We report a 28-year-old man with alcohol-induced interstitial acute pancreatitis (AP) who developed rapidly progressive anemia and thrombocytopenia beginning on hospital day two. Hemoglobin decreased from 16.5 g/dL on presentation to a nadir of approximately 5.2 g/dL, and the platelet count declined from 309×103/µL to 12×103/µL. Laboratory evaluation showed hemolysis with markedly elevated lactate dehydrogenase, undetectable haptoglobin, hyperbilirubinemia, and a peripheral smear demonstrating polychromasia with rare schistocytes and spherocytes, while the direct antiglobulin test (DAT) was negative on two occasions. Renal function, coagulation studies, and ADAMTS13 activity were normal, and broad infectious and autoimmune evaluation was unrevealing. Given the temporal association with pancreatitis, exclusion of thrombotic microangiopathy (TMA), disseminated intravascular coagulation, infection, and other evaluated causes, and hematologic improvement after intravenous immunoglobulin (IVIG) and corticosteroids, the working diagnosis was a suspected Evans syndrome-like immune cytopenia (immune thrombocytopenia with DAT-negative immune hemolysis) triggered by AP. Extended serologic testing for DAT-negative autoimmune hemolysis was negative, so the diagnosis remained a clinical working diagnosis. The patient was treated with transfusion support, IVIG, and intravenous methylprednisolone, with gradual hematologic recovery. This case underscores the importance of early hematologic evaluation and consideration of immunomodulatory therapy after exclusion of TMA and other common causes of hemolysis in patients with AP and severe cytopenias.
Ahmed et al. (2026) studied this question.