The frequency of leg ulcers did not decrease after HU. HU treatment was effective in patients for whom HU was given for frequent VOC and/or ACS ( Table 1). 20, IBM-SPSS Statistics, Chicago, IL, USA). Significance level was defined as P < 0.05 (SPSS, v. The effects of HU therapy on the different complications (VOC, ACS and other complications) were assessed by using the McNemar test. Biochemical and clinical routine parameters were compared prior to and at 12 months of HU therapy by using a paired student’s t-test. 8Ī one-way analysis of variance (ANOVA) with repeated measurements and post-hoc Tukey tests was used to study the biological changes occurring with HU therapy. The RBC disaggregation threshold (i.e., RBC aggregates strength) was determined using a re-iteration procedure. 6 RBC aggregation was determined at 37☌ via syllectometry using the LORCA (hematocrit adjusted to 40%). 7 RBC deformability was measured at 37☌ at 3 and 30 Pa by ektacytometry (LORCA, RR Mechatronics, Hoorn, The Netherlands). The hematocrit/blood viscosity ratio was calculated at 225 s and is considered an index of RBC oxygen transport effectiveness. 6 Blood viscosity was determined at native Hct, at 25☌ and at shear rates of 45, 90 and 225 s using a cone/plate viscometer (Brookfield DVII+, Brookfield Engineering Labs, Natick, MA, USA). 2 All hemorheological measurements were carried out within 4 hours of the venipuncture to avoid blood rheological alterations, and after complete oxygenation of the blood. Biochemical parameters in blood and urine (24 hours urine sample) were performed using standard methods. 2 Hematological parameters were determined using a hematology analyzer (Max M-retic, Coulter, USA). The study was performed in accordance with the Declaration of Helsinki, was approved by the IRB of the Academic Hospital of Pointe-à-Pitre (DRCI-CHUPAP 230514, Guadeloupe), and written consent was obtained from all patients.Ī diagnosis of SCA and α-thalassemia was made as previously described. Blood was sampled before HU therapy and at 1, 3, 6 and 12 months of treatment for biological measurements. The same parameters, as well as the occurrence of the above complications, were prospectively recorded for one year after the initiation of HU therapy. Routine examination before starting HU therapy included the measurements of anthropometric characteristics, blood pressure, mean hemoglobin saturation (by pulse oximetry) and heart rate. Other complications within the preceding year were listed by an experienced physician. 2 1 For the other patients (n=8), HU therapy was proposed due to their need for frequent ambulatory care for subclinical VOC and a persistent low value of hemoglobin in comparison to usual steady-state values. ACS and VOC were defined as previously described. Frequent hospitalizations for vaso-occlusive crises (VOC n=13) and/or at least one acute chest syndrome (ACS n=8) event in the preceding year were the main criteria used to propose HU therapy to these patients: 5 patients met the two criteria. We demonstrated that the improvement in RBC deformability and the decrease of RBC aggregates robustness in HU-treated patients limit the consequences of the increase of hemoglobin on blood viscosity.Ģ4 adult patients with SCA (38.3 ± 11.8 yrs, 61.9 ± 12.7 kg, 172.3 ± 10.9 cm 14 males/10 females) regularly followed by the Sickle Cell Center of Pointe-à-Pitre (Academic Hospital, Guadeloupe) and at steady-state, 2 were recruited consecutively. The aim of the present study was to test the effects of one year of HU therapy on blood rheology (RBC deformability and aggregation, blood viscosity), hematology and clinical profile in SCA adults. 5 4 However, no study has of yet investigated the effects of HU therapy on blood viscosity and RBC rheology. 3 1 Hydroxyurea (HU) therapy improves the clinical course of both children and adults with SCA. Abnormal blood rheology has been shown to modulate the clinical severity and to also be involved in several complications of SCA. The presence of sickle hemoglobin (HbS) in red blood cells (RBC) of patients with sickle cell anemia (SCA) is at the origin of their rheological abnormalities.
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