Acute myeloid leukaemia presenting as acute liver failure—a case report and literature review

Sun, Kai; Reynolds, Ryan J; Sheu, Tiffany G.; Tomsula, Jessica; Rice, Lawrence

doi:10.3332/ecancer.2019.960

Cited by 5 publications

(6 citation statements)

References 18 publications

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“…There were seven case reports described in the literature where AML presented as acute liver failure and obstructive jaundice. It is a rare presentation and gives rise to very high mortality [5]. Their presentation includes abnormal blood counts (anemia, leukocytosis, thrombocytopenia) and five of seven patients had blasts on peripheral smear, similar to our case.…”

Section: Discussionsupporting

confidence: 84%

Acute Myeloid Leukemia Masquerading as Decompensated Cirrhosis

Ahdi¹,

Mannem²,

Lakha³

2022

Cureus

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Patients with known cirrhosis who present with anemia, thrombocytopenia, acute renal failure, and confusion are usually presenting with decompensated cirrhosis. We present a patient with known alcoholic cirrhosis presenting with the above abnormalities, initially thought to be decompensated cirrhosis but found to have acute myeloid leukemia (AML) with acute blast crisis. This case was presented as a poster at the American College of Gastroenterology Annual Scientific Meeting held on October 22-27, 2021.A 59-year-old male with a history of compensated alcoholic cirrhosis presented with unresponsiveness. On physical exam, vitals were normal, he appeared lethargic with generalized pallor, and rectal exam demonstrated an empty rectal vault with no blood or stool noted. Labs were notable for hemoglobin 3.1 g/dL, platelet count 41,000/µL, creatinine 5.2mg/dL, aspartate aminotransferase (AST) 242 U/L, alanine aminotransferase (ALT) 138 U/L, bilirubin 0.8 mg/dL, lactic acid 8.5 mmol/L, international normalized ratio (INR) 1.8, ammonia 51µmol/L. Imaging with CT head was unremarkable and CT abdomen demonstrated cirrhotic morphology of the liver with a small amount of ascites. Upper endoscopy was performed with no evidence of varices. Paracentesis demonstrated a high serum-ascites albumin gradient with low total protein consistent with portal hypertension. He was intubated for airway protection due to worsening encephalopathy. A peripheral smear was performed which showed myeloblasts with no signs of hemolysis. Bone marrow biopsy was subsequently performed which revealed 38% myeloblasts and features of myelodysplastic syndrome suggestive of secondary AML. Chemotherapy was not initiated as he was acutely critically ill and he expired shortly thereafter.AML can present with symptomatic anemia, bleeding, mental status changes due to central nervous system involvement, organomegaly, and renal insufficiency. Diagnosing AML in the setting of decompensated liver cirrhosis can be difficult as the clinical presentations can be similar at times. Thus, hematological causes should be considered when there is profound anemia with no acute blood loss early in the course.

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Section: Discussionsupporting

confidence: 84%

Acute Myeloid Leukemia Masquerading as Decompensated Cirrhosis

Ahdi¹,

Mannem²,

Lakha³

2022

Cureus

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“…Hepatomegaly is a common manifestation in ALL that is seen in up to 50% of patients 33 . Acute leukemia may present with acute liver failure which adversely affects the outcome of treatment 34,35 . Hepatomegaly was also reported to associate with hyperleukocytosis and a higher rate of death in adults with chronic myeloid leukemia in the chronic phase 36 .…”

Section: Discussionmentioning

confidence: 99%

“…33 Acute leukemia may present with acute liver failure which adversely affects the outcome of treatment. 34 , 35 Hepatomegaly was also reported to associate with hyperleukocytosis and a higher rate of death in adults with chronic myeloid leukemia in the chronic phase. 36 However, The association between hepatomegaly and worse outcomes in acute leukemia was never reported previously.…”

