Could COVID-19 Be a Hemoglobinopathy?
| Autor: | Muhammad Hafeez, Arif Malik, Tania Ahmed Shakoori |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
ARDS
medicine.medical_specialty lcsh:Medicine Pulmonary Edema Altitude Sickness Hypoxemia High altitude pulmonary edema pathophysiology Hypoxic pulmonary vasoconstriction High-altitude pulmonary edema medicine Humans Intensive care medicine Altitude sickness Acute respiratory distress syndrome SARS-CoV-2 business.industry High altitude pulmonary embolism lcsh:R COVID-19 General Medicine Hypoxia (medical) medicine.disease Pulmonary edema Hemoglobinopathies Hemoglobinopathy CD147 Preliminary Communications medicine.symptom business |
| Zdroj: | Acta Clinica Croatica, Vol 59., Iss 4., Pp 740-744 (2020) Acta Clinica Croatica |
| ISSN: | 1333-9451 0353-9466 |
| Popis: | SUMMARY The world is struggling to deal with the corona pandemic. Effective therapies are still awaited due to the lack of understanding of the pathophysiological mechanism of the disease. Bearing recent research and clinical observations in mind, the authors propose a novel physiological mechanism of COVID-19 and explain development of COVID-19 related acute respiratory distress syndrome (ARDS) secondary to COVID-19 related hemoglobinopathy. It is a consistent observation that the radiological picture of COVID-19 related ARDS bears more resemblance to high altitude pulmonary edema (HAPE) than typical ARDS. There has been great controversy regarding this proposed similarity. The main argument from those objecting to this comparison is that the etiology is hypoxia in case of HAPE and inflammation in COVID-19 related ARDS. We propose that considering the recent bioinformatics prediction models, COVID-19 might first infect red blood cells via CD147 and cause hemoglobin damage. The resulting hypoxemia may cause pulmonary hypoxic vasoconstriction leading to HAPE-like lung lesions. The now introduced alveolar hypoxia further exaggerates hemoglobinopathy hypoxemia leading to a vicious cycle. In this review, the authors recommend laboratory experiments to prove these hypotheses. The proposed physiological mechanism has significant therapeutic implications. If proven, the authors suggest the use of exchange transfusion as adjunct therapy and development of anti-CD147 drugs. |
| Databáze: | OpenAIRE |
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