Fulminant Hepatic Failure Caused by Adenovirus Infection ...

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□ CASE REPORT □

Fulminant Hepatic Failure Caused by Adenovirus InfectionMimicking Peliosis Hepatitis on Abdominal Computed

Tomography Images after Allogeneic HematopoieticStem Cell Transplantation

Kiriko Terasako 1, Kumi Oshima 1, Hidenori Wada 1, Yuko Ishihara 1, Koji Kawamura 1,

Kana Sakamoto 1, Masahiro Ashizawa 1, Miki Sato 1, Tomohito Machishima 1,

Hideki Nakasone 1, Shun-ichi Kimura 1, Misato Kikuchi 1, Shinya Okuda 1, Shinichi Kako 1,

Rie Yamazaki 1, Kengo Takeuchi 2, Junji Nishida 1, Shigeki Yamada 3,

Osamu Tanaka 4 and Yoshinobu Kanda 1

Abstract

Disseminated adenovirus disease after allogeneic hematopoietic stem cell transplantation (HSCT) is lethal

in most cases, especially when it develops as fulminant hepatic failure. We encountered a patient who devel-

oped fulminant hepatic failure caused by adenovirus infection. She did not show manifestations of graft-

versus-host disease and the results of serum tests for viral infection were all negative. Abdominal computed

tomography (CT) findings were consistent with peliosis hepatitis. She died of fulminant hepatic failure, how-

ever, and pathological examinations of the liver specimen obtained after her death revealed adenovirus infec-

tion. In this report, we review the clinical characteristics and imaging findings of fulminant hepatic failure

caused by adenovirus infection.

Key words: fulminant hepatic failure, adenovirus, hematopoietic stem cell transplantation, peliosis hepatitis

(Intern Med 51: 405-411, 2012)(DOI: 10.2169/internalmedicine.51.6432)

Introduction

Adenovirus infection after allogeneic hematopoietic stem

cell transplantation (HSCT) is associated with high

transplant-related mortality. Adenovirus infection is not in-

frequently observed after allogeneic HSCT. In 1980’s, ade-

novirus was reported to be isolated from approximately 5%

of patients undergoing bone marrow transplantation (1). Re-

cently, weekly monitoring by enzyme-linked immunoassay

(ELISA) for adenovirus antigen and polymerase chain reac-

tion (PCR) for adenovirus DNA revealed that the incidence

of adenovirus infection was 29% (2). The results of nested

PCR for adenovirus DNA using samples from peripheral

blood (PB), stool, urine, and throat were positive in 27% of

patients after allogeneic HSCT (3). Another retrospective

study reported that adenovirus infection was detected in

11.5% of allogeneic HSCT recipients (4). The risk factors

for the development of adenovirus infection were graft-

versus-host disease (GVHD) and the presence of adenovirus

antibody in the donor (1, 2).

The clinical course of adenovirus infection ranges from

subclinical reactivation to fatal disseminated adenovirus dis-

ease. Shields et al (1) isolated adenovirus from 51 of 1,051

patients undergoing marrow transplantation and invasive in-

fection was histologically confirmed in 10 of the 51 pa-

tients, including those with hepatitis. We encountered a pa-

tient who developed fulminant hepatic failure caused by

１Division of Hematology, Saitama Medical Center, Jichi Medical University, Japan, ２Department of Pathology, The Cancer Institute Hospital of

Japanese Foundation for Cancer Research, Japan, ３Department of Pathology, Saitama Medical Center, Jichi Medical University, Japan and ４De-

partment of Radiology, Saitama Medical Center, Jichi Medical University, Japan

Received for publication August 22, 2011; Accepted for publication November 7, 2011

Correspondence to Dr. Yoshinobu Kanda, [email protected]

Intern Med 51: 405-411, 2012 DOI: 10.2169/internalmedicine.51.6432

406

adenovirus infection after allogeneic HSCT. Abdominal

computed tomography (CT) findings of this patient were un-

usual and resembled those of peliosis hepatitis. We could

not diagnose it as adenovirus hepatitis before her death.

Herein, we report the patient characteristics and review the

clinical and imaging findings of fulminant adenovirus he-

patic failure.

