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PubMed1995

[Peliosis hepatitis during intestinal lymphomatous polyposis treated with chemotherapy and radiotherapy. Regression after antibiotic therapy].

We report a case of regressive peliosis hepatis, which occurred in a 55 year-old woman with diffuse intestinal lymphomatous polyposis in remission after treatment with chemotherapy and radiotherapy, and which was cleared after one month treatment with erythromycin. The Warthin-Sarry stain, performed to identify a specific agent such as Rochalimaea quintana and henselae, was negative, and the polymerase chain reaction technique could not be performed. Regressive cases of peliosis hepatis are rare, and 4 out of 7 have been reported after antibiotic treatment. Two of them were observed after an antibiotic regimen with erythromycin in patients with HIV disease, and the bacilli Rochalimaea quintana and henselae were identified in liver tissue with Warthin-Starry stain and polymerase chain reaction technique. The observation and the regressive cases recently reported elsewhere, suggest that appropriate antibiotic treatment should be proposed when peliosis hepatis occurs.

Anti-Bacterial Agents↗
PubMed2006

Multiple intestinal lymphomatous polyposis in a Jindo dog.

A male, 5-year-old Jindo dog underwent enterectomy and enteroanastomosis due to ileus of the intestine at a local veterinary hospital. Grossly, the excised intestine showed markedly thickened multinodular masses in the serosal layer of the upper part, and soft-to-firm, cream-colored neoplastic masses that displayed extensive nodular mucosal protuberances into the lumen. The neoplastic masses were filled with large round cells that were ovoid in shape and they had pale and/or hyperchromatic nuclei. The neoplastic cells had mainly infiltrated into the mucosal and submucosal layers, and they had diffusely invaded the muscular and serosal layers. Therefore, the diagnosis of canine multiple intestinal malignant lymphomatous polyposis was made based on the gross and histopathological findings. The origin of these tumor cells was determined to be B-cells since they were positive for anti-CD20.

Animals↗
PubMed1979

Involvement of small intestine in familial polyposis coli.

Extracolonic intestinal manifestations of familial polyposis coli have been described in recent years, but the exact frequency is still unknown. To date the more common sites of extracolonic polyposis appear to be stomach and duodenum with true adenomas being somewhat rare in jejunum and ileum. The authors report a further two cases of ileal polyposis in siblings from a family with familial polyposis coli and conclude that this condition cannot be considered as a disease exclusively of the large bowel. They emphasize that examination of the upper gastrointestinal tract and small bowel must be included in the investigation and follow-up of patients with familial polyposis coli.

Adult↗
PubMedDate not supplied

Prevention of intussusception in Peutz-Jeghers syndrome.

Peutz-Jeghers syndrome is a familial disease characterized by mucocutaneous pigmentation and intestinal polyposis. Small-intestinal intussusception is a common complication. Preservation otion technique to prevent intussusception is described.

Humans↗
PubMed1982

Abnormal sensitivity of skin fibroblasts from familial polyposis patients to DNA alkylating agents.

