S5738 Disguised Malignancy: Acute Myeloid Leukemia Presenting as Decompensated Cirrhosis

Introduction: Acute myeloid leukemia (AML) is a malignancy of immature myeloid cells, while cirrhosis is characterized by hepatic fibrosis. Both can present with anemia and thrombocytopenia, but hematologic abnormalities warrant further evaluation when gastrointestinal bleeding is absent. Although AML in cirrhotic patients has been reported, simultaneous new-onset AML and decompensated cirrhosis remains undocumented. Case Description/Methods: A 78-year-old woman with iatrogenic hypothyroidism presented with lower extremity edema, fatigue, abdominal distension, low-grade fevers, and dyspnea. Labs revealed WBC 26.9 × 10³/µL, Hb 5.5 g/dL, platelets 34 × 10³/µL, MCV 123 fL, and 10% blasts. Peripheral smear showed macrocytosis, anisopoikilocytosis, and smudge cells. CMP showed total bilirubin 1.8 mg/dL, aspartate aminotransferase 49 U/L, and albumin 2.5 g/dL. Coagulation profile showed PT 17.1 sec, international normalized ratio 1.6. Computed tomography abdomen/pelvis showed a nodular liver, portal hypertension, large esophageal varices, and splenomegaly with infarct. EGD revealed grade 1 esophageal varices without high-risk stigmata and reactive gastropathy. Hematologic evaluation, including flow cytometry, confirmed AML. Iron studies showed elevated ferritin (1390 ng/mL), transferrin saturation (80%), and low TIBC—suggestive of hereditary hemochromatosis. Hepatitis panel, autoimmune workup, and metabolic risk factors were unremarkable. Given the absence of GI bleeding, hematologic malignancy was identified as the primary contributor to cytopenias. The patient was discharged to initiate AML treatment and outpatient follow-up was planned to include colonoscopy, capsule endoscopy if indicated and liver ultrasound elastography. Discussion: This case highlights the diagnostic complexity when new-onset AML coexists with decompensated cirrhosis. Both conditions may present with fatigue, cytopenias, and organomegaly. In our patient, the absence of high-risk varices and GI bleeding necessitated further hematologic evaluation, ultimately confirming AML. Iron overload, suspected due to elevated ferritin and transferrin saturation, may be related to hereditary hemochromatosis and may have contributed to cirrhosis. Iron overload is associated with poor AML prognosis due to oxidative stress and genomic instability but has not been shown to increase AML incidence in hereditary hemochromatosis. This case underscores the importance of a thorough, multidisciplinary approach to evaluating overlapping hematologic and hepatic abnormalities.