Gastric Acid Suppression May Lead to an Increased Risk of Vancomycin-Resistant Enterococcus Colonization: Presidential Poster Award

Objective Peritonitis caused by enteric organisms in peritoneal dialysis (PD) patients is associated with greater morbidity and mortality than peritonitis with non-enteric organisms. One reported risk factor for enteric peritonitis (EP) is gastric acid suppression, with two small studies providing conflicting results. The objective of this study was to determine, using a larger patient population, whether gastric acid suppressants are associated with an increased risk of EP. Patients and Methods Using a single-center case-control design, information on episodes of EP occurring between 2003 and 2006 was collected. Control episodes were all non-enteric episodes of peritonitis that occurred during the same time interval. Proton pump inhibitor (PPI) or H2-blocker (H2B) use prior to development of peritonitis was documented. Results A total of 228 peritonitis episodes among 137 patients met inclusion criteria. In 32% of episodes, the causative organism was enteric. Gastric acid suppressant use was documented in 46% of episodes, with the majority on PPIs. Overall, gastric acid suppression was not associated with a higher EP risk ( p = 0.17). In a post hoc analysis, PPIs were not associated with EP [odds ratio (OR) 1.3, 95% confidence interval (CI) 0.7 – 2.4; p = 0.42], whereas H2Bs were associated with a higher risk of EP (OR 2.9, 95% CI 1.1 – 7.7; p = 0.04), although the number of patients on H2Bs was small. Conclusion Overall, gastric acid suppression was not associated with an increased risk of peritonitis with enteric organisms. While PPI use appears to be safe for PD patients with appropriate indications, the potential risk of EP with H2Bs requires further investigation.

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The impact of gastric acid suppression on the developing intestinal microbiome of a child

10.1101/2021.12.21.21268064 ◽

2021 ◽

Author(s):

Andrew Spurr ◽

Wei Zhu ◽

Wendy Wong ◽

Bernadette Diez ◽

Ian Leibowitz ◽

...

Keyword(s):

Gastric Acid ◽

Beta Diversity ◽

Acid Suppression ◽

Intestinal Microbiome ◽

Alpha And Beta Diversity ◽

Clostridioides Difficile ◽

Increased Risk ◽

Before And After ◽

Gastric Acid Suppression ◽

The Impact

Gastric acid suppressing medications have been associated with an increased risk of Clostridioides difficile (C. difficile) infection, hypothesized to be due to underlying intestinal microbiome changes. Our goal is to characterize these changes in children as their microbiome is undergoing critical development. Our study included 5 children (< 3 years old) who were started on clinically indicated gastric acid suppression and 15 healthy age-matched controls. Stool samples were collected before and after 2 months of treatment. We analyzed the microbiome using 16S rRNA sequencing. Quantitative-PCR was used to detect C. difficile toxins. Subjects and controls had similar alpha and beta diversity. We found no significant change in alpha or beta diversity of subjects after treatment. C. difficile toxins were not found and there was no increase in C. difficile carriage after treatment. A significant increase in Lactobacillus was found after treatment, which has been associated with C. difficile in adults.

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Gastric Acid Suppression Is Associated with an Increased Risk of Adverse Outcomes in Inflammatory Bowel Disease

Digestion ◽

10.1159/000455008 ◽

2017 ◽

Vol 95 (3) ◽

pp. 188-193 ◽

Cited By ~ 16

Author(s):

Rajesh Shah ◽

Peter Richardson ◽

Hong Yu ◽

Jennifer Kramer ◽

Jason Ken Hou

Keyword(s):

Inflammatory Bowel Disease ◽

Gastric Acid ◽

Bowel Disease ◽

Adverse Outcomes ◽

Acid Suppression ◽

Increased Risk ◽

Inflammatory Bowel ◽

Gastric Acid Suppression

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Risk factors for Clostridioides difficile colonization among hospitalized adults: A meta-analysis and systematic review

Infection Control and Hospital Epidemiology ◽

10.1017/ice.2020.1236 ◽

2020 ◽

pp. 1-8

Author(s):

Scott Anjewierden ◽

Zheyi Han ◽

Adam M. Brown ◽

Curtis J. Donskey ◽

Abhishek Deshpande

Keyword(s):

