Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Androgenetic alopecia (a.A.) occurs quite frequently. Up to 79% of women suffer at least temporarily from varying degrees of intermittent diffuse hair loss in the centro-parietal and/or fronto-temporal regions. A.A. is caused by an androgen excess acting on the hair follicle for prolonged periods of time in the presence of a genetic predisposition. However, often hyperandrogenemia cannot be demonstrated in such patients. 125 women with clinically typical a.A. were investigated prospectively under standardized conditions. Patient age ranged from 18 to 68 years (mean +/- SD: 34 +/- 11.6). Atypical uterine bleeding such as menorrhagia, hypermenorrhea and polymenorrhea were found in 69 women. The hair loss varied between 50 and 400 hairs per day (124 +/- 125). Additional signs of hyperandrogenism, i.e. seborrhea (n = 83), acne (n = 52) and hirsutism (n = 28), were often observed. Basal levels of total and free testosterone (T and FT), dihydro-T (DHT) DHEA-sulfate (DS), delta 4-androstendione (A), 17 alpha-hydroxy-progesterone (17P), cortisol (F), progesterone (P), 17 beta-estradiol (E2), sex hormone binding globuline (SHBG), prolactin (PRL), thyreoidea-stimulating hormone (TSH), ferritin (Fe), vitamin B12 (B12) and folat (Fo) were determined by RIA. FT was also measured by equilibrium dialyses. Different methods of determining bound and unbound T were used; their diagnostic value is discussed in detail. In addition, a combined ACTH/TRH-stimulation test was performed in all patients. Pathologic changes of one parameter were detectable in 26.4% of patients, while 67.2% revealed deviations of two or more indices. Excluding clinically relevant borderline values, only 6.4% of patients were without any abnormalities. The incidence rate of pathologic parameters was as follows: FT in % = 52%, Fe = 42%, PRL = 34%, E2 = 34%, FT in pg = 29%, DHT = 28%, SHBG = 26%, TSH = 20.8%, DS = 19%, T = 14%, 17P = 11%, Fo = 7%, A = 6%, F = 6%, B12 = 5%. Group and individual case analyses revealed significant correlations between (1) the levels of the various androgens, PRL and TSH and (2) the E2, SHBG and FT values; these, in turn, were correlated to (3) the occurrence of certain bleeding anomalies (amount, duration, interval) and corresponding ferritin deficiency. Therapy was directed at normalizing the disturbed estrogen-androgen-balance. Using low-dose antiandrogens, estrogens, prolactin suppressants, corticoids, iron-II-preparations as well as estrogen-containing hair lotions hair loss was arrested in 74 of 104 treated women, while regrowth of hair was accomplished in 16 patients. 14 women did not respond to therapy.
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PMID:[Hormonal diagnosis in so-called androgenetic alopecia in the female]. 337 87

Female androgenetic alopecia or female-pattern alopecia is one of the most common causes of hair loss, affecting 50 % of women over their lifetime. The appearance of this condition is the cause of significant stress and psychological problems, making appropriate management important. Cases exist in which it is associated with hyperandrogenism. Here, we review the different clinical forms (diffuse, male-pattern, and Christmas-tree pattern), discuss the most appropriate laboratory tests (complete blood count, thyroid stimulating hormone, ferritin, prolactin, free and/or total testosterone, and dehydroepiandrosterone sulfate), and the different treatments, including finasteride.
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PMID:[Management of androgenetic alopecia in postmenopausal women]. 1839

OBJECTIVE Increased serum ferritin levels and iron stores may be involved in the development of abnormal glucose tolerance in women presenting with obesity and/or polycystic ovary syndrome (PCOS). We aimed to study the determinants of serum ferritin levels in premenopausal women among indexes of insulin resistance, adiposity, hyperandrogenism, and genotypes pertaining to inflammation, oxidative stress, and iron metabolism. RESEARCH DESIGN AND METHODS A total of 257 premenopausal women, classified depending on the presence or absence of PCOS, obesity, and/or abnormal glucose tolerance, underwent a complete metabolic evaluation, serum ferritin, haptoglobin, and C-reactive protein (CRP) measurements, and genotyping for proinflammatory and prooxidant variants and mutations in the HFE gene. RESULTS Serum ferritin concentrations were increased in women presenting with PCOS and/or abnormal glucose tolerance, independent of obesity. A stepwise multivariate linear regression analysis (R(2) = 0.18, P < 0.0001) retained menstrual dysfunction (beta = 0.14, P = 0.035), free testosterone (beta = 0.14, P = 0.052), insulin sensitivity index (beta = -0.12, P = 0.012), the His63Asp variant in HFE (beta = 0.16, P = 0.008), and abnormal glucose tolerance (beta = 0.15, P = 0.015) as significant predictors of the logarithm of ferritin levels, whereas CRP, haptoglobin, waist-to-hip ratio, or variants in the TNFalpha, TNFRSF1B, IL6, IL6ST, IL6Ralpha, PON1, and HFE Cys282Tyr mutation exerted no influence. CONCLUSIONS Androgen excess (partly because of hyperandrogenemia and partly because of menstrual dysfunction), insulin resistance, abnormal glucose tolerance, and the HFE His63Asp variant correlate with ferritin levels in premenopausal women.
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PMID:Body iron stores and glucose intolerance in premenopausal women: role of hyperandrogenism, insulin resistance, and genomic variants related to inflammation, oxidative stress, and iron metabolism. 1940 44