Microsoft Word - AHA114BF

Dr. A.K. Al-Ali, College of Medicine and Medical Sciences (43), King Faisal University, P.O. Box 2114, Dammam 31451 (Saudi Arabia) It has been reported that sickle cell anemia patients have elevated serum levels of uric acid [1, 2]. This has been ascribed to altered renal function or increased bone marrow activity [3, 4]. The majority of investigations have been carried out on subjects of African or West Indian origin. Hemolytic anemias such as sickle cell disease and glucose-6-phosphate dehydrogenase (G6PD) deficiency are known to be prevalent in the eastern province of Saudi Arabia. Perrine et al. [5] reported that due to high fetal hemoglobin, Saudi sickle cell anemia takes a benign clinical course. A slightly elevated uric acid level has been reported earlier in Saudi sickle cell patients, which proved to be statistically insignificant [6]. However, the investigators did not appraise the high prevalence of G6PD deficiency in this area, where it is also common in sickle cell disease subjects. Therefore, we have sought to establish the levels of uric acid, urea and creatinine in normal, homozygous sickle cell disease (Hb SS) and heterozygous sickle cell trait (Hb AS) subjects, with or without G6PD deficiency. Blood samples were collected in EDTA or heparin tubes from Saudi volunteers or patients from the eastern province attending Qatif Central Hospital (age range 5-25 years) and were analyzed within a 4-hour period. Hematological indices (Cell DYN 700, Sequoia Turner), cellulose acetate hemoglobin electrophoresis (Helena Laboratories, Beaumont, Tex., USA), uric acid, creatinine and urea were determined using standard procedures. G6PD activity was determined spectrophotometrically according to the method of Bat-tistuzzi [7]. All subjects were in a clinically steady state and the Hb A2 level and reticulocyte counts were determined to exclude the possibility of active hemolysis or the presence of the ß-thalassemia trait [8]. Statistical analysis was carried out by Student’s t test and ANOVA. 679 blood samples were obtained from subjects of both sexes who did not exhibit active hemolysis, ß-thalassemia or show any history of favism. Table 1 reports the hematological indices determined on both heterozygous and homozygous sickle cell subjects with or without G6PD deficiency. The indices for normal controls are similar to those reported in