Fibroblast cell strains derived from different patients all afflicted with genetic predisposing to the development of intestinal polyposis and cancer were tested for their sensitivity to the lethal effects of the DNA alkylating agents methylmethanesulfonate (MMS), ethyl methanesulfonate, N-methyl-N'-nitro-N-nitrosoguanidine, and 4-nitroquinoline 1-oxide. The genetic syndromes studied were: (a) adenomatosis of the colon and rectum only, an autosomal dominant trait; (b) Turcot's syndrome, a rare autosomal recessive polyposis syndrome also characterized by central nervous system tumors; and (c) Gardner's syndrome, an autosomal dominant syndrome which, in addition to intestinal polyposis, is also clinically characterized by osteomas and soft tissue tumors. Survival (relative clone-forming ability) of the various polyposis fibroblast strains was compared to the average survival of three normal human fibroblast strains by t test analysis of the respective values for the inverse of the slope of the survival curve (D0) and the concentration resulting in 10% survival (D10) with p less than 0.05 considered significant. Fibroblasts from the patient with adenomatosis of the colon and rectum (strain GM2355) were moderately but significantly sensitive to 4-nitroquinoline 1-oxide with D0 and D10 values of 0.069 microM (p less than 0.05) and 0.15 microM (p = 0.01), respectively, compared with the normal values of 0.10 microM and 0.26 microM. In addition, strain GM2355 was significantly more sensitive to ethyl methanesulfonate based on D10 comparison only, 24 mM versus the normal average D10 of 28 mM (p less than 0.05). Fibroblasts from the patient with Turcot's syndrome were hypersensitive to MMS, having a D0 value of 0.24 mM (p less than 0.01) versus the normal average D0 of 0.36 mM and a D10 value of 0.95 mM (p less than 0.01) compared with the normal average value of 1.3 mM. Fibroblasts from the Gardner's syndrome proband were moderately sensitive to MMS, ethyl methanesulfonate, and N-methyl-N'-nitro-N-nitrosoguanidine due to significant differences of D10 values of 0.60 mM (p less than 0.01), 15 mM (p less than 0.01), and 4.8 microM (p less than 0.025), respectively, versus the normal average values of 1.3 mM, 28 mM, and 9.4 microM. Fibroblasts from the clinically affected Gardner's syndrome daughter of the proband were significantly more sensitive to MMS treatment, D0 of 0.22 mM (p less than 0.01) versus the normal average D0 of 0.36 mM and a D10 of 0.97 mM (p less than 0.01) versus the normal average. This differential sensitivity to the several DNA alkylating agents suggests that different mechanisms of hypersensitivity to these chemicals may be associated with fibroblasts from the various forms of familial polyposis.

4-Nitroquinoline-1-oxide↗
PubMed1996

Frequency of congenital hypertrophy of the retinal pigment epithelium in familial adenomatous polyposis.

Congenital hypertrophy of the retinal pigment epithelium is a recognized clinical marker in familial adenomatous polyposis as an expression of the altered gene in this autosomal dominant disease. Ocular lesions could be discovered years before the development of intestinal polyposis. We studied 29 diagnosed patients, 38 relatives (first degree) of familial adenomatous polyposis kindreds and 26 controls (general population). Number, size and bilaterality of pigmented lesions were analysed in order to separate members affected and non affected by intestinal polyposis in familial adenomatous polyposis kindreds. Three of 26 families (23%) had patients with polyposis and normal fundus. Bilaterality and more than 4 lesions improved specificity or sensibility of the fundus examination. However, the best efficacy of the test was obtained with large lesions (sensibility 0.82 and specificity 0.97).

Adenomatous Polyposis Coli↗
PubMed1990

Ovarian sex cord tumor with annular tubules and Peutz-Jeghers syndrome.

A case of ovarian sex cord tumor with annular tubules (SCTAT) is described in a patient with Peutz-Jeghers syndrome. The patient had undergone surgery at age 19 years for intestinal invagination caused by intestinal polyposis, and the subsequently had seven pregnancies. Of the four children surviving at the time of this study, all had intestinal polyposis. The ovarian tumor was discovered during a routine examination, although the patient had suffered moderate menstrual disorders and hypermenorrhea for several months previously. Eight years after surgery the patient remains free of symptoms. A review of the bibliography shows that sex cord tumors with annular tubules are very rare. Initially described by Scully in 1970, these usually benign tumors appear frequently in patients with Peutz-Jeghers syndrome. They are considered to originate from granulosa cells, and grow in patterns reminiscent of Sertoli cells.

Adult↗
PubMedDate not supplied

Small-intestinal involvement in familial polyposis diagnosed by operative intestinal fiberscopy: report of four cases.

Operative intestinal fiberscopy, in which the duodenal fiberscope was introduced during laparotomy for colectomy in familial polyposis via the enterotomy opening, permitted the demonstration of small intestinal polyps in six of seven consecutive cases. Four of the six patients had adenomatous polyps in the proximal jejunum, including one patient with the concomitant presence of ileal adenomas. Polyposis due to lymphoid hyperplasia in the terminal ileum was found in three patients. Preoperative upper gastrointestinal surveys revealed adenomas in the duodenums of all seven patients, adenomas in the gastric antrum in three, and multiple hamartomas in the gastric corpus in two. Thus, in familial polyposis or Gardner's syndrome, more or less the entire gastrointestinal tract seems to be involved and the term "gastrointestinal polyposis" seems to describe these conditions.

Adenoma↗
PubMed1995

Malignant potential in intestinal juvenile polyposis syndromes.

