Abstract
ARTESUNATE AND ESOMEPRAZOLE ADD-ONS TO LOW-DOSE ASPIRIN IN THE PREVENTION AND TREATMENT OF PLACENTAL MALARIA, PRE-ECLAMPSIA, FETAL GROWTH RESTRICTION AND METABOLIC SYNDROME: A MECHANISTIC REVIEW AND CLINICAL REPORT
Dr. Nicholas Oriaifo, Dr. S. E.Oriaifo*, Dr. C. Iruolagbe, Prof. J. Egbeifo
ABSTRACT
Recent evidence indicates that malaria, type 2 diabetes mellitus and hypertension constitute a ‘triumvirate’ that significantly increases the suffering in Africa. The contribution of malaria to the alliance may be via the up-regulation of inflammatory and oxidative stress which attenuate factors of the insulin signalling pathway. Upregulation of immune-inflammatory cascade and ThI/Th17 reponse is a common mechanism in severe malaria, placental malaria, pre-eclampsia, hypertension, type 2 diabetes mellitus, auto-immune diseases and fetal growth restriction with placental insufficiency. Safe drugs that attenuate inflammatory and oxidative stress, decrease ThI/Th17 response, upregulate factors of the insulin signalling pathway and which kill the ring/early forms of the malaria parasite in the blood which particularly mediate the oxidative stress stand to be beneficial in these diseases. Rigorous supervision of malaria treatment with ACTs decreases umbilical artery resistance index in microscopic and submicroscopic placental malaria which has identical aetiopathogenic mechanisms with pre-eclampsia. The improved ACT campaign may have co-incided with the significant (P< 0.05) decrease in eclampsia rates observed 2012-2016. Artesunate, esomeprazole, low-dose aspirin, calcium and vitamin A supplementation may upregulate factors of the insulin signalling pathway, enhance the actions of heme oxygenase –I and endothelial nitric oxide. They thus deserve attention as emerging agents that additively may enhance insulin signalling, and down-regulate the immune-inflammatory cascade, angiogenic/anti-angiogenic imbalance in type 2 diabetes, hypertension, severe malaria, placental malaria, pre-eclampsia and fetal growth restriction.
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