Risk Factors ◽

Systematic Review ◽

Gastric Acid ◽

Meta Analysis ◽

Tube Feeding ◽

Acid Suppression ◽

Clostridioides Difficile ◽

Increased Risk ◽

Acid Suppression Therapy ◽

Gastric Acid Suppression

Abstract Objective: To identify risk factors for asymptomatic Clostridioides difficile colonization among hospitalized adults utilizing a meta-analysis, which may enable early identification of colonized patients at risk of spreading C. difficile. Design: Meta-analysis and systematic review. Methods: We systematically searched MEDLINE, Scopus, Web of Science, and EMBASE from January 1, 1975, to February 15, 2020, for articles related to C. difficile colonization among hospitalized adults. Studies with multivariable analyses evaluating risk factors for asymptomatic colonization were eligible. Results: Among 5,506 studies identified in the search, 19 studies met the inclusion criteria. Included studies reported 20,334 adult patients of whom 1,588 were asymptomatically colonized with C. difficile. Factors associated with an increased risk of colonization were hospitalization in the previous 6 months (OR, 2.18; 95% CI, 1.86–2.56; P < .001), use of gastric acid suppression therapy within the previous 8 weeks (OR, 1.42; 95% CI, 1.17–1.73; P < .001), tube feeding (OR, 2.02; 95% CI, 1.06–3.85; P = .03), and corticosteroid use in the previous 8 weeks (OR, 1.58; 95% CI, 1.14–2.17; P = .006). Receipt of antibiotics in the previous 3 months (OR, 1.37; 95% CI, 0.94–2.01; P = .10) was not associated with statistically significant effects on risk of colonization. Conclusions: C. difficile colonization was significantly associated with previous hospitalization, gastric acid suppression, tube feeding, and corticosteroid use. Recognition of these risk factors may assist in identifying asymptomatic carriers of C. difficile and taking appropriate measures to reduce transmission.

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Gastric acid suppression is associated with increased risk of pneumonia

BMJ ◽

10.1136/bmj.330.7484.0-f ◽

2005 ◽

Vol 330 (7484) ◽

Keyword(s):

Gastric Acid ◽

Acid Suppression ◽

Increased Risk ◽

Gastric Acid Suppression

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Role of gastric acid suppression in the treatment of gastro-oesophageal reflux disease.

Gut ◽

10.1136/gut.33.1.118 ◽

1992 ◽

Vol 33 (1) ◽

pp. 118-124 ◽

Cited By ~ 124

Author(s):

N J Bell ◽

R H Hunt

Keyword(s):

Gastric Acid ◽

Reflux Disease ◽

Acid Suppression ◽

Oesophageal Reflux ◽

Oesophageal Reflux Disease ◽

Gastric Acid Suppression

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Gastric Enzyme Supplementation Inhibits Food Allergy in a BALB/c Mouse Model

Nutrients ◽

10.3390/nu13030738 ◽

2021 ◽

Vol 13 (3) ◽

pp. 738

Author(s):

Nazanin Samadi ◽

Denise Heiden ◽

Martina Klems ◽

Martina Salzmann ◽

Johanna Rohrhofer ◽

...

Keyword(s):

Food Allergy ◽

Mouse Model ◽

Gastric Acid ◽

Clinical Symptoms ◽

Acid Suppression ◽

Gastric Digestion ◽

Enzyme Solution ◽

Allergic Symptoms ◽

Gastric Acid Suppression ◽

The Impact

Impaired gastric digestion due to suppressed gastric acidity enhances the risk for food allergy development. In the current study, we aimed to evaluate the impact of a supported gastric digestion via application of a pharmaceutical gastric enzyme solution (GES) on food allergy development and allergic reactions in a BALB/c mouse model. The ability of the GES to restore hypoacidic conditions was tested in mice treated with gastric acid suppression medication. To evaluate the impact on allergic symptoms, mice were orally sensitized with ovalbumin (OVA) under gastric acid suppression and subjected to oral challenges with or without GES. The immune response was evaluated by measurement of antibody titers, cytokine levels, mucosal allergy effector cell influx and regulatory T-cell counts. Clinical response was objectified by core body temperature measurements after oral OVA challenge. Supplementation of GES transiently restored physiological pH levels in the stomach after pharmaceutical gastric acid suppression. During oral sensitization, supplementation of gastric enzymes significantly reduced systemic IgE, IgG1 and IgG2a levels and allergic symptoms. In food allergic mice, clinical symptoms were reduced by co-administration of the gastric enzyme solution. Support of gastric digestion efficiently prevents food allergy induction and alleviates clinical symptoms in our food allergy model.

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