Epidemiology of active epilepsy in a suburban community in Southeast Nigeria: A door-to-door survey.

CONTEXT: Epilepsy is one of the most common neurologic conditions afflicting an estimated 65 million people the world over. Current community-based data on the prevalence of active epilepsy in Africa are sparse. AIMS: This study was aimed at determining the prevalence and profile of active epilepsy in a suburban community in Southeast Nigeria. METHODS: It was a two phase cross-sectional descriptive study. In the first phase, those with possible active epilepsy were identified in a door-to-door survey using a modification of the World Health Organization Neuroscience research protocol. In the second phase, cases of active epilepsy were identified and the clinical forms of epilepsy diagnosed based on the International League against Epilepsy guidelines 1993. RESULTS: A total of 6,800 persons was screened in the first phase of the study. There were 29 cases (16 males and 13 females) of active epilepsy. The point prevalence of active epilepsy was 4.3/1,000 (95% confidence interval (95% CI): 2.7-5.9) for the total population, 4.9/1,000 (95% CI: 2.5-7.3) for males and 3.7/1,000 (95% CI: 1.7-5.7) for females. The age-adjusted prevalence for the total population was 4.1/1,000 (US Population 2000). Classified using clinical criteria only, generalized seizures occurred in 62.1% (n=18) while partial seizures occurred in 37.9% (n=11) of cases. CONCLUSIONS: The prevalence of active epilepsy in Southeast Nigeria is comparable to that found in developed and some developing countries but less than that reported in suburban Southwest Nigeria about three decades ago.

Prevalence of hepatitis B surface antigen seropositivity among HIV-infected and non-infected individuals in Nnewi, Nigeria.

BACKGROUND: Co-infection of human immunodeficiency virus (HIV) and hepatitis B virus (HBV) is common as both viruses share common routes of transmission. HIV significantly affects the natural history of HBV, hence the need to determine the prevalence of co-infection. MATERIALS AND METHODS: This was a retrospective study between 2005 and 2009, in which is a total of 2018 subjects who reported at our University Teaching Hospital blood bank and human immunodeficiency virus clinic were studied. Hepatitis B surface antigen (HBsAg) was tested for using a one step lateral flow rapid chromatographic immunoassay (Acumen labs and diagnostic centre, Bangalore, India) and HIV 1/2 was tested using two kits, Determine (made by Abbot, Japan for Inverness Medical, Japan). RESULTS: A total of 2018 subjects were studied out of which 1176 were HIV positive (964 males and 212 females) and 842 (334 males and 508 females) were negative. The prevalence of HBsAg positivity in the study population was 5.9%. It was 6.3% and 5.6% in the HIV-infected and un-infected population, respectively. Although the prevalence was higher in those who are HIV infected, the difference was not statistically significant (P=0.52). Males who were HIV positive were found to be more likely to have co-infection than females (8.7% vs. 4.2%, P=0.02, OR=1.917). CONCLUSION: This study showed that in south-eastern Nigeria, infection with HBV is relatively common in both HIV-infected and un-infected individuals. Routine screening for HBV should be done for all HIV positive individuals.

Low-dose mercury induces testicular damage protected by zinc in mice.

OBJECTIVES: This investigation was set out to determine whether mercury at a very low dose (4ppm) induces testicular damage on murine testis, and if so whether the toxic effects of mercury could be prevented by zinc. STUDY DESIGN: One of the following solutions was administered in the drinking water of CD-1 male mice: (1) 4ppm HgCl(2); (2) 800ppm ZnCl(2); (3) 4ppm HgCl(2)+800ppm ZnCl(2); or (4) deionised water; for 12 weeks. At the expiration of the treatment period, animals were sacrificed, testes excised and weighed, and epididymal sperm number taken. The testes were processed for histological examination. RESULTS: Both zinc and mercury significantly (p<0.05) decreased the absolute and relative testicular weights, with mercury producing the highest reduction in weight. Mercury reduced significantly (p<0.05) the epididymal sperm number, while zinc and mercury/zinc produced statistically same effect with control on the sperm number. Histological study showed that mercury at the concentration employed produced remarkable degenerative lesions on the testes, as the zinc-treated group showed a normal morphology. Majority of the animals in the mercury/zinc-treated group exhibited complete or partial protection as evidenced by the morphology of the seminiferous tubules. CONCLUSION: Zinc prevents mercury-induced testicular damage in mouse. These findings highlight the risks exposure to inorganic mercury might pose to male reproduction of mice, and suggests possible therapy with zinc. Study in humans is therefore advocated.

Effects of two antihistamines on chloroquine and histamine induced weal and flare in healthy African volunteers.

This study investigated the effects of single doses of clemastine (2mg orally), mepyramine (2 micrograms intradermally) and placebo on weal and flare caused by intradermal chloroquine 2.5mg and histamine 2 micrograms in 11 healthy black subjects who experienced generalised pruritus with oral chloroquine. Compared with placebo, both antihistamines caused significant reductions in histamine-induced weal and flare. By contrast, chloroquine-induced weal and flare were not significantly altered by clemastine or mepyramine when compared with placebo. It is concluded that histamine is unlikely to be the main mediator of chloroquine-induced weal and flare. These findings are in consonance with the lack of significant effect of antihistamines on chloroquine-induced generalised pruritus.

Urine methylhistamine concentrations before and after chloroquine in healthy black subjects.

Urine concentrations of methylhistamine were measured in 11 subjects who experienced itching with chloroquine ('itchers') and in 14 who did not itch ('non-itchers'). In each group, urine methylhistamine concentrations were significantly greater at 12, 24 and 36 h after ingestion of 1 g chloroquine phosphate than before. There was no significant difference between itchers and non-itchers as regards urine methylhistamine concentrations at any time-point. Furthermore, there was no correlation between urine methylhistamine concentration and degree of pruritus in itchers. The findings suggest that histamine may be released by chloroquine, but it is unlikely to be the main cause of chloroquine-induced pruritus.