G6PD deficiency in malaria endemic areas of Nepal

Baburam Marasini,Ram Kumar Mahato,Dinesh Koirala,Arun Chaudhary,Suman Thapa,Shambhu Nath Jha,Kiran Raj Awasthi,Rahachan Gharti Magar,Pimsupah Penpitchaporn,Sanjeev Neupane,Pratik Khanal,Smriti Iama,Rajan Bhattarai ,Pramin Ghimire,Gornpan Gornsawun,Madan Koirala,Germana Bancone,Bijay Bajracharya,Suresh Bhandari,Sanjaya Acharya,Bibek Kumar Lal,Bishnu Acharya

doi:10.1186/s12936-020-03359-6

Abstract

BackgroundGlucose-6-phosphate dehydrogenase (G6PD) deficiency is currently a threat to malaria elimination due to risk of primaquine-induced haemolysis in G6PD deficient individuals. The World Health Organization (WHO) recommends G6PD screening before providing primaquine as a radical treatment against vivax malaria. However, evidence regarding the prevalence and causing mutations of G6PD deficiency in Nepal is scarce.MethodsA cross-sectional, population-based, prevalence study was carried out from May to October 2016 in 12 malaria-endemic districts of Nepal. The screening survey included 4067 participants whose G6PD status was determined by G6PD Care Start™ rapid diagnostic test and genotyping.ResultsThe prevalence of G6PD deficiency at the national level was 3.5% (4.1% among males and 2.1% among females). When analysed according to ethnic groups, G6PD deficiency was highest among the Janajati (6.2% overall, 17.6% in Mahatto, 7.7% in Chaudhary and 7.5% in Tharu) and low among Brahman and Chhetri (1.3%). District-wise, prevalence was highest in Banke (7.6%) and Chitwan (6.6%). Coimbra mutation (592 C>T) was found among 75.5% of the G6PD-deficient samples analysed and Mahidol (487 G>A) and Mediterranean (563 C>T) mutations were found in equal proportions in the remaining 24.5%. There was no specific geographic or ethnic distribution for the three mutations.ConclusionsThis study has identified populations with moderate to high prevalence of G6PD deficiency which provides strong evidence supporting the WHO recommendations to screen G6PD deficiency at health facility level before the use of primaquine-based radical curative regimen for Plasmodium vivax.

Highlights

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is currently a threat to malaria elimination due to risk of primaquine-induced haemolysis in G6PD deficient individuals
The presence of G6PD deficiency among the population is a huge challenge for malaria treatment due to the associated haemolytic risk with radical treatment using 8-aminoquinolines
G6PD-deficient individuals may suffer from acute haemolytic anaemia (AHA) when exposed to several oxidative triggers, such as fava beans, infections or anti-malarial drugs such as primaquine

Summary

Introduction

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is currently a threat to malaria elimination due to risk of primaquine-induced haemolysis in G6PD deficient individuals. Malaria remains a global problem with an estimated 228 million cases occurring globally and 405,000 deaths in 2018. It is still endemic in 91 countries with about half of the world’s population at risk, those living in lower-income countries [1]. The presence of G6PD deficiency among the population is a huge challenge for malaria treatment due to the associated haemolytic risk with radical treatment using 8-aminoquinolines. Males are historically considered more susceptible to haemolysis because the deficient phenotype is more prevalent among them, but recent evidence shows that heterozygous women with intermediate G6PD phenotypes are at risk of severe haemolysis [13, 14]

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