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Chronic Duodenitis and Celiac Disease

Duodenitis chronica

For medical students2 min readUpdated 2026-10-10

Chronic duodenitis is a long-standing inflammation of the mucosa in the proximal duodenum. The process is accompanied by impaired cellular renewal, remodeling of histoarchitecture, and the development of gastric metaplasia, which is a crucial step in the pathogenesis of duodenal ulcers.

Main triggers*H. pylori* infection and parasitic infestations (giardiasis, opisthorchiasis).
Antibody isotype switchDuring chronification, the normal IgA plasma cell phenotype shifts to an aggressive IgG phenotype.
"Semolina" signWhitish grains 5–8 mm in size on the mucosa, caused by edema and microcirculatory disturbances.
LipodystrophyAccumulation of neutral fats beneath the epithelium due to lymphatic drainage blockage by macrophages.

Etiology and Immunological Shifts

The primary damaging factor is aggressive gastric content driven by hydrochloric acid hypersecretion (peptic duodenitis). Additional causes include H. pylori infection and helminthic infestations.

Normally, the lamina propria is dominated by lymphocytes and plasma cells with an IgA phenotype. Chronic inflammation induces a phenotypic switch to IgG. Locally formed IgG–antigen immune complexes activate complement, creating a potent chemoattractant for neutrophils. Massive infiltration and apoptosis of neutrophils lead to damage of the villous stroma, deformation, and subsequent atrophy. Concurrently, the surface epithelium undergoes gastric metaplasia, which can subsequently be colonized by Helicobacter.

Morphological Findings and Severity Grades

Macroscopically, the mucosa is unevenly edematous. Hyperemia (elevated areas of 2 cm or larger) and multiple acute or chronic erosions (often 4 or more) are observed. The endoscopic "semolina" phenomenon—whitish lesions 5–8 mm in diameter—is characteristic.

Microscopically, three grades of severity are distinguished:

  1. Grade 1: Histoarchitecture is preserved; the stroma contains a dense lymphoplasmacytic infiltrate with an increased number of intraepithelial lymphocytes.
  2. Grade 2: Villi are shortened and deformed; lymphocytes dominate the lamina propria.
  3. Grade 3: Marked shortening of villi, crypt deepening, hyperplasia of duodenal glands, appearance of erosions, and gastric metaplasia.

Alcian blue staining (pH=2.5) combined with the PAS reaction reveals PAS-positive mucus in the apical part of mucocytes, clearly outlines the brush border of enterocytes, and highlights goblet cells.

Celiac Disease

The primary histological hallmark of celiac disease is pronounced mucosal remodeling. Unlike the normal intestine with tall villi, celiac disease exhibits villous atrophy (flattening) and altered overall mucosal architecture.

Tropheryma whipplei Infection and Malabsorption

Severe small bowel disease can be caused by the Gram-positive actinomycete Tropheryma whipplei. It penetrates from the intestinal lumen into the lamina propria in patients with impaired macrophage function. Due to an inadequate immune response, macrophages rupture, and bacteria enter the microvasculature, causing bacteremia.

Systemic manifestations include fever, polyadenopathy, polyarthritis, uveitis, liver, spleen, CNS involvement (dementia), and cardiac involvement (endocarditis, myocarditis, pericarditis).

The gastrointestinal tract develops malabsorption syndrome, manifested by severe diarrhea, anemia, and cachexia. The mechanism is linked to defective macrophages blocking lymphatic capillaries of the villi. This leads to subepithelial accumulation of neutral fats (intestinal lipodystrophy). Loss of proteins and electrolytes triggers severe complications, such as edema and tetany.

Mnemonic

To quickly remember the grades of duodenitis: 1 — Infiltrate (structure intact), 2 — Deformation (villi shortened), 3 — Defects (erosions, deep crypts, and metaplasia).

Frequently asked questions

What histological features characterize the small intestinal mucosa in celiac disease?

The small intestinal mucosa in celiac disease is characterized by a specific histological triad. Key morphological changes include:

  • Villous atrophy — the leading diagnostic sign, manifesting as shortening of villi up to complete mucosal flattening.
  • Crypt hyperplasia — compensatory elongation and widening of crypts (hyperplasia of the proliferative compartment).
  • Cellular infiltration — a sharp increase in intraepithelial lymphocytes, alongside massive infiltration of the lamina propria by lymphocytes and plasma cells with an admixture of eosinophils.

At the cellular level, enterocyte microvilli are deformed and shortened, and intercellular junctions are widened, leading to epithelial barrier dysfunction.

Which specific antibodies are tested for the serological diagnosis of celiac disease?

For the serological diagnosis of celiac disease using ELISA, specific IgA class autoantibodies are evaluated. The diagnostic panel includes testing for antibodies against three main targets:

  • Tissue transglutaminase (tTG).
  • Endomysium (smooth muscle connective tissue structures).
  • Deamidated gliadin peptides (and gliadin).

A mandatory prerequisite before testing is the preliminary assessment of total serum IgA to rule out false-negative results, as celiac disease frequently coexists with selective IgA deficiency. Blood collection must be performed strictly before the patient initiates a gluten-free diet.

Why do villi break down in chronic duodenitis?

Due to an immune response shift toward the IgG phenotype. Immune complexes form, activating complement which recruits neutrophils. Their massive destruction within the lamina propria damages the villous stroma.

What is the "semolina" phenomenon?

This is an endoscopic sign of duodenitis—whitish grains 5–8 mm in diameter on the mucosal surface. They appear due to marked edema and local microcirculatory disturbances.

How does Tropheryma whipplei cause malabsorption syndrome?

Bacteria are phagocytosed by macrophages, which fail to destroy them due to an immune defect. The accumulation of these macrophages blocks lymphatic drainage, leading to subepithelial fat accumulation and halted nutrient absorption.

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