BACKGROUND: Unlike familial polyposis coli, where the premalignant nature of adenomatous polyps is well established, the cancer risk in juvenile polyposis has generally been considered not increased. METHODS: This study reviews all cases of juvenile polyposis reported in the English language to date to assess the occurrence and prognosis of carcinoma in the gastrointestinal tract. RESULTS: A total of 218 patients met the inclusion criteria. Mean age at diagnosis was 18.5 years (range: 9 months to 67 years). No gender preference was identified. The most common presenting symptom was chronic anemia, followed by acute gastrointestinal bleeding, rectal prolapse of polyp, protein-losing enteropathy, and intussusception. A family history of juvenile polyposis could be established in approximately 50% of patients, and associated congenital malformations were detected in 15%. Ninety-nine patients underwent 138 gastrointestinal operations: 121 colorectal, 12 gastric, and 5 small intestinal procedures. The development of a gastrointestinal carcinoma was reported in 36 cases (17%). Mean age at diagnosis of carcinoma was 35.5 years (range: 4-60 years). Most malignancies were located in the distal colon and rectum, with only one case of gastric and one case of duodenal carcinoma. Tumor stage at diagnosis was usually advanced, with poor survival figures. CONCLUSIONS: This study shows that juvenile polyposis syndromes carry a more significant risk of carcinoma than generally appreciated. Therefore, more intense endoscopic surveillance may be warranted, and definitive surgical options should often be considered in these syndromes.

Adolescent↗
PubMed1995

Effects of docosahexaenoic acid (DHA) on intestinal polyp development in Apc delta 716 knockout mice.

Epidemiological studies and animal experiments show an association of dietary intake of fish oils and low incidence of several types of cancers. The active ingredients of fish oils appear to be polyunsaturated fatty acids of omega-3 type such as eicosapentaenoic acid and docosahexaenoic acid (DHA). We have investigated chemopreventive effects of DHA on mouse intestinal polyposis using adenomatous polyposis coli (Apc) gene knockout mice. Damage to the human APC gene is responsible for not only familial adenomatous polyposis but also many sporadic cancers of the entire digestive tract. Using homologous recombination in embryonic stem cells, we recently constructed gene knockout mice containing a truncation mutation in the Apc gene at codon 716 (Apc delta 716). The heterozygous mice developed numerous intestinal polyps, and all microadenomas dissected from the earliest polyps had already lost the wild-type allele, indicating the loss of heterozygosity [Oshima et al. (1995), Proc. Natl Acad. Sci. USA, 92, 4482-4486]. We fed Apc delta 716 heterozygotes with AIN-76A purified diet containing 3% DHA for 7 weeks, and scored the number and size of intestinal polyps. Average DHA intakes per day were 4.1 and 4.3 g/kg body wt for males and females, respectively. DHA-fed females had only 31% of polyps compared with the control females that developed about 220 polyps, whereas DHA-fed females showed no significant decrease in the polyp number. As for the polyp size, the proportion of larger polyps decreased more significantly in females than in males. This is the first demonstration that DHA inhibits intestinal polyposis induced by an Apc mutation at both its formation and growth.

Animals↗
PubMed2006

Peutz-Jeghers syndrome: clinicopathology and molecular alterations.

Peutz-Jeghers syndrome (PJS, OMIM 175200) is an unusual inherited intestinal polyposis syndrome associated with distinct peri-oral blue/black freckling. Variable penetrance and clinical heterogeneity make it difficult to determine the exact frequency of PJS. PJS is a cancer predisposition syndrome. Affected individuals are at high risk for intestinal and extra-intestinal cancers. In 1997, linkage studies mapped PJS to chromosome 19p, and subsequently a serine/threonine kinase gene defect (LKB1) was noted in a majority of PJS cases. A phenotypically similar syndrome has been produced in an LKB1 mouse knockout model. Several PJS kindred without LKB1 mutations have been described, suggesting other PJS loci. The management of PJS is complex and evolving. New endoscopic technologies may improve management of intestinal polyposis. Identification of specific genetic mutations and their targets will more accurately assess the clinical course, and help gage the magnitude of cancer risk for affected individuals.

Humans↗
PubMed2006

Proinflammatory CD4+ CD45RB(hi) lymphocytes promote mammary and intestinal carcinogenesis in Apc(Min/+) mice.

