580 LETTERS TO THE EDITOR

© 2008 The AuthorsJEADV 2009, 23, 570–620 Journal compilation © 2008 European Academy of Dermatology and Venereology

knee biarthritis especially degenerative disorders, inflammatorydiseases and infectious and crystal-related arthritis. Palmar keratosisas well as biarthritis were then concluded to be paraneoplastic.Patient underwent a lobotomy followed by a systemic chemotherapy.After a 1-year follow up period, there was a partial improvementof the knee arthritis and of the palmar keratosis, supporting theparaneoplastic nature of these two manifestations.

The term ‘tripe palms’, also known as acanthosis palmaris,pachydermatoglyphy and palmar hyperkeratosis, was initiallydescribed by Clarke in 1977.1 To the best of our knowledge,hundred cases of this rare paraneoplastic dermatosis have beendescribed.2 Cutaneous changes are more prominent over pressureareas, like thenar, hypothenar eminences and the fingertips.Recognition of this sign is crucial as it usually points to underlyingmalignancy. At least 90% of cases occur in patients with aninternal malignancy, most commonly of the gastrointestinal tractor lung (50%).3,4 TP is often associated with other paraneoplasticcutaneous syndromes especially acanthosis nigricans (72%) andsign of leser-trélat (10%).5 In our case, the patient has TP associatedwith a paraneoplastic oligoarthritis. Only one patient with thisassociation has been previously described but he has polyarthritis.4

Paraneoplastic arthritis is rarely described and is more frequentlyassociated with solid cancers especially adenocarcinoma of thelung and more rarely with haematological malignancies.6 Parane-oplastic knee monoarthritis is only recently described by Cantiniet al. In this series counting 296 isolated asymmetric non-erosiveknee monoarthritis, paraneoplastic knee monoarthritis wasobserved in only 1.7% of patients. It occurred at an early phase ofnon-SCLC, thus allowing the surgical resection of the tumour.7

When it is isolated, pachydermatoglyphy is generally associatedwith pulmonary carcinoma.8 TP as well as arthritis follow aparallel course with the underlying malignancy, usually improvingafter treatment of the neoplasia. Their persistence could reflecttreatment failure.5

Patients presenting with TP and/or mono/oligo/polyarthritis,especially heavy smokers, should be suspected to harbour anoccult malignancy, or have persistence of a known malignancy,until proven otherwise.

A Khaled,†* M Ben Abdallah,† R Tekaya,‡ M Kharfi,†

C Belhadj Yahia,‡ R Zouari,‡ MR Kamoun†

†Charles Nicolle Hospital – Dermatology, ‡Charles Nicolle Hospital-Rheumatology, Boulevard 9 Avril 1006 Tunis, Tunisia

*Correspondence: A Khaled. E-mail: aida.khaled@rns.tn

References1 Koulaouzidis A, Leiper K. Tripe palms or acanthosis palmaris. Intern Med J

2007; 37: 502.2 Cohen PR, Grossman ME, Almeida L, Kurzrock R. Tripe palms and

malignancy. J Clin Oncol 1989; 7: 669–678.3 Patel A, Teixeira F. Palmoplantar keratoderma (‘tripe palms’) associated with

primary pulmonary adenocarcinoma. Thorax 2005; 60: 976.4 Gisserot I, J.Guigay I. Des paumes en forme de tripes. Rev Med Interne 1997;

18: 489–490.

5 Pentenero M. DDS. Oral acanthosis nigricans, tripe palms and sign of leser-trélat in a patient with gastric adenocarcinoma. Int J Dermatol 2004; 43: 530–532.

6 Morel J, Deschamps V, Toussirot E et al. Characteristics and survival of 26 patients with paraneoplastic arthritis. Ann Rheum Dis 2008; 67: 244–247. Epub 2007 Jun 29.

7 Cantini F, Niccoli L. Isolated knee monoarthritis heralding resectable non-smallcell lung cancer. A paraneoplastic syndrome not previously described. Ann Rheum Dis 2007; 66: 1672–1674.

8 Devaux B, Rosenstingl S. Pachydermatoglyphie ou ‘tripe palms syndrome’ et adénocarcinome bronchique. Rev Med Interne 2006; 27: S336–S418.

DOI: 10.1111/j.1468-3083.2008.02962.xXXXOriginal ArticlesLETTERS TO THE EDITORLETTERS TO THE EDITORLETTERS TO THE EDITOR

Frontal fibrosing alopecia: treatment with oral dutasteride and topical pimecrolimus

EditorFrontal fibrosing alopecia (FFA) is a rather uncommon form ofcicatricial alopecia originally described by Kossard in 1994.1 Itis almost exclusively seen in postmenopausal women.1–3 It ischaracterized by a slowly progressive recession of the fronto-temporal hairline and, less often, loss of the eyebrows and alopeciaof the axillae, the pubic area or the limbs.2 Lichen planus andandrogenetic alopecia are the most commonly associated conditions.4

