eMedicine Specialties > Gastroenterology > Stomach

Gastritis, Acute: Treatment & Medication

Author: Mohammad Wehbi, MD, Assistant Professor of Medicine, Associate Program Director, Department of Gastroenterology, Atlanta Veterans Affairs Medical Center, Emory University School of Medicine
Coauthor(s): Nicole M Griglione, MD, Staff Physician, Department of Medicine, Emory University School of Medicine; Richard H Snyder, MD, Vice-Chair, Program Director, Department of Medicine, Norfolk General Hospital; Clinical Associate Professor, Department of Internal Medicine, East Virginia Medical School; Gwendolyn Sarver, BS, Pennsylvania State University College of Medicine; Kamil Obideen, MD, Assistant Professor of Medicine, Division of Digestive Diseases, Emory University School of Medicine; Consulting Staff, Division of Gastrointestinal Endoscopy, Atlanta Veterans Affairs Medical Center; Vincent W Yang, MD, PhD, R Bruce Logue Professor, Director, Division of Digestive Diseases, Department of Medicine, Professor of Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine
Contributor Information and Disclosures

Updated: Jul 30, 2008

Treatment

Medical Care

  • Administer medical therapy as needed, depending on the cause and the pathological findings.
  • No specific therapy exists for acute gastritis, except for cases caused by H pylori.
  • Administer fluids and electrolytes as required, particularly if the patient is vomiting.
  • Discontinue the use of drugs known to cause gastritis (eg, NSAIDs, alcohol).

Surgical Care

Surgical intervention is not necessary, except in the case of phlegmonous gastritis. With this entity, surgical intervention with resection of the affected area may be the most effective form of treatment.

Consultations

Consult a gastroenterologist in complicated cases.

Medication

Specific treatment is dependent on the etiology of gastritis.

According to the Centers for Disease Control and Prevention (CDC), the treatment of tuberculosis consists of a 2-month period of daily isoniazid, rifampin, and pyrazinamide, followed by 4 months of daily isoniazid along with rifampin. See Tuberculosis.

Medical management generally is ineffective in treating phlegmonous gastritis. No effective antiviral therapy exists for the treatment of human cytomegalovirus (HCMV) infection, though 2 agents (ie, ganciclovir, foscarnet) have been shown to be virostatic. See Cytomegalovirus.

The treatment of C albicans includes a variety of agents, including nystatin, oral clotrimazole, itraconazole, fluconazole, amphotericin B, and ketoconazole. See Candidiasis.

The treatment of disseminated histoplasmosis includes a variety of agents, including amphotericin B, itraconazole, and fluconazole. They have all been determined to be effective. See Histoplasmosis.
 
No drugs are available to treat anisakidosis. Endoscopic removal may be necessary.

Antacids

Used for general prophylaxis. Antacids containing aluminum and magnesium can help relieve symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe.


Aluminum and magnesium hydroxide, magnesia and alumina oral suspension (Rulox)

Drug combination that neutralizes gastric acidity and increases pH of the stomach and duodenal bulb. Aluminum ions inhibit smooth-muscle contraction and inhibit gastric emptying. Magnesium/aluminum antacid mixtures are used to avoid bowel function changes.

Adult

5-15 mL PO; 650 mg to 1.3 g tab PO qid

Pediatric

0.5 mL/kg PO qid prior to eating

Decreases effects of allopurinol, amprenavir, chloroquine, corticosteroids, diflunisal, digoxin, ethambutol, iron salts, H2-antagonists, isoniazid, penicillamine, phenothiazines, tetracyclines, thyroid hormones, and ticlopidine; increases effects of benzodiazepines and amphetamine; may cause aluminum toxicity with ascorbic acid; aluminum and magnesium potentiate effects of valproic acid, sulfonylureas, quinidine, and levodopa

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Antacids may mask the symptoms of internal bleeding secondary to NSAIDs; magnesium-containing antacids may cause diarrhea and potentially lead to dehydration; caution with aluminum-containing antacids in patients who recently have had a massive upper GI hemorrhage

H2 blockers

This class includes drugs whose mechanism of action is competitive inhibition of histamine at the histamine 2 (H2) receptor. Histamine plays an important role in gastric acid secretion, thereby making H2 blockers effective suppressors of basal gastric acid output and acid output stimulated by food and the neurological system. When used alone, they are frequently used as antisecretory drugs in H pylori therapy regimens. There are different drugs with different potencies and half-lives (eg, cimetidine, ranitidine, famotidine, nizatidine). Cimetidine will be discussed below as a representative of this class of drugs.


