Helmut Schöfer

Rosacea – S1 Guideline

Rosacea is a common infl ammatory skin disorder, which usually occurs in adults and primarily affects the face. The disease is characterized by a chronic, episodic course. The severity of disease varies clinically and morphologically. Initially, there may be only transient erythema on the face which becomes persistent. Telangiectases – mainly on the cheeks – are also very common. Papules and papulopustules are typical fi ndings in stage II of disease. Not only the face, but also adjacent areas, such as the neck, chest, back, and scalp, may also be affected. Other types of rosacea are characterized by lymphedema and diffuse hyperplasia affecting the connective tissue and the sebaceous glands, known as phyma (skin thickening). Skin thickening may be associated with other skin changes, or it may occur independently. Involvement of the eyes is common. The clinical appearance of papulopustular rosacea may resemble acne, although there are no comedones, and the patients are signifi cantly older than the typical acne patient. It is still under discussion whether rosacea is primarily a follicular disease. Synonyms: acne rosacea, couperosis, facial erysipelas (obsolete terms include acne erythematosa, and in German, “copper fi ns” or “red fi ns”).

Bacillary Angiomatosis in HIV-Infected Patients – An Epidemiological and Clinical Study

Background: No data were available on the epidemiological and clinical characteristics of bacillary angiomatosis (BA) in Germany. Objective: To determine epidemiological and clinical data on HIV-associated BA. Methods: A chart review of all BA cases between 1990 and 1998 was performed in 23 German AIDS treatment units. Results: A total of 21 cases of BA was diagnosed. During this period, the participating HIV centers treated about 17,000 HIV-infected patients. As a result, a BA prevalence of 1.2 cases/1,000 patients can be assumed. 19 BA were localized in the skin; in 5 cases bones and in 4 cases the liver were involved. Out of 20 patients who received antibiotic therapy, 13 had complete remission. The median time of duration up to complete remission was 32 days (9–82). During the follow-up of the 20 patients, 7 relapses were observed. Conclusion: BA is a rare HIV-associated disease with a prevalence of 1,2 cases/1,000 patients in the presented study.

Kaposi's sarcoma in HIV infection: impact on opportunistic infections and survival.

Objective:To determine the effect of Kaposis sarcoma on survival of HIV-infected patients. Methods:Retrospective cohort study to compare the survival of 241 HIV-infected homosexual patients with Kaposis sarcoma (cases) with that of 241 HIV-infected homosexual patients without Kaposis sarcoma (control subjects) but with a similar level of immunosuppression (measured by the absolute CD4+ lymphocyte count). Results:Cases and control subjects were similar in age, occurrence of previous opportunistic infections, and the use of antiretroviral therapy. The mean CD4+ lymphocyte counts were similar for cases and control subjects (185 × 106 versus 184 × 106/l, respectively). Cases had a higher incidence of opportunistic infections (5.95 versus 3.88 infections, respectively, per 100 person-months of observation) and a greater number of infections typical of late-stage HIV infection. Cases had a shorter overall survival than did control subjects (P = 0.0025). Kaposis sarcoma was associated with an increased risk of death (odds ratio, 1.28), even when adjusting for age, previous opportunistic infection, baseline CD4+ lymphocyte count, and antiretroviral therapy. Conclusion:Kaposis sarcoma appears to accelerate the clinical course of HIV infection. Opportunistic infections develop earlier and more often in patients with the disease than in control subjects. Survival was significantly shorter in patients with Kaposis sarcoma.

Chromoblastomycosis caused by Chaetomium funicola: a case report from Western Panama

Little is known about opportunistic fungi causing skin lesions in tropical countries such as Panama. We report an 83‐year‐old man from Chiriquí, Western Panama, with crusted skin lesions covering tumorous masses resembling Bowen’s disease of the skin on the dorsum of his right hand. Fungal cultures were obtained on different nutrient media from disinfected superficial skin scrapings and fragments taken from a deep skin biopsy. Deep skin biopsy showed the presence of globose, dark fungal cells in the upper and lower dermis, sometimes in abscesses or giant cells, indicating chromoblastomycosis. All fungal fragments plated on nutrient media yielded colonies of Chaetomium funicola which was identified based on morphological observations and molecular sequence data of large ribosomal subunit rDNA. Treatment with fluconazole was ineffective. Further treatments could not be applied because of the patient’s advanced age, low compliance, and limited resources in a rural, tropical environment. For the first time, C. funicola is confirmed as an opportunistic fungus causing superficial and deep cutaneous lesions. Up to now, the only known clinical record of this species is a tentative identification as an agent of deep mycosis.

