ライフサイエンスコーパス: hyperandrogenism

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1 e mild non-classic form is a common cause of hyperandrogenism.

2 the pathogenesis of "polycystic" ovaries in hyperandrogenism.

3 hrome P450c17 alpha activity and ameliorates hyperandrogenism.

4 ical hyperandrogenism as opposed to clinical hyperandrogenism alone showed a metabolic phenotype (p <

5 valent but unreliable markers of biochemical hyperandrogenism among this population.

6 ndocrine disorder of women, characterized by hyperandrogenism and chronic anovulation.

7 dition in which intrinsic functional ovarian hyperandrogenism and excess adiposity share a common ori

8 late childhood or early adulthood with mild hyperandrogenism and is an important cause of masculiniz

9 case group included girls with high (n = 40, hyperandrogenism and oligomenorrhea or amenorrhea), inte

10 pathway linking hyperinsulinism with ovarian hyperandrogenism and the infertility of obesity.

11 ncluding acanthosis nigricans, organomegaly, hyperandrogenism, and diabetes.

12 Insulin resistance and hyperandrogenism are the cardinal features of polycystic

13 COS women with both biochemical and clinical hyperandrogenism as opposed to clinical hyperandrogenism

14 sorder of unknown aetiology characterized by hyperandrogenism, chronic anovulation and defects in glu

15 is often complicated by inadequately treated hyperandrogenism, iatrogenic hypercortisolism, or both.

16 an experience iatrogenic Cushing's syndrome, hyperandrogenism, infertility, or the development of the

17 Clinical and/or biochemical hyperandrogenism is one of the diagnostic criteria for P

18 Hyperandrogenism is the most consistent PCOS characteris

19 ent etiologies of type 2 diabetes, such that hyperandrogenism may increase risk in women while decrea

20 ray of disorders, including oligo-ovulation, hyperandrogenism, obesity, hyperlipidemia, infertility a

21 The ordinary hypergonadotropic hyperandrogenism of obese women appears to be an excepti

22 matched (+/- 2 years) girls with no clinical hyperandrogenism, oligomenorrhea, or amenorrhea.

23 oint was development of PCOS components (ie, hyperandrogenism or ovulatory dysfunction).

24 Rotterdam criteria (anovulation with either hyperandrogenism or polycystic ovaries).

25 norrhea or amenorrhea), intermediate (n = 8, hyperandrogenism), or low (n = 7, oligomenorrhea or amen

26 rimary hyperaldosteronism, hypercortisolism, hyperandrogenism, or hyperestrogenism), and less than 1%

27 lin receptor (INSR) mutations develop severe hyperandrogenism secondary to hyperinsulinaemia.

28 y be associated with adverse birth outcomes, hyperandrogenism, sexual dysfunction, and impaired impla

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