Small intestine diseases

Chronic duodenitis and malabsorption syndrome

Inflammatory processes in the small intestine are often accompanied by changes in cellular composition. In chronic duodenitis, the epithelium undergoes metaplasia, and the number of goblet cells in the remaining glandular epithelium of the villi drops sharply. The pathologist assesses the degree of inflammation activity by how heavily the lamina propria is infiltrated by neutrophilic leukocytes. If a large number of eosinophils appear in the infiltrate, this is a specific signal indicating allergic reactions, helminthic invasion, or tumor growth.

Any serious mucosal damage leads to malabsorption syndrome. This is a condition in which the transport of normally digested nutrients, vitamins, and electrolytes from the intestinal lumen through the absorptive epithelium into the lymphatic and blood vessels of the villi is impaired.

There are three main groups of malabsorption:

• Congenital — characterized by genetic enzymopathy.
• Primary — associated with the pathology of the absorptive epithelium itself (celiac disease, soy enteropathy, tropical and collagenous sprue).
• Secondary — develops when individual layers or the entire intestinal wall are damaged against the background of other diseases (Whipple's disease, Crohn's disease, tuberculosis, scleroderma, amyloidosis, lymphomas, common variable immunodeficiency, and selective IgA deficiency).

Celiac disease (gluten-sensitive enteropathy)

The disease occurs due to a deficiency of enzymes that metabolize gluten, a protein found in cereal grains. The pathogenesis is based on individual sensitivity to gluten, which triggers immunologically mediated disorders of the histoarchitecture and cellular renewal of the mucosa. Clinically, this manifests as diarrhea, wasting, and steatorrhea (fatty stools).

Microscopic picture of celiac disease:

1. Villous atrophy — the leading diagnostic sign. By the end stage of the disease, the mucosa completely loses its villi.
2. Structural remodeling — shortening of the villi is accompanied by hyperplasia of the proliferative zone (crypts lengthen and widen).
3. Cellular infiltration — the lamina propria is massively infiltrated by lymphocytes and plasma cells with an admixture of eosinophils. The number of intraepithelial lymphocytes increases sharply.

At the cellular level, the enterocytes themselves suffer. Their microvilli are deformed, shortened, and lose their regularity, leading to a sharp decrease in absorptive capacity. At the same time, intercellular junctions widen. This critical change signifies a disruption of the epithelial barrier: antigens from the intestinal lumen freely penetrate into the lamina propria.

The outcome of the disease is favorable provided gluten is excluded from the diet. A strict gluten-free diet leads to complete restoration of the mucosal structure and disappearance of symptoms.

Whipple's disease (intestinal lipodystrophy)

This is a disease of presumed infectious etiology, characterized by systemic involvement with a predominant localization in the small intestine. The causative agent is the bacterium Tropheryma whipplei (a short rod-shaped species).

Pathomorphological features: The key feature of the disease is the appearance of clusters of specific macrophages in the lamina propria of the small intestine, mesentery, and regional lymph nodes. These are large polygonal cells with foamy cytoplasm containing lipid vacuoles.

Upon histological examination, the contents of these macrophages give a positive PAS reaction (PAS-positive). The mechanism of this phenomenon is that the phagocytosis of bacteria in macrophages is incomplete, and indigestible material accumulates inside the cell.

Electron microscopy makes it possible to detect the causative agent Tropheryma whipplei itself. The bacteria are localized in the intercellular spaces, inside individual enterocytes, lie freely in the lamina propria, and inside macrophages. An additional subepithelial change is the accumulation of neutral fats in dilated lymphatic vessels.

Unlike many other enteropathies, Whipple's disease has a good prognosis because it responds very well to antibiotic therapy.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of epithelial barrier disruption in gluten-sensitive enteropathy
• Secondary malabsorption syndrome: pathogenesis in Crohn's disease and amyloidosis
• Electron microscopic picture of enterocytes in celiac disease
• The role of incomplete phagocytosis in the pathogenesis of Whipple's disease

Other topics in the «Digestive System Diseases» section

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