Enhanced synthesis of Prostaglandins (PGs) has been reported in coeliac disease (CD) and a possible involvement of these substances in the pathogenesis of diarrhoea in coeliac patients has been supposed. The aim of our study was to evaluate Prostaglandin E2 (PGE2) and 6-Ketoprostaglandin F1α (6-Keto-PGF1α) synthesis in small intestinal mucosa of three groups of patients: group A, consisting of 11 children with active CD and total or subtotal mucosal atrophy, group B consisting of 7 children on a gluten free diet for at least 1 year with mild villous atrophy or nornal intestinal mucosa, group C (control) of 6 non-coeliac patients with normal intestinal mucosa. Only 6 children from group A had chronic diarrhoea while children from group B were asymptomatic. Children from group C suffered from failure to thrive; we excluded from this group children who showed diarrhoea. The amounts of PGs generated by intestinal mucosa were measured by a standard method, using a RIA system. In group A PGE2 generation was significantly higher (2052 ± 407, mean ± SE) than in group C (603 ± 140) (p<0.003). Children from group A with chronic diarrhoea and those without this symptom both showed significant higher PGE2 generation (2569 ± 687, 1431 ± 171, respectively) than group C (p<0.02). In group B PGE2 generation was higher (1632 ± 567) but not significantly different from group C. E-Keto-PGF1α generation although higher in group A and B than C did not show any statistically significant variation. Our results indicate that PGE2 generation in CD is not always related to the presence of diarrhoea. Elevated PGs levels in intestinal mucosa in CD may be due to both enhanced synthesis and decreased degradation. Alternatively, as hypothesized by Branski (J Pediatr Gastroenterol Nutr 3,672, 1984), it could be the expression of an adaptative mechanism. This latter hypothesis could explain our results of high PGE2 levels in asyntomatic coeliac children on a gluten free diet. Maybe is necessary a long period of diet before to cease this adaptative mechanism.
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