The CBC Was Screaming: Acute Myeloid Leukemia Unmasked by Gastrointestinal Bleeding

Background

Cytopenias in a patient with gastrointestinal bleeding are usually attributed to blood loss, but this framework can fail when the marrow itself is the primary site of disease. Acute myeloid leukemia (AML) presenting primarily as gastrointestinal bleeding is uncommon, and most reported cases involve thrombocytopenia or coagulopathy as the mechanism of bleeding. We describe a case in which specific CBC and differential findings, present from admission, pointed to an occult AML before the bleeding source itself was identified.

Case Presentation

An 83-year-old woman with hypertension, type 2 diabetes, and dyslipidemia was transferred for melena, hematochezia, progressive weakness, and anemia requiring transfusion. She remained afebrile and hemodynamically stable, and no active bleeding was captured on serial evaluation. Her presenting CBC showed leukopenia (WBC 3.7 x10³/µL), severe neutropenia (ANC 0.51 x10³/µL), marked monocytosis (36%), elevated red cell distribution width, circulating immature granulocytes, and nucleated red blood cells, all attributed initially to hemorrhage. EGD showed chronic gastritis, colonoscopy showed diverticulosis and hemorrhoids, and video capsule endoscopy showed nonbleeding small-bowel lesions; none explained the severity of the anemia, and the cytopenias persisted despite repeated transfusion and negative stool occult blood testing.

Results

Persistent leukopenia and monocytosis prompted hematology consultation. Peripheral blood flow cytometry identified circulating myeloblasts expressing CD34, CD117, and CD33. Bone marrow biopsy showed a hypercellular marrow largely replaced by immature, dysplastic hematopoietic cells with a prominent blast population showing monocytic differentiation and dysplasia across all three lineages, including dysplastic megakaryocytes and erythroid precursors; blasts reached 23% by manual differential. Cytogenetics revealed a complex karyotype with del(5q), del(17p)/TP53 loss, and trisomy 8. The integrated findings were consistent with AML with monocytic differentiation and myelodysplasia-related features. The patient was lost to follow-up before treatment could begin.

Discussion & Conclusion

Blood loss classically produces reactive neutrophilia, not neutropenia; monocytosis, immature myeloid forms, and nucleated red blood cells reflect disordered marrow release rather than a transient post-hemorrhagic response. In this case, these findings preceded both the endoscopic workup and hematology consultation in signaling the diagnosis, and the morphologic picture, a hypercellular marrow effaced by dysplastic blasts rather than one depleted by blood loss, confirmed a primary marrow disorder. Her adverse-risk cytogenetic profile carries a poor prognosis, which is why early recognition matters for timely hematology-oncology referral and treatment planning. Cytopenias in a patient with gastrointestinal bleeding should be interpreted independently of the presumed bleeding source rather than assumed reactive by default. When CBC abnormalities are disproportionate to identified blood loss, early hematologic evaluation should be pursued regardless of a seemingly sufficient concurrent explanation such as active bleeding.