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Notes: To characterise the new patient referrals to a combined vulva clinic and to assess the role of genitourinary services within the clinic.〈section xml:id="abs1-3"〉〈title type="main"〉MethodsA case note review of all new patients attending a monthly, multidisciplinary vulva clinic over a 12-month period.〈section xml:id="abs1-4"〉〈title type="main"〉ResultsThe mean age of the 135 women was 43 years (range 18–86 years). The majority of patients, 64 (47%), were referred by their general practitioner (GP). Using nurse and physician triage 85 (63%) patients were seen by a dermatologist, 55 (41%) by a genitourinary medicine physician, 38 (28%) by a gynaecologist and six (4%) by a psychosexual physician. Fifty-one (38%) women required a consultation by at least two specialties. Itch was the most frequent presenting symptom (70%) and 59 (44%) women had experienced symptoms for between 6 months and 2 years. A previous STD screen had been performed in only 57 (42%), which was negative in 45 (79%). The most frequent initial clinical diagnoses were lichen sclerosus (35, 26%), vaginal candidiasis (21, 16%), vulvodynia (16, 12%), lichen simplex chronicus (13, 10%) and Bowenoid papulosis (13, 10%). Thirty-eight (28%) women had microbiological investigations revealing 13/135 (10%) had vaginal candidiasis and two (2%) bacterial vaginosis, all symptomatic. A biopsy was performed in 32 (24%) confirming the initial diagnosis in 20 (63%) cases. Treatment was initiated in 101 (75%) women: 62 (46%) were prescribed steroid cream, 46 (34%) emollient cream and 22 (16%) treatment for Candida infection. Fifty-three (39%) women received more than one treatment. 94 (70%) patients were followed-up in the vulval clinic, five (4%) in the genitourinary clinic and 12 (9%) by their GP.〈section xml:id="abs1-5"〉〈title type="main"〉ConclusionsDespite having genitourinary symptoms less than half the patients had been tested for infection prior to attending the clinic. More than a third of the patients, 46 (34%), were diagnosed with a genitourinary infection. There is a significant role for genitourinary services in the diagnosis, management and ongoing care of patients in a vulva clinic.

Notes: Objective To describe and illustrate bleomycin-induced cutaneous toxicity, which may present atypically in AIDS patients with Kaposi's sarcoma.Design and subjects Case note review of all AIDS patients receiving systemic chemotherapy in the preceding year.Setting Combined oncology and HIV out-patient clinic at the Chelsea and Westminster Hospital in London.Outcome measured Cutaneous toxicity associated with intravenous bleomycin therapy.Results We report three cases of bleomycin-induced flagellate dermatitis with atypical presentation of pruritic skin lesions after relatively low doses of bleomycin.Conclusions Bleomycin usage is increasing as an effective agent in the treatment of AIDS-related Kaposi's sarcoma. Awareness that cytotoxic drugs may produce a range of unusual cutaneous adverse effects in this patient population is important for doctors of all specialities who treat HIV-infected patients. The pathomechanism of flagellate dermatitis is discussed.

Notes: A woman with a 20-year history of acral pustular psoriasis of Hallopeau and recurrent pustular lesions of the forearms and lower legs, developed a B-cell lymphoma of the lip following 4½ years of treatment with razoxane.

Notes: A randomised, double-blind, placebo-controlled trial with lithium succinate ointment was conducted in patients with UDS-associated facial seborrhoeic dermatitis. Twice daily applications of the ointment brought about a rapid (2-.S days) and highly significant (P= 0·007) improvement in the severity of the condition. Lithium succinate ointment is well tolerated and can be a useful treatment for seborrhoeic dermatitis in this group of patients.

Notes: We report a patient with the glucagonorna syndrome and octreotide-resistant necrolytic migratory erythema (NME). The NME responded on two occasions to an intravenous infusion of essential fatty acids (EFA) and ammo acids (AA). A deficit of serum EFA prior to treatment was corrected following the infusion, whilst plasma AA were low before and after treatment. These findings indicate that NME, in the glucagonoma syndrome, may respond to correction of the EFA deficit, and that NME-may be a disease of EFA deficiency.

