Methods: This research utilized data from the Demographic and Health Surveys 2014, 2016, 2014-2015, 2015-2016, and 2016 from Ghana, Ethiopia, Rwanda, Tanzania, and Uganda, respectively. Respondents were women aged between 15 and 49 years. Hemoglobin levels were measured by HemoCue hemoglobin meter. 45,299 women data were extracted from the five countries with 4,644, 14,923, 6,680, 13,064, and 5,988 from Ghana, Ethiopia, Rwanda, Tanzania, and Uganda, respectively. Association between anemia and selected predictive variables was assessed using Pearson's chi-square test statistic. Poisson regression with robust standard errors was used to estimate the prevalence rate ratios of developing anemia. The deviance goodness of fit test was employed to test the fit of the Poisson model to the data set.
Results: There was a statistically significant difference in prevalence of 1,962 (42.3%), 3,527 (23.6%), 1,284 (19.3%), 5,857 (44.8%), and 1,898 (31.7%) for Ghana, Ethiopia, Rwanda, Tanzania, and Uganda, respectively, χ 2 = 2,181.86 and p value < 0.001. Parity, pregnancy status, and contraceptives significantly increased the prevalence rate ratio of a woman developing anemia. Women in Ethiopia with a parity of six or more were 58% more likely to develop anemia than those with parity of zero. Tanzanian women who were pregnant had a 14% increased rate ratio of developing anemia. Factors that significantly decreased anemia in this study were wealth index, women's age, and women's highest level of education. Women who were in the higher education category in Ethiopia were 57% less likely to develop anemia. Ugandan women in the richest category of the wealth index were 28% less likely to develop anemia. Rwandan women in the middle category of the wealth index were 20% less likely to develop anemia. Women who were within the 45-49 age category in Ethiopia were 48% less likely to develop anemia.
Conclusion: The individual country governments should encourage the implementation of increasing female enrollment in higher education. Women in their reproductive age should be encouraged to use modern contraceptives to reduce their anemia prevalence.
METHODS AND FINDINGS: A search using Ovid MEDLINE and Embase was initially conducted to identify studies on severe Plasmodium falciparum malaria that included information on treatment delay, such as fever duration (inception to 22nd September 2017). Studies identified included 5 case-control and 8 other observational clinical studies of SM and UM cases. Risk of bias was assessed using the Newcastle-Ottawa scale, and all studies were ranked as 'Good', scoring ≥7/10. Individual-patient data (IPD) were pooled from 13 studies of 3,989 (94.1% aged <15 years) SM patients and 5,780 (79.6% aged <15 years) UM cases in Benin, Malaysia, Mozambique, Tanzania, The Gambia, Uganda, Yemen, and Zambia. Definitions of SM were standardised across studies to compare treatment delay in patients with UM and different SM phenotypes using age-adjusted mixed-effects regression. The odds of any SM phenotype were significantly higher in children with longer delays between initial symptoms and arrival at the health facility (odds ratio [OR] = 1.33, 95% CI: 1.07-1.64 for a delay of >24 hours versus ≤24 hours; p = 0.009). Reported illness duration was a strong predictor of presenting with severe malarial anaemia (SMA) in children, with an OR of 2.79 (95% CI:1.92-4.06; p < 0.001) for a delay of 2-3 days and 5.46 (95% CI: 3.49-8.53; p < 0.001) for a delay of >7 days, compared with receiving treatment within 24 hours from symptom onset. We estimate that 42.8% of childhood SMA cases and 48.5% of adult SMA cases in the study areas would have been averted if all individuals were able to access treatment within the first day of symptom onset, if the association is fully causal. In studies specifically recording onset of nonsevere symptoms, long treatment delay was moderately associated with other SM phenotypes (OR [95% CI] >3 to ≤4 days versus ≤24 hours: cerebral malaria [CM] = 2.42 [1.24-4.72], p = 0.01; respiratory distress syndrome [RDS] = 4.09 [1.70-9.82], p = 0.002). In addition to unmeasured confounding, which is commonly present in observational studies, a key limitation is that many severe cases and deaths occur outside healthcare facilities in endemic countries, where the effect of delayed or no treatment is difficult to quantify.
CONCLUSIONS: Our results quantify the relationship between rapid access to treatment and reduced risk of severe disease, which was particularly strong for SMA. There was some evidence to suggest that progression to other severe phenotypes may also be prevented by prompt treatment, though the association was not as strong, which may be explained by potential selection bias, sample size issues, or a difference in underlying pathology. These findings may help assess the impact of interventions that improve access to treatment.