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Results for “Intestinal Polyps”

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At least 325 records · Page 18Linked to original sources
PubMed1979

Desmoid tumors and mesenteric fibromatosis in Gardner's syndrome: report of kindred 109.

Kindred 109, from which Gardner's syndrome was first described, now has 224 members, 28 of whom have inherited the syndrome. Among the group of 28, desmoid tumors or mesenteric fibromatosis or both have developed in eight (29%). In four patients, the fibrous dysplasia appeared to originate in postsurgical abdominal incisional scars; in two of these cases, the mesenteric involvement resulted in death. In one patient, the process was present in the mesentery at the original operation. In three patients, the fibrous dysplastic lesions were extraincisional, with no known trauma associated with their occurrence.

Abdominal Muscles↗
PubMed1977

Diet and metabolism: large-bowel cancer.

Epidemiological data demonstrate that colon cancer incidence is associated mainly with high dietary fat consumption. Studies in metabolic epidemiology indicate that high fat intake influences both the amount and type of bile acids and neutral sterols and intestinal microflora acting on these compounds which may contain tumorigenic activity for the colon. This is compatible with the results of studies comparing populations with high or low risk for the colon cancer and patients with colon cancer.

Bacteria↗
PubMed1975

Epidermoid cysts, polyposis coli and Gardner's syndrome.

One hundred and ninety-six members of 15 families with Gardner's syndrome were investigated to determine the type of skin cyst that is part of this syndrome. These were shown to be epidermoid cysts and not pilar cysts or steatocystoma multiplex. They were solitary or multiple and seldom large and disfiguring. The skin cysts often occurred before the intestinal polyps were detectable. The presence of epidermoid cysts in children should be an indication for sigmoidoscopy when the child reaches the age of 14 years, and at 3-yearly intervals thereafter up to the age of 30 years, whether or not there is a family history of polyposis coli. At present it is not possible to say if Gardner's syndrome is the same as, or different from, familial polyposis. Until all patients with colonic polyps have a full clinical examination, looking for skin cysts and osteomas, X-rays of the skull and long bones to detect osteomas and dental X-rays for abnormalities of the teeth this question will remain unanswered.

Adolescent↗
PubMed1976

Efforts in cancer diagnosis: national task forces--large bowel cancer.

Current information from the National Large Bowel Cancer Project and other sources is given concerning new leads and avenues of research that may be used in early diagnosis or possibly in monitoring therapy. The search for biological markers has developed in two general directions: (1) to identify by genetic studies patients with a high probability of developing cancer who will provide insight into biochemical changes as premalignant lesions develop into frankly developed cancer, and (2) to fine differences between tissue and body fluid constituents in normal subjects and patients with cancer. Screening for colon cancer is discussed with a selective diagnostic approach and with emphasis on this approach in early diagnosis of asymptomatic high risk patients.

Adult↗
PubMedDate not supplied

Molecular biology of gastric cancer.

Gastric cancer involves changes in multiple oncogenes and multiple suppressor genes, and it causes genetic instability. Aberrant expression and amplification of the c-met gene, inactivation of the p53 gene, and CD44 abnormal transcripts are common events of both well differentiated and poorly differentiated gastric cancers. Amplification of the cyclin E gene is also observed in gastric cancer regardless of histologic type. Decreased expression of the pic1 (p21) gene occurs independent of the p53 mutations. In addition, K-ras mutations, c-erbB-2 gene amplification, loss of heterozygosity (LOH) and mutations of the APC gene, LOH of the bcl-2 gene, and LOH at the DCC locus are preferentially associated with well differentiated gastric cancer. Moreover, LOH on chromosome 1q is involved in the progression of well differentiated cancer. Precancerous lesions, including hyperplastic polyp, intestinal metaplasia, and adenoma, share genetic changes found in well differentiated cancers. Conversely, genetic instability may be involved in the first step of stomach carcinogenesis of the poorly differentiated type. Reduction or loss of cadherin and catenins, K-sam gene amplification, and c-met gene amplification are necessary for the development and progression of poorly differentiated or scirrhous carcinoma. Interaction between cell-adhesion molecules in the c-met expressed tumor cells and hepatocyte growth factor from stromal cells is implicated in the morphogenesis of two types of gastric cancer.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1976

[The surgical treatment of villous tumours of the large bowel (author's transl)].

The treatment of 12 patients with villous tumours of the rectum is described. In benign lesions a sphincter conserving operation should be employed. With the technique of submucosal local excision per anum which was described by A.G. Parks it is possible to remove large villous tumours of the rectum. If there is malignant change with invasion of the muscularis muscosae which is found in about 20% of the cases resection therapy is necessary.

Aged↗
PubMed1977

[Reversal of small bowel segments to delay intestinal passage after total colectomy (author's transl)].

Five female mini-pigs underwent total colectomy including resection of the ileocecal valve. Sparing the terminal rectum, we reformed an end-to-end anastomosis between terminal ileum and remaining rectal cuff. In a second series 8 female mini-pigs have been colectomized using the same model. To delay intestinal passage, in addition a 10-12 cm long reversed segment of terminal ileum has been inserted between small bowel and rectal stump. Both groups were compared with a group of normal unoperated mini-pigs in a study up to 1 year, observing intestinal transit time, blood chemistry and general development of the animals. It could be proved that the reversal of a small bowel segment in colectomized animals leads to a prolongation of the intestinal transit time, to normalization of electrolytes and general appearance. Colectomy was only survived by animals with a reversed segment. The clinical application of a reversed small bowel segment following total colectomy in 1 patient was successful.

Adult↗
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↗