Section: Discussionmentioning

confidence: 99%

The survival of childhood leukemia: An 8‐year single‐center experience

et al. 2023

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Background The survival of childhood leukemia has improved. We aimed to report the survival rate and the associated factors in children with acute leukemia during an 8‐year follow‐up. Aims This study investigates the 8‐year survival rates of children with acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) in Shiraz, the largest oncology center in Southern Iran. We also aimed to assess the independent factors associated with higher mortality in childhood leukemia. Methods Children 0–18 years with acute leukemia were followed from 2013 to 2021 in Shiraz, Iran. The 8‐year overall survival (OS) and event‐free survival (EFS) rates were estimated by the Kaplan–Meier method. Independent factors associated with survival were assessed by the Cox regression hazard modeling. Results We included 786 children, with 43.5% female, and a mean age of 6.32 ± 4.62 years. Patients with AML compared to ALL experienced more relapse (34.6% vs. 22.5%, p = .01) and death (31.7% vs. 11.3%, p < .001). The cumulative 8‐year OS and EFS were 81% (95% confidence interval (CI), 74.3% to 86.1%) and 68.3% (95% CI, 63.5% to 72.7%) in ALL patients and 63.5% (95% CI, 52.1% to 72.9%) and 43% (95% CI, 33.1% to 52.6%) in AML patients. Multivariable analysis revealed that hepatomegaly (hazard ratio = 4, 95% CI, 1.0 to 22.3, p = .05) was the main independent risk factor of death in ALL patients. No definite risk factor was defined for AML patients. Conclusion The survival of childhood leukemia has recently increased dramatically in low‐middle income countries. Hepatomegaly was introduced as a potential risk factor for lower survival in ALL patients. Further multicenter studies are needed to confirm the validity of this association.

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“…The causative mechanism of liver injury is due to sinusoid infiltration by leukemic cells that induces tissue ischemia, with raised transaminase levels, and progresses to necrosis, presenting as liver failure [ 14 , 15 ]. Another consequence of liver damage is hepatic clearance reduction, which leads to hyperlactatemia.…”

Section: Discussionmentioning

confidence: 99%

Acute hepatitis-like presentation with cholestasis of CBFB–MYH11-positive acute myeloid leukemia in an adult male: a case report

et al. 2022

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Background Liver involvement in adults with acute myeloid leukemia is uncommon. Most of the case reports describe acute liver failure or obstructive jaundice, while acute hepatitis is rarely mentioned. We report a patient with acute myeloid leukemia who presented with clinical, biochemical, and radiological signs of acute hepatitis that totally regressed after chemotherapy. Case presentation A 38-year-old Caucasian man presented with fever, cough, and mild fatigue. Laboratory workup showed anemia, thrombocytopenia, severe leukocytosis, transaminitis, and hyperbilirubinemia. Imaging of the abdomen (ultrasound and magnetic resonance) showed hepatomegaly, splenomegaly, upper limits portal veins diameters, increased thickness of the gallbladder wall, and significant abdominal lymph nodes. Peripheral blood smear and bone marrow evaluation were consistent with acute myeloid leukemia, and liver biopsy showed massive sinusoidal and portal infiltration by leukemic cells. After remission-inducing chemotherapy, there was complete normalization of liver function tests, and liver, spleen, and portal vein size. Conclusions This case highlights the importance of taking acute myeloid leukemia into account as a possible cause of liver damage to make a rapid diagnosis and start appropriate treatment that may lead to hematological remission and hepatic dysfunction resolution.

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Acute myeloid leukaemia presenting as acute liver failure—a case report and literature review

Cited by 5 publications

References 18 publications

Acute Myeloid Leukemia Masquerading as Decompensated Cirrhosis

Acute Myeloid Leukemia Masquerading as Decompensated Cirrhosis

The survival of childhood leukemia: An 8‐year single‐center experience

Acute hepatitis-like presentation with cholestasis of CBFB–MYH11-positive acute myeloid leukemia in an adult male: a case report

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