Gastrointestinal · PANCE / PANRE

Helicobacter pylori Infection

Gram-negative spiral bacterium colonizing gastric mucosa; causes gastritis, PUD, MALT lymphoma, and gastric cancer.

Also known as: H. pylori, Helicobacter pylori, HP infection

Overview

Chronic infection of the gastric mucosa by Helicobacter pylori, a microaerophilic, urease-producing, Gram-negative spiral bacterium. Classified by WHO/IARC as a Group 1 carcinogen.

Epidemiology

Estimated to colonize ~50% of the global population; prevalence 30-40% in the US (higher in immigrants, lower socioeconomic groups, and elderly). Acquired in childhood, typically via fecal-oral or oral-oral transmission. Declining incidence in developed countries.

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Risk factors

Birth or residence in high-prevalence country (Asia, Africa, Latin America, Eastern Europe)
Crowded living conditions, poor sanitation in childhood
First-degree relative with H. pylori or gastric cancer
Lower socioeconomic status

Pathophysiology

Urease hydrolyzes urea to ammonia, neutralizing gastric acid to allow colonization. Flagella enable penetration of the mucus layer. Virulence factors CagA and VacA induce epithelial injury, inflammation, and apoptosis. Chronic inflammation drives one of two patterns: antral-predominant gastritis (high acid → duodenal ulcer) or corpus-predominant atrophic gastritis (hypochlorhydria → gastric ulcer, intestinal metaplasia, dysplasia, gastric adenocarcinoma).

Clinical presentation

Symptoms

Most infections asymptomatic
Dyspepsia: epigastric pain, fullness, nausea, bloating
Symptoms of complications: PUD, GI bleed, gastric cancer, MALT lymphoma (early satiety, weight loss, anemia)

Signs / physical exam

Epigastric tenderness if active ulcer or gastritis
Pallor if iron-deficiency anemia

Classic findings

Unexplained iron-deficiency anemia, ITP, or B12 deficiency — test for H. pylori per ACG.

Differential diagnosis

Functional dyspepsia (H. pylori negative) — Same symptoms but negative testing; treat with PPI ± prokinetic
GERD — Heartburn, regurgitation; H. pylori may coexist but is not the cause
Bile reflux gastritis — Post-gastrectomy or post-cholecystectomy; bilious vomiting; bile in stomach on EGD
Autoimmune atrophic gastritis — Pernicious anemia, B12 deficiency, anti-parietal/anti-IF antibodies; corpus-predominant atrophy without H. pylori
NSAID gastropathy — NSAID exposure; erosions or ulcers without inflammatory infiltrate
Zollinger-Ellison syndrome — Refractory ulcers, diarrhea, multiple/distal ulcers; high fasting gastrin

Diagnostic workup

Labs

Urea breath test — high sensitivity and specificity (>95%); confirms ACTIVE infection; preferred non-invasive test
Stool antigen test — equivalent accuracy to UBT; useful in children and post-treatment confirmation
Serology (IgG) — limited utility; cannot distinguish active vs prior infection; reserve for low-prevalence settings or where other tests unavailable
CBC if anemia suspected; iron studies; B12

Imaging

EGD with gastric biopsy when endoscopy is otherwise indicated (alarm features, age ≥60 with new dyspepsia, refractory symptoms)
Rapid urease test (CLO test) on antral/corpus biopsy — high specificity; false-negative with recent PPI, antibiotics, or bleeding
Histology with H&E and Giemsa staining — gold standard; also identifies metaplasia/dysplasia
Culture with susceptibility testing — increasingly recommended after first treatment failure

Other studies

WITHHOLD PPI 2 weeks and antibiotics/bismuth 4 weeks before testing (except serology) to avoid false negatives
Test-and-treat strategy: non-invasive test in patients <60 with uninvestigated dyspepsia and no alarm features

Diagnostic algorithm

Test	Detects Active Infection	Affected by PPI/Abx	Use Case
Urea breath test	Yes	Yes — hold PPI 2 wk, abx 4 wk	Initial diagnosis; eradication confirmation
Stool antigen	Yes	Yes — same hold	Initial diagnosis; eradication confirmation; pediatrics
Serology IgG	No (past or present)	No	Limited; not for treatment confirmation
Rapid urease (CLO) on biopsy	Yes	Yes — false negatives	EGD already indicated
Histology with stains	Yes	Yes (less affected)	EGD; gold standard; also detects metaplasia
Culture + susceptibility	Yes	Yes	After repeated treatment failure

H. pylori diagnostic test characteristics — choose based on whether EGD is needed and recent medication exposure.

Treatment

First-line

Bismuth quadruple therapy × 14 days — PPI BID + bismuth subsalicylate QID + tetracycline 500 mg QID + metronidazole 500 mg QID — PREFERRED first-line in US (clarithromycin resistance >15% in most regions)
Clarithromycin triple therapy × 14 days — PPI BID + clarithromycin 500 mg BID + amoxicillin 1 g BID (or metronidazole if PCN-allergic) — ONLY if no prior macrolide exposure and local resistance <15%

Second-line / adjunct

Salvage regimens after first-line failure (choose a regimen the patient has NOT received):
Levofloxacin triple × 14 days — PPI BID + levofloxacin 500 mg daily + amoxicillin 1 g BID
Bismuth quadruple × 14 days (if not previously used)
Rifabutin triple × 14 days — PPI BID + rifabutin 50 mg TID + amoxicillin 1 g TID — refractory cases
Susceptibility-guided therapy after second failure
Confirm eradication 4 weeks after completing therapy by urea breath test or stool antigen

Complications

Peptic ulcer disease (duodenal > gastric)
Gastric adenocarcinoma (intestinal-type) — eradication reduces risk; most pronounced if treated before intestinal metaplasia
Gastric MALT (mucosa-associated lymphoid tissue) lymphoma — 60-80% regress with H. pylori eradication alone
Iron-deficiency anemia (refractory or unexplained)
Immune thrombocytopenic purpura (ITP)
Vitamin B12 deficiency
Functional dyspepsia symptoms (modest benefit from eradication)

PANCE pearls

Indications to test (ACG 2017): active PUD, history of PUD without prior eradication, gastric MALT lymphoma, early gastric cancer post-resection, uninvestigated dyspepsia <60 yr without alarm features, long-term NSAID/aspirin users, unexplained iron-deficiency anemia, ITP, household contacts of H. pylori carriers, family history of gastric cancer.
ALWAYS confirm eradication 4 weeks after therapy — failure rates 15-30% with first-line regimens.
Avoid clarithromycin-based regimens in patients with any prior macrolide exposure.
Bismuth turns stool and tongue BLACK — counsel patients to avoid confusing with melena.
MALT lymphoma — treat H. pylori first; surveillance EGD; chemotherapy/radiation only for non-responders or t(11;18)-positive disease.
Mass eradication is not recommended; treat only patients meeting indications.

References

ACG 2017 — Chey WD et al. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol 2017;112:212-239
Maastricht VI/Florence — Malfertheiner P et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence Consensus Report. Gut 2022;71:1724-1762
AGA 2024 — Shah SC et al. AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis. Gastroenterology 2021;161:1325-1332

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