Approach Considerations
Surgical intervention is not necessary for gastritis, except in the case of phlegmonous gastritis or acute necrotizing gastritis. With the latter entity, surgical intervention with resection of the affected area may be the most effective form of treatment.
Consult a gastroenterologist in complicated cases.
In cases of suspected upper gastrointestinal (GI) bleeding (decreased hemoglobin, melena, hematemesis), diagnostic endoscopy is mandatory to exclude bleeding ulcers, angiomatous malformations, erosions and malignant transformation. Severe cases with upper GI bleeding can be treated by cautery, hemoclips, local epinephrine injection, or hemostatic spraying of the bleeding area [15] along with an intravenous (IV) proton-pump inhibitor (PPI) bolus, then continuous infusion for 72 hours to stabilize the bleeding. [16]
Over-the-counter (OTC) drugs such as mucosal coating (sucralfate, antacids) agents or short-term histamine-2 antagonists can stabilize mild to moderate cases in the short term. [17] In the long term, treatment of the underlying cause (ie, avoid nonsteroidal anti-inflammatory drugs, caffeine, smoking; H Pylori eradication; etc.) is the most satisfactory course of action.
Proton-pump inhibitor (PPI) treatment and coronavirus disease 2019 (COVID-19) infection
There is an association between the use of PPIs and the severity of COVID-19 infection. This is explained by the increased viral infection after swallowing the viral particles in patients who have low gastric acidity, most commonly due to PPI ingestion. Viral inactivation takes place in a low acidic medium, protecting the patient from viral entry through the gastrointestinal tract. However, using PPIs does not increase the risk of acquiring infection. [18, 19, 20, 21]
Lee et al also found that increasing the dose of PPIs is associated with increased severity of COVID-19 infection. [20] Furthermore, there is a debate over whether antihistamines such as famotidine could be more protective of severe infection. It is postulated that famotidine can inhibit the replication of human immunodeficiency virus (HIV); further computational methods showed that this agent could be effective in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as well. A retrospective cohort proved this preliminary hypothesis: Hospitalized patients who received famotidine showed a lower risk of intubation or mortality than those who didn’t receive the drug. Moreover, famotidine was associated with mildly lowering ferritin levels (used as a surrogate marker for the cytokine storm). Unfortunately, when the authors repeated the study on another set of patients, the results were not replicable (ie, no protective effect of famotidine). [21, 22]
Medical Care
Administer medical therapy for patients with acute gastritis as needed, depending on the underlying cause and the pathological findings.
The US Food and Drug Administration announced voluntary recalls of ranitidine from the market between December 2019 and February 2020 [3] after raising major concerns in September 2019 about drug contamination with the impurities of the carcinogenic molecule N-nitrosodimethylamine (NDMA). [23] A total withdrawal of all ranitidine products was requested in April 2020. [24]
No specific therapy exists for acute gastritis, except for cases caused by H pylori. The American College of Gastroenterology (ACG) guidelines suggest that the current evidence does not support the notion that treating H pylori worsens gastroesophageal reflux disease (GERD). [25] For patients who need eradication of H pylori, this should not be a concern.
First-line H pylori eradication therapy
First-line therapy for H pylori eradication consists of bismuth quadruple therapy with a proton-pump inhibitor (PPI), a nitroimidazole, and tetracycline for 10-14 days or clarithromycin-based triple therapy with amoxicillin or amitronidazole and a PPI for 14 days (both strong recommendations). [25] Other first-line options are concomitant (14 days of clarithromycin, amoxicillin, and a nitroimidazole) or sequential (first week with amoxicillin and second week with clarithromycin and a nitroimidazole) or hybrid therapy (amoxicillin for 14 days, then adding clarithromycin and a nitroimidazole on the second week only). [25]
Note that the guidelines mention a nitroimidazole molecule in general (metronidazole or tinidazole), as they have similar efficacy, although tinidazole is not recommended as first-line therapy to avoid drug resistance. [25] As for levofloxacin-containing regimens, the quality of evidence is very low; these regimens could be used for 10-14 days, on a triple regimen of levofloxacin, amoxicillin, and a PPI. Another first-line therapy regimen is a fluoroquinolone sequential therapy with amoxicillin in the first week, followed by a PPI, fluoroquinolone with nitroimidazole in the second week.
Second-line or salvage therapy
Second-line therapy or salvage therapy depends on the antibiotics used in the first course of treatment and the culture results in cases of resistant strains. Levofloxacin- and rifabutin-based salvage regimens have a better degree of evidence than bismuth- or clarithromycin-based regimens. [25, 26] See the table below.
Acute Gastritis. Acute gastritis treatment options according to latest American College of Gastroenterology (ACG) guidelines are shown.
In a 2020 systematic review, investigators found nitazoxanide was effective in treatment-naïve patients as well as for salvage therapy. [27] This anti-protozoal drug increases the efficacy of multidrug regimens and could provide a good alternative in regions where multidrug resistance is endemic. Nitazoxanide is generally well tolerated and could also be of benefit in children. [27]
Other management
Administer fluids and electrolytes as required, particularly if the patient is vomiting.
Discontinue the use of drugs known to cause gastritis (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], alcohol). A long-term prospective study found that patients with arthritis who were older than 65 years and regularly took low-dose aspirin were at an increased risk for dyspepsia severe enough to necessitate the discontinuation of NSAIDs. [28] This suggests that better management of NSAID use should be discussed with older patients to reduce NSAID-associated upper gastrointestinal events.
