Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunosuppressive treatment with prednisolone and/or azathioprine has been assessed in three chronic liver diseases with immunological features, namely chronic active hepatitis, cryptogenic cirrhosis and primary biliary cirrhosis. In chronic active hepatitis, controlled prospective clinical trials have shown clinical, biochemical and hepatic histological improvement when prednisolone with or without azathioprine is employed. Azathioprine alone has no advantage over placebo tablets. Cirrhosis is probably not prevented. Selection of patients for treatment, the response and therapeutic regimes are discussed. Patients with hepatitis B surface antigen positive chronic active hepatitis have a worse therapeutic response than those patients with chronic active hepatitis who are HBsAg negative. In primary biliary cirrhosis, corticosteroid treatment is contra-indicated on account of bone thinning. Azathioprine has been used in controlled clinical trials and is of only marginal benefit.
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PMID:Immunosuppressive therapy in chronic liver disease. 71 60

A 4-year-old boy presented with mildly itchy, linear, skin lesions over the trunk, arms, and face of 3 months' duration. He had previously been admitted to a private hospital for generalized exfoliation of the skin following drug intake for fever and throat pain. The nature of the drugs was not known. The exfoliative dermatitis was treated with oral prednisolone, 10 mg daily, tapered over 3 weeks. No further topical or oral medication was given. The present skin lesions started 1 month after the cessation of the steroids. There was no family history of skin lesions, voice changes, or systemic complaints. Cutaneous examination showed multiple violaceous, linear, reticulate ridges with adherent scaling over the chest, back, and neck. There were scaly, flat-topped papules over the extensor aspects of both upper arms and the buttocks, and scaly plaques over the cheeks (Figs 1a-d and 2a,b). The scalp showed diffuse greasy scaling. There were no oral, genital, axillary, or eye lesions. The nails were normal. Systemic examination did not reveal any abnormal finding. Routine hematologic investigations, liver and kidney function tests, tests for hepatitis B and C, and enzyme-linked immunosorbent assay (ELISA) for HIV were normal. Histopathology from skin lesions on the back revealed hyperkeratosis, patchy parakeratosis, follicular plugging, alternating irregular acanthosis and epidermal thinning, basal cell degeneration, and a band-like inflammatory infiltrate of lymphocytes, histiocytes, and a few plasma cells (Fig. 3). Based on the classical clinical features and histopathology, keratosis lichenoides chronica was diagnosed, and topical 1% hydrocortisone acetate cream, twice daily, was prescribed. There was slight relief of pruritus at a follow-up visit after 3 weeks; however, the patient was subsequently lost to follow-up.
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PMID:Keratosis lichenoides chronica in an Indian child following erythroderma. 1831

A 52-year-old black woman presented with a 5-year history of gradual swelling and slowed hair growth involving the vertex and both parietal regions of the scalp. Gradually, the swelling progressed to involve the entire scalp, only sparing a peripheral crown. She reported no history of trauma or medications. Slight pruritus of the involved area was the only accompanying symptom. There was no family history of a similar condition. Her past medical history included surgery for ovarian cysts, 10 years previously, and cholelithiasis. Physical examination revealed diffuse hair thinning and alopecia, more prominent along the vertex and parietal regions (Fig. 1a). There was no evidence of scalp inflammation, scaling, or increased hair fragility. The scalp was mildly tender on palpation and had a boggy, spongy consistency. The hairs which still remained in the involved areas were thin, short, and soft (Fig. 1b). The involved area was slightly hypopigmented when compared with adjacent noninvolved scalp. The rest of the physical examination was within normal limits. No abnormalities of the hair shaft were observed on microscopic examination of several plucked hairs. Laboratory investigations, including a complete blood cell count, blood chemistry, urinalysis, sedimentation rate, antinuclear antibodies, and serologic tests for syphilis, hepatitis B and C virus, and human immunodeficiency virus, were negative. A computed tomography scan of the skull demonstrated diffuse and regular thickening of subcutaneous fatty tissue of the scalp, disclosing a maximum scalp thickness of 15 mm at the vertex (Fig. 2). The biopsy from the vertex revealed a normal epidermis and dermis, with diffuse loss of hair follicles. The most striking feature consisted of a large increase in thickness of the subcutaneous fatty tissue (Fig. 3a). Pre-existing hair follicles were replaced by vertical fibrous tracts of lamellar fibroplasia with no inflammatory infiltrate (Fig. 3b). Adipocytes showed a normal size and shape, but the connective tissue septa, which are normally present separating the subcutaneous tissue into fat lobules, were lacking, and subcutaneous fatty tissue consisted of a continuous and diffuse sheet of mature adipocytes (Fig. 3c). Orcein stain revealed normal contents of elastic fibers with foci of condensation at the sites of disappeared pre-existing hair follicles (Fig. 3d). Colloidal iron and Alcian blue (pH 2.5) stains revealed no mucin deposits.
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PMID:Lipedematous alopecia: an uncommon clinicopathologic variant of nonscarring but permanent alopecia. 1847 57