H. pylori organisms have adapted to the ecologic niche provided by gastric mucus. Although H. pylori may invade the gastric mucosa, the contribution of invasion to disease pathogenesis is not known. Four features are linked to H. pylori virulence:
Flagella, which allow the bacteria to be motile in viscous mucus
Urease, which generates ammonia from endogenous urea, thereby elevating local gastric pH around the organisms and protecting the bacteria from the acidic pH of the stomach
Adhesins, which enhance bacterial adherence to surface foveolar cells
Toxins, such as that encoded by cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer development
These factors allow H. pylori to create an imbalance forces that overcome those defenses.
MORPHOLOGYGastricbiopsyspecimensgenerallydemonstrateH. pylori ininfectedindividuals(
Fig.15.14A ).Theorganismisconcentratedwithinmucusoverlyingepithelialcellsinthesurfaceandneckregions.Theinflammatoryreactionincludesavariablenumberofneutrophilswithinthelaminapropria,includingsomethatcrossthebasementmembranetoassumeanintraepitheliallocation(
Fig.15.14B )andaccumulateinthelumenofgastricpitstocreatepitabscesses.Thesuperficiallaminapropriaincludeslargenumbersofplasmacells,ofteninclustersorsheets,aswellasincreasednumbersoflymphocytesandmacrophages.Whenintense,inflammatoryinfiltratesmaycreatethickenedrugalfolds,mimickinginfiltrativelesions.Lymphoidaggregates,somewithgerminalcenters,arefrequentlypresent(
Fig.15.14C )andrepresentaninducedformofmucosa-associated lymphoid tissue (MALT)thathasthepotentialtotransformintolymphoma.Intestinal metaplasia, characterizedbythepresenceofgobletcellsandcolumnarabsorptivecells(
Fig.15.14D ),alsomaybepresentandisassociatedwithincreasedriskofgastricadenocarcinoma.H. pylori showstropismforgastricfoveolarepitheliumandgenerallyisnotfoundinareasofintestinalmetaplasia,acid-producingmucosaofthegastricbody,orduodenalepithelium.AntralbiopsiesarethereforepreferredforevaluationofH. pylori gastritis.
In addition to histologic identification of the organism, several diagnostic tests have been developed including a noninvasive serologic test for anti–H. pylori antibodies, a stool test for the organism, and the urea breath test, based on the generation of ammonia by bacterial urease. Gastric biopsy specimens also can be analyzed by the rapid urease test, bacterial culture, or polymerase chain reaction (PCR) assay for bacterial DNA. Effective treatments include combinations of antibiotics and proton pump inhibitors. Patients with H. pylori gastritis usually improve after treatment, although relapses can follow incomplete eradication or reinfection.
Autoimmune gastritis accounts for less than 10% of cases of chronic gastritis. In contrast H. pylori-associated gastritis, autoimmune gastritis typically spares the antrum and induces marked hypergastrinemia (
Table 15.2 ). Autoimmune gastritis is characterized by the following:
Antibodies to parietal cells and intrinsic factor that can be detected in serum and gastric secretions http://ebooksmedicine.net