Esen Özkaya-Bayazit

Specific site involvement in fixed drug eruption

Abstract A total of 105 patients with established fixed drug eruption (FDE) by oral provocation were evaluated with regard to a drug-related site involvement. Cotrimoxazole was the leading causative agent (63.8%), followed by naproxen sodium (23.8%), dipyrone (5.7%), oxicams (4.8%) and other rare causes (1.9%). Cotrimoxazole most frequently induced lesions on genital mucosa; naproxen and oxicams on lips; and dipyrone on trunk and extremities. Isolated FDE on male genitalia (n = 16) was exclusively because of cotrimoxazole. A highly significant association could be established between naproxen and FDE on lips (chi-square = 28.3; corrected P = .000002). As this study represents the largest series of patients with naproxen-induced FDE, we would suggest that naproxen should be considered as an important potential cause of FDE on lips.

Intermittent use of topical dimethyl sulfoxide in macular and papular amyloidosis

Background Severe and therapy‐resistant pruritus is the most prominent feature of macular (MA) and lichen (LA) amyloidosis that leads to further amyloid deposition by recurrent frictional trauma to the epidermis. Of the various therapeutic modalities with variable success, the most encouraging and beneficial effect has been observed with topical dimethyl sulfoxide (DMSO) therapy. In a previous study, we achieved marked clinical improvement in nine of 10 patients in a daily treatment regimen over 6–20 weeks, but relapses occurred in the post‐treatment follow‐up period. The aims of this study are to investigate whether the patients would benefit from intermittent therapy and to determine the optimal application interval of DMSO to maintain the relief of symptoms.

Topical provocation in 27 cases of cotrimoxazole-induced fixed drug eruption.

The purpose of this study was to investigate the usefulness of topical provocation in the diagnosis of cotrimoxazole‐inducedxed‐drug eruption (FDE). 27 patients with established cotrimoxazoleinduced FDE by oral provocation and 20 healthy controls were tested with drugs at increasing concentrations in white petrolatum and dimethyl sulfoxide (DMSO) both on previously involved and uninvolved skin sites. Tape‐stripping occlusive patch testing in petrolatum remained negative in 19 tested patients. Open testing with drug preparations in DMSO revealed positive results in 25 of 27 tested patients. 1 patient showed an additional positive reaction on previously uninvolved skin. Lesions on male genitalia and on face reacted to testing once with 10% or 20% of the suspected drug, whereas repeated testing with concentrations up to 50% was necessary in lesions on trunk & extremities. Open testing with drug preparations in DMSO at concentrations of 10%, 20% and 50% and pure DMSO remained negative in 20 healthy controls. The present study shows that repeated open testing with graded concentrations of the drugs up to 50% in DMSO is a reliable test method in sulfamethoxazole/trimethoprim‐induced FDE. Patients and physicians should be aware of the transient irritant reaction to DMSO that is not infrequent, so as to avoid false‐positive interpretations.

Pustular psoriasis with a striking linear pattern

Pustular psoriasis has different clinicomorphologic forms such as generalized, localized (mainly palmoplantar or acral), and annular. There are also few cases with a linear distribution pattern. We report a case of pustular psoriasis with a striking linear distribution probably related to Blaschkos lines. We suggest that linear pattern should also be considered among the morphologic variants of pustular psoriasis.

Lokale DMSO-Behandlung der makulösen und papulösen Amyloidose

ZusammenfassungMakulöse Amyloidose (MA) und Lichen amyloidosus (LA) sind die zwei am häufigsten vorkommenden Varianten der primär kutanen Amyloidosen, bei denen ein heftiger Juckreiz im Vordergrund der klinischen Symptomatik steht. Leider zeigen aber die verschiedenen Therapiemaßnahmen wie Antihistaminika, Kortikosteroide, UVB, Etretinat, Dermabrasion usw. wenig oder keinen Erfolg. In den letzten Jahren wurde in der Literatur über die erfolgreiche Therapie mit lokalem Dimethylsulphoxid (DMSO) berichtet. In unserer Studie haben wir Patienten mit MA, LA und biphasischer Amyloidose mit 50%iger DMSO-Lösung lokal behandelt. Während einer Behandlungsdauer von 6–20 Wochen wurde bei 9 von insgesamt 10 Patienten klinische Besserung erzielt. Das schnelle Ansprechen des Juckreizes auf die Therapie innerhalb der ersten Woche ist auf den die Mastzelldegranulation bzw. -depletion fördernden Effekt von DMSO zurückzuführen. Mittels DMSO-Therapie wurde auch eine vollständige Rückbildung der lichenoiden papulösen Effloreszenzen innerhalb von durchschnittlich 11 Wochen erzielt, welche am ehesten durch das Abklingen des Juckreizes und des damit verbundenen Kratzeffektes erklärt werden kann. Trotz der guten klinischen Ergebnisse war histopathologisch kein Verschwinden der Amyloidmassen festzustellen. In den weiteren Verlaufskontrollen nach Ende der Therapie wurden Rezidive der klinischen Symptomatik beobachtet, wobei weitere prospektive Studien zur Bestimmung der optimalen Behandlungsdauer notwendig erscheinen.SummaryMacular amyloidosis (MA) and lichen amyloidosus (LA) are the two major variants of the primary cutaneous amyloidoses which present with severe and therapy resistent itching. Various therapeutic modalities such as antihistamines, intralesional injection or topical application of corticosteroids, etretinate, UVB irradiation and dermoabrasion have been employed with variable success. Recently, in a few case reports authors have observed encouraging beneficial clinical effects by using topical dimethyl sulphoxide (DMSO). In our study 10 patients with either MA or LA or biphasic amyloidosis were treated with a 50% solution of DMSO in water. 9 of them showed marked clinical improvement at the end of 6–20 weeks of treatment. Degranulation and depletion of the mast cells by DMSO is the most probable explanation for the rapid improvement of itching beginning within the first week of therapy. Remarkable flattening of the lichenoid papules which was obtained within 11 weeks of treatment is interpreted as a result of the improvement of itching and the related scratch effect. Histological examination after treatment revealed no disappearance of amyloid deposits in the papillary dermis. In the follow-up period relapses of itching and papules were observed. Therefore further studies are needed to find out the optimal procedure of therapy.