Case Report

Clinical course

A 52-year-old female developed aplastic anemia. Al-

though she received cyclosporine (CSA) and methenolone

acetate for 3 years, her pancytopenia gradually progressed.

Then, she received immunosuppressive treatment with CSA

and anti-thymocyte globulin (ATG), once with horse ATG

(Lymphoglobulin, Institut Pasteur Merieux; Lyon, France)

and thereafter with rabbit ATG (Zetbulin, ATG-F; Fresenius,

Munich, Germany); however, these treatments were ineffec-

tive. Her white blood cell count decreased to 1.29×109/L

with 48% neutrophils and she became transfusion dependent

for red blood cells and platelets. Therefore, she decided to

undergo allogeneic HSCT when she was 58 years old.

The conditioning regimen consisted of rabbit ATG (Thy-

moglobulin, ATG-G, Genzyme; Cambridge, MA, USA) at

2.5 mg/kg/day from day -5 to day -2, fludarabine at 30 mg/

m2/day from day -5 to day -2, cyclophosphamide at 25 mg/

kg/day from day -5 to day -2, and total body irradiation at 2

Gy on day -1 (5). She received allogeneic bone marrow

transplantation from an HLA-matched unrelated male donor.

Bone marrow graft including 4.84×108 all nucleated cells

per recipient body weight (kg) was infused on day 0. Pro-

phylaxis against GVHD included CSA at 3 mg/kg/day in

combination with methotrexate at 10 mg/m2 on day 1 and 7

mg/m2 on days 3, 6, and 11. The dose of CSA was adjusted

to maintain the blood level at 500 ng/mL (6). Prophylaxis

against bacterial, fungal and Pneumocystis jiroveci infection

consisted of levofloxacin, fluconazole, and pentamidine in-

halation. Prophylaxis against herpes simplex virus and

varicella zoster virus infection was performed with acyclovir

at 500 mg/day intravenously or at 1,000 mg/day orally from

day -7 to 35, followed by long-term low-dose (200 mg/day)

oral administration (7, 8). G-CSF (filgrastim) at 300 μg/

body/day was intravenously administered until neutrophil re-

covery was achieved. Engraftment, defined as a neutrophil

count of more than 500/mm3 for 3 consecutive days, was

achieved on day 18. Bone marrow aspiration on day 29

showed complete donor-type chimerism by sex-chromosome

fluorescent in situ hybridization (FISH). Grade II acute

GVHD limited to the skin was observed on day 19, and it

was controlled with topical steroid alone. Cytomegalovirus

(CMV) antigenemia assay using C10/C11 antibody became

positive on day 28 after HSCT and preemptive treatment

with ganciclovir (5-10 mg/kg/day) was initiated (9). High-

grade CMV antigenemia of more than 50 positive cells per

2 slides persisted until day 70, but no CMV disease was de-

tected.

On day 79, she complained of fever and fatigue. Despite

antibacterial treatment with moxifloxacin, high fever per-

sisted and she presented with sore throat. In addition, CMV

reactivation was detected again and preemptive treatment

with GCV was resumed. No other abnormalities were found

in physical examination except for swelling of pharynx.

Complete blood count revealed a white blood count (WBC)

of 1.56×103/μL, hemoglobin level of 8.7 g/dL, and platelet

count of 39×103/μL. Flow cytometric analysis of peripheral

blood showed a persistently low number of CD3+CD4+ cells

and CD3+CD8+ cells (2 and 37/μL, respectively) on day 91.

All microbiological studies were negative including culture

of blood, sputum, urine, stool, and spinal fluid. CT of the

neck and chest also revealed no significant findings. How-

ever, despite the use of various antibacterial and antifungal

agents in addition to GCV, her fever persisted (Fig. 1). Al-

though she had no abdominal symptoms, alanine aminotr-

ansferase (ALT) and aspartate aminotransferase (AST) levels

on day 96 increased to 94 mU/mL and 64 mU/mL, respec-

tively. We performed abdominal ultrasonography (US),

which showed a hypoechoic lesion in the liver. At that time,

we suspected a fungal or protozonal infection, and we ad-

ministered liposomal amphotericin B and metronidazole. We

also performed immediate abdominal contrast-enhanced CT,

which revealed multiple oval-shaped low-density lesions

from a few millimeters to about 3 cm in diameter. They

showed slow but homogeneously centripetal enhancement,

similar to that observed in hemangioma (Fig. 2). Peliosis

hepatitis was strongly suspected based on the findings of the

CT scan, but it was not compatible with the clinical course.

