Acute liver failure as the presenting manifestation of chronic lymphocytic leukemia complicated by fatal post-biopsy hemorrhage: a case report

Chronic lymphocytic leukemia (CLL) is typically an indolent B-cell malignancy involving the blood, bone marrow, lymph nodes, and spleen. Although hepatic infiltration may occur, it is usually clinically silent. Acute liver failure (ALF) as the initial presentation of CLL is exceedingly rare, and the mechanisms underlying severe hepatic dysfunction remain poorly understood. We report a 65-year-old Caucasian man with no significant prior medical history who presented with constitutional symptoms, acute encephalopathy, profound anemia, marked leukocytosis, hyperbilirubinemia, and severe hepatocellular injury. Evaluation demonstrated warm autoimmune hemolytic anemia, with positive direct antiglobulin testing (IgG), undetectable haptoglobin, elevated lactate dehydrogenase, and reticulocytosis. Imaging revealed hepatomegaly and marked splenomegaly without significant lymphadenopathy. Peripheral blood flow cytometry confirmed CLL. Additional molecular studies demonstrated deletion of 13q14.3, with negative TP53 mutation testing and no evidence of MYC, BCL6, or IGH::BCL2 rearrangements. Because the etiology of the rapidly progressive ALF remained uncertain despite extensive evaluation, an image-guided percutaneous liver biopsy was performed. Histopathologic examination demonstrated marked acute cholestasis and portal infiltration by CLL. Following the procedure, the patient developed hemorrhagic shock due to massive intra-abdominal bleeding and died within 24 h. Postmortem examination confirmed hepatic involvement by CLL and extensive intra-abdominal hemorrhage. Acute liver failure may rarely accompany newly diagnosed CLL, with hepatic dysfunction reflecting multiple concurrent mechanisms rather than leukemic infiltration alone. When liver biopsy is necessary in a coagulopathic patient, a transjugular approach should be preferred to reduce the risk of intraperitoneal hemorrhage. Transient INR improvement following blood product administration does not resolve the underlying cause of coagulopathy or establish procedural safety.