Boaz Amichai

Adverse drug reactions of the new oral antifungal agents – terbinafine, fluconazole, and itraconazole

Cutaneous side-effects Cutaneous reactions include mainly urticarial and erythematous eruptions, as well as pruritus.2 Villars and Jones4 reported mild skin eruption in 1.8% of 1440 patients receiving terbinafine in the daily recommended dose of 250 mg. More severe eruptions include erythema multiforme,5–7 toxic epidermal necrolysis,7 including a fatal case,8 and Stevens–Johnson syndrome.9 Erythema multiforme has been reported in 15 of 110,000 patients treated with terbinafine,3 which is quite a high frequency of development, and can be compared with 20 per 100,000 patients taking phenobarbital, and 3 per 100,000 for those exposed to sulfamethoxazol and trimethoprim and ampicillin.10 In most cases, the skin eruption developed during the first month of terbinafine therapy; withdrawal of the drug with or without corticosteroid treatment led to a resolution of the eruption. Other rare cutaneous sideeffects included erythema annulare-like eruption,11 fixed drug eruption,12 hair loss and alopecia areata,2 desquamation,13 and exacerbation of dermatitis.14

5α-reductase inhibitors – a new hope in dermatology?

Androgens, testosterone, and, in particular, dihydrotestosterone are prerequisites for sexual hair and sebaceous gland development. In conjunction with other regulatory factors such as insulin-like growth factors, androgens cause the prepubertal pilosebaceous unit in androgen-dependent areas to differentiate either into a terminal hair follicle or into a sebaceous follicle in which the sebaceous component proliferates and the hair remains fine. Androgens, particularly dihydrotestosterone, appear to play a major role in the pathogenesis of male-pattern baldness, hirsutism, acne, male pseudohermaphroditism, and benign prostatic hyperplasia. Antiandrogens reverse this process, causing pilosebaceous units to revert toward the vellus state. The conversion of testosterone to dihydrotestosterone is a key reaction for androgen activity. 5a-reductase is the enzyme responsible for the irreversible conversion of testosterone to dihydrotestosterone.S* , ,

Dapsone - the treatment of infectious and inflammatory diseases in dermatology.

Dapsone is known as useful in the treatment of infectious diseases. The use of the drug in infectious and inflammatory diseases in dermatology is reviewed.

Small malignant melanoma in patients with mycosis fungoides

An increased risk for a second malignancy has been reported in patients with mycosis fungoides. We describe two subjects with mycosis fungoides who developed small malignant melanoma after topical application of nitrogen mustard.

Alopecia as a rare cutaneous manifestation of POEMS syndrome

1 Romankiewicz JA. Franklin JE Jr, Allergic reactions to corticosteroid therapy, JAMA 1976: 236: 1939, 2 English JSC, Ford G, Beck MH, Rycroft R|G, Allergic contact dermatitis from topical and systemic steroids. Contact Dermatitis 1990:23: 196-7. 3 Brarabilla L, Boneschi V, Chiappino G et al. Allergic reactions to topical desoxymethasone and oral triamcinolone. Contact Dermatitis 1989; 21:272-4. 4 Rasanen L, Hasan T, Allergy to systemic and intralesional corticosteroids, BrJDermato! 199 J: 128:407-11, 5 Fernandez de Corres L. Bernaola G, Urrutia I, Munoz D. Allergic dermatitis from systemic treatment with corticosteroids. Contact Dermatitis 1990: 22: 104-6, 6 von Maur K, Rocklin RE, Stevens MB. Corticosteroid allergy in patient with systemic lupus erythematosus. Johns Hop!(ins Med j 1974; 134: 356-64, 7 Comaish S, A case of hypersensitivity to corticosteroids. Br / Dermato! 1969: 81:919-25, 8 Behan PO, Thomas M, Behan WMH. Allergic reactions to steroids presenting with neurological symptoms, Acla Neurol Scand 1982; 65:432-41 , 9 Pirila V. Endogenic contact dermatitis. Allerg Asthma 1970: 16: 15-19. 10 Fisher AA. Contact Dermatitis, 3rd edn. Philadelphia: Lea and Febiger 1986: 7 ,21 . 11 Adams RM, Occupational Skin Disease. 2nd edn, Philadelphia: W,B. Saunders 1990; 32,