Lip papillomatosis in immunodeficiency: therapy with imiquimod

Peristomal lichen sclerosus affecting colostomy sites Sir, Lichen sclerosus typically affects the genital area. We describe two patients with an unusual extra-genital presentation of lichen sclerosus. Patient 1 was a 72-year-old lady who presented with a 3-month history of a painful, ulcerated, eruption around her colostomy site. This had been fashioned 3 years earlier after emergency surgery for a large and benign diverticular mass. Recently, her stoma bag had become difficult to fit, and poor occlusion had resulted in progressive faecal leakage. Application of topical betamethasone valerate 0 ́1% (Betnovate, Glaxo-Wellcome, Uxbridge, Middlesex, U.K.) and fluocinolone acetonide 0 ́025% (Synalar, Zeneca Pharmaceuticals, Cheshire, U.K.) cream provided mild relief, but were ineffective in controlling her ulcerated eruption. She had been troubled by pruritus vulvae and ani for 12 years. On examination, there was a white circumferential indurated plaque with a rim of ulceration, purpura and bullae over the lateral edge around the colostomy site (Fig. 1a). In the anogenital region there were white atrophic patches with an erythematous edge. No other sites were affected. A biopsy from the peristomal skin showed an atrophic epidermis, homogeneous hyaline change in the papillary dermis and a dense band-like infiltrate of chronic inflammatory cells, characteristic of lichen sclerosus. Contact allergic dermatitis was excluded by negative patch-testing to the European Standard and Steroid Series, stoma bag, barrier material and adhesive. She was admitted and treated with clobetasol propionate 0 ́05% cream (Dermovate, Glaxo-Wellcome) to both peristomal and vulval areas. The peristomal inflammatory changes settled steadily over the next 2 months. Four months later, she had a relapse of her peristomal lichen sclerosus. This was controlled with clobetasol propionate 0 ́05%, neomycin 0 ́5%, nystatin 100,000 U/g cream (Dermovate-NN, Glaxo-Wellcome), applied twice daily for 2 weeks, followed by the intermittent use of clobetasol propionate 0 ́05% cream. By 2 months the peristomal skin had largely returned to normal. Patient 2 was an 84-year-old lady who presented with a 1-year history of a peristomal eruption around her colostomy site, formed after an abdominoperineal resection for a Dukes A rectal carcinoma. She had suffered from pruritus vulvae for 10 years. On examination there was a white thickened plaque with a smooth surface around the stoma (Fig. 1b). No other extragenital lesions were noted. Similar white atrophic patches were present over the vulva. A clinical diagnosis of peristomal lichen sclerosus with vulval involvement was made, and confirmed on biopsy of the vulva which showed a focal chronic inflammatory infiltrate with homogenization of the dermal collagen. She was treated with 0 ́05% clobetasol propionate (Dermovate) cream, to both her vulval and peristomal sites. The peristomal skin returned to normal within 4 weeks. There has been no relapse since and she remains well. In a review of 5207 patients diagnosed with lichen sclerosus, Meffert et al. found genital involvement alone in 85%, truncal involvement alone in 15%, and concurrent genital and truncal involvement in 7%. Infrequent sites of involvement have included the infraorbital skin, scalp, scrotum, palms and soles. To our knowledge there have been no reported cases of lichen sclerosus over the peristomal skin of a colostomy site. The more common dermatoses over peristomal sites are enzyme-induced irritant contact dermatitis, and less frequently allergic contact dermatitis to various components of the pouch, barrier materials and adhesive. A number of cases of pyoderma gangrenosum have also been described in peristomal skin. The cause of lichen sclerosus remains unclear. Mechanisms involving genetic, hormonal and autoimmune factors may all play a part. In our two patients we suspect that repeated mechanical trauma or irritancy precipitated lichen sclerosus by the isomorphic (KoÈbner) phenomenon. Other unusual sites of extragenital lichen sclerosus where the KoÈbner

Evaluation of imiquimod for the therapy of external genital and anal warts in comparison with destructive therapies.

External genital and anal warts (acuminate condyloma) were the first medical indication the topical immune response modifier imiquimod was approved for in 1997. Since then, many placebo controlled randomized clinical trials have demonstrated the efficacy and safety of this synthetic imidazoquinoline derivate for the treatment of different human papillomavirus infections and tumours. Treatment modalities for genital warts (5% cream, three times weekly, minimum duration 4 weeks, control of side‐effects) have been optimized and assured by further clinical trials and meta‐analyses. For a few years clinical studies focussed on the long‐term efficacy of the immunomodulatory therapy (sustained clearance from warts) and most recent studies compared the efficacy of ablative, destructive and imiquimod monotherapy as well as combination therapies.

