Browsing by Author "Forson, P.O."
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Item Comorbidity of Glucose-6-Phosphate Dehydrogenase Deficiency and Sickle Cell Disease Exert Significant Effect on RBC Indices(Anemia, 2019-03) Antwi-Baffour, S.; Adjei, J.K.; Forson, P.O.; Akakpo, S.; Kyeremeh, R.; Seidu, M.A.Background. Glucose-6-phosphate dehydrogenase (G6PD) converts glucose-6-phosphate into 6-phosphogluconate in the pentose phosphate pathway and protects red blood cells (RBCs) from oxidative damage. Their deficiency therefore makes RBCs prone to haemolysis. Sickle cell disease (SCD) on the other hand is a hereditary blood disorder in which there is a single nucleotide substitution in the codon for amino acid 6 substituting glutamic acid with valine. SCD patients are prone to haemolysis due to the shape of their red blood cells and if they are deficient in G6PD, the haemolysis may escalate. Reported studies have indicated variations in the prevalence of G6PD deficiency in SCD patients and as such further work is required. The aim of this study was therefore to estimate the incidence of G-6-PD deficiency among SCD patients and to determine its impact on their RBC parameters as a measure of incidence of anaemia. Methods. A total of 120 clinically diagnosed SCD patients of genotypes HbSS and HbSC were recruited into the study. About 5ml of blood was collected via venipuncture from each patient and used to run G6PD, full blood count, and haemoglobin (Hb) electrophoresis tests. The data were analyzed using SPSS version 20 and Graphpad prism. Result. G6PD deficiency was detected in 43 (35.83%) of the participants made up of 16 (13.33%) males and 27 (22.50%) females of whom 17 (14.17%) had partial deficiency and 10 (8.33%) full deficiency. Statiscally significant differences p=0.036 and p=0.038 were established between the Hb concentration of the participants having a G6PD deficiency and those with normal G6PD activity for males and females, respectively. Conclusion. From the results obtained, it implies that G6PD deficiency may increase the severity of anaemia in SCD patients. There is therefore the need to screen all SCD patients for G6PD deficiency to ensure that their condition is not exacerbated during treatment.Item Genetic Variations in Schistosoma Haematobium, Resistance and Reinfection in the Greater Accra Region(University Of Ghana, 2017-07) Forson, P.O.Background: Schistosomiasis is among the major parasitic diseases following malaria in the category of neglected tropical diseases (NTD) especially in Africa sub-Saharan region. About 93% of Schistosomiasis is believed to occur in Africa. The genus Schistosoma is the parasitic trematode worm responsible for this disease. Schistosoma haematobium is responsible for causing Urogenital Schistosomiasis. The WHO recommended drug for schistosomiasis is Praziquantel (a single dose of 40mg/kg). Resistance of Schistosomiasis using Praziquantel (PZQ) has been reported in Egypt and Senegal. However, in endemic areas, reinfection after treatment is common. Genetic variants in Schistosomes have been observed in countries like Mali and Sudan. Presently in Ghana little is known about trends of genetic variants, as well as the possibility of resistance development and reinfection. Aim: The aim of this study is to determine genetic variation in Schistosoma haematobium (ITS2, NAD1, COX1), assessment of resistance and reinfection. Methodology: Urine samples of school children were obtained with consents from parents and guardians in the two communities (Zenu and Weija) in the Greater Accra region. Microscopy with egg count as well as viability test (modified hatchability technique, vital stains, and fluorescent microscopy) was performed on the spun urine sediments after macroscopic examination. The study procedure included a follow up collection of urine samples after treatment to assess resistance and reinfection. Genetic variation was assessed from sequences of the PCR amplified products (ITS2, NAD1) by comparing with sequences from other countries. Results: The percentage reinfection was 10.4% and there was no resistance observed in this study. The mean percentage viability of all the methods used were 70% and 30% in live and dead eggs respectively at baseline. At post-treatment, the percentage viability of live and dead eggs was 13.3% and 86.6% respectively. For the ITS 2 sequences, there was genetic variation from the Kenyan strain and for the NAD 1 sequences it varied from Madagascar, Mauritius and Tanzania. Conclusion: Reinfection was recorded among the study participants however there was no resistance observed. There was effect of treatment on the viability of Schistosoma haematobium eggs using the modified hatchability technique which was complemented by the vital stains and the fluorescent microscopy. Genetic variants were identified in relation to other countries.