Acta Derm Venereol 2000; 80: 446-458

LETTERS TO THE EDITOR

Zosteriform and Disseminated Lesions in Cutaneous Leiomyoma

Sir, A 40-year-old housewife presented with multiple, erythema- tous, skin-coloured, ® rm, tender, papules and nodules (5 ± 15 mm diameter) in a zosteriform pattern con® ned to the left upper portion of the chest of 15 years duration (Fig. 1). A few similar lesions had appeared on her back within the previous 1.5 years. Pain was episodic and aggravated on exposure to cold. There was no family history of similar lesions. General physical and systemic examinations (including gynecological examinations) were normal. Biopsies from chest and back nodules showed a tumour composed of irregularly arranged interlacing bundles of smooth muscle ® bres with varying amounts of collagen bundles in the dermis (Fig. 2). Masson’s trichrome stain demonstrated the muscle ® bres. These ® ndings con® rmed the clinical diagnosis of piloleiomyoma. The patient was treated with 10 mg nifedipine three times daily Fig. 2. Microphotograph showing a tumour composed of irregu- for 2 months with some relief of pain. The patient was then larly arranged interlacing bundles of smooth muscle ® bres with lost to follow-up. varying amounts of collagen bundles in the dermis (haematoxylin and eosin staining, original magni® cation 610).

DISCUSSION (3). The lesions are often sensitive to touch, cold and emotional stress. Pain usually occurs spontaneously and Cutaneous leiomyomas are benign smooth muscle tumours may be paroxysmal in nature with stabbing, burning or derived from arrector pili muscle, media of blood vessels and pinching qualities (4). The cause of pain is unknown; dartos muscle of the scrotum, vulva or nipples. They are however, Montgomery & Winkelmann (3) postulated that it classi® ed into 3 types according to their site of origin, namely may be due to pressure on the cutaneous nerve. The piloleiomyoma, dartoic leiomyoma and angioleiomyoma (1, zosteriform pattern, with a few discrete nodules, has been 2). Piloleiomyomas are ® rm, painful, intradermal nodules, described in hereditary leiomyoma (5) and in a patient with most commonly seen in early adult life with equal incidences uterine leiomyoma (6). in males and females (1). They are usually multiple, and occur over the face, anterior trunk and the extensor surface of extremities (1, 2). They range in size from a few millimeters to REFERENCES 41 cm and the colour varies from pink to yellow or brown 1. Jolliffe DS. Multiple cutaneous leiomyomata. Clin Exp Dermatol 1978; 3: 89 ± 92. 2. Spencer JM, Amonette RA. Tumour with smooth muscle differentiation. Dermatol Surg 1996; 22: 761 ± 768. 3. Montgomery H, Winkelman RK. Smooth muscle tumours on the skin. Arch Dermatol 1959; 79: 32 ± 40. 4. George S, Pulimod S, Jacob M, Chandi SM. Pain in multiple leiomyomas alleviated by nifedipine. Pain 1997; 73: 101 ± 102. 5. Berendes U, Kuhner A, Schnyder UW. Segmentary and dis- seminated lesions in multiple hereditary cutaneous leiomyoma. Hum Genet 1971; 13: 81 ± 82. 6. Smith CG, Glaser DA, Lernardi C. Zosteriform multiple leiomyomas. J Am Acad Dermatol 2000; 38: 272 ± 273.

Accepted September 27, 2000.

Arun Agarwalla1, Amarnath Thakur2, Mary Jacob1, Arun Joshi1, Vijay Kumar Garg1 and Sudha Agrawal1 Fig. 1. Multiple, erythematous, skin-coloured papules and nodules Departments of 1Dermatology and 2Pathology, B. P. Koirala Institute con® ned to the left upper chest. of Health Sciences, Dharan, Nepal. E-mail: [email protected]

Acta Derm Venereol 80 # 2000 Taylor & Francis. ISSN 0001-5555 Letters to the Editor 447 Pigmentosa Associated with Diabetic Ketoacidosis

Sir, mononuclear in® ltration, including a small number of melanophages, Prurigo pigmentosa, reported mostly in Japan, is a distinct in the dermal papillae and super® cial reticular dermis. These clinical entity which indicates characteristic clinical pictures: histological ® ndings were compatible with prurigo pigmentosa. symmetrically distributed pruritic erythematous papules on the trunk and subsequent reticulate hyperpigmentation. Only 20 cases of non-Japanese patients have been reported (1, 2). DISCUSSION Because several cases were associated with fasting, dieting to Teraki et al. (5) suggested that ketosis may contribute to the lose body weight and diabetes mellitus (DM), ketosis may pathogenesis because ketosis was observed in 8 of 10 cases in contribute to the pathogenesis of prurigo pigmentosa (3 ± 8). their series. The present case was also associated with diabetic We report here a case of prurigo pigmentosa which triggered ketoacidosis, and the disappearance of urinary ketone a diagnosis of associating diabetic ketoacidosis, and review correlated well with the clinical course, namely, improvement the patients associated with DM. of the eruptions. We investigated all case reports of prurigo pigmentosa associated with DM, including the Japanese literature, and CASE REPORT found 18 cases of prurigo pigmentosa associated with DM A 20-year-old Japanese female came to our department in February (Table I). All cases were Japanese (5 ± 19). There were no 1998 with pruritic eruptions on her chest and back region which had reports of any non-Japanese patients associated with DM in appeared 7 days previously. She had lost 5 kg in weight during the the Western literature. These 18 patients ranged in age from past month. Although her past history was unremarkable, her family 12 to 44 years, and the mean age was 22.9 years old. No history revealed that her father had suffered from DM. Physical signi® cant differences between genders were observed in these examination revealed numerous rice-sized red papules distributed in a cases; the female to male ratio was 10:8, while the dermatosis reticulate pattern mainly on the central region of her chest and back. From the characteristic clinical picture, a diagnosis of prurigo was more common in young women. In 8 cases which were pigmentosa was made and general laboratory tests, including treated only with insulin injection, a spontaneous resolution examination for DM, were performed. On the day after her visit, of the eruptions was observed. The relationship between she started to suffer from fever, nausea and appetite loss. At the prurigo pigmentosa and DM was thus supported. Of 14 cases second visit, 4 days after the initial visit, the previous laboratory of DM which were described in detail, 10 cases were insulin- examination revealed a high value of glycohemoglobin (HbAIc dependent DM (IDDM), in spite of a high prevalence of non- 13.8%), urinary glucose (3+ ) and ketone (4+ ). Immediate blood insulin-dependent DM (NIDDM) in the total cases of DM. It and urinary tests at her second visit showed blood glucose at 533 mg/ was con® rmed that prurigo pigmentosa occurred more dl, urinary glucose at 3+ and ketone at 4+ , in addition to the frequently in IDDM, which progresses more easily to ® ndings of hemoconcentration. She was immediately admitted to ketoacidosis, than in NIDDM. We therefore speculate that hospital for the treatment of diabetic ketosis. After administration of continuous drip infusion of insulin, the eruptions gradually reduced in ketosis contributes to the pathogenesis in some cases of accordance with an improvement in her general condition and prurigo pigmentosa. In 7 of 10 patients associated with disappearance of urinary ketone. Seven days after her admission, a unnoticed and untreated DM, the eruptions occurred with biopsy specimen was obtained from the brownish erythema on her pre-existing general symptoms: extreme thirst, polyuria and/or back, which revealed slight basal pigmentation and perivascular general fatigue. Onset of the eruptions was simultaneous with

