Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intestinal Polyps”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1989

Angiodysplasia. Natural history and efficacy of therapeutic interventions.

Angiodysplasia, a disease for which the optimal treatment is uncertain, is a frequent cause of lower intestinal bleeding among older patients. To study the natural history of angiodysplasia and compare the efficacy of medical therapy, endoscopic electrocoagulation, and surgery, the course of 101 patients evaluated from 1974 through 1983 at the Massachusetts General Hospital was reviewed. Angiodysplasia caused bleeding that ranged from occult blood in stools to massive hemorrhage and was also observed incidentally in nonbleeding patients. Patients were followed for up to 10 years (mean of 22 months). Rebleeding was defined as evidence of hemorrhage requiring hospital admission, transfusion, or surgery. Thirty-one patients were treated surgically, 19 patients were treated endoscopically, and 36 patients were treated medically. Using life table analysis we observed similar rebleeding rates among medically and endoscopically treated groups. The surgically treated group had a frequency of rebleeding less than half that of the other groups (P = 0.15). A multivariate regression analysis failed to identify any factors other than coagulopathy to explain the different incidence of rebleeding in the patients treated by endoscopic electrocoagulation and surgery.

Diverticulum↗
PubMed1985

The role of bile acids in colonic carcinogenesis.

Several line of evidence suggest that bile acids may be implicated in the pathogenesis of colonic cancer. A high consumption of fat and animal protein and a low dietary intake of fiber have been shown to be related to the incidence of colonic cancer. From these epidemiologic observations the hypothesis was proposed that the correlation between diet and colon cancer might be explained by the involvement of bile acids. Populations at a high risk of developing cancer were shown to have an increased excretion both of total and bacterially modified bile acids in their feces. Animal studies demonstrated a cocarcinogenic effect of bile acids and experimental diets containing large amounts of fat did not only induce an increased bile acid excretion but also an enhanced tumor formation in the colon. Furthermore, microbial in vitro tests showed a comutagenic activity of secondary bile acids. However, case control studies comparing the fecal bile acid excretion pattern in colonic cancer patients and control subjects failed to show such a clear relationship, which might be explained by rather similar dietary habits within one population and individual differences in sensitivity to environmental factors contributing to the tumor development. Cholecystectomy, leading to an increased exposure of bile acids to the intestinal microflora, has been suggested as a predisposing factor for the development of colonic cancer, but the results of experimental and epidemiologic studies so far are rather inconsistent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Clinical and roentgen features of the intestinal polyposis syndromes.

The intestinal polyposis syndromes represent a challenging diagnostic problem for the radiologist. These syndromes include: familial multiple polyposis, Gardner's, Peutz-Jeghers, Turcot's, Cronkhite-Canada and juvenile polyposis. The polyposis syndromes can usually be differentiated from one another on the basis of the clinical history, examination of the mucocutaneous tissues and roentgen findings. Numerous other conditions, however, may mimmic a polyposis syndrome, and must be considered in the differential diagnosis.

Adolescent↗
PubMedDate not supplied

Concurrent colonic carcinoma and small-bowel carcinoid tumor. Case reports and review of the literature.

Recent reviews stressing the existence of synchronous and metachronous noncarcinoid neoplastic lesions in the same segment of an organ stimulated a review of experience with simultaneous small-bowel carcinoids and colonic carcinoma. Four cases of colonic malignancy associated with small-bowel carcinoid are presented. Included are cases with multiple carcinoids and concurrent multiple carcinomas; two metachronous carcinomas with subsequent ileal carcinoids, and three cases explored for colonic carcinoma with the discovery of incidental ileal carcinoids. There are few reports describing this variety of situations. The occurrence of concurrent malignant lesions, particularly more than one metachronous lesion in primary carcinoid cases, is uncommon.

Adenocarcinoma↗
PubMed1983

Background mucosal changes of primary advanced large intestinal cancer in patients without familial polyposis coli.

In 337 cases of primary advanced large intestinal cancer in patients without familial polyposis coli, the risk factor for cancer was discussed chiefly from the background mucosa surrounding and apart from the cancers. The following findings were obtained: (1) in the mucosa surrounding cancers, adenoma was seen in 23 cases (6.8 per cent), adenomatous changes of the basal cells in 211 cases (62.6 per cent), and hyperplastic glands in 167 cases (49.6 per cent), (2) in the mucosa at least 10 mm from the cancers, adenoma, adenomatous changes of the basal cells, and hyperplastic glands were seen in 42 cases (12.5 per cent), 129 cases (38.3 per cent), and 40 cases (11.9 per cent), respectively. Therefore, it is suggested that microscopic adenoma and adenomatous changes of the basal cells might be a sign of premalignancy in patients without familial polyposis coli.

Adenocarcinoma↗
PubMed1977

Experimental carcinogenesis in the resected colon of the rat.

Until now, carcinoma of the large intestine resected previously for benign disease has not been published. However an increasing number of patients resected for Crohn's disease, diverticulitis or trauma may reach nowadays a high lifespan. On the other hand, it is known that the gastroenteral anastomosis is predisposed to cancer development. In this study, the question of whether the large intestine following colotomy or ileotransversostomy is sensitive to carcinogenesis is examined. Male Wistar rats, subjected to colotomy or resection and ileotransversostomy, were treated weekly by subcutaneous injection of 1,2-dimethylhydrazine (12 mg/kg body weight) for seven weeks. The animals were killed 54 weeks after the first injection. At autopsy, 21 out of 29 operated rats had developed adenocarcinomas of the remaining colon. Intact control animals had the same incidence of malignant degeneration of the large bowel. When the anastomosis is chronically irritated by inflammation or by formation of a diverticulum, development, of carcinoma near the stoma was observed. This was the case in three rats of 28 animals. The results demonstrate that the resected colon of the rat is not more sensitive to experimental carcinogenesis than the intact one.

Adenocarcinoma↗
PubMed2003

Exclusion of Madh2, Madh4, and Madh7 as candidates for the modifier of Min 2 (Mom2) locus.

We recently identified the Modifier of Min 2 (Mom2) locus. Mom2 is a new modifier of intestinal tumorigenesis that resulted from a spontaneous mutation in a B6 Apc(Min)/+ mouse. The presence of one resistant Mom2(R) allele results in a significant reduction in small intestinal polyp number and colon polyp incidence in Apc(Min)/+ mice. Through linkage analysis, we previously localized Mom2 to a 14-cM region on mouse Chromosome (Chr) 18, distal to the Apc gene. This region is syntenic with human Chr 18q, which frequently undergoes loss of heterozygosity (LOH) in several human cancers, including colorectal cancer. Residing in this region are the Madh2 and Madh4 genes, which have both been implicated in human colorectal cancer. Based on meiotic recombinations within the Mom2 region in the derivation of our congenic animals, we have narrowed the location of the Mom2 locus and excluded Madh2, Madh4, and Madh7, as well as Mbd1, Mbd2, Dcc, and Tcf4, as candidates for the Mom2 gene.

Alleles↗
PubMed1998

Ruby laser therapy for labial lentigines in Peutz-Jeghers syndrome.

UNLABELLED: Some patients with Peutz-Jeghers syndrome may be disturbed by the appearance of lentigines. Such patients require management of their lentigines as well as their gastro-intestinal polyps. We describe ruby laser therapy of labial lentigines in two children with Peutz-Jeghers syndrome. The response to treatment was excellent and no sequelae or recurrence of the lesions was noted. CONCLUSION: Our experience suggests that ruby laser therapy is safe and a suitable approach for the treatment of labial lentigines in children with Peutz-Jeghers syndrome.

Child↗