198/10 35 DHB 7381 Uni Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Cellular Leiomyoma with mucoid change240 Ameena S/1203/10 40 DHB 7377 Multi Menorrhagia Fibroid uterus Bulky Coarse trabecular Leiomyoma with myxoid change241 Shantabai S/1210/10 55 AMCH 12977 Uni Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Adenomyosis242 Chandibai S/1214/10 24 DHB 7863 Uni Mass per abdomen Fibroid uterus Bulky Coarse trabecular Cellular leiomyoma with hyaline change243 Kavita S/1222/10 26 DHB 7833 Uni Mass per vagina UV Prolapse Normal Coarse trabecular Adenomyosis244 Hemmavva S/1223/10 40 AMCH 13990 Multi Menorrhagia DUB Slight Bulky Single,submucosal,Whorl pattern Leiomyoma with adenomyosis245 Neelamma S/1231/10 45 DHB 8069 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Leiomyoma with myxoid change246 Zameera S/1236/10 35 AMCH 7900 Multi Dysmenorrohea DUB Slight Bulky Unremarkable Monckebergs sclerosis in leiomyoma247 Rukasana S/1239/10 33 AMCH 14757 Multi Mass per abdomen Fibroid uterus Normal Coarse trabecular Mitotically active leiomyoma

248 Parveen S/1247/10 36 AMCH 8501 Multi Menorrhagia DUB Atropied Single,intramural,Whorl pattern Epitheloid leiomyoma249 Kamalakshi S/1256/10 27 AMCH 837 Uni Dysmenorrhea DUB Atropied Unremarkable Mitotically active leiomyoma250 Sharada S/1267/10 30 DHB 14761 Uni Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Cellular Leiomyoma251 Ansuya S/1277/10 30 AMCH 15338 Uni Menorrhagia DUB Atropied Unremarkable Cellular Leiomyoma252 Keshubai S/1281/10 45 AMCH 8368 Multi Mass per abdomen Fibroid uterus Slight Bulky Single,intramural,Whorl pattern Mitotically active leiomyoma253 Afifa S/1287/10 28 AMCH 8799 Uni Menorrhagia DUB Slight Bulky Single,submucosal,Whorl pattern Leiomyoma with adenomyosis254 Gouravva S/1289/10 45 DHB 8995 Multi Mass per abdomen Fibroid uterus Normal Unremarkable Cellular Leiomyoma255 Raziya S/1298/10 40 AMCH 16486 Multi Dysmenorrhea DUB Normal Single,intramural,Whorl pattern Leiomyoma with schwannoma like change256 Rekha S/1302/10 34 DHB 15712 Multi Mass per abdomen Fibroid uterus Normal Coarse trabecular Mitotically active leiomyoma257 Shivaganga S/1311/10 52 AMCH 9479 Multi Menorrhagia Fibroid uterus Slight Bulky Single,intramural,Whorl pattern Cellular Leiomyoma258 Mahadevi S/1313/10 48 DHB 16778 Multi Dysmenorrhea DUB Normal Coarse trabecular Mitotically active leiomyoma 259 Farheen S/1323/10 30 DHB 17654 Uni Menorrhagia DUB Slight Bulky Single,submucosal,Whorl pattern Cellular leiomyoma with hyaline change260 Rathna S/1334/10 22 DHB 9733 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Cellular Leiomyoma261 Jayashree S/1337/10 30 AMCH 21723 Uni Menorrhagia DUB Normal Single,intramural,Whorl pattern Epitheloid leiomyoma262 Sheerin S/1345/10 22 AMCH 197 Uni Menorrhagia UV Prolapse Normal Coarse trabecular Cellular leiomyoma with hyaline change263 Shashikala S/1359/10 55 DHB 12167 Multi Menorrhagia DUB Slight Bulky Single,submucosal,Whorl pattern Leiomyoma with schwannoma like change264 Girija S/1363/10 41 AMCH 635 Multi Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Mitotically active leiomyoma with necrosis265 Vani S/1373/10 32 AMCH 266 Multi Menorrhagia DUB Slight Bulky Unremarkable Cellular Leiomyoma with mucoid change266 Erravva S/1379/10 45 DHB 322 Multi Menorrhagia DUB Normal Single,submucosal,Whorl pattern Leiomyoma with schwannoma like change267 Nalini S/1386/10 35 AMCH 2778 Uni Mass per abdomen Fibroid uterus Slight Bulky Unremarkable Cellular Leiomyoma with fattychange268 Afsha S/1393/10 38 AMCH 5167 Multi Mass per vagina UV Prolapse Normal Coarse trabecular Cellular leiomyoma with hyaline change269 Zara S/1397/10 50 AMCH 8447 Multi Menorrhagia DUB Slight Bulky Single,submucosal,Whorl pattern Leiomyoma with adenomyosis270 Noorjaan S/1413/10 35 AMCH 5307 Uni Mass per vagina UV Prolapse Normal Single,submucosal,Whorl pattern Epitheloid leiomyoma271 Farha S/1415/10 40 AMCH 40169 Uni Menorrhagia DUB Slight Bulky Coarse trabecular Leiomyoma with schwannoma like change272 Saleema S/1435/10 35 AMCH 9682 Uni Menorrhagia UV Prolapse Atropied Unremarkable Cellular leiomyoma with hyaline change273 Meenakshi S/1443/10 45 AMCH 9798 Multi Menorrhagia DUB Atropied Single,submucosal,Whorl pattern Leiomyoma with schwannoma like change274 Gurubai S/1465/10 35 AMCH 6637 Uni Mass per vagina UV Prolapse Slight Bulky Coarse trabecular Epitheloid leiomyoma 275 Fauzia S/1467/10 35 DHB 6774 Multi Menorrhagia UV Prolapse Normal Coarse trabecular Cellular Leiomyoma with necrosis276 Parveen S/1471/10 35 DHB 6468 Uni Dysmenorrhea DUB Normal Single,submucosal,Whorl pattern Leiomyoma with adenomyosis