Drug-induced organ injury in coronavirus disease 2019 pharmacotherapy: Mechanisms and challenges in differential diagnosis and potential protective strategies.

The world is currently facing an unprecedented pandemic caused by a newly recognized and highly pathogenic coronavirus disease 2019 (COVID-19; induced by SARS-CoV-2 virus), which is a severe and ongoing threat to global public health. Since COVID-19 was officially declared a pandemic by the World Health Organization in March 2020, several drug regimens have rapidly undergone clinical trials for the management of COVID-19. However, one of the major issues is drug-induced organ injury, which is a prominent clinical challenge. Unfortunately, most drugs used against COVID-19 are associated with adverse effects in different organs, such as the kidney, heart, and liver. These side effects are dangerous and, in some cases, they can be lethal. More importantly, organ injury is also a clinical manifestation of COVID-19 infection. These adverse reactions are increasingly recognized as outcomes of COVID-19 infection. Therefore, the differential diagnosis of drug-induced adverse effects from COVID-19-induced organ injury is a clinical complication. This review highlights the importance of drug-induced organ injury, its known mechanisms, and the potential therapeutic strategies in COVID-19 pharmacotherapy. We review the potential strategies for the differential diagnosis of drug-induced organ injury. This information can facilitate the development of therapeutic strategies, not only against COVID-19 but also for future outbreaks of other emerging infectious diseases.

Updated information on new coronavirus disease 2019 occurrence, drugs, and prediction of a potential receptor.

The new coronavirus (COVID-19) was first reported in Wuhan in China, on 31 December 2019. COVID-19 is a new virus from the family of coronaviruses that can cause symptoms ranging from a simple cold to pneumonia. The virus is thought to bind to the angiotensin-converting enzyme 2, as a well-known mechanism to enter the cell. It then transfers its DNA to the host in which the virus replicates the DNA. The viral infection leads to severe lack of oxygen, lung oxidative stress because of reactive oxygen species generation, and overactivation of the immune system by activating immune mediators. The purpose of this review is to elaborate on the more precise mechanism(s) to manage the treatment of the disease. Regarding the mechanisms of the virus action, the suggested pharmacological and nutritional regimens have been described.