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Unilateral adrenal infarction is a rare cause of acute abdomen in pregnancy (AAP). Its presentation is non-specific and requires a high index of suspicion with a low threshold to obtain radiographic imaging for diagnosis. Evaluating AAP is challenging as diagnostic radiographic imaging is often limited in relation to radiation exposure to the developing fetus. We describe a case of a 24-year-old pregnant female who presented with severe acute abdominal pain. The patient’s pain was refractory to intravenous analgesics and ultrasonography was inconclusive. Computed tomography (CT) scan was not obtained due to the risk of radiation exposure to the developing fetus. Due to the persistence of pain and suspicions for other serious etiologies, magnetic resonance imaging (MRI) was completed and the patient was diagnosed with acute unilateral adrenal infarction. In this case report, unilateral adrenal infarction was likely secondary to elevated plasma factor VIII levels. Even with the physiological elevation of factor VIII levels during pregnancy, levels greater than 150 IU/dL confer greater than five-fold increased risk of venous thrombosis. Once hemorrhage is excluded, patients should be started on therapeutic anticoagulation to prevent progression of adrenal infarct or infarction of the contralateral adrenal gland. Prompt recognition and treatment of acute adrenal infarction during pregnancy are of paramount importance to prevent adverse outcomes for both the mother and fetus.

Summary As prospective trials failed to establish a reducedrisk of venous and arterial thrombosis in hyperho-mocysteinemic subjects after supplementation withB-vitamins, we hypothesized that an associatedcondition, rather than hyperhomocysteinemia it-self, is the thrombotic culprit.We assessed the contribution of elevated factorVIII levels to the risk of thrombosis in hyper-homocysteinemia in a retrospective family-cohortstudy. Relatives of consecutive probands, who hadvenous thrombosis or premature atherosclerosis,and hyperhomocysteinemia, elevated factor VIII le-vels, or both, were enrolled. 1052 relatives wereanalyzed. Hyperhomocysteinemic relatives hadmore often elevated factor VIII levels than normo-homocysteinemic relatives (38% versus 28%, P=0.024). Other thrombophilic defects were equallydivided.Hypertensionandsmokingweremoreoftenfound in hyperhomocysteinemic relatives than innormohomocysteinemic relatives (28% versus 48%;P=0.027, and 19% versus 38%; P=0.029). After ad-justing for these confounders, the relative risk ofvenous thrombosis in hyperhomocysteinemic rela-tives was 0.8 (95% confidence interval [CI] 0.3–1.7)and 0.9 (95% CI, 0.5–1.6) for arterial thrombosis.The absolute risk of venous thrombosis in hyperho-mocysteinemia was 0.14% (95% CI, 0.06–0.30) and0.31% (95% CI, 0.18–0.52) for arterial thrombosis.Hyperhomocysteinemia had no effect on the risk ofvenous thrombosis or arterial thrombosis in rela-tives with elevated factor VIII levels; relative risks1.0 (95% CI, 0.4–2.3) and 1.1 (95% CI, 0.5–2.5),respectively. We conclude that hyperhomocysteine-mia is not a risk factor for venous and arterialthrombosis, and is associated with elevated factorVIII levels.