Table I. Prurigo pigmentosa associated with insulin-dependent (ID) and non-insulin-dependent (NID) diabetes mellitus

Ref. no. Age (years) Gender Type of diabetes General treatment For eruptions

9 21 F ID Insulin Dapson 10 12 M ID Insulin Dapson 10 40 M NID? Unknown Dapson 11 16 F Unknown Unknown Minocycline 12 44 M ID Insulin None 13 14 F ID Insulin None 14 19 F (twin) ID Insulin None 14 19 F (twin) ID Insulin None 15 17 M NID Insulin Topical corticosteroid 5 15 M ID Unknown Unknown 6 16 F ID? Insulin None 7 30 M NID? Low-carbohydrate diet Minocycline 8 32 M NID Glibenclamide Minocycline 16 18 F NID Insulin None 17 18 F ID Insulin None 18 20 F ID Insulin Minocycline 19 41 M NID Insulin Minocycline Present case 20 F ID Insulin None F= female; M= male. Although the clinical course in the case of Ref. 5 is unknown, eruptions in all other cases improved.

Acta Derm Venereol 80 448 Letters to the Editor the symptoms, or appeared within 6 weeks after the 12. Amemori M, Nishigaki I, Ogino K, Yamashita S, Banba M, symptoms. Therefore, attention should be paid to the pre- Kosugi K, et al. A case of prurigo pigmentosa associated with existing general symptoms as listed above, and urinary ketone insulin-dependent diabetes mellitus. J Jpn Diab Soc 1989; 32: should be examined when making a diagnosis of prurigo 547 ± 551 (in Japanese). 13. Moriki T, Wainai H, Takei I, Maruyama H, Kataoka K, Saruta pigmentosa from its characteristic clinical appearance. T, Tajima S. A case of IDDM and prurigo pigmentosa which was improved with insulin treatment. Intern Med 1991; 68: 995 ± 999 REFERENCES (in Japanese). 14. Sagawa Y, Komatsu T, Hayakawa K, Nagashima M. Twin cases 1. Siragusa M, Schepis C. A case of prurigo pigmentosa successfully of prurigo pigmentosa associated with insulin-dependent diabetes treated with minocycline. J Dermatol Treatment 2000; 11: 131 ± mellitus (Abstract). Jpn J Dermatol 1992; 102: 251 (in Japanese). 135. 15. Miyauchi Y, Matsuhashi A. A case of prurigo pigmentosa in a 2. Gurses L, Gurbuz O, Demircay Z, Kotiloglu E. Prurigo young patient with non-insulin-dependent diabetes mellitus. pigmentosa. Int J Dermatol 1999; 38: 924 ± 925. Hihubyoh-Shinryoh 1997; 19: 151 ± 154 (in Japanese). 3. Wakabayashi T, Shibata A, Morishima T. Prurigo pigmentosa 16. Kametani T, Koshida H, Oshima S, Inoue T. A case of non- when fasting to lose weight. Nishinihon J Dermatol 1986; 48: insulin-dependent diabetes mellitus associated with ketoacidosis 887 ± 891 (in Japanese). and prurigo pigmentosa (Abstract). J Jpn Diab Soc 1998; 41: 861 4. Ohnishi T, Nishiyama Y, Chikakane K, Watanabe S, Takahashi (in Japanese). H. Prurigo pigmentosa in a patient on a diet. Rinsho Derma 17. Sato Y, Yamamoto T, Izaki S, Kitamura K. A case of prurigo 1997; 39: 469 ± 471 (in Japanese). pigmentosa with insulin-dependent diabetes mellitus. Jpn J Clin 5. Teraki Y, Teraki E, Kawashima M, Nagashima M, Shiohara T. Dermatol 1999; 53: 608 ± 610 (in Japanese). Ketosis is involved in the origin of prurigo pigmentosa. J Am 18. Himeno H, Maki Y, Himeno T, Yoshinari M, Fujishima M. A Acad Dermatol 1996; 34: 509 ± 511. case of IDDM associated with diabetic ketoacidosis and prurigo 6. Kobayashi T, Kawada A, Hiruma M, Ishibashi A, Aoki A. pigmentosa (Abstract). J Jpn Diab Soc 1999; 42: 882 (in Prurigo pigmentosa, ketonemia and diabetes mellitus. Dermatol- Japanese). ogy 1996; 192: 78 ± 80. 19. Saga H, Kanda N, Higaki Y, Kawashima M. A case of prurigo 7. Murao K, Urano Y, Uchida N, Arase S. Prurigo pigmentosa pigmentosa with diabetes mellitus. Jpn J Clin Dermatol 2000; 54: associated with ketosis. Br J Dermatol 1996; 134: 379 ± 382. 501 ± 503 (in Japanese). 8. Kubota Y, Koga T, Nakayama J. Bullous prurigo pigmentosa and diabetes. Eur J Dermatol 1998; 8: 439 ± 441. 9. Yamashina Y, Komatsu M, Miyakawa S, Sakamoto K. A case of Accepted September 13, 2000. prurigo pigmentosa (Abstract). Hihu 1987; 29: 1010 (in Japanese). 10. Akita N, Hanada K, Katabira Y. Prurigo pigmentosa associated with systemic disorders. Rinsho Derma 1987; 41: 231 ± 234 Takamitsu Ohnishi1, Hiromi Kisa1, Eri Ogata2 and Shinichi (in Japanese). Watanabe1 11. Aso M, Miyamoto T, Morimura T, Shimao S. Prurigo Departments of 1Dermatology and 2Internal Medicine, Teikyo pigmentosa successfully treated with minocycline. Br J Dermatol University School of Medicine, 11-1, Kaga-2, Itabashi-ku, Tokyo 1989; 120: 705 ± 708. 173-8605, Japan.

