Idiosyncratic Side Effects of Hydroxyurea in Patients with Sickle Cell Anemia

Samir K Ballas Priya Singh

doi:10.4172/2155-9864.1000162

Abstract

Hydroxyurea was approved by the Food and Drug Administration for the treatment of adults with moderate to severe sickle cell anemia and sickle-β0-thalassemia. Its major side effect is myelotoxicity, which is reversible upon discontinuation of the drug. Other side effects that have been described in animal studies but unconfirmed in humans include its teratogenic and carcinogenic potential. Additionally, hydroxyurea has idiosyncratic side effects that occur in some individuals and this may be a genetic or epigenetic phenomenon. We report three idiosyncratic side effects of hydroxyurea in four patients with sickle cell anemia (SS). Desquamating rash, decreased libido and partial complex seizures have not been previously described in patients who are hydroxyurea responders. Although these reactions are rare, they can be serious in some patients.

Highlights

Hydroxyurea (HU) was approved by the Food and Drug Administration (FDA) on February 25, 1998 to decrease the frequency of painful crises, decrease the frequency of acute chest syndrome and decrease the need for blood transfusions in adult patients with moderate to severe sickle cell anemia (SS) and sickle-β0-thalassemia (S-β0-T)
Hydroxyurea may be associated with certain idiosyncratic side effects in some patients
We reported an unusual desquamating, pruritic rash, decreased libido and a partial complex seizure in 4 patients with sickle cell anemia during treatment with hydroxyurea

Summary

Introduction

Hydroxyurea (HU) was approved by the Food and Drug Administration (FDA) on February 25, 1998 to decrease the frequency of painful crises, decrease the frequency of acute chest syndrome and decrease the need for blood transfusions in adult patients with moderate to severe sickle cell anemia (SS) and sickle-β0-thalassemia (S-β0-T). It is the only FDA approved drug for patients with SS. Proposed mechanisms include selectively killing cells in the bone marrow, and increasing the number of early erythroid progenitors such as fetal erythroblasts that lead to production of Hb F reticulocytes. We describe three idiosyncratic effects of HU in patients with SS that have not been previously reported

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