Disease relevance of Hyperandrogenism

• In the present study we evaluated the association of obesity and hyperinsulinemia with valproate-related polycystic ovaries and hyperandrogenism in women with epilepsy [1].
• Metformin improved hyperandrogenism, hyperinsulinemia, and menstrual cyclicity, most likely through its positive effect on insulin clearance and abdominal adiposity [2].
• Among post-menarcheal PP girls (n = 69), shorter CAG number (biallelic mean </=20) was associated with higher 17-hydroxy-progesterone levels post leuprolide (P = 0.009), indicative of ovarian hyperandrogenism, higher testosterone levels (P = 0.02), acne (P = 0.03) and hirsutism scores (P = 0.01), and more menstrual cycle irregularities (P = 0.04) [3].
• Children with classic congenital adrenal hyperplasia (CAH) have multiple endocrine imbalances, including prenatal glucocorticoid and adrenomedullary deficiency and androgen excess, with possible postnatal iatrogenic glucocorticoid excess, hyperandrogenism, and adrenomedullary hypofunction [4].
• Subjects with PCOS were defined by chronic amenorrhea or oligomenorrhea and clinical and/or biochemical hyperandrogenism in the absence of an adrenal or pituitary disorder [5].

Psychiatry related information on Hyperandrogenism

• Polycystic ovary syndrome (PCOS) is a serious endocrine disorder characterized by ovulatory dysfunction and hyperandrogenism that is thought to have a higher prevalence in women with epilepsy and perhaps bipolar disorder [6].

High impact information on Hyperandrogenism

• CONCLUSIONS: In obese women with the polycystic ovary syndrome, decreasing serum insulin concentrations with metformin reduces ovarian cytochrome P450c17 alpha activity and ameliorates hyperandrogenism [7].
• Hyperandrogenism in polycystic ovary syndrome [8].
• Polycystic ovaries and hyperandrogenism in women taking valproate for epilepsy [9].
• Detection of functional ovarian hyperandrogenism in women with androgen excess [10].
• To our knowledge, these are the first examples of human SHBG variants linked to hyperandrogenism and ovarian dysfunction [11].

Chemical compound and disease context of Hyperandrogenism

• Eighty percent of the women treated with valproate before the age of 20 years had polycystic ovaries of hyperandrogenism [9].
• Hormonally regulated serine phosphorylation of human P450c17 suggests a possible mechanism for human adrenarche and may be a unifying etiologic link between the hyperandrogenism and insulin resistance that characterize the polycystic ovary syndrome [12].
• Association of the steroid synthesis gene CYP11a with polycystic ovary syndrome and hyperandrogenism [13].
• Hyperandrogenism, defined as serum testosterone levels higher than the mean + 2SD in the control girls at the same pubertal stage, was seen in 38% of prepubertal, 36% of pubertal, and 57% of postpubertal girls taking valproate [14].
• Twenty-four (39%) had characteristic polycystic ovaries on ultrasound, an exaggerated response of 17-hydroxyprogesterone to leuprolide, or both, suggesting ovarian hyperandrogenism and the diagnosis of mild polycystic ovary syndrome [15].

Biological context of Hyperandrogenism

• It is thus possible that a single defect produces both the insulin resistance and the hyperandrogenism in some PCOS women (Fig. 19) [16].
• Polycystic ovary syndrome (PCOS) is a common endocrine disorder of women, characterized by hyperandrogenism and chronic anovulation [17].
• We assessed whether metformin treatment is capable of inducing ovulation in nonobese adolescents with anovulatory hyperandrogenism after precocious pubarche [18].
• These findings support the hypothesis that insulin and IGFs may have a role in the hyperandrogenism of premature adrenarche just as they do in PCOS [19].
• Flutamide-metformin plus ethinylestradiol-drospirenone for lipolysis and antiatherogenesis in young women with ovarian hyperandrogenism: the key role of metformin at the start and after more than one year of therapy [20].

Anatomical context of Hyperandrogenism

• Classic congenital adrenal hyperplasia (CAH) is characterized by a defect in cortisol and aldosterone secretion, impaired development and function of the adrenal medulla, and adrenal hyperandrogenism [21].
• PCOS was defined as 1) oligoovulation, 2) clinical hyperandrogenism (i.e. hirsutism) and/or hyperandrogenemia, and 3) exclusion of other related disorders, such as hyperprolactinemia, thyroid abnormalities, and non-classic adrenal hyperplasia [22].
• Cell facts: -ovarian androgen-producing cells; -are associated only with developing follicles; -over-activity of theca cells causes infertility due to hyperandrogenism; -under-activity of theca cells causes infertility due to lack of estrogen [23].
• High neutrophil count in girls and women with hyperinsulinaemic hyperandrogenism: normalization with metformin and flutamide overcomes the aggravation by oral contraception [24].
• Effects of chronic hyperandrogenism and/or administered central nervous system insulin on ovarian manifestation and gonadotropin and steroid secretion [25].

Gene context of Hyperandrogenism

• In conclusion, the M196R (676 T-->G) variant in exon 6 of TNFRSF1B is associated with hyperandrogenism and PCOS, further suggesting a role for inflammatory cytokines in the pathogenesis of these disorders [26].
• Moreover, the present findings indicate, for the first time, that PTH probably is also linked to PCOS-associated hyperandrogenism [27].
• CONCLUSION(S): The IGF-1 axis appears to be involved in the pathogenesis of hyperandrogenism, especially in patients with adrenal hyperandrogenism, who have a clear increase in IGF-1 levels [28].
• Mutational analysis of the melanocortin-4 receptor (MC4R) gene in children with premature pubarche and adolescent girls with hyperandrogenism [29].
• CONCLUSION(S): This SORBS1 polymorphism does not play a major role in premature pubarche, hyperandrogenism, and/or polycystic ovary syndrome in our patient population [30].

Analytical, diagnostic and therapeutic context of Hyperandrogenism

• The value of the low-dose dexamethasone suppression test in the differential diagnosis of hyperandrogenism in women [31].
• To assess the potential role of scintigraphy in the evaluation of clinically and biochemically suspect ovarian hyperandrogenism (HA), dexamethasone suppression 131I-6 beta-iodomethyl-19-norcholesterol (NP-59) scans were performed to characterize ovarian function in nine patients [32].
• Immunoradiometric assay of human intact proinsulin applied to patients with type 2 diabetes, impaired glucose tolerance, and hyperandrogenism [33].
• In addition to menstrual dysfunction and hyperandrogenism, women with polycystic ovary syndrome also may have hypothalamic-pituitary abnormalities, polycystic ovaries on pelvic ultrasonography, infertility, obesity, and insulin resistance [34].
• Increased body mass index and more pronounced abdominal fat localization resulted in basal hyperinsulinemia, markedly exaggerated glucose-induced insulin levels, and hyperandrogenism, as was evident by significantly elevated free T and low SHBG serum levels [35].

References