Blood donation among women in Nigeria: Motivators, barriers and appealing incentives.

BACKGROUND AND OBJECTIVES: Women are grossly under-represented among blood donors in Nigeria. We, therefore, determined the barriers, motivators and appealing incentives to blood donation among women in Nigeria. MATERIALS AND METHODS: This was an internet-based cross-sectional study among women aged 18-65 years. A well-structured questionnaire was used to determine sociodemographic characteristics, motivation, barriers and appealing incentives. Motivational and barrier differences in some sociodemographic characteristics were determined using the chi-squared test. A p-value of 0.05 was considered statistically significant. RESULTS: The most common motivators among blood donors were 'when family or friend is in need of blood', 'health benefits' and 'reminders to donate'. One-time donors who were willing to become regular donors were more motivated by reminders to donate than those not willing (p = 0.000). The most common barriers among non-donors were 'poor attitude of hospital staff' and 'fear of contracting infections'. Younger women and those of the Hausa tribe were more debarred by 'lack of privacy during blood donation exercise' than older women and those of the other tribes (p-values of 0.008 and 0.006, respectively). The most appealing incentives for blood donation were medical consultation and a blood donation certificate. CONCLUSION: Women's participation in blood donation in Nigeria can be improved by sending regular reminders to donors, especially one-time donors and by infrastructural adjustments to improve privacy at the blood donation sites. Specific and targeted capacity-building initiatives should also be put in place to drive a paradigm shift in the attitude of hospital staff to work in Nigeria.

The Effect of Alpha Thalassemia, HbF and HbC on Haematological Parameters of Sickle Cell Disease Patients in Ibadan, Nigeria.

BACKGROUND: Sickle cell disease is a protean disease with limited data on Nigeria's phenotypic and genetic variants. This study was conducted to provide baseline data on these variants by characterising the existing forms of sickle cell disease and correlating these with basic haematological parameters. METHODS: Adult and paediatric patients with SCD were recruited from a tertiary health centre in Nigeria. Patients were age and sex-matched with healthy controls. Blood samples were obtained for Full Blood Count, phenotyping by High-Performance Liquid Chromatography, and genotyping for alpha thalassemia by multiplex Gap-polymerase chain reaction. Data analysis was done using IBM SPSS statistics version 23. RESULTS: A total of 130 patients with sickle cell disease and 117 controls were studied. Alpha thalassemia in the study population was due to a 3.7kb deletion in the alpha-globin gene cluster at a prevalence of 45.4% in the patients and 47% in the controls. The prevalence of the various existing forms of SCD genotype was: Homozygous S without alpha gene deletion (HbSS)- 39.2%; HbSC - 10.8%; HbSSα+1- 35.4%; HbSSα+2 - 6.9% and HbSF- 7.7%. In the control population, HbAA without alpha gene deletion had a prevalence of 42.7%, HbAAα+1 was 25.6%, HbAA α+2 was 6%, HbAS- 7.7%, HbAS α+1 - 11.1%, HbAS α+2 - 2.6%, HbAC - 2.6% and HbAC α+1 - 1.7%. HbA2 was significantly elevated in HbSS individuals with two alpha gene deletions but reduced in normal controls (HbAA) with alpha gene deletions. HbF and HbA2 were negatively correlated with each other (r= -0.587, p < 0.001). Individuals with the HbSC genotype followed by HbSSα+2 had the best haematological parameters. CONCLUSIONS: Haematological parameters vary with haemoglobin genotype. The C haemoglobin and homozygous alpha-thalassemia deletion had a better ameliorating effect on SCD haematological parameters than the F haemoglobin in this population. The effect of alpha thalassemia on some haematological parameters in SCD patients are reversed in normal controls.

Assessment of hepatitis B surface antigen negative blood units for HBV DNA among replacement blood donors in a hospital based blood bank in Nigeria.