Acta Derm Venereol 80 Letters to the Editor 449

An Intensely Pruritic Eruption on the Back Occurring after Stopping Dieting

Sir, urinalysis, liver function, serum creatinine, serum protein electro- Dieting to reduce weight for cosmetic reasons is popular, phoresis, IgG, IgA and IgM. Urine was negative for ketones. especially among women. We report here the case of a The patient was told to stop using the topical medications given to Japanese woman who developed an intensely pruritic eruption her by the general practitioner, because contact allergy to them could not be excluded on the basis of the course of the disease. Although on her back, concomitantly with a modest weight gain that she followed this instruction for 1 week, there was no signi® cant occurred after she had stopped dieting. While topical improvement. Despite administering topical di¯ ucortolone valerate corticosteroids were not effective in our case, systemic for 2 weeks the eruption showed gradual exacerbation. Patch testing antibiotics, namely cefdinir and minocycline, produced with all topical medications used up to this point (clobetasol excellent effects. To our knowledge, such a case has not propionate, gentamicin sulphate and di¯ ucortolone valerate) revealed previously been described. negative reactions, even though we made observations for 7 days in order to avoid missing delayed reactions. As a trial, we administered 100 mg of the cephalosporin cefdinir (Fujisawa Pharmaceutical Co., Ltd.) three times daily, which produced signi® cant effects within 1 CASE REPORT week. However, after cefdinir was discontinued, the eruption and severe pruritus rapidly recurred. Subsequently, 100 mg of minocycline A 42-year-old woman was referred to our clinic on 17 December daily was given, resulting in a complete cure of the rash within about 1997, with a 1-month history of an intensely pruritic eruption on her 3 weeks, leaving a mottled pigmentation. After stopping minocycline, upper back. She had been treated by her general practitioner with topical clobetasol propionate and gentamicin sulphate for 2 weeks, there has been no sign of a relapse for about 2 years. but the eruption gradually spread. She was slightly obese, weighing 50 kg. She had started a low-calorie diet in spring 1997 for aesthetic reasons, and lost 3 kg slowly. She stopped dieting at the beginning of DISCUSSION November and her weight increased rapidly, returning to the pre-diet At ® rst, contact was suspected in this case on level within a month. She had had acne on the face and trunk in her clinical grounds. However, topical steroids produced no teenage years and a low-grade acneform eruption had continued into her 40s. On examination, irregular, con¯ uent, erythematous plaques with small crusted erosions were present on the upper back. In addition, 1 ± 2 mm diameter, reddish papules were found scattered on and close to the erythematous lesions (Fig. 1). The skin of the face and upper trunk showed seborrhoea. A skin biopsy taken from a solitary papule revealed that a hair follicle was located in the centre. There was a mononuclear cell in® ltrate not only in the vicinity of the hair follicle, but also in the follicular wall with spongiosis (Fig. 2). The epidermis outside the hair follicle showed mild acanthosis, exocytosis of lymphoid cells, liquefaction degeneration of the basal cells and scattered apoptotic keratinocytes. There was no evidence of amyloid or mucin deposition in the dermis. Direct immuno¯ uores- cence studies gave negative results. A culture of exudate from the erosions yielded Staphylococcus aureus. The results of the following laboratory tests were within normal limits: complete blood count,

Fig. 1. Irregular, con¯ uent, erythematous plaques with small crusted erosions present on the upper back. Reddish papules (1 ± Fig. 2. A mononuclear cell in® ltrate is seen not only in the vicinity 2 mm diameter) are seen scattered on and close to the erythema- of a hair follicle, but also in the follicular wall with spongiosis. tous lesions. Haematoxylin and eosin staining; original magni® cation 650.

Acta Derm Venereol 80 450 Letters to the Editor effects, and the results of patch testing with all the topical more, the patient developed eruption concomitantly with the medications used were all negative. It seems likely that the rapid weight gain that occurred after stopping dieting, in primary event in the in¯ ammatory cascade, leading to the contrast to prurigo pigmentosa in which the onset is often development of the unique conditions in our patient, might associated with fasting or dieting. have occurred in the hair follicles, as histopathology from a It seems unlikely that systemic antibiotics were ef® cacious solitary papule revealed that a hair follicle was located in the in our case through their activity against S. aureus because, as centre. Such histological ® ndings also argue against the mentioned above, the clinical picture and histology were quite diagnosis of . A rather bizarre morphology different from those of staphylococcal skin infections such as of the eruption might be accounted for, to some extent, by impetigo. A possible explanation for the ef® cacy of the scratching resulting from intense pruritus. However, derma- antibiotics is that they may have suppressed the normal titis artefacta could be excluded in our patient, because the resident ¯ ora on the skin, thus having a favourable effect on papular lesions which revealed the characteristic histological the course of the disease. In addition, minocycline may features are not seen in dermatitis artefacta. Impetigo might produce an excellent result through its unique, inhibitory be considered in the differential diagnosis, because a bacterial effects on the immunological system (5). culture of exudate yielded S. aureus and systemic antimicro- To our knowledge, such a case has not previously been bials produced excellent effects. However, the clinical picture described in the literature. The cause is unknown but we can and histology are quite different from those of impetigo. speculate that, in this case, the eruption occurred as a result of Nummular eczema should also be included in the the metabolic response to a rapid weight gain after stopping differential diagnosis, because it often shows a poor response dieting. High sebum secretion may have been an important to topical corticosteroids but reacts favourably to systemic precipitating factor. In addition, psychological factors, such antibiotics (1). However, histopathological ® ndings in this as disappointment and frustration that the attempt to reduce case argue against the diagnosis of nummular eczema. weight had failed, might have been involved in the aetiology Pityrosporal folliculitis involves follicles, and is often localized of the condition. on the back. However, the plaque lesions seen in our patient are not a feature of this condition (2). REFERENCES Prurigo pigmentosa, as ® rst described by Nagashima (3), is characterized by recurrent pruritic erythematous papules that 1. Burton JL. Discoid eczema. In: Champion RH, Burton JL, Ebling subside in about 1 week, leaving a peculiar, reticulate FJG, eds. Textbook of dermatology, 5th edn., Vol. 1. Oxford: hyperpigmentation. The sites of predilection are the anterior Blackwell Scienti® c, 1992: 555 ± 557. chest, back, clavicular, scapular and nuchal regions. The 2. BaÈ ck O, Faergemann J, Hornqvist R. Pityrosporum folliculitis: a common disease of the young and middle-aged. J Am Acad histological picture is characterized by a lichenoid tissue Dermatol 1985; 12: 56 ± 61. reaction with a mild degree of spongiosis, intracellular 3. Nagashima M. Prurigo pigmentosaÐ clinical observations of our oedema and exocytosis. Treatment with dapsone or minocy- 14 cases. J Dermatol 1978; 5: 61 ± 67. cline is extremely effective, whereas the response to topical 4. Teraki Y, Teraki E, Kawashima M, Nagashima M, Shiohara T. and systemic corticosteroids is poor. The cause of prurigo Ketosis is involved in the origin of prurigo pigmentosa. J Am Acad pigmentosa remains obscure, although it was recently Dermatol 1996; 34: 509 ± 511. suggested that ketosis associated with fasting, dieting and 5. Humbert P, Treffel P, Capuis J-F, Buchet S, Derancourt C, insulin-dependent diabetes mellitus may play a signi® cant role Agache P. The tetracyclines in dermatology. J Am Acad Dermatol (4). Our case has some resemblance to prurigo pigmentosa, as 1991; 25: 691 ± 697. the pruritic eruption on the patient’s back was successfully treated with minocycline, leaving a pigmentation, and the Accepted September 27, 2000. histological changes in the area outside a hair follicle resemble those of this condition. However, our case seems to be distinct Kazuhito Hayakawa and Tetsuo Shiohara from this entity because the lesions were persistent, and Department of Dermatology, Kyorin University School of Medicine, consisted mainly of con¯ uent, erythematous plaques. Further- 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan.

