Community-Acquired Pneumonia Complications in a Patient with Hereditary Glucose-6-Phosphate Dehydrogenase Deficiency

Because severe G6PD deficiency can be a phenocopy of chronic granulomatous disease with regard to the cellular and clinical phenotype, careful evaluation of neutrophil function seems mandatory in these patients to decide on appropriate anti-infective preventive measures. Determining the level of G6PD enzyme activity should be followed by analysis of reactive oxygen species production and NET formation to decide on required antibiotic and antimycotic prophylaxis.

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Severe glucose-6-phosphate dehydrogenase deficiency leads to susceptibility to infection and absent NETosis

Siler

Romão

Tejera

et al. 2017

Journal of Allergy and Clinical Immunology

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Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling

Chiu

Lin

et al. 2015

Viruses

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Glucose-6-phosphate dehydrogenase (G6PD)-deficient cells are highly susceptible to viral infection. This study examined the mechanism underlying this phenomenon by measuring the expression of antiviral genes—tumor necrosis factor alpha (TNF-α) and GTPase myxovirus resistance 1 (MX1)—in G6PD-knockdown cells upon human coronavirus 229E (HCoV-229E) and enterovirus 71 (EV71) infection. Molecular analysis revealed that the promoter activities of TNF-α and MX1 were downregulated in G6PD-knockdown cells, and that the IκB degradation and DNA binding activity of NF-κB were decreased. The HSCARG protein, a nicotinamide adenine dinucleotide phosphate (NADPH) sensor and negative regulator of NF-κB, was upregulated in G6PD-knockdown cells with decreased NADPH/NADP+ ratio. Treatment of G6PD-knockdown cells with siRNA against HSCARG enhanced the DNA binding activity of NF-κB and the expression of TNF-α and MX1, but suppressed the expression of viral genes; however, the overexpression of HSCARG inhibited the antiviral response. Exogenous G6PD or IDH1 expression inhibited the expression of HSCARG, resulting in increased expression of TNF-α and MX1 and reduced viral gene expression upon virus infection. Our findings suggest that the increased susceptibility of the G6PD-knockdown cells to viral infection was due to impaired NF-κB signaling and antiviral response mediated by HSCARG.

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An Assessment of Frequent Haemolytic Crisis in G6PD Deficiency Subjects Linked with Chronic Disease States in Al Ahsa Community, Saudi Arabia

Emeka¹,

Hilal²,

Asif³

et al. 2015

Health

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The main treatment strategy for glucose-6-phosphate dehydrogenase (G6PD) deficiency is averting the use of oxidative precipitants like drugs or foods that trigger haemolysis. However, subjects could experience acute crisis in a comorbidity state of diabetes, hypertension or infection. In addition, the condition could in turn predispose carriers to these chronic diseases. Aim of the study was to evaluate the frequency of haemolytic crisis in carriers with attendant chronic diseases, and also assess awareness and knowledge of aggravated reactions from these conditions. 282 subjects consented and participated in the study. A cross-sectional semi-structured interview questionnaire conducted from May to August 2013 was adopted. Questions focused on demographics, awareness and when disease was diagnosed, type and frequency of crisis, family history, screening and presence of other diseases and awareness of trigger from these conditions. A total of 69.9% were G6PD deficiency gene carriers and mostly fell within the age group of 31 -40 (43.6%). 75.6% of the carriers were not aware that other disease conditions could exacerbate crisis. Non-drug related crisis was 85.3% compared with 14.7 drug related reactions. Out of the 69.9% carriers, 17.3% are diabetics, 18.3% of them are hypertensive and 25.9% are with bleeding disorders. Also, 29.1% had frequent episodes with bacterial infection. Symptoms experienced that were not drug related included, 44.8% attacks of pallor, 25.3% jaundice, 28.5% with shortness of breath, while 21.7% had dark urine frequently. No routine screening for other diseased conditions was carried out for these subjects despite experiencing frequent crisis that were not drug related. Carriers * Corresponding author. P. Emeka et al. 626with other diseased conditions experienced more non-drug related crisis and were not aware of it.

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Community-Acquired Pneumonia Complications in a Patient with Hereditary Glucose-6-Phosphate Dehydrogenase Deficiency

Cited by 3 publications

References 5 publications

Severe glucose-6-phosphate dehydrogenase deficiency leads to susceptibility to infection and absent NETosis

Severe glucose-6-phosphate dehydrogenase deficiency leads to susceptibility to infection and absent NETosis

Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling

An Assessment of Frequent Haemolytic Crisis in G6PD Deficiency Subjects Linked with Chronic Disease States in Al Ahsa Community, Saudi Arabia

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