S2624 Liver Injury in Acute Myeloid Leukemia

Abstract

INTRODUCTION: Hepatic involvement in acute myeloid leukemia (AML) is rare and associated with a high mortality rate. Given the potential hepatotoxicity of chemotherapy, treating patients with hepatic dysfunction requires administering attenuated doses or delaying therapy resulting in possible worse outcome. We report a case of a patient with elevated transaminases at the time of diagnosis of AML in whom treatment with attenuated dose chemotherapy was promptly started. CASE DESCRIPTION/METHODS: A 66-year-old male with no pertinent history came to the emergency room with neck fullness and right sided tooth pain associated with a 10lb weight loss. On admission he was febrile to 100.4F, vitals otherwise normal. Laboratory results revealed leukocytosis with WBC 138.8 (abs neutrophil count 1.4 Thou/mL and 25 Thou/mL of blasts), Hb 11.9, Hct 37.2, PLT 16,000. A CT neck showed right 2nd molar infection and lytic lesions of the maxilla. A peripheral flow cytometry and bone marrow biopsy were consistent with AML. The LFTs showed T bili 1.2, AST 163, ALT 138, ALP 114. Further workup including, abdominal ultrasound, viral hepatitis, ANA and anti-smooth muscle antibody were unremarkable. On day 2, T bili 3.2, AST 524, ALT 587, ALP 169. At this time, it was thought that the transaminitis was secondary to AML and induction chemotherapy with cytarabine and daunorubicin (50% reduction) was started. On day 7 of chemotherapy, the transaminases improved to normal limits indicating the liver injury was reversible and secondary to AML (Figure 1). Unfortunately, our patient did not achieve remission and died 35 days after admission. DISCUSSION: Although liver infiltration by AML is rare, it should be considered early. It usually presents with elevated LFTs in a mixed hepatocellular and cholestatic pattern. In addition to our case, there are several case reports suggesting AML as an etiology of elevated LFTs. Definitive diagnosis relies on liver biopsy which can be difficult to obtain in the presence of coagulopathy. The improvement of transaminases after initiating chemotherapy and negative work-up for other etiologies suggests that AML is the cause of hepatitis. Prompt initiation of chemotherapy in AML patients is of utmost importance. Studies suggest that semi intensive dosing or delays in chemotherapy initiation result in decreased survival and higher mortalities. It is important to recognize AML as a possible, and potentially reversible, cause of hepatic dysfunction in order to prevent treatment delays and poor outcomes.Figure 1.: Level of transaminases throughout admission. Dashed orange line corresponds to the time that chemotherapy was initiated.Table 1.: Laboratory, imaging and treatment findings in eight previous studies reporting liver involvement in AML