This medication works through inhibition of the enzyme ribonucleotide reductase. This enzyme reduces ribonucleotides into deoxyribonucleotides, which are necessary for DNA synthesis.
By inhibiting ribonucleotide reductase with hydroxyurea, DNA synthesis is decreased.
Hydroxyurea leads to prolonged inhibition of DNA replication, and as a result, cellular division is arrested in the S phase. This is also known as activating the S phase "checkpoint." Thus, by inhibiting DNA replication, hydroxyurea stops or severely slows down the cell replication cycle.
This medication is also used to treat malignant melanoma.
This medication is used to treat chronic myelogenous leukemia (CML). Its use has been largely replaced by imatinib, but is still used because of cost-effectiveness.
Hydroxyurea is a mainstay of therapy in sickle cell disease, because it effectively reverses sickling of cells. It causes an increase of Fetal hemoglobin (HbF), and inhibits Hemoglobin S (HbS) aggregation.
This drug enhances fetal hemoglobin (HbF) production. Fetal hemoglobin's reduction in the severity of the disease comes from its ability to inhibit the formation of hemoglobin aggregates within red blood cells that contain hemoglobin S (HbS), which is seen in sickle cell anemia.
A very common side effect of hydroxyurea is bone marrow depression; patients often develop neutropenia and thrombocytopenia. Hematologic recovery usually happens 2 weeks after stopping medications administration, however.
Hydroxyurea can lead to acute mucocutaneous toxicity. Patients can have severe GI distress, with diarrhea, constipation, nausea and vomiting.
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