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Background <p>The transformation of Fanconi anemia into a hematological malignancy is consistent with the natural history of the disease. Few cases have been reported on acute myeloid leukemia, and even fewer cases involving coexistence with sickle cell anemia. Acute myeloid leukemia development is postulated to follow a multihit hypothesis where preleukaemic cells progress into leukemia through a second promotional mutation. Fever is a predominant clinical presentation, with blasts usually observed on peripheral blood smear and the immunophenotype confirmed with flow cytometry. In this case report from Tanzania, we present a case of acute myeloid leukemia with a failed induction in a patient with Sickle cell anemia and&#xa0;suspected Fanconi anemia.</p> Case presentation <p>A 6-year-old Haya boy from northern Tanzania presented to Muhimbili National Hospital with a congenital malformation of the left hand, short stature, and multiple café-au-lait spots distributed over the trunk, face, and limbs. He had experienced recurrent fever for 8 months, accompanied by headache, weight loss, and abdominal distension. Laboratory evaluation confirmed acute myeloid leukemia and sickle cell anemia with clinically suspicious features of Fanconi anemia. The patient was initiated on institutional treatment for acute myeloid leukemia. He had a failed induction and subsequently transitioned to home-based palliative care after prognostic counseling with the family. Thereafter, he had several admissions, mostly for blood product support, and eventually died 7 months post-discharge.</p> Conclusion <p>The onset of acute myeloid leukemia in this case could be attributed to a malignant transformation from an underlying cancer predisposition syndrome. Our particular focus was on the leukemia treatment response where we observed a failed induction, prompting the need for alternative treatment approaches in this category of patients with acute myeloid leukemia in order to realize better treatment outcomes.</p>

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Managing acute myeloid leukemia in the context of sickle cell anemia and suspected Fanconi anemia in Tanzania: a case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月2日

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  • Amosi Kilipamwambu,
  • Irene Msirikale,
  • Bernice Mukuria,
  • Koga Luhulla,
  • Trish Scanlan,
  • Godlove Sandi,
  • Peter Swai,
  • Khadija Mwamtemi,
  • Lulu Chirande,
  • Nana Nakiddu

摘要

Background

The transformation of Fanconi anemia into a hematological malignancy is consistent with the natural history of the disease. Few cases have been reported on acute myeloid leukemia, and even fewer cases involving coexistence with sickle cell anemia. Acute myeloid leukemia development is postulated to follow a multihit hypothesis where preleukaemic cells progress into leukemia through a second promotional mutation. Fever is a predominant clinical presentation, with blasts usually observed on peripheral blood smear and the immunophenotype confirmed with flow cytometry. In this case report from Tanzania, we present a case of acute myeloid leukemia with a failed induction in a patient with Sickle cell anemia and suspected Fanconi anemia.

Case presentation

A 6-year-old Haya boy from northern Tanzania presented to Muhimbili National Hospital with a congenital malformation of the left hand, short stature, and multiple café-au-lait spots distributed over the trunk, face, and limbs. He had experienced recurrent fever for 8 months, accompanied by headache, weight loss, and abdominal distension. Laboratory evaluation confirmed acute myeloid leukemia and sickle cell anemia with clinically suspicious features of Fanconi anemia. The patient was initiated on institutional treatment for acute myeloid leukemia. He had a failed induction and subsequently transitioned to home-based palliative care after prognostic counseling with the family. Thereafter, he had several admissions, mostly for blood product support, and eventually died 7 months post-discharge.

Conclusion

The onset of acute myeloid leukemia in this case could be attributed to a malignant transformation from an underlying cancer predisposition syndrome. Our particular focus was on the leukemia treatment response where we observed a failed induction, prompting the need for alternative treatment approaches in this category of patients with acute myeloid leukemia in order to realize better treatment outcomes.