Sinusoidal obstruction syndrome (SOS) was unlikely, as she

did not have any other symptoms of SOS including body

weight gain or right upper quadrant pain. On day 98, the se-

rum ALT and AST level increased to 178 U/L and 121 U/L,

respectively (Fig. 1). We analyzed various serum markers

for viral infection. She was positive for HBsAb and negative

for HBsAg, HBV DNA, HCV-Ab, and HIV. Her serum IgG

titers for HSV and VZV were positive and the correspond-

ing serum IgM titers were negative. Further, CMV antigene-

mia had decreased with GCV therapy. The PCR for ade-

novirus DNA using whole blood sample was positive, while

adenovirus was not detected in the nasopharyngeal swab by

direct immunofluorescence. PCR for EB virus DNA using

whole blood sample was also positive (1.8×103 copies/106

cells). Thereafter, the patient’s liver function rapidly pro-

gressed to fulminant hepatic failure with a peak in AST and

ALT levels of 6,800 U/L and 2,400 U/L, respectively, on

day 106. She developed grade II hepatic encephalopathy on

day 108. In addition, the prothrombin time was elongated to

43.4% on day 108, 33.3% on day 109, and 26.9% on day

110. Although we started plasmapheresis, she died of fulmi-

nant hepatic failure on day 109. All blood, stool, and urine

cultures were persistently negative for bacteria and fungi be-

fore her death. Chronic GVHD was never observed through-


407

Figure　1.　Clinical course of the patient with fulminant hepatic failure after allogeneic hematopoi-etic stem cell transplantation. ALT: alanine aminotransferase, ALP: alkaline phosphatase, T.Bil: total bilirubin, CFPM: cefepime, MEPM: meropenem, TEIC: teicoplanin, ITCZ: itraconazole, L-AMPH: liposomal amphotericin. MCFG: micafungin, GCV: ganciclovir, PE: plasma exchange, MV: mechanical ventilation.

out the clinical course. Immune recovery, in particular the T

lymphocyte recovery, was delayed and the WBC, lympho-

cyte, CD3+CD4+ T cell, and CD3+CD8+ T cell count was

1,830, 275, 2, 37/μL, respectively, on day 91.

Pathological findings

Pathological examinations using the liver specimen ob-

tained percutaneously under an ultrasound-guided procedure

after her death revealed large, random foci of hepatocytic

necrosis (Fig. 3). The multiple oval-shaped low-density le-

sions detected by CT scan were thought to be hepatic necro-

sis. Although mild inflammation was present, there was no

significant inflammatory response suggesting acute GVHD.

Intranuclear inclusions with characteristic Cowdry bodies

and chromatin margination were found in some hepatocytes.

Immunostaining for adenovirus (MAB805, blend of clones

20/11 and 2/6; CHEMICIN International Inc., Temecula,

CA, USA) showed diffusely positive nuclear staining, while

those for CMV and EB virus were negative.

Discussion

The main causes of liver injury after HSCT vary depend-

ing on the timing after SCT. Sinusoidal obstruction syn-

drome and drug-induced hepatotoxicity are frequently ob-

served in the first few weeks after SCT. Subsequently, acute

GVHD, viral infection, chronic GVHD, and nodular regen-

erative hyperplasia develop (10). Adenovirus is one of the

causes of fulminant hepatic failure after HSCT. Acute or ful-

minant adenovirus hepatic failure is not an uncommon com-

plication after HSCT. As shown in Table 1, however, there

are differences in the timing after SCT, symptoms, and

speed of progression.

Adenoviral disease can be diagnosed by histology, im-

munocytochemistry and culture of biopsied specimen. How-

ever, its diagnosis is hampered by the difficulty to obtain an

appropriate specimen. In particular, liver biopsy is difficult

to perform due to the high risk of bleeding. Therefore, im-

aging studies may be useful if there are some specific find-

ings for adenovirus hepatitis. To date, there have been few

reports on the imaging findings of severe liver injury after

HSCT. SOS after HSCT shows specific Doppler sonography

findings, including reversed or “to and fro” flow in the por-

tal vein and/or a decreased flow in the portal vein (11).