Acta Derm Venereol 80 Letters to the Editor 451

Topical Tacrolimus is Effective for Facial Lesions of Psoriasis

Sir, ment. Complete remission was obtained in 5 cases, and partial Tacrolimus (FK 506) is an immunosuppressive agent isolated remission was noted in 5 cases. The one patient who was from fermentation broth of Streptomyces tsukubaensis (1). resistant to tacrolimus had presented with severe facial Although tacrolimus has a spectrum of activity that is very lesions. The mean PASI score had decreased from 1.5 to similar to that of cyclosporine, tacrolimus is a more potent 0.6 in erythema and from 1.4 to 0.6 in in® ltration after 4 inhibitor of T-cell activation (2). weeks. In general, desquamation was mild or faint in facial Like other immunosuppressiveagents, such as cyclosporine, lesions even before therapy. The maximum amount of oral tacrolimus has been shown to be effective for the ointment used during the 4-week trial did not exceed 5 g in treatment of severe, chronic plaque-type psoriasis. It has also total. No adverse effects on liver or renal function were noted. been topically applied for chronic psoriatic plaques in pilot Topical application of tacrolimus has recently been shown studies (3, 4). No statistically signi® cant difference in effect to be effective in the treatment of certain in¯ ammatory skin was found between tacrolimus ointment and placebo (3). It disorders. Our trial was limited to facial lesions associated can be speculated that this lack of effect may be due to low with psoriasis. Usually, facial psoriasis lesions are not covered absorption of the drug through thick psoriatic scales. with thick scales, which may have been of bene® t in this The forehead, cheeks and nasolabial areas of the face are study. We conclude that topical tacrolimus is effective for often involved in psoriasis. Although these lesions may not be facial psoriasis lesions. severe they occasionally cause discomfort to patients. We used topical tacrolimus for the treatment of facial psoriasis in 11 REFERENCES patients and obtained an acceptable effect after a short treatment period. 1. Kino T, Hatanaka H, Miyata S, Inamura N, Nishiyama M, Eleven patients with psoriasis vulgaris (6 males and 5 Yajima T, et al. FK-506, a novel immunosuppressant isolated from females; 31 ± 64 years of age; mean 49.3 years) were enrolled a streptomyces. II: immunosuppressive effect of FK-506 in vitro. J in this study. All of the patients had typical extra-facial Antibiot (Tokyo) 1987; 40: 1256 ± 1265. 2. Schreiber SL, Grabtree GR. The mechanism of action of psoriasis. Three patients exhibited sebopsoriasis-type psoriasis cyclosporin A and FK 506. Immunol Today 1992; 13: 136 ± 142. on the forehead and frontal scalp. None of the patients 3. Zonneveld IM, Rubins A, Jablonska S, Dobozy A, Ruzicka T, received any systemic treatment before or during the trial. Kind P, et al. Topical tacrolimus is not effective in chronic plaque Five patients had been treated with tacalcitol ointment which, psoriasis. Arch Dermatol 2000; 134: 1101 ± 1102. however, had not been effective. After receiving informed 4. Remitz A, Reitamo S, Erkko P, Granlund H, Lauerma AI. consent, 0.1% tacrolimus ointment (Fujisawa Pharmaceutical Tacrolimus ointment improves psoriasis in a microplaque assay. Br Co. Ltd., Tokyo, Japan) was applied twice a day. The disease J Dermatol 1999; 141: 103 ± 107. severity of the facial lesions was assessed by the PASI score (degree of erythema, in® ltration and desquamation) after 2 Accepted September 7, 2000. and 4 weeks of treatment. Laboratory examination, including liver and renal function tests, was carried out before treatment Toshiyuki Yamamoto and Kiyoshi Nishioka and after 4 weeks of treatment. Department of Dermatology, Tokyo Medical and Dental University, After 2 weeks, we observed a marked improvement in 6 School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, cases. After 4 weeks, all except 1 patient showed improve- Japan.

Acta Derm Venereol 80 452 Letters to the Editor

An Unusual Location of Nodular Elastosis with Cysts and Comedones (Favre ± Racouchot’s Disease)

Sir, remarkable cutis rhomboidalis nuchae, deep wrinkles and multiple In 1951, Favre & Racouchot described a disease characterized actinic lentigo on the face and the dorsal surface of the hands. A large by nodular elastosis with cysts and comedones (1). The cafe au lait spot was detectable on the left abdomen. He was in good disease is localized on the lateral canthi of the eyes, temples, general condition: all blood and urine tests were within normal limits and X-rays of the left scapular girdle were normal. The lesions did not cheeks, nucha, retro-auricular regions and, more rarely, on impede movements of the left arm. Histologic examination of a the chin and nose. The skin is wrinkled and intensely dark biopsy specimen of a papulonodular lesion showed no alterations of over the lesions. The disease develops gradually in elderly the epidermis, but a well-de® ned pluristrati® ed epithelium cyst in the males and is frequently associated with cutis rhomboidalis mid-dermis and remarkable dermal elastosis. On this basis, Favre ± nuchae and disorders due to sun exposure. Racouchot’s disease, over an atypical area, was diagnosed.

