Case Presentation: A 56-year-old male with type II diabetes presented to the hospital with 3 weeks of oral ulcers involving the left buccal region with spread to the palate and tongue. He also reported odynophagia, poor oral intake, and 40-lb weight loss. He had not responded to outpatient amoxicillin, fluconazole, and nystatin swish and swallow. On physical exam, he was febrile to 38.2 °C, tachycardic, and had multiple oral necrotic ulcers with fibrinous debris. Labs were remarkable for white blood cell count of 13.1 K/uL (normal range: 4 to 11 K/uL). Tissue cultures revealed normal oral flora and biopsy showed non-specific inflammation. Serologies were negative for viral, syphilitic, or autoimmune etiologies. His ulcers improved on antimicrobials, but he subsequently developed a recurrent fever and a progressive, worsening pancytopenia. MRI of the jaw was obtained to assess for further infection and showed osteomyelitis with an incidental finding of hematopoietic bone marrow reconversion. Due to his worsening pancytopenia, recurring fevers, and apparent immunosuppression, a bone marrow biopsy was obtained which showed 25% blasts in hypocellular marrow consistent with acute myeloid leukemia.
Discussion: Acute myeloid leukemia (AML) is a hematologic cancer characterized by the abnormal proliferation of myeloid blasts in the bone marrow, blood, and other tissues. Expansion of blasts in the bone marrow can impair development of normal hematopoietic cell lines, resulting in cytopenias. AML is classically suspected based on signs and symptoms of anemia, thrombocytopenia, or leukopenia, such as weakness, bleeding, or infections.1 Oral presentations of AML have been previously reported, mainly in the dental literature, and commonly manifest as gingival hyperplasia, petechiae, or ulcerations.2,3,4,5 Our patient presented with infected oral ulcers that improved on antimicrobials and initially normal hematologic findings. We postulate that his infections led to a leukemoid reaction and a reactive thrombocytosis that masked his hematologic dyscrasias, delaying his diagnosis. The patient’s jaw MRI revealed an incidental finding of bone marrow reconversion from fatty to red marrow, indicating increased hematopoietic activity. During normal bone aging, conversion of red bone marrow to yellow marrow occurs in predictable anatomic patterns.6 Bone marrow reconversion is the reverse of this normal process, and is a response to increased hematopoietic demand. In the setting of new-onset pancytopenia, the finding of bone marrow reconversion in our patient suggested dysfunctional bone marrow activity concurrent with increased metabolic demand. This combination of bone marrow findings was suspicious for a neoplastic process, in our case characterized by the malignant proliferation of blast cells disrupting normal hematopoiesis.
Conclusions: This case illustrates an unusual, nonspecific initial presentation of AML as oral ulcers and the challenges of recognizing AML when first-line laboratory tests are normal. It is important to redirect clinical decision-making and have a low threshold for suspecting AML in the appropriate clinical setting with pancytopenia, infections, fever, and suggestive MRI findings.