Dystrophic epidermolysis bullosa associated with eosinophilic infiltrate and elevated serum IgE

An infiltrate of eosinophils is rarely seen in epidermolysis bullosa. We describe a child with dystrophic epidermolysis bullosa associated with a marked eosinophilic tissue infiltrate and elevated serum IgE.

Chronic trichophytic granuloma and abscesses in an immunocompetent patient

histiocytosis most often occurring in adults. On review of the literature, we found 21 GEH cases, only seven of them involving children [7-lOJ (Table 1). When analyzing all eight cases, it seems clear that lesions tend to appear between 4 months and 9 years of age, witJi periods of self-healing of varying duration (up to 5 years) and affect the two sexes equally. In summary, an exceptional case of pediatric GEH is reported. The absence of progression to other forms of non-X histiocytosis after a 3-year follow-up supports the concept of GEH as a specific diagnostic entity within the group of non-X histiocytosis, and, as a consequence, the recommendation that it be included in the differential diagnosis of this disease group in pediatric subjects.

An immunohistochemical study of bcl-2 protein expression in keratoacanthoma, as compared to squamous cell carcinoma and basal cell carcinoma

dust and extravasal erythrocytes (Fig. 2). A diagnosis of vasculitis in course of hyper IgE syndrome was therefore formulated. The therapy prescribed was 3 g oral ampicillin daily in accord with the antibiogram for 2 weeks, followed by maintenance therapy with diaminocillin (1 200000 UI) every 2 weeks until now. The patient experienced complete clearing of the lesions in the 10 month follow-up period with no relapses. Usually HES occurs early in infancy with eczematoid skin lesions c]ose]y resembling those of atopic dermatitis [3], which is more responsive to topical steroids, emollients and antihistamines, is seasonally related and when it is cornplicated with Gratii^ bacteria infections these tend to be more superficial than in HES [4]. Our case presents some typical features of HES, such as higb level of IgE, eosinophitia, coarse facies with broad nasal bridge and irregularly proportioned cheeks and jaws. However, the late onset of the disease and the vasculitic aspect of the lesions localized on the limbs and the face sparing the folds were atypical. It can be suggested that bacterial infections typical of HES might be the etiologic factor of the vasculitic process [5]. Bacteria may cause damage to vessel walls by activation of coagulation and platelet aggregation, acting as antigens in immune complexes or as toxins directly damaging the endothelial cells [6]. Altbough the management of patients with HES is considered difficult and dicloxacillin is the most effective treatment [7], our case responded dramatically to penicillin. The vasculitic skin lesions completely disappeared confirming that the bacterial infections were the cause of vasculitis. In conclusion, in cases of recurrent vasculitis the dosage of total serum IgE should be performed to detect Jobs syndrome with unusual clinical presentation.

Erythrodermic bullous pemphigoid

We report a case of erythrodermic type of bullous pemphigoid which is a rare variant of bullous pemphigoid. Our patient had a peculiar clinical presentation with bullae, erosions and extensive erythrodermic areas, and distinct direct immunofluorescent findings which included linear IgG and C3 deposits in the basement membrane and also IgG in the intercellular spaces. Very high levels of serum IgE were also detected in our patient.

Eruptive pseudoangiomatosis induced by gestodene in an oral contraceptive

We describe a case of eruptive pseudoangiomatosis triggered by the oral contraceptive Minulet® containing gestodene and ethinyloestradiol. A possible immunological mechanism in the induction of the skin lesions is suggested by the histopathological findings and a positive macrophage migration inhibition factor (MIF) test for the progesterone components in Minulet®.