| BRIEF COMMUNICATION |
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| Year : 2021 | Volume
: 12
| Issue : 1 | Page : 35 |
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Pulmonary Covid fibrosis a new pharmaceutic approach
Roberto Menicagli1, Mario Limodio2, Marta Limodio3, Maria Teresa Casotti4, Laura Menicagli5
1 Biochemistry, Senior Scientist, University Milan Consultant, Italy
2 Researcher UOC, Infectious and Tropical Diseases, Spaziani Hospital Frosinone, Italy
3 Pharmacological Researcher, ASST Frosinone, Italy
4 Radiodiagnostic Department, Pisa University, Italy
5 Policliclinico San Donato Radiodiagnostic Department, Milan University, Italy
Correspondence Address:
Roberto Menicagli
Biochemistry, Senior Scientist, University Milan Consultant, Mediglia - 20060
Italy
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijpvm.IJPVM_462_20
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Background: Patient's post-COVID may develop chronic irreversible respiratory failure with “widespread signs of pulmonary fibrosis.” Our study analyzed the causes of this fibrosis to propose a therapeutic protocol. Methods: Identification of the biochemical causes of fibrosis in COVID-19 analysing the literature and chest CT. Results: The CT imaging shows pulmonary fibrosis. The viral infection produces “interleukin-6”, which binds to its receptor, in MUC1 of lung epithelial cells. The biochemical response of the cells promotes an over-expression of MUC1 with fibrosis. Interleukin6 also causes a metabolic imbalance in NO that promotes clots and atherosclerosis of the pulmonary vessels. These results show to promote NO endothelia's formation to block both the excessive expression of MUC1 and the atherosclerosis effect of the vessels. Conclusions: This study proposes to inhibit phosphodiesterase by vasodilatation of the pulmonary vascular bed and the MUC1 over expression by interleukin6, the Sildenafil with the SGLT2 and N-Acetylcysteine.
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