Question
Asked 8th Jul, 2020

Do you accept the empirical use of famotidine in COVID patients?

Empirical use of non-harmful drugs for patients is superior to evidence-based medicine ... or not
Does anyone use famotidine in COVID?

Most recent answer

12th Jul, 2020
Robert John Wolff
South University
I should probably also add that in addition to the increased risk for COVID-19 infections, using the drugs may increase the risk of other gastrointestinal infections for other pathogens. This would increase overall pathology as well as risk for any of these infections. Nutritional damage and other effects may also occur, even if not severe.
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All Answers (6)

8th Jul, 2020
Muhammad Yousuf
King Abdulaziz Medical City (KAMC), King Saud bin Abdulaziz University for Health Sciences (KSAU-HS)
I would preferably use famotidine or other H2-receptor blockers icompared to proton pump inhibitors (PPI) in severe or critical COVID-19 patients because H2RB have immune modulatory properties (1-3). Furthermore, PPI can increase the risk of pneumonia (4), and fatality in COVID-19 pneumonia (5).
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10th Jul, 2020
Muhammad Yousuf
King Abdulaziz Medical City (KAMC), King Saud bin Abdulaziz University for Health Sciences (KSAU-HS)
Recent evidence indicates proton pump inhibitors (PPI) are related to increased COVID-19 risk, therefore Histamine 2 receptor blockers (H2RB) should be preferred in the times of COVID-19 pandemic.
Proton Pump Inhibitors Tied to COVID-19 Risk
1 Recommendation
11th Jul, 2020
Iman Hassan Ibrahim
Al-Azhar University
No drug is non-harmful when the patient don't need it. Drug use in general MUST be rational.Otherwise, one might do empirical study, but not clinical practice.
12th Jul, 2020
Robert John Wolff
South University
While the use of famotidine (and others in category) may be helpful and useful for COVID-19 the question is incorrect as there is really almost no data to support the effectiveness, dosage, time length, and other pathology factors in COVID-19. Therefore the use of this (and most other drugs) is not based on 'empiracal' data for treating COVID-19 but simply our best 'guesses.'
12th Jul, 2020
Robert John Wolff
South University
I also must agree with Iman Hassan Ibrahim that there is not any drug which may be completely harmless (even our foods can have risks) especially when we are now finding out that PPI's seem to increase the risk of infections from SARS-CoV-2 and this may also include this acid blocker category. The lack of acid may increase the risk that some of the viruses survive the stomach and infect the intestines.
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Similar questions and discussions

Chloroquine effective in COVID-19: True or false?
Discussion
197 replies
  • Prashant WankhadePrashant Wankhade
Chloroquine effective in COVID-19: True or false?
Dr. Prashant R. Wankhade
Hypothesis:
It has been proposed that these viruses are internalized by receptor mediated endocytosis and delivered to lysosomes. At acidic pH, the membrane surrounding the virus fuses with the membrane of lysosome, allowing the nucleic acid of virus to cross lysosomal membrane and enter the cytoplasm where the virus replicates. Infection of tissue culture cells by these viruses can be prevented by chloroquine, an agent that blocks function of lysosome. Chloroquine is a weak base that diffuses in lysosome and raises the pH of lysosome causing impairment of function of lysosomal enzymes. Viruses that requires acidic pH to fuse with cell membrane can no longer do so in the presence of chloroquine and the cells are protected from infection.
Facts:
1. Aim of the virus is to reach the destination where it can replicate. This destination is cytoplasm for RNA viruses and nucleus for DNA viruses.
2. Normally viruses enter the cell by direct membrane fusion or endocytosis-based mechanism.
3. Exact mechanism of COVID-19 entry in cell isn’t clear (https://www.ncbi.nlm.nih.gov/books/NBK92477/). If its entry is via membrane fusion then there is no need for COVID-19 to cross Lysosome as the virus particles will get direct entry in cytoplasm. Even if the entry is endocytosis-based then also it is less likely to cross Lysosome.
4. Chloroquine and hydroxychloroquine are known to alter Lysosomal function. But there are discrepancies in the literature about whether or not chloroquine raises the lysosomal pH (Autophagy. 2018; 14(8): 1435–1455). Some studies do not support this fact whereas others state that the change in pH may not last longer than 1 to 4 hours. So, the fact that Chloroquine will cause alteration in viral cell cycle is not clear.
5. Viruses like polio virus and Hepatitis-C virus enters the cell via endocytosis; in that case Chloroquine would have helped in controlling these infections also, but no guidelines recommend its use.
6. This hypothesis related to Chloroquine and Viral infection is not new. One of the articles published in 2003 advocates its possible role in treatment of HIV infection but none of the guidelines has yet recommended (Lancet Infect Dis. 2003 Nov;3(11):722-7).
The same article advocates its possible role in clinical management of Corona related Middle East Respiratory syndrome (MERS) and Corona related severe acute respiratory syndrome (SARS) but no further data available on its definite role.
7. RNA viruses including COVID-19 can replicate in cytoplasm and need not require entry in the nucleus like DNA viruses. Chloroquine doesn’t have any effect on cytosolic pH to alter the replication of virus and in fact that will be hazardous for cell itself.
8. Thus, these facts put question mark on above hypothesis.
9. And finally, in this era of evidence-based medicine we need concrete evidence to support the hypothesis; as it’s not necessary for every hypothesis to reflect vis a vis in clinical applicability.

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