Pace BS, Qian XH, Sangerman J, et al. Hydroxyurea treatment of patients with sickle-cell disease increases fetal hemoglobin (HbF), which reduces hemoglobin S polymerization and clinical complications. Obtain HbF levels every 3 to 4 months. This analysis is composed of all children (<19 years of age) with SCA (HbSS/HbSβChildren with SCA treated at St. Jude were followed by a multidisciplinary staff trained to provide comprehensive care including physicians, nurses, nurse case managers, social workers, psychologists, child life specialists, nutritionists, pharmacists, and advanced practitioners (nurse practitioners and physician assistants).
Sustained long-term hematologic efficacy of hydroxyurea at maximum tolerated dose in children with sickle cell disease.
Kinney TR, Helms RW, O’Branski EE, et al.
These two drugs serve as cytidine analogs that are incorporated into DNA, where they form covalent bonds with DNMT, leading to depletion of functional enzyme.The leading hypothesis for the mechanism of induction of HbF by butyrate is that it increases the transcriptional activity of the γ-globin promoters by increasing the level of histone acetylation.
Carcinogenicity and haemoglobin synthesis induction by cytidine analogues. Hydroxyurea enhances fetal hemoglobin production in sickle cell anemia. Hydroxyurea, an inducer of HbF, has already …. Means and standard deviations are reported, if not otherwise specified. Hematologic responses of patients with sickle cell disease to treatment with hydroxyurea. Maintenance of elevated fetal hemoglobin levels by decitabine during dose interval treatment of sickle cell anemia. In Model #2, HbF% was categorized into 2 groups (≤20% and >20) and the GEE model was utilized to calculate the odds ratios (OR) and 95% confidence intervals (95% CI) for hospitalization within each HbF% category during each interval. Bailey K, Morris JS, Thomas P, Serjeant GR. At full dose, the medicine should slightly reduce the number of blood cells in the body.
Interestingly, decitabine treatment resulted in an increase rather than a decrease in platelet count. Multiple drugs including 5-azacytidine (and decitabine), hydroxyurea, butyrate and erythropoietin were shown to induce HbF 5-Azacytidine was the first prototype of an agent that induces HbF by targeting epigenetic silencing. Natural history and determinants of clinical severity of sickle cell disease. All statistical testing was two-sided and no multiplicity was corrected.The 383 subjects had a median enrollment age of 31.0 (range 18–74) years with equal gender proportions (184 subjects, 48% male), and sixty-six percent (n = 253) had ever been treated with hydroxyurea. Requirement of GATA-1 and p45 NF-E2 expression in butyric acid-induced erythroid differentiation. As a result of the recent introduction of decitabine as a new DNA hypomethylating agent and follow-up animal studies which showed that hypomethylating agents could reduce the incidence of tumors, there has been a renewed interest in the use of DNA hypomethylation therapy for inducing HbF in patients with SCD. Hydroxyurea, an inducer of HbF, has already been approved for the treatment of patients with moderate and/or severe SCD. Partington GA, Patient RK. Platt OS, Brambilla DJ, Rosse WF, et al.
Yang AS, Estecio MR, Garcia-Manero G, Kantarjian HM, Issa JP. The MSH did not specifically report fetal hemoglobin (HbF) responses, although other reports have shown that hydroxyurea largely exerts its effect by increasing HbF and inhibiting RBC sickling [ 11, 12 ]. 44 A reduction of WBC and ANC did favorably influence the odds of hospitalization, but HbF level was the dominant variable supporting this effect. Reactivation of fetal hemoglobin (HbF) expression is an important therapeutic option in patients with hemoglobin disorders. Cox regression analysis revealed deceased subjects had more hepatic dysfunction (elevated alkaline phosphatase, Hazard Ratio = 1.005, 95% CI 1.003–1.006, p<0.0.0001), kidney dysfunction (elevated creatinine, Hazard Ratio = 1.13, 95% CI 1.00–1.27, p = 0.043), and cardiopulmonary dysfunction (elevated tricuspid jet velocity on echocardiogram, Hazard Ratio = 2.22, 1.23–4.02, p = 0.0082). The most common identifiable causes of death were pulmonary (N = 11, First we compared characteristics at enrollment where deceased subjects (n = 59) were significantly older at enrollment (41.8 versus 32.5 years, p = 0.0067), had lower maximum HbF (p = 0.0044), were less likely to have taken hydroxyurea (56% versus 68%, p = 0.040, hazard ratio 0.58, 95% confidence interval 0.34, 0.97), and had a lower proportion prescribed hydroxyurea within the recommended dosage range (29% versus 46%, p = 0.0039, Multivariable Cox regressions using age as the time-scale were performed to further identify baseline factors that are associated with survival time.
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