Chronic Gastritis

Overview
  • Chronic Gastritis does not refer to a unique pathophysiological entity but is rather a histological description of chronic inflammation occurring in the gastric mucosa often with subsequent mucosal atrophy and eventual metaplasia. Chronic gastritis is caused by two basic etiologies: Infection with Helicobacter pylori and by autoimmune disease. Regardless of the etiology, chronic gastritis displays a common histomorphology and is typically subclinical; however, nausea and vomiting and mild epigastric pain can occur. Additionally, dysplastic changes of the gastric mucosa observed in chronic gastritis increases the risk of gastric carcinoma. Following a discussion of the general morphology of chronic gastritis we discuss a variety etiology-specific features of the disease.
Morphology
  • Chronic Gastritis is characterized by the presence of lymphocytes and plasma cells in the superficial gastric mucosa, esp. in the gastric lamina propria. With time, progressive atrophy of the gastric mucosa and distortion of oxyntic glands and pyloric glands is observed. Eventually, Intestinal metaplasia can be observed which involves replacement of the gastric mucosa with columnar epithelium containing goblet cells more akin to small intestine mucosa. In long-standing cases, dysplasia of the gastric mucosa can be observed which increases the risk of progression to gastric carcinoma.
H. Pylori Chronic Gastritis
  • Chronic Inflammation is due to the immune response to the Helicobacter pylori (see page for more information). Bacteria can be observed overlying, but never actually invading, the gastric mucosa. Often the gastric Mucosal Associated Lymphoid Tissue (MALT) can be expanded, due to chronic microbial stimulation of immune cells which increases the risk of concomitant gastric lymphoma. It should be noted that chronic gastritis due to H. pylori infection often occurs in concert with Peptic Ulcer Disease.
Autoimmune Gastritis
  • Overview
    • Autoimmune Gastritis is an autoimmune disease essentially caused by a Type II Hypersensitivity reaction in which auto-antibodies are developed against the HK ATPase present in parietal cells. This leads to destruction of parietal cells which are critical for stomach acid secretion and production of Intrinsic Factor secretion. Consequently, the primary clinical consequences of autoimmune gastritis are sequelae of reduced levels of Intrinsic Factor along with reduced stomach acid, termed achlorydria.
  • Loss of Intrinsic Factor:
    • Absence of intrinsic factor results in an inability to absorb Vitamin B12 which leads to megaloblastic anemia or pernicious anemia.
  • Achlorydria
    • Recall that gastrin is a peptide hormone secreted by G Cells that induces stomach acid secretion from parietal cells (See Stomach Acid Secretion). Normally, secretion of gastrin is feedback inhibited by the presence of stomach acid in the stomach. However, the absence of stomach acid caused by parietal cell destruction results in lifting of this negative feedback and thus hyper-secretion of gastrin. Importantly, gastrin is also a trophic hormone for the entire gastric mucosa but especially for enterochromaffin cells which normally secrete histamine. Sustained enterochromaffin cell trophic stimulation leads to their hyperplasia which can eventually lead to their neoplastic transformation and thus generation of a carcinoid tumor.
Epidemiology
  • Chronic Gastritis due to Helicobacter pylori is very common especially among the elderly where incidence can approach 100% by the eighth decade. In contrast, autoimmune chronic gastritis is much less common.