A ribonucleotide reductase inhibitor, has been used to treat patients with myeloproliferative cancers, and patients with sickle cell disease.

The drug is used to increase fetal hemoglobin levels.

Short-term hydroxyurea therapy can result in a substantial reduction in the frequency of painful episodes and acute chest syndrome in sickle cell disease.

Long-term therapy can result in reduced mortality in sickle cell disease.

Rare side effect is melanonychia.

Trade names Apo-Hydroxyurea, Droxia, Hydrea

Oral agent.

Hepatic metabolism.

Biological half-life 2-4 hours.

Excretion renal and lungs.

An antineoplastic drug used in myeloproliferative disorders, specifically polycythemia vera and essential thrombocythemia.

It is also used to reduce the rate of painful attacks in sickle-cell disease and has antiretroviral properties in diseases such as HIV/AIDS.

Used for the following indications:

Myeloproliferative disease (primarily polycythemia vera and essential thrombocytosis). It has been found to be superior to anagrelide for the control of ET.

Sickle-cell disease

AIDS as an adjunct to ddI in combination antiretroviral therapies

Second line treatment for psoriasis

Systemic mastocytosis

Chronic myelogenous leukemia

Reported side-effects are: drowsiness, nausea, vomiting and diarrhea, constipation, mucositis, anorexia, stomatitis, bone marrow toxicity (dose-limiting toxicity; may take 7–21 days to recover after the drug has been discontinued), alopecia, skin changes, abnormal liver enzymes, creatinine and blood urea nitrogen.

Monitoring of the blood count, renal function, uric acid and electrolytes, as well as liver enzymes should be performed.

Ued primarily for the treatment of myeloproliferative diseases, which has an inherent risk of transforming to acute myeloid leukemia.

There has been concern that it carries a leukemia risk, but large studies have shown that the risk is either absent or very small.

Decreases production of deoxyribonucleotides via inhibition of the enzyme ribonucleotide reductase by scavenging tyrosyl free radicals.

In the treatment of sickle-cell disease, it increases the concentration of fetal hemoglobin.

Increases nitric oxide levels, causing soluble guanylyl cyclase activation with a resultant rise in cyclic GMP, and the activation of gamma globin chain synthesis necessary for fetal hemoglobin production.

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