Cancers of breast and bowel are increasingly frequent in humans. Chronic inflammation is known to be a risk factor for these malignancies, yet cellular and molecular mechanisms linking inflammation and carcinogenesis remain poorly understood. Here, we apply a widely used T-cell transfer paradigm, involving adoptive transfer of proinflammatory CD4+ CD45RB(hi) (T(E)) cells to induce inflammatory bowel disease (IBD) in mice, to investigate roles of inflammation on carcinogenesis in the Apc(Min/+) mouse model of intestinal polyposis. We find that transfer of T(E) cells significantly increases adenoma multiplicity and features of malignancy in recipient Apc(Min/+) mice. Surprisingly, we find that female Apc(Min/+) recipients of T(E) cells also rapidly develop mammary tumors. Both intestinal polyposis and mammary adenocarcinoma are abolished by cotransfer of anti-inflammatory CD4+ CD45RB(lo) regulatory lymphocytes or by neutralization of key proinflammatory cytokine tumor necrosis factor-alpha. Lastly, down-regulation of cyclooxygenase-2 and c-Myc expression is observed coincident with tumor regression. These findings define a novel mouse model of inflammation-driven mammary carcinoma and suggest that epithelial carcinogenesis can be mitigated by anti-inflammatory cells and cytokines known to regulate IBD in humans and mice.

Adenocarcinoma↗
PubMed2001

A solitary gastric Peutz-Jeghers type polyp: report of a case.

Peutz-Jeghers type polyps of the stomach are rare and almost always associated with intestinal polyposis and mucocutaneous pigmentation; a condition known as Peutz-Jeghers syndrome. The case presented in this report refers to a woman found to have a large solitary Peutz-Jeghers type polyp of the stomach, with a maximal diameter of 7cm. Extended investigation did not reveal intestinal polyposis or any other sign of Peutz-Jeghers syndrome. Because of the size of the polyp, a partial gastrectomy was performed. To the best of our knowledge, there are only three other reports in the literature of a solitary Peutz-Jeghers type gastric polyp occurring in the absence of Peutz-Jeghers syndrome. This patient is scheduled to undergo a follow-up examination every 2 years to detect any sign of the development of Peutz-Jeghers syndrome or malignancies commonly associated with it.

Female↗
PubMedDate not supplied

[Gardner's syndrome].

Gardner's syndrome is a dominant, familial cancer syndrome. It is characterized by intestinal polyposis, multiple osteomas, especially of the skull, and various soft tissue tumors (such as epidermal cysts or desmoid tumors). Late age of onset is the main feature distinguishing it from other polyposis syndromes. The risk of malignancies developing during adult life is virtually 100%, and colectomy is mandatory. Since extracolonic manifestations are very often the first symptoms seen by the physician, it is very important to know that they are indicative of Gardner's syndrome and associated with intestinal polyposis.

Adult↗
PubMed1994

Familial juvenile polyposis. Study of a kindred: evolution of polyps and relationship to gastrointestinal carcinoma.

Familial juvenile polyposis is a rare intestinal polyposis that has recently been associated with gastric and colonic adenocarcinoma. The authors report a kindred of 41 members, 11 of whom have familial juvenile polyposis. In these patients, random sections of otherwise grossly normal-appearing colonic mucosa showed a dense population of mixed inflammatory cell infiltrates in the superficial third of the lamina propria. Fine nodular mucosa was noted focally and diffusely in six of eight colons resected. These consisted of foci of dense inflammatory cell infiltrates in the mucosa with slight crypt architectural abnormalities. The majority of lesions were typical juvenile polyps. Dysplastic changes were noted in the polyps that were 1-2.9 cm or larger. The largest polyps contained foci of villous adenoma and juvenile polyp. A focus of adenocarcinoma of the colon was noted at the base of the villous adenoma portion of the largest polyp. The gastric polyps were histologically identical to hyperplastic polyps of the stomach. This report represents the largest number of patients (eight) in a single family with familial juvenile polyposis studied histologically. This is also the first time that the changes in the nonpolypoid colonic and gastric mucosa have been reported. The pattern of inheritance in this family suggests that the trait for familial juvenile polyposis segregates as an autosomal dominant.

Adenocarcinoma↗