CASE REPORT DISCUSSION An 80-year-old male patient (phototype IV) presented with many Our patient had worked for many years as a bricklayer, rounded, well-de® ned, yellowish, hard, papulonodular lesions, both carrying weights on his left shoulder only. The association of separated and coalescing in plaques, about 7 cm in diameter, localized prolonged sun exposure and repeated pressure on the left on the left scapular girdle (Fig. 1). Some large comedones were also scapular girdle might have caused degenerative alterations of present, but no greasy substance emerged upon squeezing. The skin the dermis, unilaterally, over an unusual area with a ¯ at over the lesions was thin and wrinkled. The ® rst asymptomatic lesions appearance of the lesions; in contrast the classical form of had appeared approximately 30 years earlier and had not been Favre ± Racoucht’s disease is characterized by a prominent preceded by in¯ ammatory events. The patient also presented with a lesional aspect. To our knowledge, only one case of Favre ± Racouchot’s disease has previously been reported over an atypical area (2). We consider the present case to be the second such observation in the literature.

REFERENCES 1. Favre M, Racouchot J. L’e laste idose cutanee nodulaire aÁ kystes et aÁ come dons. Ann Dermatol Syph 1951; 78: 681 ± 702. 2. Degos R, Delort J, Durant J. Forme aÁ topographie atypique d’e lastoidosie cutane e nodulair aÁ kystes et come dons (maladie de Favre et Racouchot). Bull Soc Fr Dermatol Syph 1954; 61: 27 ± 28.

Accepted September 9, 2000.

Maddalena Siragusa1, Emilia Magliolo2, Dario Batolo2 and Carmelo Schepis1 1Unit of Dermatology, Oasi Institute (IRCCS), Via Conte Ruggero Fig. 1. Rounded, yellowish papulonodular lesions on the left scapu- 73, 94018 Troina, Italy. E-mail: [email protected] and 2Department lar girdle. of Human Pathology, University of Messina, Messina, Italy.

Acta Derm Venereol 80 Letters to the Editor 453

The Coexistence of Amyopathic Dermatomyositis and Fibromyalgia

Sir, prednisolone, 20 mg daily, which were tapered off after 6 weeks. The Amyopathic dermatomyositis (ADM) is an uncommon patient underwent extensive investigation for associated malignancy variety of dermatomyositis (DM) and affects patients without but this was not found. She was later referred to the National muscle weakness or laboratory evidence of muscle involve- Hospital, University of Oslo, and was examined at the Department of Dermatology and the Center for Rheumatic Diseases. Her skin ment (1 ± 3). In primary idiopathic DM up to one-third of symptoms were at that time in regression but the diagnosis of patients present initially with only skin changes which may ® bromyalgia was sustained. Muscle biopsy and electromyography last for several years before muscle weakness develops (1 ± 7). (EMG) were normal. A few cases have been followed for as much as 10 ± 12 years The patient has been followed for 5 years without laboratory signs without signs of muscle involvement. It has been suggested of muscle involvement. Because of her ® bromyalgia symptoms she has that nearly 10% of all patients with DM describe their disease now received a disability pension. Recurrence of her skin symptoms as ADM (2 ± 4). necessitates treatment with prednisolone. Her laboratory data, Criteria for the diagnosis of ADM include pathognomonic including muscle enzymes and antinuclear antibodies (ANA), are Gottron’s papules, together with the characteristic heliotrope, normal. periorbital, violaceous erythema associated with oedema. Other characteristic skin lesions include periungual telangiec- DISCUSSION tasia and macular, violaceous erythema on the hands, arms, chest, neck or shoulders. One or two pathognomonic signs By de® nition the term ADM should be reserved for those associated with one or more characteristic signs and a patients who have characteristic and pathognomonic skin compatible skin biopsy are required for the diagnosis of lesions of DM without any evidence of muscle disease at any ADM. Several other skin manifestations have been described, time during the course of the disease. As some cases may such as pruritus, photosensitivity, poikiloderma, scalp invol- develop signs of muscle involvement after 4 years, one could vement with alopecia and a seborrhoeic pattern of cutaneous use the term premyopathic DM (8). EMG and muscle involvement (1, 6, 8, 9). enzymes are not always correlated and muscle histology may The prevalence of ® bromyalgia in another connective-tissue depend on the biopsy site; however, it is dif® cult to convince a disease, systemic erythematosus, is high (10), but has patient to undergo another muscle biopsy. MRI may be not been described in connection with DM. Such a case is warranted in patients with ADM (1, 7) and would certainly reported here. have been of use in the present case. The cutaneous manifestations of DM are polymorphic and may be misleading in the absence of overt muscle involve- CASE REPORT ment, as was the case at the initial examination of our patient. Although the skin symptoms responded to oral corticosteroid A 52-year-old woman had initially presented about 5 years previously therapy, regression was not complete. This patient had typical with an erythematous, slightly scaly, eruption on her face involving ® bromyalgia with subjective and objective manifestations but the front, the cheeks and particularly the facial fold. She also had an surprisingly there were no laboratory ® ndings of muscle erythematous rash on her breast. The diagnosis was or perhaps psoriasis and she was prescribed a mild steroid disease. There are several overlapping symptoms in DM and cream with an antifungal component. Four months later she returned ® bromyalgia, e.g. lethargy, fatigue, arthralgia and, of course, because of worsening symptoms; on this occasion her skin muscle weakness (6). This can lead to misinterpretation and manifestations consisted of periocular, heliotrope, violaceous also to a delay in diagnosis and therapy. Our patient ful® lled erythema associated with oedema with extension to the front. On the ACR-90 classi® cation criteria of ® bromyalgia (11), with the trunk, including the upper part of the abdomen, the breast region, chronic widespread pain for 43 months and 11 tender the neck and shoulders, there was a reddish-blue erythema with points. According to these criteria a distinction between telangiectasia. Erythema and papules were noted on the bony primary and secondary ® bromyalgia is no longer made and prominences of the elbows, hips and knees. Her ® ngers were the presence of associated symptoms is not required. erythematous and felt swollen. She ascribed her symptoms to sun Furthermore, a second clinical disorder does not exclude exposure. The diagnosis was changed to DM and a biopsy was obtained from the diagnosis of ® bromyalgia. the trunk and processed for routine histologic staining and direct We do not know the ultimate outcome of ADM with immuno¯ uorescence (DIF) studies. Using light microscopy a regard to the development of malignancy and muscle perivascular lymphocytic in® ltration was observed in the dermis involvement. ADM has been regarded as one end of a while DIF examination showed a bandlike deposition of IgM, clinical spectrum, with the combination of skin and muscle complement and ® brin. Serum levels of creatine phosphokinase, symptoms in the middle and polymyositis at the other end (3, aldolase and lactic acid dehydrogenase were normal. Antinuclear 6). It is not yet known if all patients with ADM will antibodies were not detected. The patient was about 20 kg over- eventually develop muscle disease. It has been advocated that weight. She was periodically depressed, had dif® culty sleeping, did not an aggressive approach to treating the skin disease may feel refreshed in the morning and complained of general fatigue and prevent the development of muscle disease in patients who widespread pain above and below the waist (arms, shoulders, back, thighs and knees) which had lasted for several years. On examination initially have only skin involvement (3). Only prospective she experienced extreme pain upon pressure (4 kg) at 12 ® bromyalgia studies can prove this proposal. Corticosteroids may induce tender points and her muscles felt hypertonic. Muscle strength was myopathy but there seems to be no such relationship in the apparently normal. Because of progressing skin symptoms, which present case as the therapy was begun years after the caused her much distress, she was treated with moderate doses of symptoms of ® bromyalgia ® rst appeared. The coexistence of