However, no specific findings on imaging studies have been

reported thus far about adenovirus hepatitis after HSCT. As

shown in Table 2, the results of imaging studies of adenovi-

rus hepatitis after HSCT have been described in 3 patients.

One of the 3 patients showed diffuse nonspecific changes by

ultrasound and magnetic resonance scans of the liver (12),


408

Figure　2.　Abdominal CT findings. (A) Arterial phase of abdominal CT with contrast enhance-ment. (B) Portal venous phase of abdominal CT with contrast enhancement. Multiple oval-shaped low-density lesions from a few millimeters to about 3 cm in diameter are observed. These lesions show slow but homogeneous centripetal enhancement.

A B

Figure　3.　Histopathological examinations of the liver specimen. (A) Hematoxylin and Eosin stain-ing (10×0.45), (B) Hematoxylin and Eosin staining (40×0.95) and (C) immunohistochemistry staining for adenovirus proved nuclear staining. (MAB805 40×0.95).

while the other 2 showed no abnormality (13, 14). With re-

gard to solid organ transplantation recipients, Gupta et al.

reported adenoviral hepatitis in a cardiac transplant recipi-

ent (15). Abdominal CT scan showed multiple indeterminate

low-attenuation masses in the liver. Similarly, Saad et al de-

scribed a patient with adenovirus hepatitis after an ortho-

topic liver transplantation (16). CT scans of the liver showed

multiple low-density ill-defined lesions. Among hematologi-

cal disorder patients other than HSCT recipients, the ab-

dominal CT scan of an 84-year-old man with B-cell lym-

phoma who developed adenovirus-induced acute liver failure

showed innumerable small hypoattenuating lesions, which

probably corresponded to the areas of hepatic necrosis ob-

served in autopsy (Table 3) (17). Hough et al reported 3

acute lymphoblastic leukemia patients with hepatomegaly

and abnormal findings by ultrasound scan (18).


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Table　1.　Characteristics and Outcomes of Adult Allogeneic HSCT Patients with Adenovirus Fulminant Hepatic Failure

No. Age Sex Disease Diagnosticapproach

Diagnostic sites Serotype Onset Image Other organ involvement

AcuteGVHD

Treatment Outcome Use of steroid

Ref

1 24 F AML His Liver 1 N.A. Noimage

N.A. + N.A. Dead N.A. [1]

2 22 M CML His Liver 2 Day 136

Noimage

- GradeIII

IVIG Dead + [20]

3 21 M ALL His,Cul Liver , blood N.A. 4months

Noimage

- GradeIII

N.A. Dead N.A. [21]

4 23 N.A. CML Cul Liver 1 Day 112

Noimage

- - Cidofovir, IVIG Alive - [22]

5 39 M ALL Cul Sigmoid N.A. Day 68 Noimage

Colitis - Cidofovir, IVIG Dead - [22]

6 43 M AML Cul Liver, BAL 1 Day 187

Noimage

Pneumonia N.A. Cidofovir, IVIG Alive + [22]

7 73 M AML Cul Sigmoid 1 Day 64 Noimage

Colitis + Cidofovir, IVIG Dead + [22]

8 35 F MDS PCR Blood, BAL 3 and 34

Day 45 Noimage

Nephritis,pneumonia, colitis

- Ganciclovir, IVIG

Alive + [23]

9 22 F N.A. His or Cul Liver, stool, urine N.A. Day 19 Noimage

- - Ribavirin Dead - [24]

10 38 M N.A. His or Cul Liver, stool, throat, sputum

N.A. Day113

Noimage

- GradeIII

No specific treatment

Dead + [24]

11 44 F N.A. His or Cul Liver N.A. Day 17 Noimage

N.A. GradeIV

No specific treatment

Dead + [24]

12 24 F ALL Cul Liver, urine, blood, throat

N.A. N.A. Noimage

- - N.A. Dead N.A. [25]

13 44 M CML Cul,PCR,His

Stool, blood, sputum, liver

2 30weeks

Noimage

- + Ribavirin Dead + [26]

