首页> 外文期刊>Pediatric Research >PROSTAGLANDINS IN SHALL INTESTINAL MUCOSA OF CHILDREN WITH ACTIVE COELIAC DISEASE AND ON A GLUTEN FREE DIET
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PROSTAGLANDINS IN SHALL INTESTINAL MUCOSA OF CHILDREN WITH ACTIVE COELIAC DISEASE AND ON A GLUTEN FREE DIET

机译:患有主动性小肠疾病和无谷蛋白饮食的儿童小肠黏膜中的前列腺素

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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.
机译:在乳糜泻(CD)中,前列腺素(PGs)的合成得到了增强,据推测这些物质可能与乳糜泻患者的腹泻发病有关。我们研究的目的是评估三组患者小肠粘膜中前列腺素E2(PGE2)和6-酮戊二烯F1α(6-Keto-PGF1α)的合成:A组,由11名活动性CD患儿和全部或次要患儿组成黏膜萎缩,B组由7名儿童接受无麸质饮食,至少1年,伴轻度绒毛萎缩或正常肠黏膜,C组(对照组)为6例正常肠黏膜的非乳糜泻患者。 A组仅6名儿童患有慢性腹泻,而B组则无症状。 C组儿童壮成长;我们排除了出现腹泻的儿童。由肠粘膜产生的PG的量使用RIA系统通过标准方法测量。 A组的PGE2生成量显着高于C组(603±140)(2052±407,均值±SE)(p <0.003)。患有慢性腹泻的A组儿童和没有这种症状的儿童均显示出比C组明显更高的PGE2产生(分别为2569±687、1431±171)(p <0.02)。 B组中PGE2的产生较高(1632±567),但与C组无显着差异。E-Keto-PGF1α的产生虽然在A和B组中均高于C,但无统计学意义。我们的结果表明CD中PGE2的产生并不总是与腹泻的存在有关。 CD肠道粘膜中PGs水平升高可能是由于合成增强和降解降低所致。另外,正如布兰斯基(Branski)(J Pediatr Gastroenterol Nutr 3,672,1984)所假设的那样,它可能是适应性机制的表达。后一种假设可以解释无麸质饮食的无症状腹腔儿童中高PGE2水平的结果。在停止这种适应性机制之前,可能需要长期饮食。

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