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The added value of pirfenidone to declare war on inflammation and the fibrotic state induced by Sars Cov 2
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  • Francesco Ferrara,
  • Giovanni Granata,
  • Chiara Pelliccia,
  • Raffaele La Porta,
  • Antonio Vitiello
Francesco Ferrara
Azienda Unità Sanitaria Locale Umbria 1
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Giovanni Granata
Local Health Authority Salerno
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Chiara Pelliccia
Azienda Unità Sanitaria Locale Umbria 2
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Raffaele La Porta
ASUR Marche
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Antonio Vitiello
Azienda Unità Sanitaria Locale Umbria 1
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Abstract

Reduction of pulmonary fibrotic status and reduction of hyperinflammation is essential to combat SARS-CoV-2 and avoid death. Many authors have divided the SARS-CoV-2 infection into three stages, the second and third of which are purely inflammatory and fibrotic. Waiting for the development of antiviral drugs and vaccines to give good results, the best pharmacological goal is the reduction of proinflammatory molecules. This leads to less formation of fibrotic tissue and to the resolution of the patient’s respiratory problems. In fact, in phase 3, the most serious, there is a state of overexpression of the immune system with consequent assault on all tissues and damage to the lungs. Sars cov 2 pneumonia is characterized by “cytokine storm” and can lead to death. Acting early and with pirfenidone combination therapy can be effective. The IL-6 or IL-1 inhibitors, chloroquine / hydroxychloroquine and colchicine, which are demonstrating their anti-inflammatory efficacy, when combined with an anti-inflammatory and antifibrotic agent, such as pirfenidone, can have a winning result. The effective combined terepia allows to use non-lethal dosages and affects all the pathological steps induced by the virus. Pirfenidone has been used for years in lung diseases and has been shown to have good clinical success and good safety and tolerability.The purpose of this study is to explain the pharmacological logic behind the use of a combination therapy as an effective and safe remedy to reduce pneumonia and the consequent death from Sars CoV 2. Keywords: pirfenidone, fibrotic, inflammation, cythokine, interleukin, Sars-CoV-2.