Fig. 15.14 Chronicgastritis.(A)Spiral-shapedHelicobacter pylori bacilliarehighlightedinthisWarthin-Starrysilverstain.Organismsareabundantwithinsurfacemucus.(B)Intraepithelialandlaminaproprianeutrophilsareprominent.(C)Lymphoidaggregateswithgerminalcentersandabundantsubepithelialplasmacellswithinthesuperficiallaminapropriaarecharacteristicof
H. pylori gastritis.(D)Intestinalmetaplasia,recognizableasthepresenceofgobletcellsadmixedwithgastricfoveolarepithelium,candevelopandisariskfactorfordevelopmentofgastricadenocarcinoma.
Vitamin B12 deficiency leading to pernicious anemia and neurologic changes
Autoimmune gastritis is associated with immune-mediated loss of parietal cells and subsequent reductions in acid and intrinsic factor secretion. Deficient acid secretion stimulates gastrin release, resulting in hypergastrinemia and hyperplasia of antral gastrin-producing G cells. Lack of intrinsic factor disables ileal vitamin B12 absorption, leading to B12 deficiency and a particular form of megaloblastic anemia called pernicious anemia (Chapter 12). Reduced serum concentration of pepsinogen I reflects chief cell loss. Although H. pylori can cause hypochlorhydria, it is not associated with achlorhydria or pernicious anemia, because the parietal and chief cell damage is not as severe as in autoimmune gastritis.
MORPHOLOGYAutoimmunegastritisischaracterizedbydiffusedamage of the oxyntic (acid-producing)mucosa withinthebodyandfundus.Damagetotheantrumandcardiatypicallyisabsentormild.Withdiffuse atrophy, theoxynticmucosaofthebodyandfundusappearsmarkedlythinned,andrugalfoldsarelost.Neutrophilsmaybepresent,buttheinflammatoryinfiltratemorecommonlyiscomposedoflymphocytes,macrophages,andplasmacells;incontrastwithH. pylori gastritis, theinflammatoryreactionmostoftenisdeepandcenteredonthegastricglands.Parietal and chief cell loss canbeextensive,andintestinal metaplasia maydevelop.
Antibodies to parietal cells and intrinsic factor are present early in the disease, but B12 deficiency and pernicious anemia develop in only a minority of patients. The median age at diagnosis is 60 years, and there is a slight female predominance. Autoimmune gastritis often is associated with other autoimmune diseases but is not linked to specific human leukocyte antigen (HLA) alleles.
There are three important complications of chronic gastritis: Peptic ulcer disease, mucosal atrophy and intestinal metaplasia, and dysplasia. Each of these is discussed shortly.
Peptic ulcer disease (PUD) most often is associated with
H. pylori infection or NSAID use. The imbalances of
Table 15.2 Characteristics of Helicobacter pylori–Associated and Autoimmune Gastritis
Feature H. pylori–Associated Autoimmune
InflammatoryinfiltrateNeutrophils,subepithelialplasmacellsLymphocytes,macrophages
SerologyAntibodiestoH. pylori Antibodiestoparietalcells(H+,K+-ATPase,intrinsicfactor)
SequelaePepticulcer,adenocarcinoma,lymphomaAtrophy,perniciousanemia,adenocarcinoma,carcinoidtumor
AssociationsLowsocioeconomicstatus,poverty,residenceAutoimmunedisease;thyroiditis,diabetesmellitus,Gravesdiseaseinruralareas http://ebooksmedicine.net