Therapeutic Status of Famotidine in COVID-19 Patients: A Review

Author:

Mohseni Moein1,Raissi Vahid2,Sharifan Yasamin3,Barikro Kimia1,Amiri Sasan4,Mohseni Maedeh Sadat5,Raeisi Farid6,Masoumi Kimia1,Khodakarami Sina1,Raiesi Omid7ORCID

Affiliation:

1. Pharmaceutical Sciences Research Center, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran

2. Department of Medical Parasitology and Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran

3. Students Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran

4. Emam Reza Hospital, Sirjan School of Medical Sciences, Sirjan, Iran

5. Department of Engineering and Technology, Islamic Azad University, Sari Branch, Sari, Iran

6. Department of Nursing and Midwifery of Dezful Islamic Azad University, Dezful, Iran

7. Department of Parasitology, School of Allied Medical Sciences. Ilam University of Medical Sciences, Ilam, Iran

Abstract

Abstract:The novel coronavirus, SARS-coV-2, which emerged in Wuhan in November 2019, has increasingly spread worldwide. More than 272 million cases of infection have been identified. COVID-19 has affected 223 countries and territories across the world. The principal target of the SARS-CoV-2 infection is the lower respiratory tract. Series of moderate to non-specific severe clinical signs and symptoms appear two to fourteen days after exposure to SARS-CoV-2 in patients with COVID-19 disease, including cough, breath deficiency, and at least two of these symptoms: headache, fever, chills, repeated rigor, myalgia, oropharyngitis, anosmia, and ageusia. No therapeutic agents have been validated to have substantial efficacy in the clinical care of COVID-19 patients in large-scale trials, despite worsening infected rates of COVID-19. Early clinical evidence from many sources suggests that treatment with famotidine may decrease COVID-19-related morbidity and mortality. The mechanism by which famotidine could improve the outcomes of COVID-19 is currently unknown. A more recent postulated mechanism is that the effect of famotidine is mediated by histamine-2 receptor antagonism or inverse agonism, inferring that the SARS-CoV-2, resulting in COVID-19 infection, at least partially leads to the abnormal release of histamine and perhaps dysfunction of mast cells.

Publisher

Bentham Science Publishers Ltd.

Subject

Microbiology (medical),Pharmacology,Molecular Medicine,General Medicine

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