Its therapeutic effectiveness could also benefit healed individuals with effects on lung cells with a state of fibrosis

Its therapeutic effectiveness could also benefit healed individuals with effects on lung cells with a state of fibrosis. combination with anti-inflammatory medicines to manage and control complications of SARS-CoV-2 illness. Results Based on the medical literature and epidemiological results and considering the pathophysiological, biological, and molecular characteristics of SARS-CoV-2, an antifibrotic drug such as pirfenidone as monotherapy or in combination with anti-inflammatory drugs can be SRPKIN-1 (acting early, at the right doses and at the right time) therapeutically effective to avoid severe complications during viral illness. The same approach can also be effective as postinfection therapy in individuals with residual pulmonary fibrotic damage. Management of inflammation and fibrotic status with a combination therapy of pirfenidone and IL-6 or IL-1 inhibitors could represent a pharmacological synergy with added value. Conclusion In this article, we consider the part of antifibrotic therapy with pirfenidone in individuals with SARS-CoV-2 illness on going or in the stage of postinfection with pulmonary fibrotic effects. The medical rationale for its use is also explained. strong class=”kwd-title” Keywords: Pirfenidone, Fibrotic, Swelling, Cytokine, Interleukin, SARS-CoV-2 Intro PSTPIP1 The current global SARS-CoV-2 pandemic (COVID-19) represents a health problems with few precedents in history; at the time of writing this short article, SARS-CoV-2 caused about 6.42 million infected and about 383,000 deaths [1]. SARS-CoV-2 illness, in the most severe cases, can cause cells hyperinflammation, fibrosis and scarring, lung collapse, multi-organ dysfunction, and patient death. [2] To date, no effective or antiviral vaccines against SARS-CoV-2 are available, so it is very important to decrease the aggressiveness of the viral contamination, avoiding serious complications and patient death. The excessive inflammatory state, associated with the presence of fibrotic tissue induced by SARS-CoV-2, has been shown to play a key role in clinical cases considered more crucial. [3] In the more severe stages of viral contamination, excessive release of pro-inflammatory mediators, such as cytokines, leads to lung damage with extensive fibrosis and rapid onset of respiratory distress syndrome. [4, 5] The use of agents to prevent or reduce fibrotic status, such as pirfenidone, may be therapeutically SRPKIN-1 effective in preventing serious or fatal complications. Pirfenidone is the drug of choice in the SRPKIN-1 treatment of idiopathic pulmonary fibrosis (IPF) [6] and with a pleiotropic mechanism of action reduces the fibrotic and inflammatory state of lung tissue. Its therapeutic efficacy could also benefit healed patients with consequences on lung tissue with a state of fibrosis. In addition, a combination therapy of anti-inflammatories and antifibrotics such as pirfenidone could lead to additional clinical benefits, using low dosages and decreasing the risk of toxicity. The clinical aspects of the three phases of SARS-CoV-2 contamination and similarities with IPF The first cases of SARS-CoV-2 contamination were recorded in November 2019 in China; then, rapidly, they spread to all countries around the world causing thousands of deaths. SARS-CoV-2 contamination in the most severe stages can rapidly cause respiratory distress syndrome. According to observational studies conducted, the majority of patients considered severe cases present bilateral interstitial pneumonia and a hyperactive inflammatory state that is not only localized in lung tissue but in all tissues of the body causing multi-organ dysfunction [7, 8]. SARS-CoV-2 contamination has, according to scientific advice, been divided into three stages, the first as asymptomatic or slightly symptomatic with symptoms such as moderate sore throat and abdominal pain and the second and third more severe stages presenting a generalized inflammatory state and respiratory distress syndrome. Studies have shown that bilateral interstitial pneumonia, so called because it attacks the tissue covering the pulmonary alveoli, is associated with the presence of fibrotic tissue caused by extra collagen (fibrosis) in the pulmonary interstitium with hyperinflammation present [9]. Phases two and three are the most severe, and the presence of inflammation in the lungs and fibrotic tissue requires timely immunomodulatory and anti-inflammatory treatment. However, based on descriptions of symptomatology and diagnostic investigations of early observational studies, one might think that the use of a drug currently indicated for pulmonary fibrosis such as SRPKIN-1 pirfenidone could bring great additional benefits both during viral contamination and in the post-healing phase with residual pulmonary fibrotic damage [10]. The rationale for using antifibrotic therapy is based on the characteristics of pulmonary fibrosis observed in COVID-19, ranging from fibrosis associated with organic pneumonia to severe acute lung injury, SRPKIN-1 where a rapid evolution towards widespread fibrotic change is usually observed [11]. In the most severe and fatal.