Notes: Langerhans cells (LC) are antigen-presenting CD4+ dendritic cells in the skin which may become infected by the human Immunodeficiency virus (HIV). Decreased LC function could account for the cutaneous manifestations seen in HIV disease. Previous studies of epidermal LC density in HIV-infected subjects have produced conflicting results. A definitive, prospective, case-control study was performed lo determine whether there is an association between epidermal LC density mid HIV clinical disease stage. Skin cryosections were stained with the CD1 monoclonal antibody using a three-step immunoperoxidase method. LC were counted by light microscopy and epidermal dimensions calculated with computer-assisted planimetry. The stage of the HIV clinical disease correlated with epidermal LC densities was quantified by three different methods: mean LC numbers per mm length of basement membrane, mean LC per mm2 of epidermal area, and mean LC population per mm of epidermal surface length. Seventy-one subjects, recruited from a large out-patient HIV clinic in London, comprised 56 HIV-positive men and 15 male HIV-negative controls. Contrary to previous smaller studies, there was no detectable association between epidermal LC density (quantified by any of the three methods) and the stage of the HIV clinical disease. Given that HIV infects large numbers of CD4+ cells, we propose possible hypotheses to account for the apparent preservation of static LC numbers in the skin, further studies of LC kinetics and function are required to elucidate their role in the natural history of HIV infection.

Notes: Summary Langerhans cells (LCs) subserve an important antigen-presenting function in the skin immune system. They bear CD4 receptors, which make them potential targets for infection with the human immunodeficiency virus (HIV-1).The observation of reduced numbers of LCs in the skin of patients with the acquired immunodeficiency syndrome (AIDS), and the association of severe psoriasis with HIV-1 infection, raise interesting questions regarding the role of LCs in the skin of HIV-1-positive psoriatic patients.In this study, LCs were quantified in the lesional and non-lesional skin of seven HIV-1-positive psoriatic patients, and the results were compared with age-, sex- and site-matched HIV-1-negative psoriatic patients. The number of LCs was determined by staining skin sections with S-100 polyclonal antibody, using the three-step avidin—biotin immunoperoxidase method. The S-100-positive cells above the basal layer were quantified in two ways: cells/mm2 of epidermal area, and cells/mm of length of basement membrane.HIV-1-positive psoriatic patients showed a reduction in the number of epidermal LCs compared with HIV-1-negative psoriatic patients using both methods of quantification, in both lesional and non- lesional skin (P 〈0·05, Mann-Whitney test). In addition, a reduction in the number of LCs in lesional compared with non-lesional skin was observed in both HIV-1-positive and -negative patients when LCs were quantified per mm2 of epidermal area (P〈0·05, Wilcoxon test). This reduction was also observed when LCs were quantified per mm length of basement membrane, but the reduction was not statistically significant in the control group of HIV-1-negative psoriatic patients. Our findings of a reduced number of LCs in the epidermis of HIV-1 -positive psoriatic patients may be associated with the clinical deterioration of psoriasis in these patients.

Notes: Factor XLLLa-positive dermal dendrocytes (FXIIIa+ dd) may have an important role in the pathogenesis of psoriasis, in that their numhers are increased in lesional skin compared with non-lesionai skin. Moreover, in AIDS-associated Kaposi's sarcoma the number of these cells is also increased, in comparison with the classical type of Kaposi's sarcoma. In addition, patients suffering from HIV-1 infection may develop severe psoriasis.The aim of this study was to examine the distribution of FXIIIa+ dd in lesional and non-lesional skin from seven psoriatic patients with positive HIV-1 serology. and compare the results with age-, sex-, and site-matched HIV-1-negative psoriatic patients. In both patient groups there was an increase of FXIIIa +dd in the papillary dermis in lesional skin, compared with non-lesional skin (HIV+ [P=0.0007]: HIV− [P=0.0006]). Positive cells were also observed within the epidermis in lesional skin in both groups. However, there was no significant difference between HIV-1+ and HIV-1− groups in the number of FXIIIa+ dd in the epidermis and dermis (P〉0.05). These findings suggest that, if FXIIIa+ dd do have a role in psoriasis, deterioration of this condition in HIV-1+ patients is not due to proliferation of dermal dendrocytes.