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Biomedical subjects

R Höpfl

Publications and source records attributed to R Höpfl.

30 records · Page 2Linked to original sources
PubMed1994

Buschke-Loewenstein tumour infiltrating pelvic organs.

We report a 42-year-old HIV-negative patient with a 12-year history of exceptionally extensive genital warts and coexisting verrucous carcinoma of the anogenital region (Buschke-Loewenstein tumour). Masses of both tumour and viral papillomas infiltrated the external genitalia, perineum and buttocks, pelvic diaphragm and parts of the lesser pelvis, as well as the urethra, prostate and parts of the urinary bladder, necessitating repeated surgical intervention and plastic reconstruction. Adjuvant interferon-alpha therapy was given without any lasting effects. Human papillomavirus type 6 was detected by DNA in situ hybridization and Southern blot analysis.

Adult↗
PubMed1994

[Pyoderma gangraenosum: differential diagnosis in ulcus cruris and postoperative exacerbating processes].

A case of pyoderma gangrenosum that was initially misdiagnosed as postthrombotic ulcers is described. Surgical debridement triggered postoperative exacerbation. Dermatologic examination was then initiated and the diagnosis pyoderma gangrenosum was established. No underlying illness was detectable. Immunosuppressive therapy stopped disease activity promptly and as previously reported low-dose cyclosporine was also effective in our exceptionally therapy resistant case. Pyoderma gangrenosum should be considered as a rare, but important differential diagnosis of leg ulcers and postoperative progressive exacerbation. Timely diagnosis based on clinical suspicion is pertinent for correct therapy and to avoid iatrogenic deterioration of the disease.

Diagnosis, Differential↗
PubMed1990

[Long-term danazol therapy for hereditary angioedema].

Three patients with hereditary angio-oedema, two men of 19 and 35 years and a woman of 69 years, have been treated for 10 years with danazol, an androgen preparation with diminished androgenic effects. The 19-year-old man started taking it at the age of nine years and continued throughout puberty. Maintenance therapy with 200 mg twice a week, together with occasional booster doses of 200 mg daily, started at the age of 16 years and given when required cut the frequency of attacks from one a week to roughly six a year and greatly reduced their severity. Sexual maturation was entirely normal. The 35-year-old man, who had previously had three severe attacks a week, became symptom-free on a dose of 200 mg four or five times a week. During treatment he fathered a healthy child. The 69-year-old woman had had attacks every four weeks after the menopause, but obtained complete relief from a dose of 200 mg six times weekly. C1-Esterase inhibitor--originally depressed to around 30% of normal in all these patients--rose to about 50% during treatment. Endocrine, metabolic and toxic side-effects were minimal.

Adult↗
PubMed1990

[Eruptive viral warts of the burn area].

Eruptive viral warts were observed in a second-to-third degree burn area in a 68-year-old woman; the warts healed spontaneously and completely after approximately 3 weeks. HPV-2-related DNA was demonstrated by Southern blot analysis.

Aged↗
PubMed1989

[Benign prostatic hyperplasia: a stromal disease].

Morphometric studies show that benign human prostatic hyperplasia is a stromal disease caused by the activation of smooth muscle cells. This activation manifests itself in increased amounts of cytoplasmic organelles, which are preferably localized in the perinuclear region. Moreover, marked vesicular activity is present. Besides considerable overproduction of type I and III collagens, the architecture of the extracellular matrix is altered distinctly. In spite of strong evidence that androgens and estrogens regulate the growth of epithelial and stromal cells in the prostate and the induction of fibromuscular overgrowth in various animal models, the exact role of steroids in the pathogenesis of benign prostatic hyperplasia still remains to be elucidated.

Androgens↗
PubMed1988

Rejection, after a slightly prolonged survival time, of Langerhans cell-free allogeneic cultured epidermis used for wound coverage in humans.

Autologous cultured epidermis (CE) grown from small skin biopsies in vitro has been successfully applied for wound grafting in humans. Since it has been reported recently that allogeneic CE might be tolerated as permanent wound cover, we investigated the properties of CE and its use as autologous and allogeneic grafts. Except for some differences, such as the absence of Langerhans cells and the lack of a stratum corneum, CE resembled its natural analogue. Autologous CE applied for grafting of leg ulcers and various surgical skin defects adhered firmly and permanently to the wound bed within 2 weeks, became regularly stratified, and formed a stratum corneum. Langerhans cells gradually entered the grafts; the dermis contained no inflammatory infiltrate. Allogeneic CE unmatched for MHC and blood group antigens used to partially cover tangentially excised third-degree burns, donor sites of split-thickness skin, and a defect after tumor excision initially survived well like the autografts. However, they were completely rejected after 10-22 (mean, 14.5) days, which is 4-5 days later than reported for split-thickness skin allografts. Clinically, rejection presented as "melting" of the graft. (Immuno)histologically, we found a dense mononuclear dermal infiltrate consisting predominantly of activated T cells, vacuolization, and single-cell necrosis of keratinocytes, as well as HLA-DR expression on keratinocytes, and finally separation and lysis of the epidermis. Limiting dilution analysis in 2 out of 4 allograft recipients revealed a considerable increase of circulating donor-specific cytotoxic T cell precursors during graft rejection. We conclude that grafting of allogeneic CE does not lead to permanent but to slightly prolonged graft survival.

Adolescent↗
PubMed1988

[Amyloid K].

Electron-microscopic, histochemical and immunological studies have shown that the deposits of primary and secondary localized cutaneous amyloid (amyloid K) consist mainly of keratin filament material. The amyloid P component is the second most significant constituent. Pathogenetically, defective keratinocyte apoptosis is the most likely mechanism of generation for amyloid K. Apoptosis is a distinct mode of cell death according to which individual basal keratinocytes disintegrate in physiological and pathological conditions to form membrane-bound "apoptotic" bodies consisting mainly of keratin filament aggregates. These lose their protective membrane and drop into the upper dermis, where they present as keratin (Civatte, cytoid) bodies, which are regularly coated with immunoglobulins. Overproduction of keratin bodies and/or a defect in their degradation by enzymatic digestion or phagocytosis by macrophages and fibroblasts, followed by conversion into amyloid fibrils, may be responsible for the generation of deposits of amyloid K.

Amyloid↗