Acute Myeloid Leukemia (AML) is an uncommon neoplasia, and its treatment is challenging. The AZAVIT-ABCEF protocol (Plataforma Brasil-CAAE: 53015421.0.0000.5463) is of low intensity and reasonably well-tolerated.

To report a clinical case of a patient with AML in complete remission (CR) with the protocol, cycles of 7 days every 28 days.

Descriptive work carried out through data collection from medical records.

A 62-year-old woman, whose mother died from AML and did not wish to undergo intensive chemotherapy. Hb was 6.5 g/dL, leukocytes 33,800/mm3 with 43% blasts, and platelets 107,000/mm3. Myelogram was refused, and peripheral blood immunophenotyping was positive for: CD11b, CD13, partial CD14, CD15, CD33, CD36, CD64, partial CD117, weak CD123, HLA-DR, and MPO. Diagnostic AML with monocytic component in December 2020. In the first cycle, she presented non-pruritic hyperemic lesions on her face and upper limbs, and vespertine fever. Skin biopsy showed neutrophilic infiltrate, sweet syndrome. The patient left the hospital and returned 1 month later with anemia and thrombocytopenia. She complained of significant pain in the hip joint, and MRI showed soft tissue edema with moderate joint effusion. Corticosteroid therapy was initiated, resolving the inflammatory condition. Marrow examination in March 2021 and April 2022 showed CR. In April 2023, she decided to stop the protocol, and 3 months later she presented with pancytopenia, marrow with dysplastic changes and 15% blasts (CD13, CD123, CD33, CD38, CD117, TdT, and MPO).

The possible mechanism of action: Azacitidine - reactivation of tumor suppressor genes, transcription of differentiating genes, action on protein metabolism and microRNA inhibition, increased VDR (vitamin D receptor) expression in primitive hematopoietic cells promoting differentiation, transcription of genes related to autoimmunity, making leukemic cells visible to the immune system, reactivation of antiviral activity, and differentiation of mesenchymal cells. Vitamin B1 - cofactor in the pyruvate dehydrogenase enzyme complex, as thiamine triphosphate, which prevents the transformation of pyruvate into lactate and favors respiration through the Krebs cycle, cofactor in the metabolism of alpha-ketoglutarate, and decreases the formation of 2-hydroxyglutarate (DNA methylation), activation of the immune system, and increased neoplastic cell death via P53 (non-canonical pathway, PUMA and NOXA). Vitamin C - cofactor in the Krebs cycle reaction involving the TET2 and IDH2 genes, promoting DNA demethylation, immunomodulatory effects activating antiretroviral reactions, and increased VDR expression in primitive hematopoietic cells. Vitamin D - decreases the function of myeloid suppressor cells, increases T cell immune response, modifies the tumor microenvironment, and favors autoimmunity. It promotes differentiation by binding to VDR, which interacts with nuclear proteins that bind to vitamin A. Erythropoietin and filgrastim are differentiating agents for the erythroid and granulocytic lineages, respectively.

The patient achieved CR with the treatment, and its discontinuation may have favored the appearance of previously unreported dysplasia, as well as an increase in the number of blasts. Prospective studies are needed to assess the effectiveness of the protocol.