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Focal nodular hyperplasia of the liver in a patient with primary aldosteronism

cardiolipin antibody, with both anticardiolipin IgG and IgM serotypes detected. Imaging showed hepatosplenomegaly and there were multiple discrete lesions in the liver and spleen consistent with hepatic and splenic infarcts, and minimal ascites. There was no dilatation of the biliary tree. Liver biopsy showed discrete foci of hepatic infarction with venular and arteriolar fibrin. There was no evidence of vasculitis, central vein fibrosis, zone 3 congestion or erythrocytes within the space of Disse. The hepatic parenchyma adjacent to the coagulative necrosis was normal. There was some sinusoidal dilatation in response to small vein thrombosis, but no other evidence to suggest Budd–Chiari syndrome. Skin biopsy also showed small vessel fibrin thrombi with no evidence of vasculitis. The patient rapidly responded to intravenous hydrocortisone with resolution of his symptoms and improvement in liver chemistries (Table 1), and was discharged on a reducing dose of prednisolone. The patient was non-compliant with follow up, and was admitted to hospital with recurrent catastrophic APS on a further 17 occasions over the next 7 years. Recurrent episodes of catastrophic APS primarily involved the liver with symptoms of jaundice and ascites. The patient responded rapidly to steroids on each occasion. The addition of cyclophosphamide, gglobulin and quinine did not result in a more durable remission. A brief trial of low-molecular-weight heparin was complicated by antithrombin III deficiency and was ceased, and anticoagulation with warfarin was contraindicated because of patient non-compliance. Gastrointestinal system involvement is common in catastrophic APS, with a recent review finding that 22% of patients manifest with abdominal discomfort, and that hepatic, gastrointestinal and pancreatic involvement occur in 30%, 14% and 9% of cases, respectively. Approximately 50% of patients survive their initial episode of catastrophic APS. The majority of surviving patients are managed with anticoagulation, and recurrent catastrophic APS is seen in only 26% of cases. Few patients have previously been managed with corticosteroid therapy alone, and it has been concluded that steroids do not improve the chance of recovery. In the indexed case of catastrophic APS, steroid therapy was associated with rapid recovery from catastrophic APS on numerous occasions. This suggests that steroids, in contradistinction to previous evidence, may assist in the recovery from catastrophic APS, but do not prevent recurrent disease when stopped.