Over the past 3 months, medical experts have been debating on whether ACE inhibitors, especially, Losartan, can make COVID-19 more deadly or less! ACEIs & ARBs are used by millions of patients across the world for almost all cardiovascular diseases ranging from basic hypertension to chronic heart failure.
Although initial studies had proposed that Losartan reduces morbidity and hospitalizations, by blocking ACE-2 receptors, which have been proven to be the doorway novel coronavirus uses to gain entry to cells, but most recent studies have warned of more severe infections, with justifications both at molecular level and statistical studies from hospitalized patients. The statistical studies couldn’t really answer the chicken-, egg- situation: Did these coronavirus patients, who tended to be older, fare worse because of their high blood pressure or other chronic illnesses, or because of drugs they were taking to treat chronic illnesses — or both? And at the molecular level it is known that patients who are chronically on ACEIs/ARBs have increased numbers of ACE2 receptors in their lungs for coronavirus Spike (S) proteins to bind to, they may be at increased risk of severe disease outcomes due to SARS-CoV-2 infections.
While limited clinical studies are underway to check for both theories, Losartan provides an interesting aspect on complex scenarios each medication provides, and why clinical studies take multiple years before even existing medications are approved for a particular disease. In this case, Losartan may provide an interesting aspect on how chronic use of some drugs can actually be detrimental to the use of the same drug for other health problems. Also, this opens a wide scope for testing how other chronic medications can open gateways to other infective diseases by minimal changes at the microscopic level, which may not help acutely in COVID infections, but will bring long term changes in the management of infections in patients with chronic diseases.
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