Potassium is the principal intracellular cation with sodium being the principal extracellular cation. Maintenance of the distribution of potassium and sodium between the intracellular and the extracellular compartments relies on several homeostatic mechanisms. This study analysed the effect of blood storage on the concentrations of potassium and sodium in stored blood and also determine any variations that may exist in their concentrations. 50mls of blood was sampled each from 28 units of evenly mixed donated blood in citrate phosphate dextrose adenine (CPDA-1) bags immediately after donation into satellite bag and stored at 4oC. Potassium and sodium concentration determinations were done on each of the 28 samples on day 0 (before blood was initially stored in the fridge), day 5, day 10, day 15 and day 20 of storage using the Roche 9180 ISE Electrolyte Analyser (Hoffmann-La Roche Ltd, Switzerland). data analysis showed significant changes in the potassium and sodium concentrations with a continuous rise in potassium and a continuous fall in sodium. A daily change of 0.59mmol/l and 0.50mmol/l was observed in the potassium and sodium concentrations respectively. We showed steady but increased daily concentrations of potassium and decrease concentrations of sodium in blood stored over time at 4oC.

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IntroductionSports anaemia is a physiological activity that occurs amongst footballers and may be due to poor diet, over-training, as well as an increase in plasma volume in endurance training activities. High plasma volume leads to changes in haematological parameters that may impact on endurance of footballers. The objective of the study was to determine the correlation between haematological and an-thropometric indices and their role in sports anaemia in a tropical setting.MethodsVenous blood was taken into EDTA for 12 soccer players of KNUST soccer team before training and after training for the first (W1) and fifth (W5) weeks of training sessions. Complete blood count analysis was done for each blood sample and anthropometric parameters such as height, weight, body mass index, body fat percent and lean body mass were also measured. Cross-tabulations with mean and standard deviation or median and range were computed. Paired t-test & and Mann-Whitney test for parametric and non-parametric data computations were carried out and a p-value ≤ 0.05 was taken to rep-resent significant difference between data groups.ResultsThere was significant reduction in haemoglobin (p = 0.003), haematocrit (p = 0.002), mean cell volume (MCV) (p = 0.034) and red blood cell (RBC) count (p = 0.011) as a result of a significant expansion of plasma volume (p= 0.006). Neutrophil, lymphocyte and eosinophil counts were reduced significantly (p= 0.043, 0.001 and 0.007, respectively) after the training at W5. Lean body mass (LBM) inversely correlated with haemoglobin (r = -0.787, p = 0.002) and haematocrit (r = -0.588, p = 0.044). Body fat percentage (BFP) also negatively correlated with lymphocyte count (r = -0.700, p = 0.011). Furthermore, there was a positive correlation between body mass index (BMI) and plasma volume change after the training programme (r = 0.689, p = 0.013).ConclusionThe results suggest that sports anaemia was induced by an increase in plasma volume that resulted in changes in haematological parameters.

Weak Rh D phenotypes are very frequent in Africans. They are capable of causing alloimmunization in Rh D-negative individuals. Some weak Ds may elude routine typing using direct agglutination techniques. This study aimed at determining the prevalence of weak D phenotype among Rhnegatives, using indirect antiglobulin technique. A total of 400 donors between the ages of 16 and 35 years who were grouped by the blood bank were randomly sampled over a period of 2 months.Three hundred and sixty nine (92.25%) were typed as Rh D-positive and 31 (7.75%) RhD-negative. Two (6.45%) of the Rh D-negative donors were weak D positive while 29 (93.55%) were weak D negative. Among the males 25 (9.43%) were Rh D-negative and 240 (90.57%) RhD-positive. Two (8%) of the 25 males were weak D positive. Among the females, 6 (4.44%) were Rh D-negative and 129 (95.56%) RhD-positive. This implies that, there are people in Kumasi with weak D phenotype which cannot be detected by the direct monoclonal anti-D agglutination. Consequently, indirect antiglobulin test may be indicated for such individuals typed Rh D-negative. This study has shown the need for a comprehensive policy on appropriate testing of donors and newborns, and management of Rh D-negative mothers in the Region. This should include weak D testing of all Rh Dnegative blood donors before transfusion in Rh D-negative patient.

Background: Plasmodium falciparum malaria remains one of the world's major infectious diseases that cause most morbidity and mortality, particularly in children. In Ghana, most children below the ages of 5 years depending on the severity of the infection often lose their lives. However, it is still debatable why infection with falciparum malaria contributes to thrombocytopenia. Methods: This study sought to investigate the expression of the various platelet indices and activation markers in children with falciparum malaria. Platelet indices (Platelet count [PLT], Plateletcrite [PCT], Mean Platelet Volume [MPV], Platelet Distribution Width [PDW] and Platelet-Large Cell Ratio [P-LCR]) and platelet surface membrane glycoproteins (GPIIb/IIIa [PAC-1], P-selectin [CD62p] and GPIV [CD36]) expressions were determined in children with falciparum malaria (cases) and healthy children (controls) using automated blood cell analysis and flow cytometry techniques, respectively.Results: Except for P-LCR, all the other platelet indices (PLT, MPV, PDW, and PCT) were significantly lower in the cases than the controls (P < 0.05). Also, it was observed that the level of expression of the activation markers; PAC 1 and CD62p showed a significant (P < 0.05) decreased before and after activation in falciparum malaria cases than in the controls. On the contrary, CD36 expression in the controls did not differ significantly (p > 0.05) from the malaria cases. Platelet activation markers were known to be associated with increased risk of falciparum malaria with the mean fluorescence intensity of PAC1 (Odds Ratio [OR] 34.0, Relative Risk [RR] 4.47, 95% Confidence Interval [CI] 4.904-235.7; p < 0.0001) and CD36 (OR 4.2, RR 1.82,; p = 0.04). Moreover, the percentage expression of CD62p (OR 4.0, RR 1.80, 95% CI 0.59-27.24; p = 0.19) was also observed to be probably associated with increased risk of falciparum malaria although not statistically significant (p > 0.05). Conclusion:Plasmodium falciparum malaria has been known to be associated with platelet activation markers, which probably contributes to thrombocytopenia.

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