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Aims-Determine the proportion of infants whose celiac disease (CD) was confirmed in childhood and evaluate their prognosis in adulthood. Patients and methods-The diagnosis of CD was established between 1971 and 1982 in 84 infants based on intestinal biopsy data; a gluten-free diet was prescribed and the cohort followed prospectively. Results-Thirty-six infants were followed less than 5 years. A second biopsy was performed in 25. Mucosa had healed in 13 and remained atrophic in 12. Three children developed partial villous atrophy between 6 and 12 years of age in spite of the gluten-free diet. Forty-five patients underwent a gluten challenge between 5 and 10 years of age: in 41 histological lesions relapsed, in two mucosa remained normal and clinical and immunological relapse developed in two. Among those 45 patients, 18 were examined after 18 years follow-up: the exclusion diet was resumed in four, overt clinical relapse developed in four and four experienced intermittent gastrointestinal disorders. All biopsies performed during a period of normal diet showed villous atrophy (except in one patient) without correlation with clinical symptoms. Conclusion-The diagnosis of celiac disease in infants was confirmed in nearly all cases in childhood. When they reached adulthood, these patients had few symptoms but their histological lesions persisted. These data are in favor of a lifelong exclusion diet.
Aims-Determine the proportion of infants whose celiac disease (CD) was confirmed in childhood and evaluate their prognosis in adulthood. Patients and methods-The diagnosis of CD was established between 1971 and 1982 in 84 infants based on intestinal biopsy data; a gluten- A second biopsy was performed in 25. Mucosa had healed in 13 and remained atrophic in 12. Three children developed partial villous atrophy between 6 and 12 years of age in spite of the gluten-free diet. Forty-five patients underwent a gluten challenge between 5 and 10 years of age: in 41 histological lesions relapsed, in two mucosa remained normal and clinical and immunological relapse developed in two. Among those 45 patients, 18 were examined after 18 years follow-up: the exclusion diet was resumed in four, overt clinical relapse developed in four and four experienced intermittent gastrointestin al-bi disorders. All biopsies performed during a period of normal diet showed villous atrophy (except in one patient) without correlation with clinical symptoms. Conclusion-The diagnosis of celiac disease in infants was confirmed in nearly all cases in childhood. When they reached adulthood, these patients had few symptoms but their histological lesions persisted. These data are in favor of a lifelong exclusion diet.