Cimetidine (Tagamet)

Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

Adult

150 mg PO qid; not to exceed 600 mg/d
50 mg/dose IV/IM q6-8h; not to exceed 400 mg/d

Pediatric

Not established
Suggested dose is 10-20 mg/kg/d PO/IV divided q6h; not to exceed 40 mg/d

Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Elderly may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur; may increase risk of necrotizing enterocolitis in premature infants

Proton pump inhibitors

Proton pump inhibitors are potent inhibitors of the proton (acid) pump (ie, the enzyme H+,K+-ATPase), located in the apical secretory membrane of the gastric acid secretory cells (parietal cell). Proton pump inhibitors can completely inhibit acid secretion and have a long duration of action. They are the most effective gastric acid blockers. Omeprazole will be discussed as a representative of this class of drugs.


Omeprazole (Prilosec)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATPase pump.

Adult

20 mg PO bid

Pediatric

Not established

May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Bioavailability may increase in the elderly

Antibiotics

Bacterial infections also can cause gastritis. The most common causative organism is H pylori. A number of therapeutic regimens are effective against H pylori. Single antimicrobial agents generally are not recommended because of the potential development of resistance.

Dual therapy includes a proton pump inhibitor plus amoxicillin (no longer recommended because eradication rates are 30-80%) or a proton pump inhibitor plus clarithromycin (eradication rate of roughly 71%). Adding a second antimicrobial agent is recommended for successful eradication.

Triple regimens are preferred in clinical practice. One drug is a proton pump inhibitor or a bismuth-based drug, the second drug is clarithromycin, and the third drug is amoxicillin or metronidazole. Quadruple therapy regimens (ie, 2 antibiotics, bismuth, antisecretory agent) generally are effective; however, because more drugs are prescribed and taken, increased adverse effects and decreased patient compliance can occur. This regimen is used in the event that triple therapy fails.

The decision of which medications to use is based on the following 4 criteria: (1) the different toxicities of the various medications, (2) the relative costs of each medication and regimen, (3) the emergence of antimicrobial-resistant bacteria, and (4) the level of patient compliance.


Amoxicillin (Amoxil, Trimox)

Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Adult

500 mg PO qid

Pediatric

Not established

Reduces the efficacy of oral contraceptives

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in patients with renal impairment


Tetracycline (Sumycin)

Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).

Adult

500 mg PO qid

Pediatric

<8 years: Not recommended
>8 years: Not established

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants

Documented hypersensitivity; severe hepatic dysfunction

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in patients with renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines


Metronidazole (Flagyl)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa.

Adult

250 mg PO qid

Pediatric

Not established

Cimetidine may increase toxicity of metronidazole; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with orally ingested ethanol

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in patients with hepatic disease; monitor for seizures and development of peripheral neuropathy


Clarithromycin (Biaxin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes and causing RNA-dependent protein synthesis to arrest.

Adult

500 mg PO bid/tid

Pediatric

Not established

Toxicity increases with coadministration of fluconazole, astemizole, and pimozide; clarithromycin effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors; serious cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents

Documented hypersensitivity; coadministration of pimozide or cisapride

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; administer one half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies

Antidiarrheal agents

Used in combination with antibiotics and proton pump inhibitors/H2 receptor antagonists to eradicate H pylori.


Bismuth subsalicylate (Bismatrol, Pepto-Bismol)

Drug combination that treats active duodenal ulcer associated with H pylori.

