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Acute pancreatitis as the initial manifestation of acute myeloid leukemia: a case report and literature review.

Created on 15 Aug 2026

Authors

Dandan Chen, XianYi Lin, Xiaohong Cai, Xiangqi Huang, Churong Lin, Ruijuan Wen, Xiangzhong Zhang, Xudong Li, Lingling Liu

Published in

Frontiers in medicine. Volume 13. Pages 1924463. Epub Jul 31, 2026.

Abstract

Acute myeloid leukemia (AML) presenting with acute pancreatitis (AP) as the initial symptom is extremely rare. Severe AP (SAP) has a significant death rate and advances quickly. Therefore, it is crucial to identify the predisposing factors in the early stages of SAP, assess the condition, establish the prognosis, develop treatment plans and prevent a recurrence. Here, we describe a case of AP associated with AML infiltration involving the pancreatic segment of the common bile duct.
A 34-year-old man arrived to the hospital complaining of persistent abdominal pain. Blood analysis presented elevated serum lipase levels, leukocytosis, and severe thrombocytopenia. Computed tomography examination of the abdomen revealed necrotizing pancreatitis, accompanied by significant stenosis of the pancreatic segment of the common bile duct due to extrinsic compression, and moderate dilatation of the proximal bile duct and intrahepatic biliary ducts. The patient had no typical etiologies of acute pancreatitis except a history of type 2 diabetes mellitus, which alone could not account for the significant thrombocytopenia observed concurrently. Finally, the bone marrow aspirate and smear examination identified the acute myeloid leukemia (AML) which was considered as the primary cause of pancreatitis.
Acute leukemia, particularly AML, is an uncommon cause of AP via direct pancreatic infiltration by leukemic cells. Although AP rarely presents as an extramedullary manifestation in AML patients, it should be considered in the etiological workup of AP. Early recognition and targeted etiological management can optimize clinical outcomes and prevent ineffective treatment.

PMID:
42601859
Bibliographic data and abstract were imported from PubMed on 15 Aug 2026.

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