Medical expert of the article
New publications
Chronic duodenitis - Pathogenesis
Last reviewed: 06.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Pathogenesis of secondary chronic duodenitis
The pathogenesis of primary chronic duodenitis is not completely known. The role of immune mechanisms, disorders of neurohumoral regulation of the duodenal function, and the direct influence of etiological factors on the mucous membrane of the duodenum are assumed.
Pathogenesis of secondary chronic duodenitis
One of the main etiologic factors of secondary chronic duodenitis is Helicobacter infection. Chronic duodenitis usually develops against the background of chronic Helicobacter gastritis and metaplasia of the gastric epithelium in the duodenum. H. pylori colonizes areas of metaplastic gastric epithelium in the duodenum and causes an inflammatory process. The foci of metaplastic epithelium are easily damaged by acidic gastric contents, and erosions develop in the areas of metaplasia. Duodenitis caused by H. pylori is usually localized in the bulb of the duodenum. In gastric ulcer, secondary chronic duodenitis develops as a result of the damaging effect of the aggressive acid-peptic factor and H. pylori on the mucous membrane of the duodenum. In chronic hepatitis and chronic pancreatitis, the development of chronic duodenitis is caused by increased absorption of pancreatic enzymes; decreased secretion of bicarbonates, which contributes to acidification of the duodenal contents and the action of aggressive factors of gastric juice; decreased resistance of the mucous membrane of the duodenum; in diseases of the lungs and cardiovascular system, the development of chronic duodenitis is facilitated by hypoxia of the mucous membrane of the duodenum. In chronic renal failure, the development of chronic duodenitis is caused by the release of toxic products of nitrogen metabolism through the mucous membrane of the duodenum.
Intestinal microflora plays an important role in the development of chronic duodenitis in diseases of the biliary tract. This factor plays a particularly large role in gastric achylia. Dysbacteriosis easily develops under these conditions; the proximal sections of the small intestine, including the duodenum, are populated by bacterial flora unusual for these sections.
Depending on the nature of morphological changes, duodenitis is classified as superficial, diffuse, atrophic and erosive.
In superficial duodenitis, dystrophic changes in the superficial epithelium (flattening and vacuolization of the prismatic epithelium), stromal edema, lymphocytic and plasmacytic cell infiltration are observed.
In diffuse chronic duodenitis, the above-described changes are expressed more significantly. In superficial and diffuse duodenitis, hyperplasia and hypersecretion of the superficial epithelium, an increase in the number of goblet cells, and an increase in their secretory function are observed. The indicated changes should be considered as compensatory-adaptive in response to the impact of aggressive factors that damage the mucous membrane of the duodenum.
In atrophic chronicduodenitis, the mucous membrane is atrophied, thinned, and its villi are flattened.
With erosive duodenitis, single or multiple erosions appear on the mucous membrane of the duodenum.
Depending on the extent of the inflammatory process in the duodenum, a distinction is made between diffuse (total) and local (limited) duodenitis, which includes proximal duodenitis (bulbite), papillitis (inflammation of the major papilla of the duodenum), and distal duodenitis.
[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ], [ 9 ], [ 10 ]