There has been a growing concern in recent years regarding the interaction between PPIs and clopidogrel. A decrease in the antiplatelet activity of clopidogrel with a possible increase in adverse cardiac events is postulated. Pharmacokinetically, it has been shown that omeprazole and lansoprazole interact significantly with clopidogrel, and that omeprazole, rabeprazole, and esomeprazole interact with prasugrel. Pantoprazole has been shown to have the least interaction and, thus, pantoprazole has low CYP2C19-inhibiting properties. [29, 30]
PPIs when used with clopidogrel will increase the risk of myocardial infarction and stent thrombosis, but this combination will not increase the risk of death or bleeding after percutaneous coronary intervention according to a 2019 meta-analysis. [31] Pantoprazole and lansoprazole have shown the least interaction with clopidogrel and appear to be safer than esomeprazole and omeprazole according to the latest FDA recommendations. [31]
Rebamipide is a drug that provides mucosal protection through activation of prostaglandins and inhibition of neutrophil response in the stomach lining, thus increasing the mucosal healing in NSAID-induced gastritis and H pylori infection. In separate 2018 and 2019 meta-analyses, rebamipide was effective when combined with H pylori eradication dual-therapy regimens, although its effect could be limited by ethnicity (ie, effective in Asian but not Caucasoid populations). This drug is not approved by the FDA, but it is used extensively in Korea, Japan, and Russia. [32, 33]
In 2015, a relatively new group of reversible PPIs known as potassium-competitive acid blockers (PCAB) was first approved in Japan. Vonoprazan causes 350 times more inhibition of acid secretion than lansoprazole does. [34] In May 2022, the FDA approved vonoprazan (the first in the PCAB class) for the treatment of H pylori as a part of triple therapy. Two combination packs are available: vonaprazon + amoxicillin and vonoprazan + amoxicillin + clarithromycin.
Recommendations for using vonoprazan in erosive esophagitis in induction and maintenance therapy were presented in the 2022 AGA and Chinese guidelines. [35] The FDA had been expected to make a decision in January 2023 for the use of vonoprazan for erosive esophagitis; it is now requiring the manufacturer to provide additional stability data that demonstrates levels of a nitrosamine impurity (N-nitroso-vonoprazan [NVP]), which had been detected in trace amounts in commercial batches, remain below acceptable daily intake limits (96 ng/day) throughout the product's proposed shelf life. [36]
In a meta-analysis that examined the efficacy and safety of vonoprazan in the eradication of H pylori as compared to that of PPI-based triple-therapy, vonoprazan was associated with greater eradication (91.4% vs 74.8%) and fewer adverse events (32.7% vs 40.5%) in treatment-naïve patients. [37]
In H pylori eradication, vonoprazon action is not affected by changes in pH, thereby increasing its potency up to twice that of PPIs along with good cost-effectiveness. [38] In addition, 1-week of vonoprazan-based triple therapy had similar efficacy (87.4%) as 2-weeks of PPI-based triple therapy (88%), without an increase in the adverse events. [39]
However, Japanese investigators have noted the prevalence of gastric mucosal redness, as detected by upper gastrointestinal endoscopy, was highest in patients who received vonoprazan (8.7%), as compared to those taking PPIs (6.2%) or antihistamines (1.5%), and relative to a control group (1.9%). [40]
Moreover, a 2022 postmarketing report raised a safety concern for vonoprazan-related nephrotoxicity. Time-to-onset (TTO) analysis until the occurrence of interstitial nephritis revealed a shorter TTO in those taking vonoprazan (average: 25 days) than those receiving PPIs (average: 41 days), whereas the TTO for acute kidney injury was similar for vonoprazon (average: 10.5 days) and PPIs (average: 11 days). These results have yet to be validated, and the impact of concomitant medications such as NSAIDs or chemotherapy remains unknown. Potential causes of such nephrotoxicity may be related to the mechanism of action of the drug, in which vonoprazon competes reversibly with the K+ ion on the H+–K+ pump. [34] Also, vonoprazon may induce the immune system through antigen mimicry, new antigen formation, or haptenization. [34]
Prevention
In patients with gastritis, it is recommended to eradicate H pylori infection before starting nonsteroidal anti-inflammatory drug (NSAIDs)/aspirin treatment for the first time, as this will decrease the possibility of inducing gastroduodenal ulceration. Unfortunately, this therapy's effectiveness decreases with chronic use. However, chronic NSAIDs/aspirin users with known history of peptic ulcer or gastrointestinal bleeding could benefit from H pylori eradication by reducing the rebleeding risk. [41]
Long-Term Monitoring
H pylori eradication testing can be performed 4 weeks after completing therapy for gastritis. It is carried out using either rapid urease breath testing or stool antigen testing. However, this is not cost effective and is not always done.
The current recommendation is that patients with ulcers from H pylori, mucosa-associated lymphoid tissue (MALT) lymphoma, a history of gastric cancer, and those with no improvement of symptoms despite treatment must be checked for resolution of H pylori infection. [25]
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Acute Gastritis. Acute gastritis with superficial erosions is observed.
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Acute Gastritis. This image reveals mucosal erythema and edema consistent with acute gastritis.
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Acute Gastritis. A management algorithm for acute gastritis is depicted.
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Acute Gastritis. Acute gastritis treatment options according to latest American College of Gastroenterology (ACG) guidelines are shown.