In most cases, the disease tends to spontaneous stabilization.The aetiopathogenesis is largely unknown. It has been speculated

that targeted follicles might express specific antigens that inducea T-lymphocyte–mediated reaction leading to follicular destruction.5,6

In addition, the localization at the frontal hairline, the predomi-nance of postmenopausal women and the clinical improvementobtained with antiandrogens suggest that androgens may also play animportant role.2,7,8 Even the true nature of FFA is questioned. It is notclear if it represents a variant of lichen planopilaris with selectivetopography,3,7–9 or a distinct type of lymphocytic cicatricial alopecia.6,9

A 55-year-old woman presented with an asymptomatic recessionof the fronto-temporal hairline and marked thinning of theeyebrows (Fig. 1a,b) of 1-year duration. She had also partial loss ofthe axillary hair, dating back 10 years ago. There were no otherskin, mucosal, or nail abnormalities. She was on iatrogenicmenopause for 15 years due to hysterectomy with ovarectomy forthe treatment of early-stage cervical cancer. Her personal, family,and drug history was otherwise unremarkable. The patient hadbeen treated with topical corticosteroids without success.

Histologic examination revealed a perifollicular and perivascularlymphocytic inflammatory infiltrate, associated with perifollicularfibrosis. Laboratory investigation including complete blood cellcount, thyroid function tests, antinuclear antibodies, and sex hor-mone levels were within normal limits. Based on clinical andhistological grounds, a diagnosis of FFA was made.

LETTERS TO THE EDITOR 581

© 2008 The AuthorsJEADV 2009, 23, 570–620 Journal compilation © 2008 European Academy of Dermatology and Venereology

After obtaining her informed consent, we started treatmentwith oral dutasteride, 0.5 mg daily for 6 months, and pimecrolimus1% cream, twice daily for 3 months. A significant regrowth wasobserved in the eyebrows and the axillae and a moderate improvementin the scalp (Fig. 2). Regrowth was evident even from the one-month follow up visit. On the 4-month visit, loss of the medialpart of the eyebrows was noted. The patient was instructed toreapply pimecrolimus 1% for 3 more months. After 1 month, theeyebrows were restored. No side effects were reported during thetreatment period, except for constipation.

No recurrences have been noted 6 months since the completionof treatment.

Treatment of FFA is challenging. Corticosteroids are thefirst-line therapy, especially in the early inflammatory stage,2 butrelapse is the rule on their discontinuation. Intralesional triam-cinolone acetonide provided a response rate of 40%, but it mayworsen fibrosis and atrophy of the advanced stages.8 Antimalarials

have been tried with inconsistent results.2,3 Oral finasteride(2.5 mg/day) combined with 2% minoxidil halted the progressionof FFA in four of eight patients, after 12–18 months.7

Dutasteride is a 5α-reductase inhibitor that blocks both type Iand II isoenzymes. It is about three times as potent as finasterideat inhibiting type II 5α-reductase and more than a 100 times aspotent at inhibiting type I enzyme. Dutasteride can decreaseserum dihydrotestosterone (DHT) by more than 90%.10

In the literature, there is no previous experience with dutasteridein FFA. Georgala et al. (data under review) treated with oraldutasteride (0.5 mg daily for 12 months) 11 postmenopausalwomen with FFA. Six (54.5%) of the patients showed a completearrest of the disease. Improvement began after 6 months of treat-ment. Data regarding the use of calcineurin antagonists in FFA arelacking.

Our rational to combine dutasteride with pimecrolimus wasbased on the current pathogenetic theories for FFA that involveboth a T-cell–mediated inflammatory reaction and androgens.Dutasteride by achieving greater suppression of DHT can perhapssucceed better results than finasteride. The addition of pime-crolimus improved and accelerated the therapeutic outcome.

In conclusion, our case suggests that the combination of oraldutasteride with a topical calcineurin inhibitor may represent asafe and effective therapeutic alternative for FFA.

A Katoulis,* S Georgala, E Bozi, E Papadavid,D Kalogeromitros, N Stavrianeas

2nd Department of Dermatology and Venereology, National andKapodistrion University of Athens, ‘Attikon’ University Hospital, 1 Rimini Str

Athens 12462, Greece*Correspondence: A Katoulis. E-mail: alexanderkatoulis@yahoo.co.uk

Figure 1 Female patient with frontal hair line recession (a) and loss of the medial part of the eyebrows (b).

Figure 2 After treatment with oral dutasteride and topical pimecrolimus, significant regrowth is evident in the fronto-parietal scalp and the eyebrows.

582 LETTERS TO THE EDITOR

© 2008 The AuthorsJEADV 2009, 23, 570–620 Journal compilation © 2008 European Academy of Dermatology and Venereology

References1 Kossard S. Postmenopausal frontal fibrosing alopecia. Scarring alopecia in a

pattern distribution. Arch Dermatol 1994; 130: 770–774.2 Moreno-Ramirez D, Ferrandiz L, Camacho FM. Diagnostic and therapeutic

assessment of frontal fibrosing alopecia. Actas Dermosifiliogr 2007; 98: 594–602.

