Type B Insulin Resistance Masquerading as Ovarian Hyperthecosis

被引：22

作者：

Brown, Rebecca J. ^{[1
]}

Joseph, Jalaja ^{[1
]}

Cochran, Elaine ^{[1
]}

Gewert, Cornelia ^{[2
,3
]}

Semple, Robert ^{[2
,3
]}

Gorden, Phillip ^{[1
]}

机构：

[1] NIDDK, NIH, Bldg 10-CRC,Room 6-5942,10 Ctr Dr, Bethesda, MD 20892 USA

[2] Univ Cambridge, Metab Res Labs, Wellcome Trust, MRC,Inst Metab Sci, Cambridge CB2 OQQ, England

[3] Cambridge Biomed Res Ctr, Natl Inst Hlth Res, Cambridge CB2 OQQ, England

来源：

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM | 2017年 / 102卷 / 06期

基金：

英国惠康基金;

关键词：

CLINICAL-COURSE; RECEPTOR AUTOANTIBODIES; HYPERANDROGENISM;

D O I：

10.1210/jc.2016-3674

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Context: Hyperinsulinemia can lead to pathologic ovarian growth and androgen production. Case Description: A 29-year-old woman developed an autoantibody to the insulin receptor (type B insulin resistance), causing extreme insulin resistance and hyperinsulinemia. Testosterone levels were elevated to the adultmale range. Treatment with gonadotropin-releasing hormone (GnRH) analog led to normalization of testosterone, despite persistent extreme insulin resistance. Conclusions: This case demonstrates that gonadotropins are necessary for insulin to cause pathologic ovarian androgen production. Suppression of gonadotropins with GnRH analogs may be a useful therapeutic option in patients with severe hyperandrogenism or ovarian enlargement because of hyperinsulinemia.

引用

页码：1789 / 1791

页数：3

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