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RAPIDLY PROGRESSIVE AND SEVERE HIRSUTISM FROM HYPERREACTIO LUTEINALIS WITHIN A BACKGROUND OF POLYCYSTIC OVARY SYNDROME

OBJECTIVEGestational trophoblastic disease and hyperreactio luteinalis (HL) are rare, but important, etiologies of hyperandrogenism that need to be further studied. METHODSWe present a case of rapidly progressing hirsutism and marked biochemical androgen excess in the context of pregnancy. RESULTSA...

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Bibliographic Details
Published in:AACE clinical case reports 2019, Vol.5 (2), p.e86-e90
Main Authors: Mathew, Hannah Miriam, Lee, Christopher Wang, Haddady, Shirin
Format: Report
Language:English
Online Access:Get full text
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Summary:OBJECTIVEGestational trophoblastic disease and hyperreactio luteinalis (HL) are rare, but important, etiologies of hyperandrogenism that need to be further studied. METHODSWe present a case of rapidly progressing hirsutism and marked biochemical androgen excess in the context of pregnancy. RESULTSA 26-year-old woman with a past medical history of obesity, prediabetes, and polycystic ovary syndrome presented with worsening hirsutism and markedly elevated testosterone levels. She was subsequently found to be pregnant, with extremely elevated levels of serum β-human chorionic gonadotropin. Subsequent work-up led to the identification of molar pregnancy and bilaterally enlarged ovaries, suggestive of HL. Following surgical intervention and therapy with methotrexate for invasive mole, she experienced improvement in both biochemical and clinical androgen excess features. CONCLUSIONWith the prevalence of polycystic ovary syndrome, many women present to medical providers with hirsutism or other findings of hyperandrogenism. However, rapid progression of existing hirsutism or severe hirsutism should prompt more extensive evaluations to rule out rare etiologies. One such etiology found in pregnancy is HL, in which high levels of β-human chorionic gonadotropin can stimulate production of benign theca lutein cysts, leading to marked hyperandrogenism and virilizing symptoms.
ISSN:2376-0605
DOI:10.4158/ACCR-2018-0294