14 39 F HD His Liver 2 Day 233

Reported*1

N.A. N.A. DLI Dead N.A. [12]

15 34 M NHL His Liver 5 Day 58 Reported*2

N.A. Grade I N.A. Dead + [13]

16 43 M N.A. His or Cul Liver, stool, throat 2 Day 202

Noimage

N.A. GradeIII

Ribavirin Dead + [27]

17 22 F N.A. His or Cul Liver, stool, urine 2 Day 19 No image

- - Ribavirin Dead - [27]

18 60 M CLL Cul, PCR Intestine, stool, blood 1 Day 148

Noimage

N.A. N.A. Cidofovir Dead N.A. [28]

19 39 M NHL PCR, His

Liver, blood, duodenum, Colon, stool, multiorgan

2 Day 82 Noimage

N.A. - Ribavirin,cidofovir, IVIG

Dead + [29]

20 51 F ALL PCR, His Blood, liver N.A. Day142

Reported*3

N.A. GradeII

Plasma exchange

Dead + [14]

*1 , *2 , *3 : refer to Table2. AML : acute myelocytic leukemia, ALL : acute lymphocytic leukemia, CML : chronic myelogenous leukemia, MDS : myelodysplastic syndrome, HD : Hodgkin’s disease , NHL : Non Hodgkin’s lymphoma, His : histopathology, Cul : culture, PCR : polymerase chain reaction, BAL : bronchoalveolar lavage, IVIG : intravenous immunoglobulin, DLI : donor lymphocyte infusion, N.A.: not available.

Table　2.　Images of Adult Allogeneic HSCT Patients with Adenovirus Fulminant Hepatic Failure

No. Age Sex Disease Donor Image Ref

14 39 F HD rBMT Ultrasound and magnetic resonance scans of the liver were abnormal with diffuse non-specific changes.

[12]

15 34 M NHL rBMT Ultrasound scan of the liver showed no focal abnormality. [13]20 51 F ALL uBMT Imaging studies of the liver revealed no apparent space occupying lesion. [14]

The current patient also showed multiple hypoattenuating

lesions mimicking peliosis hepatitis on CT scan. Peliosis

hepatitis is a rare condition characterized by multiple small

blood-filled spaces in the liver parenchyma. CT scan shows

oval-shaped lesions that are homogeneously enhanced after

intravenous injection of contrast agents (19). The liver speci-

men obtained after her death revealed that these lesions cor-

respond to areas of hepatic necrosis, as previously pointed

out in some cases.

We conclude that adenoviral hepatitis should be consid-

ered as a possible cause of liver injury in allogeneic HSCT

recipients with multiple low-density lesions of the liver ob-

served in the CT scan, although such findings are not spe-

cific to adenovirus infection. Accumulation of imaging find-

ings of adenovirus hepatitis is necessary to determine the

characteristic and diagnostic imaging findings of acute or


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Table　3.　Characteristics and Outcomes of Hematological Disorder Patients other than SCT Recipients with Images of Adeno-virus Fulminant Hepatic Failure

No. Age Sex Disease Diagnosticapproach

Diagnosticsites Image Treatment Outcome Other organ

involvement Reference

1 84 y M NHL Histopathology Liver CT : Innumerable small hypoattenuating lesions Cidofovir Died of disseminated

adenoviral infection N.A. [17]

2 4 m F ALL Histopathology LiverUST : Hepatomegaly with multiple intrahepatic microabscesses.

IVIGDied of acute subarachnoidhemorrhage

Colitis [18]

3 2 y M ALL Histopathologyand culture

Stool,throat, and vesicularfluid

UST : Gross hepatomegaly with abnormal heterogeneous echotexture,and ascites.

IVIG, cidofovir and G-CSF

Died of hepatic encephalopathy

Colitis,Skinirritation

[18]

PCR Blood

4 21m M ALL Histopathology Stool UST: Hepatomegaly to the level of the umbilicus.

IVIG and cidofovir

Died of hepatic encephalopathy N.A. [18]

PCR Blood

m : months, y : years, NHL : non-Hodgkin lymphoma, ALL : acute lymphoblastic leukemia, IVIG : intravenous immunoglobulin.

fulminant adenovirus hepatic failure.

The authors state that they have no Conflict of Interest (COI).

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