Acta Derm Venereol 80 454 Letters to the Editor

ADM and ® bromyalgia in this patient is probably a 7. Stonecipher MR, Jorrizo JL, White WL, Walker FO, Prichard E. coincidence, but certainly an interesting one. Cutaneous changes of dermatomyositis in patients with normal muscle enzymes: dermatomyositis sine myositis? J Am Acad Dermatol 1993; 28: 951 ± 956. REFERENCES 8. Trautmann C, Abdel-Naser MB, Soehnchen R, Detmar M, Orfanos CE. Pramyopathische versus amyopathische Dermato- 1. Kovacs SO, Kovacs SC. Dermatomyositis. J Am Acad Dermatol myositis. Hautarzt 1995; 46: 47 ± 52. 2000; 39: 899 ± 920. 9. Katayama I, Sawada Y, Nishioka K. The seborrhoeic pattern of 2. Cosnes A, Amaudric F, Gherardi R, Verroust J, Wechsler J, dermatomyositis. Br J Dermatol 1999; 140: 978 ± 979. Revuz J, et al. Dermatomyositis without muscle weakness. Long- 10. Grafe A, Wollina U, Tebbe B, Sprott H, Uhlemann C, Hein G. term follow-up of 12 patients without corticosteroids. Arch Fibromyalgia in lupus erythematosus. Acta Derm Venereol 1999; Dermatol 1995; 131: 1381 ± 1385. 79: 62 ± 64. 3. Euwer RL, Sontheimer RD. Amyopathic dermatomyositis: a 11. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Rombardier C, review. J Invest Dermatol Suppl 1993; 100: 124 ± 127. Goldenberg DL, et al. The American College of Rheumatology 4. Rockerbie NR, Woo TY, Callen JP, Giustina T. Cutaneous 1990 criteria for the classi® cation of ® bromyalgia. Arthritis changes of dermato-myositis precede muscle weakness. J Am Rheum 1990; 33: 160 ± 179. Acad Dermatol 1989; 20: 629 ± 632. 5. Caproni M, Salvatore E, Bernocchi E, Fabri P. Amyopathic dermatomyositis: report of three cases. Br J Dermatol 1998; 139: Accepted September 8, 2000. 1116 ± 1118. 6. Euwer RL, Sontheimer RD. Amyopathic dermatomyositis (dermatomyositis sine myositis). Presentation of six new cases Per Thune and review of the literature. J Am Acad Dermatol 1991; 24: 959 ± Dermatology Section, OMNIA Romeriksklinikken, NO-2010 Strù m- 966. men, Norway.

Acta Derm Venereol 80 Letters to the Editor 455

Serum Interleukin-15 Levels are not Elevated in Patients with Stage I and II Mycosis Fungoides

Sir, Table I. Serum interleukin-15 (IL-15) levels in patients with Interleukin-15 (IL-15) is a newly described cytokine that was mycosis fungoides ® rst characterized from the culture supernatants of a simian kidney epithelial line, CV-1/EBNA (1). IL-15 shares with IL-2 No. Age/sex Stage Epidermotropism PUVA IL-15 sIL-2R (pg/ml) (U/ml) the ability to bind to the b- and c-chains of the IL-2 receptor complex and to stimulate the growth of CD4+ and CD8+ T 1 64/F Ia + + 59 N.D. cells (1). Recently, IL-15 was found to be a growth factor for 2 65/M Ia + ± 15.7 558 the Sezary cell line SeAx and immunohistological analyses of 3 65/F Ia + + 152.5 323 skin biopsy samples of Sezary syndrome and mycosis 4 67/M Ia + ± 195.7 N.D. fungoides (MF) patients showed immunoreactivity for IL-15 5 50/F Ib + + 69.8 231 in basal cell layer keratinocytes and in® ltrating lymphocytes 6 57/M Ib + + 71.4 N.D. (2). Therefore, we measured serum IL-15 levels in patients 7 62/F Ib + ± 60.8 355 with MF and examined whether they can be a marker for the 8 70/F Ib + ± 79.7 508 disease activity of MF. 9 57/M IIb + + 102 654 10 73/M IIb ± ± 135.9 7837

