Myelodysplastic syndrome (MDS) is a group of medical conditions derived from progressive bone marrow failure that result in ineffective production of blood cells. Depending on the severity, MDS reduces the quality of life to the point of being life-threatening. There is a probability of death at all stages of the disease, due to complications and co-morbidities, with progression to acute myeloid leukemia (AML) being the worst evolution. Azacytidine is a nucleosidic analog with original epigenetic mechanism of action that is widely used for treating a variety of myelodysplasic syndromes. Although generally well tolerated, severe and sometimes life-threatening toxicities were unexpectedly observed in some patients. Genetic polymorphism affecting cytidine deaminase (CDA), the liver enzyme responsible for azacytidine detoxification step, could be responsible for poor clinical outcome due to on the one hand to severe toxicities in deficient patients, and on the other hand on treatment failure in ultrametabolizer patients.This clinical study aims at correlating the values in CDA levels with the risk of drug-related toxicities and to the clinical response to azacytidine treatment.

Inclusion Criteria:

• The patients have to be capable of submitting themselves at the rate of the visits, in the plan of treatmen, in the balance assessments of laboratory and other procedures of the study.
• Patient treated by azacytidine

Exclusion Criteria:

• Patients having an infection unchecked who could compromise the participation in the study
• Patients having other grave and/or unchecked concomitant diseases which could compromise the participation in the study