The Effects of Malaria On Some Laboratory Parameters in Sierra Leonean Children

Forty two (42)blood samples were collected from children showing clinical symptoms of malaria Trophozoites and/or gametocytes of P. falciparum were identified by microscopic examination of giemsa stained films in 22 samples (52.4%). Haemaglobin (Hb), Glutamate Pyruvate Transaminase (GPT), Bilirubin, Glucose and Ketone concentrations of these parasitaemia samples were compared with those of a non equivalent control group (n-31) of healthy children who were matched for age and sex, as far as possible with malarious group. There was a significant difference in the mean Hb concentration between the patients and controls with values of 6.14mg/dl and 10.15mg/dl respectively. The PCV levels also showed a similar pattern (25.95% to 35.95%). Higher bilirubin (22.15 to 0.98mg/dl) and GPT (61.32 to 22.831U/Ml) levels in the patients indicates some degree of haemolysis of red cells and necrosis of liver cells. The plasma glucose levels were lower in the patient compared with the controls (2.60 to 4.96mmol/l). Ketones were detected in 13(59%) of the 22 samples which tested positive for malaria parasites and none in the control group. These variations in Haematological and Biochemical parameters should enhance our knowledge in the pathogenesis of malaria in Sierra Leonean children. Nigerian Quarterly Journal of Hospital Medicine Vol.9, No.1 pp. 1-

Tuberculosis and cardiovascular disease: linking the epidemics

The burden of tuberculosis and cardiovascular disease (CVD) is enormous worldwide. CVD rates are rapidly increasing in low- and middle-income countries. Public health programs have been challenged with the overlapping tuberculosis and CVD epidemics. Monocyte/macrophages, lymphocytes and cytokines involved in cellular mediated immune responses against Mycobacterium tuberculosis are also main drivers of atherogenesis, suggesting a potential pathogenic role of tuberculosis in CVD via mechanisms that have been described for other pathogens that establish chronic infection and latency. Studies have shown a pro-atherogenic effect of antibody-mediated responses against mycobacterial heat shock protein-65 through cross reaction with self-antigens in human vessels. Furthermore, subsets of mycobacteria actively replicate during latent tuberculosis infection (LTBI), and recent studies suggest that LTBI is associated with persistent chronic inflammation that may lead to CVD. Recent epidemiologic work has shown that the risk of CVD in persons who develop tuberculosis is higher than in persons without a history of tuberculosis, even several years after recovery from tuberculosis. Together, these data suggest that tuberculosis may play a role in the pathogenesis of CVD. Further research to investigate a potential link between tuberculosis and CVD is warranted