Chronic Duodenitis and Malabsorption Syndrome
Inflammatory processes in the small intestine are frequently accompanied by changes in cellular composition. In chronic duodenitis, the epithelium undergoes metaplasia, and the number of goblet cells in the preserved glandular epithelium decreases sharply. The pathologist assesses the grade of inflammation activity by the extent of neutrophil infiltration within the lamina propria. The appearance of numerous eosinophils in the infiltrate is a specific indicator pointing toward allergic reactions, helminthiasis, or tumor growth.
Any severe mucosal injury leads to malabsorption syndrome. This condition impairs the transport of normally digested nutrients, vitamins, and electrolytes from the intestinal lumen across the absorptive epithelium into the lymphatic and blood vessels of the villi.
Malabsorption is divided into three main categories:
- Congenital — characterized by genetic enzymopathies.
- Primary — related to pathology of the absorptive epithelium itself (celiac disease, soy protein-induced enteropathy, tropical and collagenous sprue).
- Secondary — develops due to injury of specific layers or the entire intestinal wall in the setting 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 arises from a deficiency of enzymes that metabolize gluten, a protein found in cereal grains. The pathogenesis is rooted in an individual's sensitivity to gluten, which triggers immunologically mediated alterations in the histoarchitecture and cellular renewal of the mucosa. Clinically, this manifests as diarrhea, wasting, and steatorrhea (fatty stools).
Microscopic findings in celiac disease:
- Villous atrophy — the leading diagnostic feature. In late stages, the mucosa completely loses its villi.
- Architectural remodeling — shortening of the villi is accompanied by hyperplasia of the generative zone (crypts elongate and widen).
- Cellular infiltration — the lamina propria is heavily infiltrated by lymphocytes and plasma cells with an admixture of eosinophils. The number of intraepithelial lymphocytes increases sharply.
Enterocytes themselves suffer at the cellular level. Their microvilli deform, shorten, and lose regularity, resulting in a dramatic reduction in absorptive capacity. Simultaneously, intercellular junctions widen. This critical change represents a breakdown of the epithelial barrier, allowing antigens from the intestinal lumen to freely penetrate the lamina propria.
The prognosis is favorable provided gluten is excluded from the diet. A strict gluten-free diet leads to complete restoration of mucosal architecture and resolution of symptoms.
Whipple's Disease (Intestinal Lipodystrophy)
This is a disease of presumed infectious etiology characterized by systemic involvement with a primary predilection for the small intestine. The causative agent is the bacterium Tropheryma whipplei (a short rod-shaped organism).
Pathomorphological features: The hallmark of the disease is the appearance of clusters of specific macrophages within 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 yield a positive PAS reaction (Periodic Acid–Schiff). The mechanism behind this phenomenon is that bacterial phagocytosis by macrophages is incomplete, causing indigestible material to accumulate intracellularly.
Electron microscopy reveals the Tropheryma whipplei organisms themselves. The bacteria are localized in intercellular spaces, within individual enterocytes, lying freely in the lamina propria, and inside macrophages. An additional subepithelial finding is the accumulation of neutral fats within dilated lymphatic vessels.
Unlike many other enteropathies, Whipple's disease carries a favorable prognosis because it responds exceptionally well to antibiotic therapy.