Proton Pump Inhibitors are Risk Factors for Viral Infections: Even for COVID-19?

Bruno Charpiat1, Nathalie Bleyzac2,3, Michel Tod2,3

  • 1Service Pharmacie, Hôpital de La Croix-Rousse, Groupement Hospitalier Nord, Hospices Civils de Lyon, 103 Grande Rue de la Croix-Rousse, 69004, Lyon, France. bruno.charpiat@chu-lyon.fr.

Insights

Proton pump inhibitors (PPIs) may increase the risk of SARS-CoV-2 infection. Reduced stomach acid from PPIs might hinder the body's defense against ingested viruses like SARS-CoV-2.

Area of Science:

  • Gastroenterology
  • Infectious Diseases
  • Pharmacology

Background:

  • Gastric acid plays a crucial role in inactivating ingested pathogens.
  • Proton pump inhibitors (PPIs) reduce gastric acid production.
  • Previous studies link PPIs to increased risk of viral infections like rotavirus, norovirus, and MERS-CoV.

Purpose of the Study:

  • To evaluate the potential increased risk of SARS-CoV-2 infection in patients using proton pump inhibitors.
  • To highlight the importance of risk-benefit assessment for PPIs during the COVID-19 pandemic.

Main Methods:

  • This study is a review and hypothesis generation based on existing literature.
  • Analysis of the known mechanisms of gastric acid in pathogen defense.
  • Correlation of PPI use with documented risks of other viral infections.

Main Results:

  • Proton pump inhibitors may compromise the natural defense mechanism of gastric acid against swallowed microorganisms.
  • Evidence suggests PPIs are associated with increased susceptibility to enteric and respiratory viral infections.
  • The fecal-oral transmission route of SARS-CoV-2 supports the potential for gastrointestinal entry.

Conclusions:

  • Patients treated with proton pump inhibitors may be at a higher risk of SARS-CoV-2 infection.
  • Further research is warranted to confirm the association between PPI use and COVID-19 susceptibility.
  • Clinicians should carefully consider the risks and benefits of prescribing PPIs during the pandemic.

Related Concept Videos

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
715
Pharmacokinetics: Drug–Food and Drug–Viral Interactions01:26

Pharmacokinetics: Drug–Food and Drug–Viral Interactions

A drug interaction occurs when the concurrent use of another drug, food, or an external substance alters the pharmacological activity of a drug. This interaction can modify the action of the original drug, affecting its effectiveness and safety.Drug–food interactions are significant as they impact drug absorption, metabolism, and excretion. For example, grapefruit juice is a well-known disruptor of drug metabolism. It inhibits the cytochrome P450 3A4 enzyme, crucial for the metabolism of...
136
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
784
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
1.0K
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
944
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
539