Oxidative imbalance in HIV infected patients

We present an outline of the complex interplay of oxidants and antioxidants in infectious diseases in general, and in particular with reference to the HIV infection, and subsequent opportunistic infections. Viral and opportunistic infections may directly or indirectly cause an imbalance in prooxidant/antioxidant mechanisms and result in generation of increased steady state concentrations of reactive oxidants. In HIV patients a prooxidant state could lead to a self-perpetuation of infection via stimulated expression of genes carrying the virus genome, and subsequently to immunosuppression, and promotion of initiated cells to neoplastic growth.

Syphilis. Leitlinie der Deutschen STD Gesellschaft zur Diagnostik und Therapie der Syphilis

no. 2004; MoPeB3283. Korting HC, Walther D, Riethmüller U et al. Comparative in vivo susceptibility of Treponema pallidum to ceftizoxime, ceftriaxone and penicillin G. Chemotherapy. 1986; 32: 352–355. Larsen SA, Steiner BM, Rudolph AH. Laboratory diagnosis and interpretation of tests for syphilis. Clin Microbiol Rev

Short German guidelines: angiosarcoma and Kaposi sarcoma.

Definition Angiosarcoma is a rare highly malignant endothelial tumor which accounts for only 1-2% of all soft tissue sarcomas. The most common sites are the skin and superficial subcutaneous tissue, especially of the head and neck region. However, angiosarcomas can also develop in almost every internal organ. Post-radiation angiosarcoma is an increasing problem, especially with increasing use of radiation therapy for breast carcinoma. The average age of angiosarcoma patients is 65-70 years. Angiosarcomas do occur in children and adolescents, but then more often in internal organs or in association with a vascular malformation such as Klippel-Trenaunay syndrome. Angiosarcomas of the breast and deeper soft tissue also affect a younger patient group. The prognosis is guarded, despite many advances in therapy, especially because of the diffuse infiltrative and discontinuous or even multifocal growth pattern. The most important pathogenetic factor is persistent lymphedema. Post-mastectomy lymphedema is most common but any persistent lymphedema can be involved including congenital lymphedema. Radiation-induced angiosarcoma, in the absence of lymphedema, appears on average 6 years after exposure. Other associated factors are arteriovenous fistulas, for example involving the shunt arm for renal dialysis, most commonly when such patients then receive renal transplantation and immunosuppression. The role of carcinogens and foreign bodies for cutaneous angiosarcoma is unclear, but in the liver Thorotrast, arsenic and vinyl chloride are all definitely associated. Rarely angiosarcomas develop within benign tumors such as leiomyoma or neurofibroma; they are even rarer within benign vascular tumors. Angiosarcomas have no relation to human herpesvirus 8 (HHV-8)

CLASTOGENIC FACTORS IN PLASMA OF HIV-1 INFECTED PATIENTS

The objective of this study was to investigate the clastogenic activity of plasma ultrafiltrates from HIV-1 infected patients. Clastogenic factors are chromosome-damaging agents with low molecular weight (< 10,000 daltons) which cause chromosome aberrations, sister chromatid exchanges, DNA strand breakage, and gene mutation. They have first been described in the plasma of irradiated persons, but they are also found in hereditary breakage syndromes and chronic inflammatory diseases with autoimmune reactions. Their formation and their clastogenic effects are modulated by superoxide anion radicals. We analyzed a total of 22 HIV-1 positive patients in comparison to 20 reference plasma samples from healthy HIV negative blood donors of similar age. The plasma ultrafiltrates (filter cutoff 10,000 daltons) from patients induced a statistically significant increase in chromosomal breakage in the cytogenetic test system (20.5 +/- 6.8 aberrations per 100 cells), while no increase was observed in test cultures exposed to plasma ultrafiltrates from healthy blood donors (6.3 +/- 2.9 aberrations per 100 cells). The breakage values were slightly, but not significantly, lower in the 10 patients with more than 200 T-helper cells/ml (18 +/- 4 aberrations per 100 cells), than in the 12 patients with less than 200 T-helper cells/ml (22.3 +/- 7.9 aberrations per 100 cells). HIV patients with high clastogenic activity (induction of more than 20 aberrations per 100 cells, range 20 to 39) showed higher plasma levels for malondialdehyde than those with lower clastogenic activity (less than 20 aberrations per 100 cells, range 12 to 18). However, the difference was statistically not significant. Another lipid peroxidation product, 4-hydroxynonenal, was increased equally in both groups. There were no significant differences in water- and lipid-soluble plasma antioxidants between the low- and high-breakage group. In agreement with previous findings, the clastogenic effects of plasma ultrafiltrates in the test cultures were reduced by the antioxidant enzyme superoxide dismutase. The presence of clastogenic factors in the plasma of HIV patients is further evidence for a prooxidant state in these persons. Since clastogenic factor formation appears to occur at an early stage of the disease, it may be significant for virus release or activation, because of the superoxide anion stimulating effects of clastogenic factors. From a practical standpoint, clastogenic factors may be useful for evaluation of promising drugs.