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J Am Acad Dermatol. 2001 Jan;44(1):129-31.
Inflammatory vitiligo in Vogt-Koyanagi-Harada disease.

Tsuruta D, Hamada T, Teramae H, Mito H, Ishii M.

Departments of Dermatology and Ophthalmology, Osaka City University Medical School, Japan.

Vogt-Koyanagi-Harada disease is a rare disease characterized by uveitis, meningitis, dysacusis, alopecia, poliosis, and vitiligo. We describe a 48-year-old patient with Vogt-Koyanagi-Harada disease associated with thin inflammatory raised erythema and plaque-type inflammatory erythema superimposed on vitiligo. Interestingly, inflammatory raised erythema was separated from the perfect vitiligo, and the incomplete vitiligo lay between them initially. Thereafter, incomplete vitiligo became completely depigmented with diminution of inflammatory raised erythema. This is the second case of vitiligo with inflammatory raised borders associated with Vogt-Koyanagi-Harada disease. Our results of immunohistochemical and electron microscopic studies suggested the involvement of T-cell-mediated cytotoxicity and apoptosis in the development of skin lesions.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11148490&dopt=Abstract



Plast Reconstr Surg. 1999 Dec;104(7):2108-11.
Repair of wide coup de sabre without cutaneous excision by means of pericranial-galeal padding flap.

Danino AM, Ichinose M, Yoshimoto S, Wako M, Servant JM.

Department of Plastic and Reconstructive Surgery, Chiba University Hospital, Japan.

A case of double linear scleroderma of the forehead (coup de sabre) is described. The histopathology of this rare lesion is now well known with a normal epidermis and a sclerotic dermis. The correction was done with an original two-stage procedure: the lesion with alopecia was first treated by excision-suture and a transfer of the involved subcutaneous tissue along the right inner canthus; 1 year later, by a hemicoronal incision, we transferred a galeal-pericranial flap beneath the wider forehead lesion. We think that the use of a filling flap to correct wide coup de sabre lesions without cutaneous excision can be a simple alternative to the classic treatment by complete excision and flap reconstruction. The subcutaneous fascial system of the scalp can provide a good donor site with minimal morbidity.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11149775&dopt=Abstract



Horm Res. 2000;53(5):260-6.
Apparent cortisone reductase deficiency: a rare cause of hyperandrogenemia and hypercortisolism.

Biason-Lauber A, Suter SL, Shackleton CH, Zachmann M.

Department of Pediatrics, University of Zurich, Switzerland. alaubeispi.unizh.ch

A 55-year-old woman presented with androgenetic alopecia which had started at age 40. Her clinical history revealed that, unlike her younger sister, she was unable to conceive and was diagnosed as being sterile at age 30. At age 45, 21-hydroxylase deficiency (late-onset CAH) was assumed and glucocorticoid treatment suggested, but not initiated. There was slight hirsutism, but no other sign of virilization. Retesting of plasma steroids revealed elevated 17-OH-progesterone and free testosterone. Treatment with prednisone, cyproterone acetate, and spironolactone was started with significant clinical success. Surprisingly, the analyses of urinary steroid metabolites revealed a pattern that did not support the diagnosis of 21-hydroxylase deficiency (pregnanetriolone absent, pregnanediol, 17-OH-pregnanolone and pregnanetriol not increased). Abdominal CT showed bilateral adrenal hyperplasia and masses in both ovaries. Bilateral adnexectomy was performed, and cystic teratomas were diagnosed. Postoperative urinary steroid analyses showed a decreased tetrahydrocortisol/tetrahydrocortisone ratio (values around 0.08 as compared to age- and sex-matched controls with a ratio of about 0.5-0.8). Plasma cortisol appeared to be repeatedly elevated with exogenous sources excluded. Mass spectrometry showed that, while the tetrahydro metabolites were mainly cortisone-derived, the metabolites not reduced in A ring were mostly cortisol derivatives. This constellation clearly indicates cortisone reductase deficiency, a defect of hepatic 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD1). This enzyme catalyzes the oxidation of cortisol to cortisone and the reduction of cortisone to cortisol. In contrast to the corresponding kidney enzyme (11 beta-HSD2), its primary activity is, however, reductive. Although this is only the fifth reported case of that defect, more attention should be paid to this condition in hyperandrogenic women, even if elevated 17-OH-progesterone and testosterone suggest a more frequent cause. 2000 S. Karger AG, Basel


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11150889&dopt=Abstract








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