HELICOBACTER PYLORI – A DANGEROUS PRIMARY CARCINOGEN (with new MCQs)
H. Pylori MCQs given on the right side of the article
By Dr Sijil Sivaraman MD DM Gastroenterologist Email for Questions: firstname.lastname@example.org
- Conventional thinking before 1982/1983 was that no pathogen can live in stomach due to the acidic nature. Dr Barry J. Marshall and Dr J. Robin Warren of western Australia discovered Helicobacter pylori during their research about gastric ulcer and later awarded Nobel prize.
- H pylori has some unique features suited to live in the acidic stomach. It is gram-negative spiral bacillus with multiple unipolar flagella and fastidious in terms of growth requirements with strictly micro-aerophilic requiring C02 for growth. It most commonly colonise in the gastric antrum and present in the mucus that overlies the mucosa and move freely in gastric mucous layer. It produce large amount of urease which hydrolyze urea to alkaline ammonia and co2
- It is the most common chronic bacterial infection worldwide with more than 50 % of world population been infected. In developing countries it is more common and acquired during childhood and with life cycle of Spontaneous elimination and subsequent reinfection.
Risk factors of acquiring H pylori:
The important risk factors for acquiring H pylori are low socioeconomic status, housing density, crowded conditions which leads to contaminated water. Major Reservoir of H pylori is man and there is person to person transmission.
Where it colonise :
H. Pylori colonise in Gastric epithelium, gastric metaplasia of esophagus and duodenum and meckel’s diverticulum.
The natural history of chronic H. pylori infection includes (1) superficial gastritis, (2) duodenal ulcer phenotype, and (3) gastric ulcer/gastric cancer phenotype
The pattern of colonization is an important determinant of H. pylori disease manifestations. Antral colonization leads to hyperacidity leads to duodenal ulcer. Gastric ulcers and gastric adenocarcinoma occur more often with is proximal colonization of the stomach.
Gastric adenocarcinoma remains the second major cause of cancer death in the world. The burden of risk of gastric cancer is considered largely attributable to H. pylori infection, with cag PAI–bearing strains having a higher association with gastric cancer .
The increased risk of development of gastric carcinoma depends on factors including the strain of bacteria, host genetic factors, the duration of infection, and the presence or absence of other environmental risk factors.
Infection by H. pylori is present in 90% of cases of gastric MALT lymphoma.
H. PYLORI INFECTION AND ASSOCIATIONS
H. pylori has been strongly associated with Peptic ulcer disease, Gastric carcinoma and MALT lymphoma.
Other well established Associations are coronary artery disease, Immune thrombocytopenia purpura and Iron deficiency anemia
TESTS FOR H. PYLORI
|NON ENDOSCOPIC TESTS:||ADVANTAGES|
|Serology (qualitative immunoglobulin G [IgG])||Widely available and inexpensive|
|Urea breath test (13C or 14C)||Identifies active infection, useful both before and after treatment|
|Stool antigen test||Identifies active infection, useful both before and after treatment|
|Histology||Excellent specificity and provides additional information about gastric mucosa|
|Rapid urease test||Rapid results, it is accurate in patients not using PPIs or antibiotics|
|Culture||It has high specificity and allows antibiotic sensitivity testing|
Rapid Urease test
- It is performed during endoscopy , with antral biopsy specimen placed into a medium containing urea and an indicator
- The urease produced by the active H pylori hydrolyzes urea to ammonia, which raises the pH of the medium and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE)
Helicobacter pylori Treatment:
Initial treatment for H. pylori, a 10- to 14-day course of standard PPI triple therapy. and appropriate alternative is 10-day sequential regimen. If infection persists after this, bacteria are likely resistant to clarithromycin so retreatment should be with one of the PPI triple regimens noted earlier that incorporates a different combination of medications or a bismuth-based therapy for 14 days.
Triple therapy :
PPI, clarithromycin, amoxicillin
PPI, clarithromycin, metronidazole
PPI, amoxicillin, levofloxacin
PPI, amoxicillin, rifabutin
PPI, bismuth subsalicylate/subcitrate, metronidazole, tetracycline
PPI, amoxicillin followed by PPI, clarithromycin and Tinidazole
This regimen appears highly effective despite clarithromycin resistance