Introduction:
Acute fatty liver of pregnancy (AFLP) and HELLP syndrome share overlapping features, often complicating clinical differentiation. While both require expedited delivery, accurate distinction is critical for maternal risk assessment, neonatal outcomes, and future pregnancy planning. The Swansea criteria, though widely used, lack specificity, with many HELLP cases also meeting its diagnostic thresholds.1 Alternative biochemical markers such as hypocholesterolaemia, reduced antithrombin III and fibrinogen, and elevated soluble Fms-like tyrosine kinase-1 (sFLt-1) may provide improved accuracy over the Swansea criteria.2-4
Case Presentation:
A 31-year-old primigravida at 37 weeks presented with hypertension, polyuria, hyperuricaemia, transaminitis, and acute kidney injury. She fulfilled six Swansea criteria but had profound hypocholesterolaemia (nadir 1.4 mmol/L) and low antithrombin III (26%). Labour was induced, resulting in vaginal delivery of a healthy male infant weighing 3000 g. Postpartum recovery was rapid, with normalization of hepatic and coagulation markers. Her pre-pregnancy cholesterol was 4.6 mmol/L, reinforcing that hypocholesterolaemia was an acquired pregnancy-related feature.
Discussion:
Physiological cholesterol elevation occurs in late pregnancy.5 Thus, marked hypocholesterolaemia may serve as an early sign of AFLP, preceding coagulopathy (Table 1). Retrospective reviews show consistently lower cholesterol in AFLP compared with HELLP.4,6-10 Additionally, low antithrombin III and elevated sFlt-1 may enhance diagnostic precision.2,4 Given cholesterol testing is widely available, its use—especially alongside antithrombin III—could improve bedside differentiation of AFLP from HELLP, particularly where advanced laboratory resources are limited.
Conclusion:
In resource-limited settings, profound hypocholesterolaemia may serve as an accessible, cost-effective diagnostic aid for AFLP, supporting early risk stratification in urgent obstetric scenarios.