Adult

525 mg PO qid

Pediatric

Not established

Coadministration with anticoagulants may increase risk of bleeding; may increase toxicity of aspirin and hypoglycemics; decreases effects of tetracyclines and uricosurics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause temporary and harmless darkening of tongue and/or black stool; alcohol consumption may cause abdominal cramps, nausea, and vomiting

More on Gastritis, Acute

Overview: Gastritis, Acute
Differential Diagnoses & Workup: Gastritis, Acute
Treatment & Medication: Gastritis, Acute
Follow-up: Gastritis, Acute
Multimedia: Gastritis, Acute
References
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References

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  2. Beers M, Berkow R, eds. Gastritis. In: The Merck Manual of Diagnosis and Therapy. 18th ed. 2006:Section 3, Chapter 23. [Full Text].

  3. Feldman. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th ed. 2002:810-823.

  4. Ford A, Delaney B, Forman D. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database Syst Rev. 2004;CD003840.

  5. Gelfand DW, Ott DJ, Chen MY. Radiologic evaluation of gastritis and duodenitis. AJR Am J Roentgenol. Aug 1999;173(2):357-61. [Medline].

  6. Gisbert JP, Pajares JM. Diagnosis of Helicobacter pylori infection by stool antigen determination: a systematic review. Am J Gastroenterol. Oct 2001;96(10):2829-38. [Medline].

  7. Haruma K. Helicobacter heilmannii: a spiral shaped organism other than Helicobacter pylori. Intern Med. Mar 1999;38(3):217-8. [Medline].

  8. Iwakiri Y, Kabemura T, Yasuda D, et al. A case of acute phlegmonous gastritis successfully treated with antibiotics. J Clin Gastroenterol. Mar 1999;28(2):175-7. [Medline].

  9. Kasper DL, Braunwald E, Fauci A, et al. Gastritis. In: Harrison's Principles of Internal Medicine: Companion Handbook. 16th ed. McGraw-Hill: 2006:Part 12, Chapter 274.

  10. Richieri JP, Pol B, Payan MJ. Acute necrotizing ischemic gastritis: clinical, endoscopic and histopathologic aspects. Gastrointest Endosc. Aug 1998;48(2):210-2. [Medline].

  11. Soltermann A, Koetzer S, Eigenmann F, et al. Correlation of Helicobacter pylori virulence genotypes vacA and cagA with histological parameters of gastritis and patient's age. Mod Pathol. Aug 2007;20(8):878-83. [Medline]. [Full Text].

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Further Reading

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Keywords

acute gastritis, gastric mucosa inflammation, inflamed gastric mucosa, pangastritis, antral gastritis, erosive gastritis, nonerosive gastritis, non-erosive gastritis, Helicobacter pylori, H pylori, Candida albicans, C albicans, alcoholic gastritis, NSAIDs, nonsteroidal anti-inflammatory drugs, analgesic-induced gastritis, cytomegalovirus, fungal infection, histoplasmosis, stomach irritation, stomach ache, upset stomach

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Contributor Information and Disclosures

Author

Mohammad Wehbi, MD, Assistant Professor of Medicine, Associate Program Director, Department of Gastroenterology, Atlanta Veterans Affairs Medical Center, Emory University School of Medicine
Mohammad Wehbi, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Nicole M Griglione, MD, Staff Physician, Department of Medicine, Emory University School of Medicine
Nicole M Griglione, MD is a member of the following medical societies: American Medical Association and Illinois State Medical Society
Disclosure: Nothing to disclose.

Richard H Snyder, MD, Vice-Chair, Program Director, Department of Medicine, Norfolk General Hospital; Clinical Associate Professor, Department of Internal Medicine, East Virginia Medical School
Richard H Snyder, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Gwendolyn Sarver, BS, Pennsylvania State University College of Medicine
Disclosure: Nothing to disclose.

Kamil Obideen, MD, Assistant Professor of Medicine, Division of Digestive Diseases, Emory University School of Medicine; Consulting Staff, Division of Gastrointestinal Endoscopy, Atlanta Veterans Affairs Medical Center
Kamil Obideen, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Vincent W Yang, MD, PhD, R Bruce Logue Professor, Director, Division of Digestive Diseases, Department of Medicine, Professor of Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine
Vincent W Yang, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Nothing to disclose.

Medical Editor

Waqar A Qureshi, MD, Chief of Endoscopy, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and VA Medical Center
Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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