Gastritis and Carditis

Abstract

Dyspepsia is a common clinical problem. Its causes include peptic ulcer disease, gastroesophageal reflux, and functional (nonulcer) dyspepsia. A detailed clinical description of pain does not reliably differentiate the cause. Approximately 80% of gastroscopies are performed for the investigation of dyspepsia. "Gastritis" is diagnosed endoscopically in 59% of all stomachs, although in only 3% are the changes severe. Pathologic examination of unselected gastric biopsy specimens reveals that abnormalities are present in 62-73%, but there is only a weak correlation between endoscopic and histologic findings. For these reasons, it is recommended that endoscopic examination should always be accompanied by biopsy. Ideally, biopsies should be taken in a systematic fashion to include sampling of antrum and corpus. Recent evidence suggests that gastric infection by Helicobacter pylori initially presents as a superficial gastritis. Later it may become atrophic with development of intestinal metaplasia. The onset of atrophic changes may be related to the duration of infection, the strain of the infecting organism, associated dietary factors, or as-yet undefined host factors related to immunity. Persistent superficial gastritis predisposes to duodenal ulcer and gastric mucosa-associated lymphoid tissue lymphoma. Atrophic gastritis predisposes to gastric ulcer and adenocarcinoma. Evidence is accumulating that in some patients, pernicious anemia may be an end result of H. pylori-induced atrophic gastritis. Reactive gastropathy is a relatively common finding in gastric biopsies; in most instances it is associated with either reflux of duodenal contents or therapy with nonsteroidal anti-inflammatory drugs. Lymphocytic gastritis, eosinophilic gastritis, and the gastritis associated with Crohn's disease are distinct morphologic entities. Most gastroscopies are performed for the investigation of dyspepsia (1-7). This is a common clinical problem but is rarely life-threatening. The causes of dyspepsia include peptic ulcer disease (30%), gastroesophageal reflux (29%), and nonulcer (functional) dyspepsia (40%). The cause of functional dyspepsia is unclear at the present time, although in many instances it may be related to abnormalities of gut motility. In Ͻ1% of cases is gastric cancer a cause of dyspepsia. A detailed description of the symptoms of dyspepsia does not reliably differentiate the cause, although the presence of heartburn strongly suggests a component of gastroesophageal reflux. Correlations among patient symptoms, endoscopic appearances, and biopsy findings of gastritis are imperfect (4 -6). Agreement is best in cases where peptic ulcer or another focal lesion is identified. A study by Khakoo et al. (7) from the United Kingdom illustrates the problems encountered. Endoscopic and histologic findings were reviewed in 167 patients who underwent gastroscopy for dyspeptic symptoms. Of these, 98 patients (57%) had endoscopic evidence of gastritis. In 42% of patients, gastritis involved the antrum alone, in 7% it involved the...

Participation of Capsaicin-Sensitive Afferent Nerves in the Gastric Mucosa of Patients with Helicobacter pylori-Positive or-Negative Chronic Gastritis

“…Acute and chronic gastritis can be differentiated on the basis of the development and process of the disease. Chronic gastritis may be caused by different factors such as Helicobacter pylori infection, bacterial overgrowth in a hypochlorhydric stomach, autoimmune mechanisms, or chemical agents such as long-term nonsteroidal anti-inflammatory drug (NSAID) treatment, and bile reflux [1,2]. Nowdays, the importance of Helicobacter pylori infection is increasing as the main causative factor in gastric diseases in humans.…”

Impact of spinal kyphosis on gastroesophageal reflux disease symptoms in patients with osteoporosis

“…Although evidence supports a good safety profile for these agents, numerous gastrointestinal adverse events have been associated with their use [24,25], because oral bisphosphonates must be taken in a fasting state at least 30 min before consuming food or beverages (other than water). Reactive gastropathy has also been estimated to occur in one third to one half of patients taking NSAIDs [26].…”

Gastritis staging in clinical practice: the OLGA staging system

“…[1][2][3][4][5][6] The phenotypic spectrum of chronic gastric inflammation is well established, and the basic distinction between non-atrophic and atrophic patterns is both internationally accepted and consistent. [7][8][9] Atrophy is defined as ''loss of appropriate glands'' and is subtyped into two main histological variants: atrophy resulting from the disappearance of glands and replacement with fibrosis of the lamina propria; and glandular loss resulting from replacement of native glands with metaplastic, ''inappropriate for location'' glandular structures.…”