3 Kossard S, Lee MS, Wilkinson B. Postmenopausal frontal fibrosing alopecia: a frontal variant of lichen planopilaris. J Am Acad Dermatol 1997; 36: 59–66.

4 Faulkner CF, Wilson NJ, Jones SK. Frontal fibrosing alopecia associated with cutaneous lichen planus in a premenopausal woman. Australas J Dermatol 2002; 43: 65–67.

5 Vaisse V, Matard B, Assouly P, Jouannique C, Reygagne P. Postmenopausal frontal fibrosing alopecia: 20 cases. Ann Dermatol Venereol 2003; 130: 607–610.

6 Zinkernagel MS, Trueb RM. Fibrosing alopecia in a pattern distribution. Arch Dermatol 2000; 136: 205–211.

7 Tosti A, Piraccini BM, Iorizzo M, Mischiali C. Frontal fibrosing alopecia in postmenopausal women. J Am Acad Dermatol 2005; 52: 55–60.

8 Moreno-Ramirez D, Camacho Martinez F. Frontal fibrosing alopecia: a survey in 16 patients. J Eur Acad Dermatol Venereol 2005; 19: 700–705.

9 Poblet E, Jimenez F, Pascual A, Pique E. Frontal fibrosing alopecia versus lichen planopilaris: a clinicopathological study. Int J Dermatol 2006; 45: 375–380.

10 Olsen EA, Hordinsky M, Whiting D et al. Dutasteride Alopecia Research Team. The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. J Am Acad Dermatol 2006; 55: 1014–1023.

DOI: 10.1111/j.1468-3083.2008.02963.xXXXOriginal ArticlesLETTERS TO THE EDITORLETTERS TO THE EDITORLETTERS TO THE EDITOR

Acquired leucoderma after henna tattoo in an Indian girl

EditorHenna is a popular vegetable dye which is used for decoratingbody and is obtained from the dried leaves of Lawsonia inermis.The active dye agent of henna is 2-hydroxy-1,4-naphthoquinone(Lawsone). Reports of contact allergic reactions1 and immediatehypesenstivity2 to henna are rare events as traditionally henna isused as a pure dye prepared from the stems and the leaves of theplant, with addition of coffee or tea for enhancing the colour ofhenna. The growing practice of mixing up of various chemicaldyes such as paraphenylendiamine (PPD; a known chemical sensitizer)for enhancing the properties of henna has resulted in an increasein the adverse allergic reactions caused by these tattoos.3–5

An 8-year-old Indian girl sought consultation for an area ofdepigmentation over the site of henna tattoo which was applied3 days ago on the dorsum of her right hand. The tattoo had to beremoved partially due to unbearable itching at the site of contactand a depigmented patch was noted by the mother. There was nofamily history of vitiligo, any prior contact with a similar tattoo inthe past or exposure to other dye. A well-defined patch ofdepigmentation was noticed on the dorsum of right hand, exactly

confirming to the lines of the Arabic henna tattoo (Fig. 1). Therewas no erythema or vesiculation. Leucoderma caused by the PPDin the henna paste was considered as the most probable cause.Mometasone furoate cream was given for itching. Patch testing toPPD or pure henna could not be performed due to its non-availability. Skin biopsy was not performed considering thecosmetic importance of the area. The child was lost to follow-up;hence, the course of depigmentation could not be ascertained.Allergic contact dermatitis to black henna has been reported in childrenrarely. Valsecchi et al. reported post-inflammatory hypopigmen-tation in the same area of a pre-existent acute contact eczema fromhenna tattooing.6 They later described two more patients: a 7-year-old boy and a 14-year-old girl who developed a severe,moderately painful and pruritic reaction to a paint on henna tattooexactly at the site of the tattoo. They tested positive for PPD on apatch test.7 Similar reaction to henna tattoo was also reported inan 11-year-old Austrian girl.8 The onset of reaction in 3–4 daysafter the application of tattoo in our case suggests an allergic reactionto the black henna (Arabic henna). However, the same could notbe confirmed in our case without the patch test. Contact leucodermahas been described following use of agents such as monobenzylether of hydroquinone, phenol and catechol derivatives. The shorttime interval suggests a direct toxic effect of PPD or some otherchemical ingredient of the henna paste in these tattoos. The contactleucoderma has been found to persist up to 2 years.7 Long-termfollow-up is required to assess repigmentation in these cases.Histopathological and electronmicroscopic studies can provideclues to the pathophysiological mechanisms involved.

V Mendiratta*Lady Hardinge Medical College and Assoc. Hospitals, New Delhi, India

*Correspondence: V Mendiratta. E-mail: vibhumendiratta@rediffmail.com

Figure 1 Multiple, depigmented macules under the henna tattoo over the dorsum of left hand.

© 2008 The AuthorJEADV 2009, 23, 570–620 Journal compilation © 2008 European Academy of Dermatology and Venereology