Endocrine Abstracts

Background: Physiological rise in lipids is expected in pregnancy, but pathological hypertriglyceridemia carries potential feto-maternal complications. Evidence to guide management is sparse and decision-making is often based on case reports. This case illustrates the diagnostic and therapeutic challenges of severe hypertriglyceridemia in pregnancy.

Case: A 32-year-old woman at 32+3 weeks gestation, with gestational diabetes on metformin, initially presented with proximal leg DVT and was treated with enoxaparin. Three weeks later, she re-presented with chest tightness, abdominal discomfort, and persistent tachycardia. Despite raised CRP and ongoing abdominal pain, clinical attention was focused on excluding cardiopulmonary causes. The initial lipemic sample showing hypertriglyceridemia (TG-57.6 mmol/l) and raised lipase of 500 U/l (8-78 U/l) consistent with acute pancreatitis secondary to hypertriglyceridemia, was only acknowledged retrospectively 10 days later. By then, TG had spontaneously fallen (21 mmol/l), possibly due to reduced intake or partial saponification. Intravenous insulin and omega-3 fatty acids were initiated, with dietary restrictions. However, intolerance to IV insulin necessitated transition to subcutaneous insulin. Despite adherence, TGs fluctuated between 17–33 mmol/l. Chylomicrons were positive. Lipoprotein electrophoresis was inconclusive. She was closely monitored in the joint antenatal-endocrine clinic.

Outcome: After multidisciplinary consensus, early delivery was performed at 37 weeks. TG normalised rapidly post-delivery, without needing ongoing treatment.

Learning points: • Lipaemic samples should trigger urgent review; overlooking them risks significant feto-maternal morbidity. • Increased plasma viscosity poses the risk of thrombotic events as in this case, DVT. However, prolonged enoxaparin may paradoxically worsen TGs via lipoprotein lipase depletion. • Spontaneous TG reduction without therapy raised suspicion of saponification at the pancreatic bed, although dietary restriction likely contributed more significantly. • Fenofibrate remains a therapeutic dilemma in pregnancy due to limited safety data. • Complete postpartum resolution highlights uncertainty over the relative contribution of gestational physiology, diet, enoxaparin exposure, and possible genetic predisposition.