Complete, Rapid Resolution of Severe Bilateral Pneumonia and Acute Respiratory Distress Syndrome in a COVID-19 Patient: Role for a Unique Therapeutic Combination of Inhalations With Bromhexine, Higher Doses of Colchicine, and Hymecromone.

An otherwise healthy, 35-year-old man was hospitalized for the management of acute respiratory failure due to coronavirus disease 2019 (COVID-19)-related severe bilateral pneumonia and acute respiratory distress syndrome (ARDS). The patient therapeutic regimen included the widely accepted standard combination of oxygen, anticoagulation therapy; corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), and antibiotics. A novel combination of colchicine, hymecromone, and bromhexine inhalations was added to the therapeutic regimen as part of our unique COVID-19 management institutional protocol. COVID-19-related severe bilateral pneumonia and acute respiratory distress syndrome (ARDS). The patient therapeutic regimen included the widely accepted standard combination of oxygen, anticoagulation therapy, corticosteroids, NSAIDs, and antibiotics. A novel combination of colchicine, hymecromone, and bromhexine inhalations was added to the therapeutic regimen as part of our unique COVID-19 management institutional protocol. Rapid clinical response on day 2, with a significant improvement of radiographic pulmonary changes on day 5, and improvement of laboratory results on days 5-7 were observed. The administration of inhalatory bromhexine in combination with high-dose colchicine and hymecromone was crucial for the positive outcome of the disease. This treatment regimen resulted in a four to five-fold decrease in the mortality of hospitalized patients.

Role of endothelial dysfunction in the severity of COVID­19 infection (Review).

COVID­19 patients with severe infection have been observed to have elevated auto­antibodies (AAs) against angiotensin II receptor type 1 (AT1R) and endothelin (ET) 1 receptor type A (ETAR), compared with healthy controls and patients with favorable (mild) infection. AT1R and ETAR are G protein­coupled receptors, located on vascular smooth muscle cells, fibroblasts, immune and endothelial cells, and are activated by angiotensin II (Ang II) and ET1 respectively. AAs that are specific for these receptors have a functional role similar to the natural ligands, but with a more prolonged vasoconstrictive effect. They also induce the production of fibroblast collagen, the release of reactive oxygen species and the secretion of proinflammatory cytokines (including IL­6, IL­8 and TNF­α) by immune cells. Despite the presence of AAs in severe COVID­19 infected patients, their contribution and implication in the severity of the disease is still not well understood and further studies are warranted. The present review described the major vascular homeostasis systems [ET and renin­angiotensin­aldosterone system (RAAS)], the vital regulative role of nitric oxide, the AAs, and finally the administration of angiotensin II receptor blockers (ARBs), so as to provide more insight into the interplay that exists among these components and their contribution to the severity, prognosis and possible treatment of COVID­19.