Bullous acral erythema and concomitant pigmentation on the face and occluded skin

To the Editor We report a patient with acute myeloid leukaemia who concomitantly developed bullous acral erythema of the hands and hyperpigmentation during chemotherapy with daunorubicin, cyclosporin and high dose cytarabine. Although hyperpigmentation is well known after daunorubicin and cyclosporin, and bullous acral erythema after cytarabine, the combined occurrence of the two conditions due to cytarabine, daunorubicin or cyclosporin has not been reported before. A 38-year-old caucasian woman with acute myeloid leukaemia (AML-M4) was on the fourth cycle of a combination chemotherapy. She was treated with cyclosporin A 2.5-mg/kg on days 0, 1, 2, 3 and 7, 8, 9, 10; cytarabine 2 g/m 2 on days 1, 2, 3; daunorubicin 50 mg/m 2 on days 1, 2, 3 and etoposide 200 mg/m 2 on days 8, 9, 10. On the second day of this chemotherapy regimen, painful erythema occurred on palmar surfaces of both hands, followed by involvement of the dorsum of the hands within 48 h. The eruption soon became purpuric and hyperpigmented; it progressed to severe oedema and bullae within a few days (fig. 1). Concomitantly, an erythematous eruption developed and evolved into a peculiar hyperpigmentation that was intense on the face (fig. 2), intertriginous areas such as neck, submammary and inguinal regions, and on skin occluded by adhesive tape. Total alopecia and severe mucositis accompanied the lesions. The acral erythema healed with desquamation and shedding of the fingernails within 4 weeks and the hyperpigmentation regressed completely within 6 weeks. Histopathological examination of the punch biopsy material obtained from the dorsal surface of the left hand revealed interface dermatitis with diffuse vacuolar degeneration of basal keratinocytes, numerous dyskeratotic cells, mild acanthosis, pigmentary incontinence and mild perivascular inflammatory infiltration consisting of lymphomonocytes on the upper dermis; all of which supported the diagnosis of bullous acral erythema. Acute graft vs. host disease was excluded because there had been no bone marrow transplantation or blood transfusions. There were no signs of vessel wall damage or eccrine sweat gland/duct changes. No punch biopsy material could be obtained from the hyperpigmented lesions. Chemotherapy-induced acral erythema (CAE) is an uncommon and self-limited localized cutaneous reaction in patients receiving systemic chemotherapy that is characterized by painful, symmetric, well-defined swelling and erythema predominantly on the palms and sometimes also on the soles. 1

Trimethoprim‐induced fixed drug eruption: positive topical provocation on previously involved and uninvolved skin

eczematous eruption on and around the hyperpigmented areas. Patch tests with the GEIDC standard series proved negative. A patch test with the entire Kojicol PlusA product was ππ after 4 days. The patient was later tested with all the individual components of the product, including hydroquinone 1% pet. and with aqueous kojic acid solutions of 5%, 1%, 0.5% and 0.1%. All the patches with kojic acid were positive after 2 and 4 days (ππ to 5% and 1%). Patch tests with the other components of the product were negative. 20 controls tested with the same kojic acid solutions were negative. We recommend 1% aq. for patch testing kojic acid.

Carbamazepine induced eczematous eruptionclinically resembling atopic dermatitis

[ 11 Bauer EA, Bnggaman RA. Hereditary epidermolysis bullosa. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al, editors. Dermatology in general medicine, fourth ed. New York: McGrawHill, 1993;60:654-669. [2] Vichinsky E, Fridje J. Correction of the anemia of epidermolysis bullosa with i.v. iron and trythropoietin. Blood 1996;88(Suppl. I , Pt. 2):15b. [3] Eschbach JW, Kelly MR, Haley NR. Treatment of the anemia of progressive renal failure with recombinant human erythropoietin. N Engl J Med 1989;321;158-163. * Corresponding author: ServiCo de Dermatologia e Venereologia, Hospital de S%o Joio, Porto, Portugal. Tel.: +351-2-527151; fax: +351-2-5510119.