Coeliac Disease in Children
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Direct answer
Coeliac disease is immune-mediated enteropathy against dietary gluten in genetically susceptible children — over 90 per cent carry HLA-DQ2 and most of the rest DQ8 — producing villous atrophy of the proximal small bowel that recovers on a gluten-free diet. The classic Indian child is a wheat-fed toddler with chronic diarrhoea, abdominal distension, failure to thrive and irritability after weaning onto gluten; the modern child is more often an asymptomatic short stature or refractory iron deficiency picked up on screening. Diagnosis rests on anti-tissue transglutaminase IgA with a total IgA level, confirmed — except in selected high-titre cases — by duodenal biopsies showing villous atrophy, crypt hyperplasia and intraepithelial lymphocytosis. Treatment is lifelong gluten exclusion from wheat, rye and barley.
What you must remember
- Serology of choice: anti-tTG IgA, with total serum IgA measured simultaneously, because IgA deficiency (commoner in coeliac disease) renders the test falsely negative — switch to IgG-based assays such as deamidated gliadin peptide IgG.
- Classic presentation at 6–24 months after gluten introduction: chronic diarrhoea, distension, wasting of buttocks, irritability and failure to thrive; non-classic presentations dominate today — short stature, refractory iron-deficiency anaemia, pubertal delay, rickets and dental enamel defects.
- Screen at-risk groups: type 1 diabetes, Down syndrome, Turner syndrome, selective IgA deficiency, autoimmune thyroiditis and first-degree relatives.
- Biopsy (multiple duodenal plus one bulb specimen, taken while on gluten) shows the Marsh spectrum: intraepithelial lymphocytosis, crypt hyperplasia, villous atrophy —Marsh 3 is the classic lesion.
- ESPGHAN allows a no-biopsy pathway in symptomatic children when anti-tTG IgA exceeds ten times the upper limit of normal, endomysial antibody is positive on a separate sample, and HLA-DQ2/DQ8 is present.
- The treatment: strict, lifelong gluten-free diet — eliminate wheat, rye and barley; uncontaminated oats are generally acceptable; dietitian supervision with micronutrient replacement is standard.
- Serology falls over months on the diet and is used to monitor adherence; symptoms should improve within weeks, and failure to improve demands a search for ongoing gluten exposure first.
- Never test a child already on a gluten-free diet — serology and histology normalise; diagnosis then needs a supervised gluten challenge of several weeks first.
- Long-term risks of untreated disease: osteoporosis, ulcerative jejunitis and small-bowel lymphoma in adulthood, alongside autoimmune thyroid and type 1 diabetes associations.
- Dermatitis herpetiformis — the itchy, vesicular, extensor-surface rash — is the skin counterpart, diagnosed on skin biopsy with granular IgA deposition.
How to work through a case
A four-year-old from a wheat-eating family has dropped from the 25th to below the 3rd centile over a year, with a capricious appetite, occasional loose stools and haemoglobin of 9.6 g/dL with low ferritin. Step one is serology with total IgA: anti-tTG IgA returns seven times the upper limit of normal. Step two is confirmation — at this titre with positive endomysial antibody and an appropriate HLA type, European guidance permits diagnosis without biopsy, though many Indian centres still proceed to endoscopy with multiple duodenal biopsies plus one from the bulb. Step three is treatment and surveillance: dietitian-led gluten exclusion, micronutrient replacement, and repeat serology at six and twelve months, which should fall with recovering height velocity.
The trap case is the child who "feels better gluten-free" and arrives already off wheat for two months with negative serology. There is nothing to test — either accept clinical uncertainty or perform a structured gluten challenge before serology and biopsy. A second trap: the weakly anti-tTG-positive toddler with normal IgA — low-titre positivity occurs in other enteropathies, and the biopsy decides. And screen the unscreened type 1 diabetes or Down syndrome clinic patient: silent coeliac disease is common in both, and the growth chart plus ferritin are where it first shows.
Where students slip
Candidates lose marks by ordering anti-tTG IgA without total IgA, by diagnosing coeliac disease in a gluten-free child with negative serology, and by equating a positive serology alone with disease in low-titre situations where histology is needed. Another favourite slip is listing rice among the foods to avoid — rice, maize and millets are the Indian staples of the gluten-free diet. And forgetting to rescreen growth after treatment misses that first-year catch-up growth is one of the diet's most satisfying confirmations.
Frequently asked questions
Which serological test is first-line and what must accompany it?
Anti-tissue transglutaminase IgA, always with total IgA — selective IgA deficiency is enriched in coeliac disease and causes false-negative results, requiring IgG-based alternatives.
What histology defines coeliac disease on duodenal biopsy?
Villous atrophy with crypt hyperplasia and increased intraepithelial lymphocytes (Marsh 3), taken while still consuming gluten.
When can coeliac disease be diagnosed without biopsy in children?
In a symptomatic child with anti-tTG IgA more than ten times the upper limit of normal, positive endomysial antibody on a separate sample and HLA-DQ2 or DQ8 positivity, per ESPGHAN criteria.
Which grains must be eliminated and which are allowed on a gluten-free diet?
Wheat, rye and barley are eliminated; rice, maize, millets and uncontaminated oats form the substitutes — making Indian rice-based diets relatively adaptable.