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At least 19 recordsLinked to original sources
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↗
PubMed1975

[Differentialdiagnosis and surgical treatment of the familial intestinal polyposis (author's transl)].

Between 1959 and 1974 we observed 18 patients with familial intestinal polyposis. 4 patients were from one family. Two brothers refused the operation and died 7 respectively 8 years after diagnosis had been made. The typical symptoms, the diagnostic procedure and the therapy are demonstrated. We prefer the proctocolectomy (eventually with the "Kock-Ileostoma"), because we observed a lot of recidivs after ileorectostomy. The prognosis of the familial intestinal polyposis is good, if the operation is performed early (also in cases of carcinomatosis). Only those patients died, who rejected the operation or were operated too late.

Adolescent↗
PubMed1991

Association between neuroepithelial tumor and multiple intestinal polyposis (Turcot's syndrome): report of a case and critical analysis of the literature.

We report a case of association of a brain tumor with multiple intestinal polyposis (Turcot's syndrome) and offer a critical analysis of the relevant literature with a view to revising the classification of the syndrome in relation to familial multiple polyposis and Gardner's syndrome. For this purpose, we considered only cases of intestinal polyposis associated with a primary neuroepithelial tumor (medulloblastoma, glioma, or glioblastoma) as originally described by Turcot. Differences emerged, depending on the central nervous system tumor type, which suggests that this neoplastic association may be classified as two distinct syndromes.

Adenomatous Polyposis Coli↗
PubMed1960

Clinical and genetic problems in familial in-intestinal polyposis.

The history of a family suffering from familial intestinal polyposis is presented, showing how a delayed onset of symptoms together with a lack of knowledge of affected relatives may obscure the familial nature of the disease. The necessity of examining all accessible relatives, irrespective of their advancing years, is stressed. Further, it is shown that in the absence of any familial incidence the proper diagnosis of an isolated case of polyposis is that the disease is the result of a fresh mutation.The possibility of a non-familial form of this disease cannot be proved at present and will require a special genetic investigation. It is emphasized that the diagnosis of non-familial polyposis should not be made, as this will lead to a relaxation of the vigil that should be kept on the descendants of all patients with polyposis.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Hereditary intestinal polyposis syndromes.

BACKGROUND: Colorectal cancer is one of the most common cancers in the world, with overall mortality exceeding 40% even with treatment. Effective efforts for screening and prevention are most likely to succeed in patient groups identified as high risk for colorectal cancer, most notably the hereditary intestinal polyposis syndromes. In these syndromes, benign polyps develop throughout the intestinal tract prior to the development of colorectal cancer, marking the patient and associated family for precancer diagnosis followed by either close surveillance or preventive treatment. PURPOSE: This review article was undertaken to discuss the most recent developments in the knowledge of hereditary intestinal polyposis syndromes, emphasizing the clinical approach to diagnosis and treatment relative to preventing the development of cancer. RESULTS: The most common of the hereditary polyposis syndromes is familial adenomatous polyposis (FAP), which is characterized by the development of hundreds to thousands of adenomatous polyps in the colon followed at an early age by colorectal cancer. Colorectal cancer can be prevented in this autosomal dominant condition by prophylactic colectomy, though a risk for other tumors, including periampullary cancers, remains throughout life. Variant of FAP associated with fewer and smaller polyps (hereditary flat adenoma syndrome), or even CNS tumors (Turcot's syndrome) also carry this high risk of colorectal cancer. Hereditary hamartomatous polyposis syndromes such as juvenile polyposis and Peutz-Jeghers syndrome (also autosomal dominant) are characterized by less frequent polyps. Though these are generally benign polyps, they are also associated with a significant risk of colorectal and other cancers. Other polyposis syndromes, including neurofibromatosis and Cowden's disease, do not carry this increased risk of colorectal cancer, and therefore affect different treatment strategies. Analysis of genetic factors responsible for these and other hereditary syndromes with predisposition to colorectal cancer has not only contributed to our molecular understanding of colorectal cancer, but opened the door to DNA testing and treatment strategies for these diseases. CONCLUSIONS: The treatment advances that are discussed and careful screening in appropriate families will effectively reduce the risk of death from colorectal cancer.

Adenomatous Polyposis Coli↗
PubMed2001

Acceleration of intestinal polyposis through prostaglandin receptor EP2 in Apc(Delta 716) knockout mice.

Arachidonic acid is metabolized to prostaglandin H(2) (PGH(2)) by cyclooxygenase (COX). COX-2, the inducible COX isozyme, has a key role in intestinal polyposis. Among the metabolites of PGH(2), PGE(2) is implicated in tumorigenesis because its level is markedly elevated in tissues of intestinal adenoma and colon cancer. Here we show that homozygous deletion of the gene encoding a cell-surface receptor of PGE(2), EP2, causes decreases in number and size of intestinal polyps in Apc(Delta 716) mice (a mouse model for human familial adenomatous polyposis). This effect is similar to that of COX-2 gene disruption. We also show that COX-2 expression is boosted by PGE(2) through the EP2 receptor via a positive feedback loop. Homozygous gene knockout for other PGE(2) receptors, EP1 or EP3, did not affect intestinal polyp formation in Apc(Delta 716) mice. We conclude that EP2 is the major receptor mediating the PGE2 signal generated by COX-2 upregulation in intestinal polyposis, and that increased cellular cAMP stimulates expression of more COX-2 and vascular endothelial growth factor in the polyp stroma.

Adenoma↗
PubMedDate not supplied

[Juvenile intestinal polyposis. Importance of the endoscopic diagnostic contribution].

We describe three cases of juvenile intestinal polyposis in children aged 9-13 years. Ulcerative colitis in two of them and Crohn's disease in one of them were initially diagnosed. These subjects came to us for symptom persistence in spite of medical (sulfasalazine and or corticosteroids) and dietetic therapy. Further an appropriate investigations were therefore necessary; endoscopy and histological study of the specimen drawn by fibroscopy were decisive for the diagnosis. The accuracy of the endoscopy is of valuable help in uncertain situations as in those described.

Adolescent↗