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Notes: Aim We aimed to clarity the effectivenes of our staging of LM over a I-year period.Background Cryosurgery has become accepted as a simple and effective treatment for lentigo maligna (LM) but not necessarily lentigo maligna melanoma (LMM). Pigmented epithelial cells are extremely sensitive to cold injury. If adequate freezing is delivered to the proper depth into the dermal appendages, LM should be eradicated. However, if the initial staging does not detect invasion the lesion may be inadequately treated.Methods Over 1 year prospectively. all patients presenting with LM(n= 12) wore stayed clinically by experienced dermatologists and by a single punch biopsy. This was then checked by complete excision of the lesion.Results In 9 patients the clinical and punch biopsy diagnosis was confirmed after excision. Two melanomas were missed clinically but detected on punch biopsy. In one patient the punch biopsy described a “LM with probable invasion elsewhere in the lesion”. Surgical excision yielded a melanoma, 0.8 mm thick. Clark's level 4. In a second patient, punch biopsy diagnosed superficial spreading melanoma (-SSM) in situ, confirmed on excision.Conclusions We therefore feel that clinical diagnosis combined with a single punch biopsy will diagnose invasion when present. We emphasise that cryotherapy should not be performed without punch biopsy confirmation of the clinical diagnosis.

Notes: Aims To establish the skin changes found in epileptics, and to relate these changes to drug therapy.Background Skin changes in epileptics, although welt acknowledged, have been subjected to few recent large-scale surveys. Newer anti-epileptic drugs, in addition to the older therapies, including phenytoin, phenobarbitone and primidone, are now popular. In an effort to update our knowledge of skin changes in epileptics, a study of 200 patients in a long-term epilepsy hospital was performed.Methods The study included taking a history, recording drug therapy and examining the skin of 200 patients.Results Patients ranged in age from 21 to over 70. 60% were men and 40% women. Their epilepsy was mostly well controlled, varying in length from less than 10 to greater than 40 years. 57.5% had post traumatic scars. 32.5% had gum hypertrophy, only half having dental caries. Dupuytren's contracture occurred in 24.5%. Seborrheic dermatitis was seen in 15%. 12.5% had coarse facial features and 11.5% had acne. 57.5% of women had facial hirsutes. 17.5% of all patients had sacral hirsutes, which is an unique feature in this group of patients. These clinical findings were correlated with drugs taken at the time, the age of the patients and length of epilepsy. 52% were on carbamazepine, 48% on phenytoin and 42% on primidone or phenobarbitone, singly or in combination.Conclusions A number of skin conditions are more common among epileptics. Phenytoin and phenobarbitone are linked to gingival hypertrophy, palmar fibromatosis, hypertrichosis, coarse fades and acne. Carbamazepine, too, may be implicated in gum hypertrophy, palmar fibromatosis, hypertrichosis, more specifically sacral hirsutes, seborrheic dermatitis, acne and coarse facies.

Notes: We have assessed the cutaneous signs in 73 patients with systemic lupus erythematosus (SLE), seen during a 5-year period in an English hospital. Most previous information about the cutaneous manifestations of SLE has been obtained from studies performed in the U.S.A. We classified lesions as specific cutaneous and mucosal LE (acute, subacute and chronic) or non-specific LE-related, e.g. photosensitivity, urticaria, erythema, Raynaud's phenomenon or vasculitis. Acute cutaneous LE lesions included a butterfly rash with erythematous macules, telangiectasia or papulosquamous lesions, seen in 37 patients (51%) and facial oedema seen in four patients (5%). Five patients (7%) had psoriasiform subacute cutaneous LE, Chronic cutaneous LE was common: 18 patients (25%) had chronic discoid lesions (DLE) and, in 12 (15%), these had preceded systemic disease. One patient had facial lupus profundus. Ten patients (14%) had scarring alopecia secondary to DLE. Fifteen patients (20.5%) had chronic chilblain lupus. Twenty-three patients (31.5%) had a history of mouth ulceration. Of these, 11 (15%) gave a history of ulcers at the onset of their disease. Three (4%) had erythema and superficial ulceration of the palate, not typical of aphthous ulcers, and three (4%) had chronic buccal plaques. Cheilitis due to DLE was seen in three (4%), episcleritis in three (4%), five (7%) had nasal disease, six (8%) bullous skin eruptions, one ‘the bullous eruption of SLE’, four bullae associated with cutaneous vasculitis, and one bullae associated with ultraviolet radiation. Forty-six (63%) observed photosensitivity. A non-scarring alopecia occurred in 29 (40%). Vascular phenomena were common: three patients (4%) had chronic palmar erythema. Raynaud's phenomenon occurred in 44 patients (60%), chronic urticaria, worsened by sun exposure, was noted by 32(44%) (in whom the lesions often lasted more than 36h), eight (11%) had cutaneous vasculitis and three (4%) livedo reticularis.Skin changes play a prominent part in SLE and may provide helpful diagnostic information. In this British population, chilblains and urticaria were particularly common. Lesions of subacute cutaneous LE were relatively unusual in this group of patients with SLE.

