ГоловнаЗворотній зв'язок

Гастроэнтерология (анг,рус)


Gastritis is a histological diagnosis, although it can sometimes be recognised at endoscopy. 

Acute gastritis 

Acute gastritis is often erosive and haemorrhagic. Neutrophils are the predominant inflammatory cell in the superficial epithelium. Many cases result from aspirin or NSAID ingestion (see Table 1). Acute gastritis often produces no symptoms but may cause dyspepsia, anorexia, nausea or vomiting, haematemesis or melaena. Many cases resolve quickly and do not merit investigation; in others, endoscopy and biopsy may be necessary to exclude peptic ulcer or cancer. Treatment should be directed to the underlying cause. Short-term symptomatic therapy with antacids, acid suppression (e.g. H2-receptor antagonists) or antiemetics (e.g. metoclopramide 10 mg 3 times a day) may be necessary. 

Table 1. Common cause of gastritis   

Chronic gastritis due to Helicobacter pylory infection

The most common cause of chronic gastritis is H. pylori (see Table 1). The predominant inflammatory cells are lymphocytes and plasma cells. Correlation between symptoms and endoscopic or pathological findings is poor. Most patients are asymptomatic and do not require any treatment. Patients with dyspepsia and H. pylori-associated gastritis may benefit from H. pylori eradication.  H. pylori bacterium plays a role in the development of gastric mucosal-associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma also.

The bacterium, initially named Campylobacter pyloridis, is a gram-negative microaerophilic rod found most commonly in the deeper portions of the mucous gel coating the gastric mucosa or between the mucous layer and the gastric epithelium. It is S-shaped and contains multiple flagella. H. pylory produces some enzymes such as urease,  catalase, lipase; also adhesins, platelet-activating factor, VacA, VacC and others. It is strategically designed to live within the aggressive environment of the stomach. Urease produces ammonia from urea,   facilitate essential step in alkalinizing the surrounding pH.  Initially, H. pylori resides in the antrum but, over time, migrates toward the more proximal segments of the stomach. The organism is capable of transforming into a coccoid form, which represents a dormant state that may facilitate survival in adverse conditions. It is possible that the different diseases related to H. pylori infection can be attributed to different strains of the organism with distinct pathogenic features.


The prevalence of H. pylori varies throughout the world and depends largely on the overall standard of living in the region. In developing parts of the world, 80% of the population may be infected by the age of 20, whereas the prevalence is 20–50% in industrialized countries. Two factors that predispose to higher colonization rates include poor socioeconomic status and less education. Other risk factors for H. pylori infection are (1) birth or residence in a developing country, (2) domestic crowding, (3) unsanitary living conditions, (4) unclean food or water, and (5) exposure to gastric contents of an infected individual. Transmission of H. pylori occurs from person to person, following an oral-oral or fecal-oral route.

The particular end result of H. pylori infection (gastritis, PUD, gastric MALT lymphoma, gastric cancer) is determined by a complex interplay between bacterial and host factors.