Celiac disease is a permanent, immune-mediated intolerance of gluten, the protein found in wheat, barley and rye, that damages the mucosa, the lining of the small intestine. It is treated with diet rather than with drugs, and the diet is not a course. The intolerance is permanent even when the mucosa has healed, so the treatment is lifelong, and most of the clinical work sits in adherence and follow-up rather than in the choice of therapy. The diagnosis behind it — serology, the pathway without biopsy and the biopsy protocol — is set out in Diagnosing Celiac Disease in Children.
The gluten-free diet
Treatment is a strict, lifelong gluten-free diet. The cereals to exclude are wheat and its variants (spelt, kamut), barley, rye and triticale, a wheat–rye hybrid; rice and naturally gluten-free grains are not restricted. The diet is not a matter of reducing gluten. Mucosal inflammation is triggered by very small amounts, so contamination — shared cooking surfaces, flour in the air, sauces thickened with wheat — matters as much as the obvious sources.
A dietitian experienced in celiac disease is part of the treatment, not an optional extra, because the diet is the therapy and its practical details are where adherence is won or lost during childhood and adolescence.
Follow-up and adherence
Follow-up is scheduled rather than symptom-driven, because symptoms are a poor guide once the mucosa has partially healed. The usual framework is clinical review every 6 to 12 months, including growth and pubertal progress, resolution of symptoms and a dietary review, with anti-tTG IgA (the antibody against tissue transglutaminase used at diagnosis) and a blood count, iron, folate, vitamin B12 and liver enzymes.
Adherence monitoring depends on both serology and a direct conversation about the diet. Anti-tTG IgA normalizes over months on a strict diet and is a useful marker of major gluten exposure, but it is not sensitive enough to detect small amounts of gluten; a normal result does not prove the diet is strict. Adolescents are the group at highest risk of abandoning the diet for social reasons, so the review has to ask about the diet directly rather than only measuring antibodies.
Long-term risks, and why the diet is permanent
Long-term risks in celiac disease — a small increase in the risk of enteropathy-associated T-cell lymphoma (a lymphoma arising in the intestinal wall) and other malignancies, reduced bone density and an association with other autoimmune diseases — are the reason the diet is permanent rather than convenient.
The excess risk is associated with continuing gluten exposure and persistent villous atrophy, the flattened intestinal lining of active disease, which is the practical argument for staying on the diet.
The gluten-free diet works because celiac disease has a known trigger that can be taken away. Inflammatory bowel disease, the other chronic disease that often first shows itself in a child as prolonged loose stools, has no equivalent: its cause is unknown, so there is no single dietary trigger to remove.