Spontaneous ovarian hyperstimulation syndrome in early singleton pregnancy with hepatic involvement: two case reports of atypical presentations.

Authors

M J Nuñez Burbano, Sergio Andrés Escobar, Dayanna Pinto-Martínez, Víctor S Rangel, Ricardo García Yepes, Yaisa Maritza Castaño Toro, Jorge L Campo

Published in

Frontiers in reproductive health. Volume 8. Pages 1872608. Epub Jun 24, 2026.

Abstract

Ovarian hyperstimulation syndrome (OHSS) is typically an iatrogenic complication of assisted reproductive techniques. Spontaneous OHSS is rare, particularly in singleton pregnancies and in the absence of known risk factors, and may present with atypical systemic manifestations such as hepatic involvement.
We report two cases of spontaneous OHSS in early singleton pregnancies with hepatic involvement. The first case was a 21-year-old woman presenting with abdominal distension, ascites, and hyperbilirubinemia, with imaging revealing markedly enlarged ovaries and no evidence of primary hepatic pathology, although biliary tract findings consistent with cholelithiasis were identified. The second case involved a 23-year-old woman with abdominal pain, bilious vomiting, and elevated liver enzymes, with ultrasound findings of bilateral ovarian enlargement and cholelithiasis. In both cases, the diagnosis was established based on clinical and imaging findings after exclusion of other causes. Management was conservative, including close clinical and laboratory follow-up; however, one patient required laparoscopic cholecystectomy due to symptomatic biliary disease.
These cases highlight that spontaneous OHSS should be considered in pregnant patients presenting with abdominal symptoms, ovarian enlargement, and abnormal liver function tests, even in the absence of assisted reproduction. The relationship between spontaneous OHSS and hepatic abnormalities remains incompletely understood, particularly in the presence of concomitant biliary disease. Further studies are needed to better characterize the hepatic manifestations, epidemiology, and underlying genetic mechanisms of this condition.

PMID:
42422460
Bibliographic data and abstract were imported from PubMed on 09 Jul 2026.

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