Impact of glucose-6-phosphate dehydrogenase deficiency on dengue infection in Myanmar children

Abstract

Glucose-6-phosphate dehydrogenase (G6PD) deficiency may affect the clinical presentation of dengue due to the altered redox state in immune cells. We aimed to determine the association between G6PD deficiency and severity of dengue infection in paediatric patients in Myanmar. A cross-sectional study was conducted among paediatric patients aged 2–13 years with dengue in Yankin Children Hospital, Myanmar. One hundred and ninety-six patients positive for dengue infection, as determined via PCR or ELISA, were enrolled. Dengue severity was determined according to the 2009 WHO classification guidelines. Spectrophotometric assays determined G6PD levels. The adjusted median G6PD value of males in the study population was used to define various cut-off points according to the WHO classification guidelines. G6PD genotyping for Mahidol, Kaiping and Mediterranean mutations was performed for 128 out of 196 samples by real-time multiplex PCR. 51 of 196 (26.0%) patients had severe dengue. The prevalence of G6PD phenotype deficiency (< 60% activity) in paediatric patients was 14.8% (29/196), specifically, 13.6% (14/103) in males and 16.2% (15/93) in females. Severe deficiency (< 10% activity) accounted for 7.1% (14/196) of our cohort, occurring 11.7% (12/103) in males and 2.2% (2/93) in females. Among 128 samples genotyped, the G6PD gene mutations were detected in 19.5% (25/128) of patients, with 20.3% (13/ 64) in males and 18.8% (12/64) in females. The G6PD Mahidol mutation was 96.0% (24/25) while the G6PD Kaiping mutation was 4.0% (1/25). Severe dengue was not associated with G6PD enzyme deficiency or presence of the G6PD gene mutation. Thus, no association between G6PD deficiency and dengue severity could be detected.Trial registration: The study was registered following the WHO International Clinical Trials Registry Platform (WHO-ICTRP) on Thai Clinical Trials Registry (TCTR) website, registration number # TCTR20180720001

Indications for blood and blood products transfusions among children in a semi-urban tertiary hospital in Nigeria

“…NADPH is essential for both oxidant and antioxidant systems of cells. [23] The low number of transfusions among children with G6PD deficiency, as observed in the present study, may be attributed to the presence of G6PD mutation variants which usually do not have severe haemolytic anaemia, since heterogeneity may occur within and between populations. [24]…”

The Many Faces of Hemolysis

“…As previously mentioned, the body has several pathways for clearing red cell byproducts and may be able to handle the spill without serious consequence. If all these pathways are overloaded, symptoms, in part, will be related to the following48,49:…”

“…G6PD is a protective agent that prevents oxidative stress on the cell. In its absence, the cell is unable to maintain its own protective environment and breaks down when introduced to oxidative stressors 38,49. The disorder is rarely fatal but may cause bouts of severe anemia.…”

Dengue complicated by acute haemolysis, methaemoglobinemia, hepatitis and rhabdomyolysis in a patient with G6PD deficiency

“…Severe intravascular haemolysis in G6PD deficiency can lead to acute renal failure via a multitude of mechanisms including deposition of iron in the kidneys 6,7 . Although there is no clear association between G6PD deficiency and dengue severity or viral replication in general 8 , dengue infection, like other infections, can trigger intravascular haemolysis in patients with G6PD deficiency. There are reported cases suggesting that G6PD deficient patients suffer more from Dengue Haemorrhagic Fever compared to normal G6PD subjects 9 .…”