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Results for “Intestinal Polyposis”

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PubMedDate not supplied

[Small intestinal polyposis in Peutz-Jeghers syndrome: combined treatment with surgery and intra-operative endoscopy].

Polyps occur throughout the gastrointestinal tract in Peutz-Jeghers syndrome, but the most serious problems are encountered in the management of small bowel polyposis. We report here on a case of Peutz-Jeghers syndrome admitted to hospital for intestinal obstruction and anaemia. The patient was submitted to colonoscopy, oesophagogastro-duodenoscopy and small bowel enema. At laparotomy, multiple intussusceptions were found and we conducted a combined surgical-endoscopic approach. Most of the polyps were identified and removed endoscopically (snare polypectomy). Five enterotomies were performed to remove 18 very large polyps (> 3 cm). Finally, a limited portion of the jejunal tract (20 cm) was resected owing to the presence of multiple, large, obstructive polyps. None of the polyps showed cancerous transformation. The shortcomings of the traditional surgical approach include repeated small bowel resections and often early reoperation to manage complications caused by polyps missed at the time of previous surgery. If surgical intervention is required, intraoperative endoscopy is always indicated. Conservative surgical management, the role of intraoperative endoscopy, planned medical follow-up and the need for a national registration system are stressed.

Adult↗
PubMed2000

Suppression of intestinal polyposis in Apc(delta 716) knockout mice by an additional mutation in the cytosolic phospholipase A(2) gene.

Arachidonic acid is a precursor for biosynthesis of eicosanoids, including prostaglandins, thromboxanes, leukotrienes, and lipoxins. Cytosolic phospholipase A(2) (cPLA(2)) plays a key role in the release of arachidonic acid as the substrate of cyclooxygenase-1 (COX-1) or COX-2. We found that the level of cPLA(2) mRNA was markedly elevated in the polyps and correlated with the polyp size in the small intestine of the Apc(delta)(716) knockout mouse, a model for human familial adenomatous polyposis. To determine the role of cPLA(2) in intestinal tumorigenesis, we then introduced a cPLA(2) gene mutation into Apc(delta)(716) mice. In the compound mutant mice, the size of the small intestinal polyps was reduced significantly, although the numbers remained unchanged. These results provide direct genetic evidence that cPLA(2) plays a key role in the expansion of polyps in the small intestine rather than in the initiation process. In contrast, colonic polyps were not affected in either size or number. Interestingly, group X sPLA(2) was constitutively expressed in the colon at much higher levels than in the small intestine. These results suggest that in the colon, group X sPLA(2) supplies arachidonic acid in both the normal epithelium and the polyps even in the absence of cPLA(2).

Animals↗
PubMed2003

Cooperation of cyclooxygenase 1 and cyclooxygenase 2 in intestinal polyposis.

Membrane arachidonic acid is converted by cyclooxygenase (COX) into prostaglandin (PG) G(2) and then to PGH(2) which is subsequently metabolized to PGE(2) by PGE synthase (PGES). Both COX-1 and COX-2 play critical roles in intestinal polyp formation, whereas COX-2 is also expressed in cancers of a variety of organs. Likewise, inducible microsomal PGES (mPGES-1) is expressed in several types of cancer, although its role in benign polyp formation has not been investigated. We demonstrated recently that most COX-2-expressing cells in the polyps are stromal fibroblasts. Here we show colocalization of COX-1, COX-2 and mPGES in the intestinal polyp stromal fibroblasts of Apc(Delta 716) mice, a model for familial adenomatous polyposis. Contrary to COX-2 that was induced only in polyps >1 mm in diameter, COX-1 was found in polyps of any size. In polyps >1 mm, not only COX-2 but also mPGES was induced in the stromal fibroblasts where COX-1 had already been expressed. Although polyp number and size were markedly reduced in COX-1 (-/-) or COX-2 (-/-) compound mutant Apc mice, both COX-2 and mPGES were induced in the COX-1 (-/-) polyps, whereas COX-1 was expressed in the COX-2 (-/-) polyps. We found also in human familial adenomatous polyposis polyps that COX-2 and mPGES were induced in the COX-1-expressing fibroblasts. On the basis of these results, we propose that COX-1 expression in the stromal cells secures the basal level of PGE(2) that can support polyp growth to approximately 1 mm, and that simultaneous inductions of COX-2 and mPGES support the polyp expansion beyond approximately 1 mm by boosting the stromal PGE(2) production.

Animals↗
PubMed2001

Suppression of intestinal polyposis in Apc(Min/+) mice by inhibiting nitric oxide production.

Inducible nitric oxide synthase (iNOS) was shown to be expressed in normal mucosa and adenoma of small and large intestines of Apc(Min/+) mice by reverse transcription-PCR and immunohistochemistry. Administration of the iNOS inhibitor aminoguanidine (1.5 g/liter) in drinking water or an L-arginine-deficient diet to Apc(Min/+) mice resulted in a significant decrease in adenoma development in the small but not the large intestine. Similarly, iNOS-gene knockout Apc(Min/+) mice (Apc(Min/+) iNOS(-/-) or Apc(Min/+) iNOS(-/+)) developed significantly fewer adenomas in both small and large intestines than Apc(Min/+) iNOS(+/+) mice. These results suggest that iNOS-selective inhibitors could be used as a potential chemopreventive agent for colorectal cancers.

Adenoma↗
PubMed1989

[Intestinal polyposis in children. Description and differential diagnosis of 2 cases].

The case of a 21-month-old girl with lymphoid nodular hyperplasia and the case of a 9-year-old girl with familial adenomatous polyposis are described. Both patients presented rectal bleeding. A defect of secretory IgA was found in the first patient. In both cases diagnosis was based on medical history, barium enema with aircontrast technique, colonscopy, and endoscopic biopsy. Differential diagnosis and diagnostic procedures in these two diseases are discussed.

Adenomatous Polyposis Coli↗