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Type B Insulin Resistance Masquerading as Ovarian Hyperthecosis
Rebecca J Brown1, Jalaja Joseph1, Elaine Cochran1
1National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
The Journal of Clinical Endocrinology and Metabolism
|December 3, 2016
Summary
Extreme insulin resistance caused by an autoantibody led to high testosterone levels. Gonadotropin-releasing hormone (GnRH) analog treatment normalized testosterone, suggesting GnRH analogs can treat hyperandrogenism linked to hyperinsulinemia.
Area of Science:
- Endocrinology
- Reproductive Endocrinology
- Immunology
Background:
- Hyperinsulinemia is linked to pathological ovarian enlargement and androgen overproduction.
- Autoimmune conditions can cause extreme insulin resistance, as seen in type B insulin resistance.
Observation:
- A 29-year-old woman with type B insulin resistance presented with extreme insulin resistance and hyperinsulinemia.
- Her testosterone levels were significantly elevated, reaching adult male ranges.
- She was treated with a gonadotropin-releasing hormone (GnRH) analog.
Findings:
- Treatment with a GnRH analog normalized testosterone levels.
- This normalization occurred despite the persistence of extreme insulin resistance.
- The case highlights the crucial role of gonadotropins in mediating insulin-induced ovarian androgen production.
Implications:
- Gonadotropin suppression via GnRH analogs may be a viable therapeutic strategy.
- This approach could benefit patients experiencing severe hyperandrogenism or ovarian enlargement due to hyperinsulinemia.
- Understanding the interplay between insulin, gonadotropins, and ovarian function is critical for managing these conditions.
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