BACKGROUND: Hepatitis B virus infection is one of the greatest threats to blood safety all over the world. The laboratory algorithm based on only the detection of hepatitis B surface antigen (HBsAg) leaves a gap for infected HBsAg negative donors to donate blood during the "window period" (WP) and late stages of infection. OBJECTIVE: To estimate the frequency of the presence of HBV deoxyribonucleic acid (DNA) in HBsAg negative blood units screened using two different assays for HBsAg in a high endemic region. METHODS: Frozen serum aliquot of 100 replacement blood donors who donated blood units that were HBsAg negative were retrieved and tested for HBV DNA. Sample positive for HBV DNA was sequenced by Sanger's method, genotyped and the viral load was determined. RESULTS: One sample (1%) was positive for HBV DNA. The HBV viral load of the sample was 768,000 IU/ml. The partial S-gene of the Hepatitis B virus isolated was genotype E using the NCBI viral genotyping tool. CONCLUSIONS: There is still a risk of HBV infected blood unit escaping detection when donor testing is limited to HBsAg screening. The use of NAT which can substantially reduce HBV infected blood donors from the donor pool should be considered.

The effect of the coinheritance of Glucose-6-phosphate dehydrogenase deficiency on the severity of sickle cell disease.

BACKGROUND: Sickle cell disease (SCD) and glucose-6-phosphate dehydrogenase (G6PD) deficiency are inherited disorders associated with chronic haemolysis. Therefore, coinheritance of both disorders could worsen haemolysis in the former and compound a haemolytic crisis. This study compared clinical and laboratory features of deficient and non-deficient SCD patients and the G6PD activities of SCD patients and apparently healthy controls. MATERIALS AND METHODS: This is a case-control study of 175 SCD patients and 166 non-SCD controls. G6PD assay was carried out on haemolysate from washed red cells. The G6PD activity was measured by spectrophotometry. RESULTS: The mean age of patients and controls was 27.3 ± 9.4 and 35.9 ± 9.7 years, respectively, with 75 (46.2%) and 87 (52.4%) being males, respectively. G6PD activity was similar in cases and controls (6.7 ± 3.3 vs. 6.9 ± 3.0 IU/gHb), respectively (P = 0.6). The prevalence of G6PD deficiency was higher in patients than controls (28.6% vs. 22.3%, P = 0.18), and SCD patients were twice more likely to have enzyme activities below 3.0 IU/gHb. No significant difference was observed in the clinical parameters between deficient and non-deficient patients. Deficient patients were more likely to have lower haematocrit (22.8 ± 3.9% vs. 24.5 ± 5%, P = 0.04) and non-significantly higher bilirubin and reticulocyte counts. Furthermore, in patients, severe deficiency resulted in higher bilirubin than in those with mild deficiency (60.5 vs. 21.7 IU/L, P < 0.001). G6PD activity correlated positively with haematocrit (r = 0.91, P = 0.01) and mean corpuscular haemoglobin concentration (r = 0.17, P = 0.02). CONCLUSIONS: Coinheritance of both disorders could worsen haemolysis in SCD patients, and care should, therefore, be taken in the choice of drugs in deficient SCD patients.

Defective lipid metabolism in sickle cell anaemia subjects in vaso-occlusive crisis.

BACKGROUND: Abnormal lipid homeostasis has been reported in sickle cell anaemia (SCA) as well as in other haematological disorders. However, there is little information on the lipid profile of SCA subjects in vaso-occlusive crisis (VOC). This study determined the lipid profile of adult SCA subjects in VOC and in steady state (SSCA). MATERIALS AND METHODS: Fifty-eight (58) adults with HbSS (30 in steady state and 28 in vaso-occlusive crisis) and 24 age-matched healthy individuals with HbAA genotype were recruited into this study. Standard methods were used for the determination of blood pressure (BP), packed cell volume (PCV), total white blood cell count (WBC) and haemoglobin phenotype. After an overnight fast, 5 ml of venous blood was obtained from each SSCA and the controls while samples were collected upon admission in the VOC group. Plasma lipid profile was determined using enzymatic method. Differences between two groups were determined using independent Student's t-test or Man-Whitney U as appropriate. P-values less than 0.05 were considered significant. RESULTS: Plasma total cholesterol (TC) and high density lipoprotein (HDL) were significantly lower while the ratio of triglyceride (TG) to HDL (TG/HDL) was significantly higher in SSCA compared with the controls. Low density lipoprotein (LDL) and TC were significantly lower in SCA subjects in VOC compared with controls. However, TC, TG, LDL and TG/HDL were significantly lower while HDL was significantly higher in VOC compared with SSCA. CONCLUSION: Sickle cell anaemia subjects have defective fasting lipid metabolism which becomes pronounced with VOC.