Notes: We have examined the action of cantharidin on the skin of patients with Darier's disease, and used immunohistological techniques to determine the distribution of desmosomal components, keratin intermediate filaments, and proteases in cantharidin-induced blisters. Cantharidin induced acantho- lysis, but the presence of acantholysis did not trigger the development of the characteristic warty, dyskeratotic papules in patients with Darier's disease.The distribution of desmosomal components. keratins and proteases within the acantholytic keratinocytes in the cantharidin-induced blisters was similar to that previously found in acantholytic cells within lesions of Darier's disease: peripheral staining for extracellular desmosomal components was reduced: some desmosomal components were detected diffusely in the acantholytic cells: basal cell keratin markers were expressed by some suprabasal acantholytic cells, and plasminogen was detected in association with acantholytic cells. Cleavage of desmosomes did not reveal the underlying abnormality in Darier's disease.

Notes: Summary Blistering in systemic lupus erythematosus has been divided into three groups.1 A specific subgroup of ‘bullous systemic lupus erythematosus’ has been defined by Gammon et al. on the basis of a number of criteria.2 From our experience of seven patients with bullous systemic lupus erythematosus, and after reviewing the literature, we suggest that the current classification is too narrow. Our patients displayed clinical and immunohistolegical (based on direct and indirect immunofluorescence and Western immunoblotting) heterogeneity. Sera from two patients bound to epidermal epitopes in sodium chloride-split skin, but immunoblotting was negative. In neither of these patients could the target antigen be type VII collagen, the only antigen identified as pathogenic in this disease. Patients with epidermal binding should not be excluded from a diagnosis of bullous systemic lupus erythematosus. SLE is a disease in which there is a genetic predisposition to form antibodies to type VTI collagen, along with other autoantibodies, many of which may be implicated in blistering. We suggest that the criteria for the diagnosis of BSLE should be revised. We define this disease as an acquired subepidermal blistering disease in a patient with SLE, in which immune reactants are present at the basement membrane zone on either direct or indirect immunofluorescence.

Notes: Summary The behaviour of cutaneous disease in systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE), under the influence of various hormonal states, was studied in 68 patients. In 28 pregnancies, cutaneous disease was essentially unchanged. In a total of 57 patients whose lupus erythematosus (LE) had been diagnosed prior to the menopause, 20% described a premenstrual cutaneous exacerbation. Only three patients had taken an oestrogen-containing contraceptive. The duration of oral contraceptive treatment before the onset of lupus varied: 1 month in a patient presenting with the acute malar rash of SLE, 2 months in a patient who presented with annular weals and later developed systemic features, and 12 months in a patient who developed generalized DLE. Thirty-three patients were menopausal at the time of the study; 4% had noticed a perimenopausal cutaneous flare. There was no deterioration in the skin of the five patients on hormone replacement therapy.

Notes: Summary Acantholysis is a feature of disorders such as Hailey-Hailey disease and Darier's disease. Immunocytochemical studies have shown internalization of desmosomal components after acantholysis. Basal cytokeratins show suprabasal expression in lesional Darier's disease. The exact mechanisms of acantholysis are still unclear. Cantharidin induces blistering, with suprabasal keratinocyte acantholysis, possibly by protease activation. Plasmin has been implicated in the pathogenesis of acantholysis in Darier's disease and Hailey-Hailey disease. We examined the distribution of desmosomal components, proteases and cytokeratins in cantharidin blisters, to compare them with those previously found in Darier's disease and Hailey-Hailey disease. Two drops of cantharidin collodion were applied to the skin of five normal volunteers. A 4-mm punch biopsy of the blister was taken, and snap frozen. Sections were stained with antibodies to desmosomal proteins (dp) 1/2, dp 3, desmosomal glycoproteins (dg) 1, 2/3, extracellular carbohydrate residues, using the lectins peanut agglutinin (PNA) and soybean agglutinin (SBA), proteases and cytokeratins. Acantholytic cells were stained diffusely with dp l/2: there was markedly reduced or absent peripheral staining for dp 3, dg l, dg 2/3, PNA and SBA. There was no clumping of stain. Plasminogen, fibrinogen and urokinase were expressed in some acantholytic cells. Basal keratin markers were expressed suprabasally in acantholytic cells. These results are similar to those previously obtained in Darier's disease, but different from the staining obtained in Hailey-Hailey disease. Extracellular glycosylated portions of adhesion molecules may be lost after acantholysis, perhaps as a result of conformational changes, internalization of extracellular domains, or proteolysis. The changes in the expression of plasminogen, fibrinogen, urokinase and cytokeratins in acantholytic cells in cantharidin-induced blisters are, as in Darier's disease and Hailey-Hailey disease, probably secondary to acantholysis, and changes in the shape of cells. We conclude that cantharidin blisters may be a useful model for the study of acantholysis in Darier's disease.

Notes: A 79-year-old virgo intacta presented with a 20-year-history of intertrigo. and a 3-month history of superimposed warty masses beneath both breasts and in the groin and perianal areas. There was no evidence of immunosuppression. Histology of the warty lesions showed squamous papillomata. with evidence of wart virus infection. Human papillomavirus (HPV) type 6 was identified by in situ DNA hybridization, in the submammary lesions. This is an unusual manifestation of both intertrigo and wart virus infection. HPV-6 is classically found in anogenital warts. We assume that these warts were acquired by a non-venereal route and/or by congenital infection some 78 years ago. We suggest that it is the warm, moist environment, rather than the specific site, which encourages HPV-6 to flourish.