The term celiac disease was first used by Gee in 1988; the harmful eff
ects of gluten, the concept of gluten intolerance, and the beneficial
effects of a gluten-free diet were discovered by Dicke in 1950. Nearly
half a century later, celiac disease is still a focus of active inter
est. Although the pathophysiology of celiac disease remains obscure, t
here is strong evidence that humoral and cellular immune factors play
a central role. In addition, a close association has been found betwee
n celiac disease and major histocompatibility genes and molecules on c
hromosome 6. HLA phenotype studies have identified B8, DR3, and/or DR7
in nearly 80% of patients and DQW2 in 90% to 100% of patients. Specif
ic phenotypic differences explain the wide variability in sensitizatio
n to gluten, in clinical symptoms, and in serologic test results. Assa
ys for IgG and IgA antibodies to gliadin, reticulin, and endomysium ha
ve been developed as means of evaluating reactivity to gliadin peptide
s. It has been suggested that the standard diagnostic strategy involvi
ng three intestinal biopsies (before treatment, under a gluten-free di
et, and after a gluten challenge) may no longer be warranted. The anti
body assays have allowed to identify celiac disease in patients with a
typical symptoms, no symptoms, or concomitant diseases (e.g., diabetes
mellitus, seizures). A gluten-free diet should be instituted at diagn
osis. Duration of the gluten-free diet (for a limited time or for life
), long-term acceptance of the diet by patients, whether a full recove
ry can be achieved, the impact of celiac disease on statural growth, a
nd the risk of cancer are issues that continue to cause concern pediat
ricians and gastroenterologists.