Etiology and immunological shifts
The main damaging factor is aggressive gastric contents against the background of hydrochloric acid hypersecretion (peptic duodenitis). Additional causes include H. pylori infection and helminthic infestations.
Normally, the lamina propria of the mucosa is dominated by lymphocytes and plasmocytes with an IgA phenotype. In chronic inflammation, the phenotype shifts to IgG. Locally, "IgG-antigen" immune complexes form and activate complement. This creates a potent chemoattractant for neutrophils. Massive death of infiltrating neutrophils leads to damage of the villous stroma, their deformation, and subsequent atrophy. Concurrently, the surface epithelium changes: foci of gastric metaplasia appear, which can later be colonized by Helicobacter.
Morphological picture and grades of severity
Macroscopically, the mucosa is unevenly edematous. Hyperemia is observed (protruding areas of 2 cm or more) and defects in the form of multiple acute and chronic erosions (often 4 or more). The endoscopic "semolina" phenomenon is characteristic — whitish eruptions with a diameter of 5–8 mm.
Microscopically, three degrees of severity are distinguished:
- First degree: histoarchitectonics is preserved, a dense lympho-plasmacytic infiltrate is present in the stroma, and the number of intraepithelial lymphocytes is increased.
- Second degree: villi are shortened and deformed, lymphocytes dominate in the lamina propria.
- Third degree: pronounced shortening of villi, deepening of crypts, hyperplasia of duodenal glands, appearance of erosions and gastric metaplasia.
When staining the micropreparation with Alcian blue (pH=2.5) combined with the PAS reaction, PAS-positive mucus is revealed in the apical part of mucocytes, the brush border of enterocytes is clearly outlined, and goblet cells are visualized.
Celiac disease
The main histological sign of celiac disease is pronounced remodeling of the mucosa. Unlike a normal intestine with tall villi, celiac disease shows their atrophy (flattening) and a change in the overall mucosal structure.
Tropheryma whipplei infection and malabsorption
Severe small intestine lesions can be caused by the Gram-negative bacterium Tropheryma whipplei (taxonomically related to actinomycetes). It penetrates from the intestinal lumen into the lamina propria of the mucosa in patients with impaired macrophage function. Due to the lack of an adequate immune response, macrophages are destroyed, and bacteria enter the microvasculature, causing bacteremia.
Systemic manifestations include fever, polyadenopathy, polyarthritis, uveitis, liver, spleen, CNS (dementia), and heart (endocarditis, myocarditis, pericarditis) involvement.
In the gastrointestinal tract, malabsorption syndrome develops, manifesting as severe diarrhea, anemia, and cachexia. The mechanism is related to the fact that defective macrophages block the lymphatic capillaries of the villi. This leads to subepithelial accumulation of neutral fats (intestinal lipodystrophy). Loss of proteins and electrolytes provokes the development of severe complications — edema and convulsive syndrome.
Briefly: answers to topical questions
What histological signs are characteristic of the small intestinal mucosa in celiac disease?
The small intestinal mucosa in celiac disease is characterized by a specific triad of histological signs. The main morphological changes include:
- Villous atrophy — a leading diagnostic sign manifested by their shortening up to complete flattening of the mucosa.
- Crypt hyperplasia — compensatory elongation and widening of the crypts (hyperplasia of the generative zone).
- Cellular infiltration — a sharp increase in the number of intraepithelial lymphocytes, as well as massive infiltration of the lamina propria by lymphocytes and plasma cells with an admixture of eosinophils.
At the cellular level, deformation and shortening of enterocyte microvilli are noted, as well as widening of intercellular contacts, which leads to disruption of the epithelial barrier.
What specific antibodies are tested for the serological diagnosis of celiac disease?
For the serological diagnosis of celiac disease by enzyme-linked immunosorbent assay (ELISA), specific IgA-class autoantibodies are investigated. The diagnostic panel includes the determination of antibodies to three main targets:
- Tissue transglutaminase (tTG).
- Endomysium (mucosal structures).
- Deamidated gliadin peptides (and gliadin).
A mandatory prerequisite before conducting the study is a preliminary assessment of the total blood IgA level. This is necessary to exclude false-negative results, as celiac disease is often combined with selective IgA deficiency. Blood sampling should be carried out strictly before the patient switches to a gluten-free diet.
For quick memorization of duodenitis grades: 1 — Infiltrate (cellular structure), 2 — Deformation (villi shortened), 3 — Defects (erosions, deep crypts, and metaplasia).
Class and exam questions
Why do villi break down in chronic duodenitis?
Due to the shift in the immune response to the IgG phenotype. Immune complexes are formed, complement is activated, attracting neutrophils. Their massive death in the lamina propria destroys the villous stroma.
What is the "semolina" phenomenon?
This is an endoscopic sign of duodenitis — whitish granules 5–8 mm in diameter on the mucosa. They appear due to pronounced edema and local microcirculation disorders.
How does Tropheryma whipplei cause malabsorption syndrome?
Bacteria are engulfed by macrophages, which cannot destroy them due to an immune defect. The accumulation of such macrophages blocks lymphatic drainage, leading to the accumulation of fats under the epithelium and cessation of absorption.
What else to study on this topic
- Mechanisms of gastric metaplasia development in the intestine
- The role of H. pylori in the pathogenesis of peptic duodenitis
- Histological differential diagnosis of duodenitis stages
- Systemic manifestations of bacteremia in T. whipplei infection
- Pathophysiology of electrolyte loss in malabsorption syndrome
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