Celiac disease (gluten enteropathy) is a disease characterized by chronic small bowel mucosal damage developing from an autoimmune response to gluten intake. In genetically HLA-DQ2/DQ8 positive individuals, an immune response is triggered against gliadin in wheat, barley, and rye. Incidence is 0.5-1% with female predominance. Histologically, villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis are diagnostic. The characteristic imaging finding is 'jejunal fold reversal' (jejunoileal fold pattern reversal) — normal jejunal folds decrease while increased folds are seen in the ileal region. CT/MR enterography may show diffuse jejunal wall thickening, mesenteric lymphadenopathy, and increased mesenteric vascularity. Refractory celiac disease and enteropathy-associated T-cell lymphoma (EATL) are important complications.
Age Range
15-55
Peak Age
35
Gender
Female predominant
Prevalence
Uncommon
In celiac disease, the autoimmune response to gliadin (gluten protein) forms the basis of intestinal mucosal damage. HLA-DQ2/DQ8 molecules present deamidated gliadin peptides to T-cells → CD4+ T-cell activation → pro-inflammatory cytokine release (IFN-γ, TNF-α) → epithelial damage. Simultaneously, tissue transglutaminase (tTG) antibodies are produced — both a serological diagnostic marker and an effector of tissue damage. Consequently, villous atrophy develops → absorptive surface area decreases dramatically → malabsorption. Crypt hyperplasia is a compensatory mechanism but cannot provide adequate absorption. On imaging, the 'jejunal fold reversal' phenomenon reflects fold loss in the proximal jejunum due to villous atrophy and fold increase in the ileum due to compensatory hyperplasia — this is the radiological counterpart of the bowel mucosa's adaptive response. Increased mesenteric vascularity (comb sign) reflects vasodilation and neovascularization due to chronic inflammation.
Loss of normally prominent folds in the proximal jejunum and increase of normally sparse folds in the distal ileum — radiological counterpart of mucosal villous atrophy and compensatory hyperplasia. Considered pathognomonic for celiac disease.
Jejunoileal fold reversal on CT enterography — valvulae conniventes (Kerckring's folds) normally prominent in the proximal jejunum are decreased or absent, while folds normally sparse in the distal ileum are increased. This 'fold pattern reversal' is considered the pathognomonic characteristic finding for celiac disease. The jejunum acquires a smooth wall ('featureless') appearance while the ileum becomes prominently folded.
Report Sentence
Jejunoileal fold reversal is observed — fold loss in jejunum and increased folds in ileum — consistent with celiac disease.
Diffuse, symmetric wall thickening (>3 mm) in the jejunum on portal venous phase — submucosal edema may create mural stratification ('target sign'). Thickening is more prominent in the jejunum compared to ileum. Wall enhancement is increased due to mucosal hyperemia. Long-segment involvement and symmetry differ from inflammatory causes.
Report Sentence
Diffuse symmetric wall thickening and submucosal edema in the jejunum are observed, consistent with celiac disease.
Prominent dilation and engorgement of mesenteric vascular structures in the arterial phase — 'comb sign'. Vasa recta (straight vessels) are dilated, appearing as parallel vessels extending perpendicularly from mesentery to bowel wall. This finding reflects the vascular component of the chronic inflammatory condition and is an important supportive finding for celiac disease.
Report Sentence
Increased vascularity and 'comb sign' in the jejunal mesentery are observed, consistent with chronic inflammatory enteropathy.
Mesenteric and retroperitoneal lymphadenopathy on portal venous phase — may be low-density or cavitary. Cavitary lymphadenopathy (central necrosis) is an important complication sign of celiac disease and should raise suspicion for refractory celiac or enteropathy-associated T-cell lymphoma (EATL). Non-cavitary reactive lymphadenopathy is more common and correlates with disease activity.
Report Sentence
Mesenteric lymphadenopathy is observed, consistent with celiac disease; in the presence of cavitary lymph nodes, EATL complication should be excluded.
Jejunal wall thickening and submucosal T2 hyperintensity — edema — on T2-weighted MR enterography images. Compensatory fold increase in the ileum is better visualized on MRI than CT. Mild diffusion restriction may be seen in actively inflamed segments on DWI. Gadolinium-enhanced MR enterography shows mucosal enhancement increase and comb sign.
Report Sentence
Jejunal wall thickening and submucosal T2 hyperintensity on MR enterography are observed, consistent with enteropathy due to celiac disease.
Transient non-obstructive intussusception in the small bowel on CT — 'bowel within bowel' appearance. Frequently seen in celiac patients (15-20%) and generally asymptomatic. Short segment and spontaneously reduces. Etiology is not definitively known but thought to be related to dysmotility and bowel wall edema.
Report Sentence
Transient non-obstructive intussusception in the small bowel is observed, evaluated as a frequent finding in celiac disease.
Criteria
Malabsorption symptoms + positive serology + villous atrophy
Distinct Features
Diarrhea, weight loss, abdominal pain, iron deficiency. Fold reversal prominent on imaging. Dramatic improvement with gluten-free diet.
Criteria
Persistent villous atrophy despite strict gluten-free diet after 6-12 months
Distinct Features
Type I (normal phenotype IEL): good prognosis. Type II (aberrant phenotype IEL): high EATL risk. Cavitary lymphadenopathy, increasing wall thickening, and obstruction should raise suspicion.
Criteria
Enteropathy-associated T-cell lymphoma developing on celiac background
Distinct Features
Newly developed focal wall thickening, mass, or stricture. High risk of ulceration and perforation. Cavitary lymphadenopathy. Increased FDG uptake on PET-CT.
Distinguishing Feature
In Crohn's, skip lesions, asymmetric involvement, and fistula/sinus tracts; in celiac, diffuse symmetric jejunal involvement and fold reversal
Distinguishing Feature
In lymphoma, focal mass or aneurysmal dilation; in celiac, diffuse fold reversal and wall thickening — but EATL complication should be excluded
Distinguishing Feature
In Whipple disease, low-density mesenteric lymphadenopathy ('fat halo' sign) and jejunal fold thickening; in celiac, fold reversal and cavitary lymphadenopathy
Distinguishing Feature
In angioedema, acute onset, drug history, and rapid resolution; in celiac, chronic course, positive serology, and fold reversal
Urgency
routineManagement
medicalBiopsy
NeededFollow-up
6-monthCeliac disease diagnosis is made with serology (anti-tTG IgA, anti-endomysium) and duodenal biopsy (Marsh classification). The foundation of treatment is lifelong gluten-free diet — villous atrophy and symptoms generally improve in 3-6 months. Role of imaging: (1) detect complications (EATL, refractory disease, cavitary lymphadenopathy), (2) evaluate extent of malabsorption, (3) exclude other causes. When cavitary lymphadenopathy or new focal mass is seen, biopsy is required for EATL exclusion. Hyposplenism (splenic atrophy) is common in celiac patients and pneumococcal vaccination is recommended.
Celiac disease is controlled with a gluten-free diet. In refractory cases, the risk of T-cell lymphoma (EATL) and small bowel adenocarcinoma is increased. Serological tests (anti-tTG, anti-endomysium) are used for screening.