MATERIAL AND METHODS sIL-2R: soluble IL-2 receptor. N.D.= not determined. Serum samples were obtained from 10 patients affected with MF (5 males and 5 females; mean age 63+7 years; range 50 ± 73 years). The activity. Serum levels of IL-15 in patients with MF have not diagnosis of MF was established by clinical and histopathological been discussed so far. Our study suggests that, at least in examinations. The clinical stages of the patients were as follows: stage stages I and II, they cannot be used as a marker of disease Ia, 4 cases; stage Ib, 4 cases; and stage IIb, 2 cases [TNM activity like sIL-2R levels, which were elevated in our 2 stage classi® cation (3)]. Ten healthy age- and sex-matched subjects served IIb patients. as controls, after giving their informed consent. IL-15 concentrations in serum samples were measured using ELISA kits (Genzyme, Cambridge, MA). Serum levels of soluble IL-2 receptor (sIL-2R) were REFERENCES also measured using ELISA kits (Yamanouchi Co., Tokyo, Japan) in 1. Grabstein KH, Eisenman J, Shanebeck K, Rauch C, Srinivasan S, some patients. The normal range of sIL-2R levels in our institution is Fung V, et al. Cloning of a T-cell growth factor that interacts with 167 ± 497 pg/ml. the beta chain of the interleukin-2 receptor. Science 1994; 264: 965 ± 968. RESULTS 2. Dobbeling U, Dummer R, Laine E, Potoczna N, Qin JZ, Burg G. Interleukin-15 is an autocrine/paracrine viability factor for Serum IL-15 levels were not elevated in the patients (mean cutaneous T-cell lymphoma cells. Blood 2000; 92: 252 ± 258. 94.2+53.1 pg/ml; range 15.7 ± 195.7 pg/ml) compared with 3. Bunn PA Jr, Lamberg SI. Report of the Committee on Staging and the controls (mean 89.5+46.7 pg/ml; range 0 ± 195.7 pg/ml) Classi® cation of Cutaneous T-cell Lymphomas. Cancer Treat Rep (p= 0.81) (Table I). Clinical stage, history of PUVA therapy, 1979; 63: 725 ± 728. epidermotropism of tumor cells and sIL-2R levels had no 4. Dalloul A, Laroche L, Bagot M, Mossalayi MD, Fourcade C, Thacker DJ, et al. Interleukin-7 is a growth factor for Sezary association with serum IL-15 levels. We also measured serum lymphoma cells. J Clin Invest 1992; 90: 1054 ± 1060. IL-15 levels in 2 stage IIb patients after therapy. In 1 patient, 5. Asadullah K, Haeussler A, Friedrich M, Siegling A, Olaizzola- serum IL-15 levels decreased (from 102.0 pg/ml to 66.5 pg/ml) Horn S, Trefzer U, et al. IL-7 mRNA is not overexpressed in as the skin lesions disappeared. In the other, serum IL-15 mycosis fungoides and pleomorphic T-cell lymphoma and is likely levels increased (from 135.9 pg/ml to 283.5 pg/ml). to be an autocrine growth factor in vivo. Arch Dermatol Res 1996; 289: 9 ± 13. 6. Wasik MA, Vonderheid EC, Bigler RD, Marti R, Lessin SR, DISCUSSION Polansky M, et al. Increased serum concentration of the soluble One important feature of MF is that lymphocyte proliferation interleukin-2 receptor in cutaneous T-cell lymphoma. Clinical and remains restricted to the skin and, therefore, some cytokines prognostic implications. Arch Dermatol 1996; 132: 42 ± 47. or chemokines may be essential for the disease. Previously, keratinocytes derived from interleukin-7 (IL-7) proved to be necessary to cultivate freshly isolated Sezary cells and some Accepted September 11, 2000. established Sezary cell lines (4). The importance of IL-7 in the pathogenesis of MF, however, remains controversial (5). Makoto Sugaya, Koichiro Nakamura and Kunihiko Tamaki Serum concentrations of sIL-2R in patients with MF are Department of Dermatology, University of Tokyo, Faculty of found to be increased (6) and are a good marker of disease Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.

Acta Derm Venereol 80 456 Letters to the Editor

Discoid and Subacute Cutaneous Lupus Erythematosus: Detection of Differences in Peripheral Lymphocyte Numbers

Sir, Reduced leukocyte and lymphocyte counts are a well-known phenomenon in patients with systemic lupus erythematosus (SLE) and are included in the classi® cation of the American College of Rheumatology (1). However, in patients with cutaneous lupus erythematosus absolute counts of peripheral lymphocytes have only been sporadically investigated. Gilliam & Hurd (2) in 1976 analyzed circulating lymphocytes in patients with discoid lupus erythematosus (DLE). They found normal T-cell numbers in these patients. In 1986 Kind et al. (3) reported on T- and B-cell abnormalities in cutaneous lupus erythematosus. They showed that patients with subacute cutaneous lupus erythematosus (SCLE) had sig- ni® cantly diminished mean numbers of CD3+ CD8+ cells compared to healthy controls. A similar difference could not be found between patients with DLE and healthy controls. Fig. 1. Mean (+SEM) lymphocyte numbers/ml in LE subsets. Both studies were done on fairly small patient groups: 24 and *po 0.05; **po 0.01. 18 patients with LE, respectively. Therefore, in this study we analyzed circulating lymphocytes in a larger group of patients lymphocytes: DLE and SCLE patients differed in their pro® le with LE. of B-cells, T-cells, CD3+ CD4+ cells and CD3+ CD8+ cells. We agree with Kind et al. that DLE and SCLE are separate MATERIAL AND METHODS entities of cutaneous LE with different immunologies and clinical presentations. We analyzed absolute numbers of peripheral lymphocytes in 80 Interestingly, we found no signi® cant differences between patients with LE (40 females and 40 males; age range 21 ± 86 years; DLE patients and healthy controls on the one hand and mean age 46 years; DLE: n= 47; SCLE: n= 19; SLE: n= 14) and in 20 between SLE and SCLE patients on the other. This may be a healthy controls (10 females and 10 males; mean age 51 years) using ¯ ow cytometry. The following subsets were included: B-lymphocytes hint that different pathogenetic features play a role in these (CD19+ ), T-lymphocytes (CD3+ ), T-helper cells (CD3+ CD4+ ) LE subtypes. The immunological disturbances in SCLE point and cytotoxic T-cells (CD3+ CD8+ ). The mean cell numbers of the to a closer correlation between this subtype and SLE. lymphocyte subsets of the different forms of LE were evaluated and However, it remains unclear whether the described diminished differences between them were checked for signi® cance using mean lymphocyte numbers and numbers of lymphocyte Student’s t-test. subsets are primary or secondary in the pathogenesis of SCLE and SLE. Further investigations are warranted to answer this question. RESULTS AND DISCUSSION Overall, our data showed normal numbers of peripheral REFERENCES lymphocyte subsets in DLE patients, while cell counts in SCLE and SLE patients were diminished (Fig. 1). We found a 1. Tan EM, Cohen AS, Fries JF. The 1982 revised criteria for the signi® cant difference (po 0.01) between mean lymphocyte classi® cation of systemic lupus erythematosus. Arthritis Rheum counts of DLE and SCLE patients. Mean counts of all 1982; 25: 1271 ± 1277. investigated lymphocyte subsets (B-lymphocytes, T-lympho- 2. Gilliam JN, Hurd ER. Comparison of circulating T and B cytes, CD3+ CD4+ and CD3+ CD8+ cells) showed signi® - lymphocytes in discoid versus systemic lupus erythematosus. Clin Immunol Immunopathol 1976; 6: 149 ± 155. cant differences between the following LE forms: B-, T- and 3. Kind P, Lipsky PE, Sontheimer RD. Circulating T- and B-cell T-helper cells (po 0.01); cytotoxic T-cells (po 0.05). Differ- abnormalities in cutaneous lupus erythematosus. J Invest Dermatol ences between DLE patients and healthy controls and 1986; 86: 235 ± 239. between SCLE and SLE patients were not signi® cant. Previously, Kind et al. (3) were able to show that mean Accepted September 27, 2000. absolute counts of CD3+ CD8+ cells differed signi® cantly between DLE and SCLE patients. Furthermore, we were able Joerg Wenzel, Ralf Bauer, Thomas Bieber and Ingrid Boehm to show signi® cant differences between DLE and SCLE Department of Dermatology, University of Bonn, Sigmund-Freud- patients in all of the investigated subtypes of circulating Strasse 25, 53105, Bonn, Germany. E-mail: [email protected]

