Gastric Infections

Helicobacter pylori

The discovery of Helicobacter pylori has dramatically transformed the approach to diagnosis and treatment of peptic ulcer disease. It is now known that H. pylori accounts for >70% of duodenal ulcers, 60-90% of gastric ulcers, and is also a cause of atrophic gastritis. H. pylori is also found in nearly 100% of individuals with chronic active gastritis. In addition, H. pylori has been classified as a type I carcinogen by the World Health Organization and has a strong association with gastric cancer and lymphoma. H. pylori is a helical Gram-negative rod that produces a variety of enzymes that help the organism adapt to its acidic environment. It is found only in gastric epithelium; however, it can be found in other areas of the gastrointestinal tract secondary to gastric metaplasia (11).

H. pylori is found worldwide, with a higher incidence in underdeveloped and third world countries. It is reported that two-thirds of the world's population is infected with H. pylori and random testing of blood donors reveals that the prevalence in the general population in the United States is around 50%. The transmission of H. pylori is via the fecal-oral route. Symptoms of infection with H. pylori may include those associated with gastritis or peptic ulcer disease, such as epigastric pain, bloating, early satiety, nausea, and vomiting. Many individuals, however, are asymptomatic.

There are several tests available to detect infection with H. pylori. These include serology, urea breath test, or endoscopy with biopsy to perform both rapid urease test and culture. Serology has limited usefulness to detect active infection and may remain positive even after eradication of the bacteria has been achieved (11).

Table 1

Current Treatment Options for H. Pylori Infection

OC 40 mg Omeprazole p.o. qd + 500 mg clarithromycin t.i.d. x 2 wk, then 20 mg omeprazole p.o. qd x 2 wk

RC 400 mg Ranitidine bismuth citrate (RBC) b.i.d.

+ 500 mg clarithromycin t.i.d. x 2 wk, then 400 mg RBC b.i.d. x 2 wks

BMT 525 mg Bismuth subsalicylate (Pepto BismolĀ®)

q.i.d. + 250 mg metronidazole q.i.d. + 500 mg tetracycline q.i.d. x 2 wk + H2RA therapy x 4 wk

LAC 30 mg Lansoprazole b.i.d. + 1 g amoxicillin b.i.d.

+ 500 mg clarithromycin t.i.d. x 10 d

LA 30 mg Lansoprazole t.i.d. + amoxicillin 1 g t.i.d. x 2 wk (restricted labeling for those who are allergic or intolerant of clarithromycin)

RC 400 mg Ranitidine bismuth citrate (RBC) b.i.d. + 500 mg clarithromycin b.i.d. x 2 wk, then 400 mg RBC b.i.d. x 2 wk

OAC 20 mg Omeprazole b.i.d. + 500 mg clarithromycin b.i.d. + 1 g amoxicillin b.i.d. x 10 d

LAC 30 mg Lansoprazole b.i.d. + 500 mg clarithromycin b.i.d. + 1 g amoxicillin b.i.d. x 10 d

MOCa 20 mg Omeprazole b.i.d. + 500 mg metronidazole b.i.d. + 500 mg clarithromycin b.i.d. x 7 d

MOAa 20 mg Omeprazole b.i.d. + 1 g amoxicillin b.i.d.

RCAa 400 mg RBC b.i.d. + 500 mg clarithromycin b.i.d. + 1 g amoxicillin q.i.d. x 10 d a Not FDA Approved.

Data from refs 10-13.

Efficacy: 70-75%

Efficacy: 73-84%

Efficacy: 88-90% With omeprazole 84-92%

Efficacy: 92% Efficacy: 50-60%

Efficacy: 75%

Efficacy: 86-95% Efficacy: 86-91% Efficacy: 89% Efficacy: 75-83% Efficacy: 62-75%

Multiple drug regimens are effective for eradication of H. pylori (Table 1). Individuals who should be treated for H. pylori are those with peptic ulcer disease who are H. pylori positive, ulcer patients in remission who also test positive for H. pylori, and those with mucosal-associated lymphoid tissue (MALT) lymphoma. Patients with a first-degree relative who has gastric carcinoma should also be considered for therapy. In patients with complicated ulcer disease or MALT lymphoma, eradication should be confirmed by urea breath test or biopsy 1 mo after completion of therapy.

Compliance with treatment regimens is a very important issue, and there is evidence for emerging antibiotic resistance to H. pylori. Metronidazole resistance is common worldwide and clarithromycin resistance is increasing in many regions. Although resis tance has been shown to effect cure rates of therapy in some studies, data remain scarce and the clinical impact of resistance is unclear (16). Most triple-drug-based therapies containing the proton pump inhibitors as well as two antibiotics remain highly effective for eradication. Methods for routine culture of H. pylori and sensitivity determination have not been established in many hospitals, and access to these remains predominantly in academic centers. Consideration for determination of resistance should be restricted to those individuals who do not respond to primary therapy (15). Noncompliance with treatment regimens remains problematic and further increases the risk of antimicrobial resistance. At this point in time, there are no recommendations regarding treatment of those individuals with nonulcer dyspepsia. A drawback of using empiric therapy is the potential for development of resistance (11).

Other

CMV is the next most common infectious etiology of gastritis. It has been reported in healthy individuals; however, it is more common in those who are immunocompromised. Rarely gastritis occurs as a result of HSV infection or syphilis. The only fungal infection that is recognized to occur in the stomach is histoplasmosis. Treatment for this should be approached as for other gastrointestinal organs (11).

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