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Short Report
Swaminathan P. Iyer
University of Texas MD Anderson Cancer Center
Corresponding Author
ORCiD: https://orcid.org/0000-0002-1646-813X
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This work is licensed under a CC BY 4.0 License. Read Full License
Declarations:
Declarations
- This study involved human subjects.
- The author confirmed that all appropriate ethical guidelines for the use of human subjects have been followed, any necessary IRB and/or ethics committee review has been obtained, and information about the IRB/ethics committee is included in the manuscript.
- The author has confirmed that all necessary patient/participant consent or assent has been obtained and the appropriate institutional forms have been archived. If the IRB/ethics committee waived the requirement for patient/participant consent or assent, an explanation for the waiver is included in the text.
- The author has confirmed that a statement listing potential conflicts of interest or lack thereof is included in the text.
The severe pneumonia caused by the human Coronavirus (hCoV)- SARS-CoV-2 has inflicted heavy casualties, especially among the elderly and those with co-morbid 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 (G6PDd), and 11 with normal levels. The two groups (Normal and G6PDd) were comparable in terms of age, sex and co-morbidities, and laboratory parameters-LDH, IL-6, CRP, and Ferritin, respectively. Thirteen patients needed ventilatory support with 8 in the normal group and 5 in the G6PDd group (72% vs.83%). The main differences indicating increasing severity in normal vs. G6PDd groups included G6PD levels (12.2 vs. 5.6, P=0.0002), PaO2/FiO2 ratio (159 vs. 108, P=0.05), 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). Only one patient with G6PDd died; 16 were discharged home. Our clinical series ascribes a possible biological role for G6PDd in SARS-CoV2 viral proliferation. It is imperative that further studies are performed to understand the interplay between the viral and host factors in G6PDd that may lead to disparity in outcomes.
Keywords
COVID19, G6PD, African American, X-linked
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A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Short Report
Swaminathan P. Iyer
University of Texas MD Anderson Cancer Center
Corresponding Author
ORCiD: https://orcid.org/0000-0002-1646-813X
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
View the published article at Annals of Hematology.
Version 2
Posted 16 Dec, 2020
No community comments so far
No comments provided
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Declarations:
Declarations
- This study involved human subjects.
- The author confirmed that all appropriate ethical guidelines for the use of human subjects have been followed, any necessary IRB and/or ethics committee review has been obtained, and information about the IRB/ethics committee is included in the manuscript.
- The author has confirmed that all necessary patient/participant consent or assent has been obtained and the appropriate institutional forms have been archived. If the IRB/ethics committee waived the requirement for patient/participant consent or assent, an explanation for the waiver is included in the text.
- The author has confirmed that a statement listing potential conflicts of interest or lack thereof is included in the text.
View the published article at Annals of Hematology.
The severe pneumonia caused by the human Coronavirus (hCoV)- SARS-CoV-2 has inflicted heavy casualties, especially among the elderly and those with co-morbid 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 (G6PDd), and 11 with normal levels. The two groups (Normal and G6PDd) were comparable in terms of age, sex and co-morbidities, and laboratory parameters-LDH, IL-6, CRP, and Ferritin, respectively. Thirteen patients needed ventilatory support with 8 in the normal group and 5 in the G6PDd group (72% vs.83%). The main differences indicating increasing severity in normal vs. G6PDd groups included G6PD levels (12.2 vs. 5.6, P=0.0002), PaO2/FiO2 ratio (159 vs. 108, P=0.05), 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). Only one patient with G6PDd died; 16 were discharged home. Our clinical series ascribes a possible biological role for G6PDd in SARS-CoV2 viral proliferation. It is imperative that further studies are performed to understand the interplay between the viral and host factors in G6PDd that may lead to disparity in outcomes.
Figure 1
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