G6PD deficiency and severity of COVID19 pneumonia and acute respiratory distress syndrome: Tip of the iceberg?

ABSTRACT

The severe pneumonia caused by the human Coronavirus (hCoV)-SARS-CoV-2 has inflicted heavy causalities, especially among the elderly and those with comorbid illnesses irrespective of their age. The high mortality in African-Americans and males, in general, raises the concern for a possible X-linked mediated process that could affect the viral pathogenesis and the immune system. We hypothesized that G6PD, the most common X linked enzyme deficiency associated with redox status, may have a role in severity of pneumonia. Retrospective chart review was performed in hospitalized patients with COVID19 pneumonia needing supplemental oxygen. A total of 17 patients were evaluated;six with G6PD deficiency, and 11 with normal levels. The two groups (Normal and G6PD def) were comparable in terms of age, sex and co-morbidities, and laboratory parameters-LDH, IL-6, CRP, and Ferritin, WHO ordinal scale respectively. Thirteen patients needed ventilatory support with 6 in the G6PD group (83% vs.72%). The main differences indicating increasing severity in G6PD def group included G6PD levels (12.2 vs. 5.6, P=0.0002), PaO2/FiO2 ratio (159 vs. 108, P=0.05), days before intubation (2.5 vs. 4.8 P= 0.03), days on mechanical ventilation (10.25 vs. 21 days P=0.04), hemoglobin level (10 vs. 8.1 P=0.03) and Hematocrit (32 vs. 26 P=0.015) and Mean WHO ordinal Scale at discharge (0.73 Vs 4.67 P=0.001). Only one patient with G6PD deficiency died;16 were discharged home. Our clinical series ascribes a possible biological role for G6PD deficiency in SARS-CoV2 viral proliferation. It is imperative that further studies are performed to understand the interplay between the viral and host factors in G6PD-deficiency that may lead to disparity in outcomes.