Objective:To evaluate the rate of seropositivity to hepatitis B and C and Human Immunodeficiency Virus (HIV) infections among children with β-thalassemia major receiving multiple transfusions in Ahmedabad, India, compared with healthy controls.Materials and Methods:The study was performed during January 2007 to January 2009 on multi-transfused children suffering with β-thalassemia major registered in the Prathama Blood Centre, Ahmedabad; Jeevandeep hospital, Ahmedabad; and Red Cross Blood Centre, Ahmedabad, and investigated for the prevalence and development of transfusion-transmitted infections. Hepatitis B surface Antigen (HBsAg), anti-Hepatitis C Virus (HCV) Antibodies (Ab), and HIV Ab were checked using a fourth-generation Enzyme-Linked Immunosorbent Assay (ELISA). Positive tests were confirmed by western blots. Healthy blood donors were used for the control group.Results:Hepatitis B surface antigen, anti-HCV Ab, and HIV Ab were positive in one of 96 (1.04%; 95% Confidence Interval (CI) = 0.17–1.3), 24 of 96 (25%; 95% CI = 11.4–14.2), and one of 96 (1.04%; 95% CI = 0.12–1.3), respectively. The rate of anti-HCV Ab was significantly higher in multi-transfused children suffering with β-thalassemia major. In thalassemia patients, the rate of positive anti-HCV Ab was significantly higher than that for positive HBsAg (P<0.001) and HIV Ab (P<0.001).Conclusion:It is concluded that HCV is the current major problem in multi-transfused children with thalassemia major and more careful pretransfusion screening of blood for anti-HCV must be introduced in blood centers.
Life long red blood transfusion remains the main treatment for b thalassemia major patients. The development of alloantibodies complicates transfusion therapy in thalassemia patients. Alloimmunization to red cell antigens is one of the most important immunological transfusion reaction and causes delayed type of transfusion reaction. A prospective study was conducted from January 2007 to January 2010. This was a cohorts of 115 patients were selected from regular transfusion group and they were followed for two and half year. They were followed up for the effect of transfusion during study period. There was a decline in patient number from 115 to 96 due to mortality and transfer of patient. A total of 96 multiply transfused thalassemia patients were prospectively included in this study and three consecutive samples collected after every 6 months and investigated for the development of alloantibody to red cell antigens. Tests for antibody screening and identification were performed on preserved sample to investigate prevalence and development of red cell alloimmunization by standardized laboratory techniques by same person at Prathama Blood Centre. A total of 96 patients were included in the study. 63 patients were males and 33 females. A total of five single alloantibodies were formed in five patients out of them four (80 %) belonged to Kell blood group system and one (20 %) from Rh system. It was observed that two (1.92 %) of new thalassemia patients developed red cell alloantibodies during study period. Red cell alloimmunization should be kept in mind in the patients receiving multiple transfusions. In present study, alloimmunization rate was 5.21 %. Mean transfusion duration in these patients was 23.90 days, probably due to presence of alloantibody. RBC alloantibody detection on regular interval and corresponding antigen negative blood transfusion is strongly recommended in transfusion dependent thalassemia patients.
Twenty-five of thirty NIDDS who remained hypertensive (diastolic greater than 95 mmHg supine) after 4 weeks on bendrofluazide 2.5 mg daily (B), completed a single-blind, observer-blind randomized crossover study, in which the additional use of atenolol (50 mg daily) (A), slow-release nifedipine (20 mg twice daily) (N), and captopril (25 mg twice daily) (C) was compared. Patients took each drug for 8 weeks with dose doubling at 4 weeks if supine diastolic remained greater than 90 mmHg. All three combinations were more effective than bendrofluazide alone (p less than 0.01). In nine patients studied 2 h after tablets at the end of each treatment period nifedipine was more effective than the other two drugs (B:174/104 mmHg, A:162/95 mmHg, -8%, N:141/88 mmHg, -17%, C:157/94 mmHg, -10%, supine), whereas in 16 patients studied 15 h after their evening dose there was no significant difference. Fasting insulin and HbA1 levels were not significantly different between groups. No drug had a significant adverse effect on creatinine, glomerular filtration rate, overnight urinary albumin excretion or foot transcutaneous oxygen levels (43 degrees C). All three drugs studied were effective without deleterious effects on renal function or peripheral blood flow.
A case is described here of drug-induced immune hemolytic anemia (DIIHA) due to cefotetan administered to a post-partum woman who received the drug for infection prophylaxis at the time of caesarean section. Renewed fatal hemolysis occurred when the drug was given a second time 12 days after the first dose. The initial immunohematologic findings included a positive direct antiglobulin test (DAT) due to IgG and complement coating of the patient’s RBCs as well as an eluate that did not react with RBCs in the absence of drug. The antibody was drug-dependent, reacting with both drug-coated RBCs as well as when the drug was added to a mixture of her serum and donor RBCs. Cefotetan has been a common cause of this uncommon problem. The clinical features of cefotetan DIIHA, classification of drug-induced antibodies, and the differential diagnosis of a positive DAT are briefly discussed.
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