T3 therapy for COVID-19 patients with Acute Respiratory Distress Syndrome

Thyroid hormones play a role in lung function. Both hypothyroidism and hyperthyroidism cause respiratory muscle weakness and decrease pulmonary function. Hypothyroidism can led to a wide range of respiratory problems, starting with a mild dyspnea up to overt respiratory failure.

Acute respiratory distress syndrome (ARDS) is a severe, life threatening form of respiratory failure due to reduced alveolar fluid clearance. ARDS is characterized by pulmonary edema, inflammation, and hypoxemia. The COVID-19 pandemic has seen a surge of patients with acute respiratory distress syndrome (ARDS) in intensive care units across the globe.

Furthermore, coronavirus infections cause a systemic disease that injures many organs. These patients show hormonal and metabolic instabilities. Changes in thyroid, pancreas and adrenal glands have been reported in detail in both SARS-CoV and SARS-CoV-2 infections.

Fortunately, more and more lives are saved compared to the first months of the COVID-19 pandemic. Drugs like Remdesivir and Dexamethasone help saving lives. Blood thinners are also routinely used in COVID-19 therapy.

There is growing interest in treating lung disease with thyroid hormone (T3) in pulmonary edema and ARDS. The problem in ARDS is that lungs get filled with fluid, making the gas exchange impossible. The hormone reduces inflammation and helps epithelial cells in the lungs absorb fluids.

If it proves to be safe and effective, the T3 therapy will not just help COVID-19 patients who develop ARDS, but any other patient suffering from other medical conditions that can lead to the serious respiratory complication.



Dipak K. DasHarry Steinberg, Thyroid Hormone Actions in the Lung, Hormonal Actions in Non-endocrine Systems pp 123-146

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Samiaa Hamdy Sadek, Walaa Anwar Khalifa,1 and Ahmad Metwally Azoz, Pulmonary consequences of hypothyroidism, Ann Thorac Med. 2017 Jul-Sep; 12(3): 204–208. doi: 10.4103/atm.ATM_364_16: 10.4103/atm.ATM_364_16

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