Acta Derm Venereol 80 Letters to the Editor 457

Stevens ± Johnson Syndrome Associated with Beza® brate

Sir, day) and azelastine hydrochloride (2 mg/day). After 3 days her Beza® brate is a ® bric acid derivative, widely used for patients symptoms were alleviated and the erythema and erosion began to with hyperlipidemia, and is considered to be a safe medication heal. Oral prednisolone was tapered and the patient was discharged (1). We report here the ® rst case of Stevens± Johnson 10 days later. A skin patch test and a drug lymphocyte stimulation test for allergy to beza® brate were negative. syndrome associated with beza® brate treatment.

DISCUSSION CASE REPORT A 42-year-old female with slight hyperlipidemia was treated with Fever, joint pain and involvement of conjunctival and labial beza® brate in the hospital of her general practitioner. On the 13th day mucous membranes indicated erythema multiforme major, i.e. of treatment she noticed fever, joint pain and exanthema on her Stevens ± Johnson syndrome. The present case clearly indi- extremities. She stopped taking beza® brate and referred herself to the cated that beza® brate caused this eruption, although skin same hospital. She was treated with an oral steroid and antibiotics patch and drug lymphocyte stimulation tests were negative. and the symptoms disappeared within a week. As there was no strong However, clo® brate, another ® bric acid derivative, has been indication not to take beza® brate, she restarted taking the drug and 5 found to induce erythema multiforme (2) and Stevens± days later developed an erythematous eruption on the whole of the Johnson syndrome (3). body, fever, joint pain and edema of the face. Examination revealed multiple generalized erythematous macules, target lesions and erosions on her trunk and extremities. We also found pigmentation REFERENCES resulting from previous skin lesions. She had shallow erosions on her lips and hard palate, and redness of her conjunctiva. At admission to 1. Olsson AG, Lang PD. One-year study of the effect of beza® brate on serum lipoprotein concentrations in hyperlipoproteinemia. our hospital, laboratory tests revealed a low hemoglobin level (9.6 g/ dl). The leukocyte count was 14,000/mm3, with 82% polymorphs, 14% Atherosclerosis 1978; 31: 429 ± 433. 2. Murata Y, Tani M, Amano M. Erythema multiforme due to lymphocytes and 4% monocytes. Blood biochemistry and urine and stool examinations were normal. Serological tests for mycoplasma clo® brate. J Am Acad Dermatol 1988; 18: 381 ± 382. 3. Wong SS. Stevens-Johnson syndrome induced by clo® brate. Acta and herpes viruses were negative. Chest X-ray and electrocardiogram Derm Venereol 1994; 74: 475. were normal. A biopsy specimen revealed hydropic degeneration of basal cells and numerous scattered necrotic keratinocytes with eosinophilic cytoplasm (colloid bodies) in the epidermis. A dense Accepted August 30, 2000. super® cial perivascular mononuclear cell in® ltrate was found around super® cial blood vessels. In some areas, hydropic degeneration caused subepidermal separation and all keratinocytes appeared necrotic. Daisuke Sawamura and Kaoru Umeki We made a diagnosis of Stevens± Johnson syndrome caused by Department of Dermatology, Hakodate Municipal Hospital, 2-33 beza® brate. The patient was treated with oral prednisolone (30 mg/ Yayoi-cho, Hakodate 040-8505, Japan

Acta Derm Venereol 80 458 Letters to the Editor

Antimalarial Drugs and Pruritus in Patients with Lupus Erythematosus . Sir, chloroquine than with hydroxychloroquine and that it was It was with great interest that we read the paper by Holme & apparently not related to lupus activity (4). Holmes entitled ``Hydroxychloroquine-induced pruritus’’, in which they presented a case of this condition in a woman with REFERENCES lupus erythematosus (1). However, these authors wrongly described their case as the ® rst one to be published. Based on 1. Holme SA, Holmes SC. Hydroxychloroquine-induced pruritus. our experience in this area, we wish to expand the knowledge Acta Derm Venereol 1999; 79: 333. of antimalarial drug-induced pruritus in some patients with 2. Jime nez-Alonso J, Tercedor J, Ja imez L, Garcõ Âa-Lora E. Antimalarial-induced aquagenic-type of pruritus in some patients lupus erythematosus. with lupus erythematosus. Arthritis Rheum 1998; 41: 744 ± 745. Two years ago we published a paper describing a series of 3. Karch FE, Lasagna L. Towards the operational identi® cation of 136 patients with lupus erythematosus. Of these, 104 were adverse drug reactions. Clin Pharmacol Ther 1977; 21: 247 ± 254. given antimalarial drugs treatment and 6 (5.77%) developed 4. Jime nez Alonso J, Reche I, Ja imez L, Tercedor J, Gutie rrez probable or de® nitive pruritus relating to the antimalarial Cabello F, Lo pez de la Osa A, et al. Prurito en enfermos de lupus drugs (2), according to Karch-Lasagna criteria (3). These 6 tratados con antipalu dicos: estudio prospectivo durante 18 meses. patients had an aquagenic or post-wetness type of pruritus, An Med Interna 1998; 15 (Suppl I): 29. usually located in the lower extremities and back, without Accepted May 29, 2000. visible skin changes. It appeared &1 ± 3 weeks after initiation of antimalarial drugs therapy and developed mainly after a J. Jime nez-Alonso, J. Tercedor and I. Reche on behalf of the members hot shower, beginning within minutes of water contact, of ``Grupo Lupus Virgen de las Nieves’’ persisting at a high intensity for approximately 10 min and Autoimmune Diseases Unit, Service of Internal Medicine, ``Virgen de then remaining at a low intensity for several hours. Also, las Nieves’’ University Hospital, 9a planta, Avda. Fuerzas Armadas we found that pruritus was slightly more intense with s/n, 18012 Granada, Spain. E-mail: [email protected]

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