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PubMed2005

Is Cronkhite-Canada Syndrome necessarily a late-onset disease?

Cronkhite-Canada Syndrome is a non-inherited, non-congenital disease characterized by juvenile hamartomatous gastrointestinal polyps with a typically late onset. In the case described herein the disease was diagnosed in a 17-year-old male with type I diabetes and thalassaemia minor, in coincidence with severe symptomatic intestinal candidiasis. Following the disappearance of the mycosis and correction of the protein and electrolyte imbalance, the ectodermal abnormalities returned to normal and the patient remained asymptomatic during a 7-year follow-up period, despite proteinuria resulting from membranous glomerulopathy. The concept that Cronkhite-Canada Syndrome is a late-onset disease should probably be reconsidered as it may remain asymptomatic, and thus not diagnosed, for a long a time.

Adolescent↗
PubMed2003

Dose-dependent suppression of hyperlipidemia and intestinal polyp formation in Min mice by pioglitazone, a PPAR gamma ligand.

In our previous study, a peroxisome proliferator-activated receptor gamma (PPAR gamma) agonist, pioglitazone, suppressed both hyperlipidemia and intestinal polyp formation in Apc(1309) mice at doses of 100 and 200 ppm in the diet. In contrast, it has been reported that doses of 1500 or 2000 ppm of another PPAR gamma agonist, troglitazone, enhanced colon polyp development in Min mice. In the present study, we therefore investigated the effects of a wide range of pioglitazone doses on both hyperlipidemia and intestinal polyp formation in Min mice. Serum triglycerides and very low density lipoprotein (VLDL) cholesterol in the basal diet group were elevated to levels 13-15 times higher than those in the wild-type counterparts at 20 weeks of age. They were reduced dose-dependently by treatment with 100, 200, 400 and 1600 ppm pioglitazone from 6-20 weeks of age with suppression to almost the wild-type level at the highest dose. Moreover, up-regulation of the liver mRNA levels for lipoprotein lipase (LPL) was evident in the pioglitazone-treated animals. Dose-dependent reduction of intestinal polyps was observed in Min mice given 100-1600 ppm for 14 weeks, total numbers being decreased to 63-9% of the control value. A suppressive effect of pioglitazone on colon polyp formation was also found. The PPAR gamma agonist, pioglitazone, may thus be a promising candidate chemopreventive agent for colon cancer.

Animals↗
PubMed2003

Genetic screening for Peutz-Jeghers syndrome.

Peutz-Jeghers syndrome is clinically characterized by mucocutaneous melanocytic pigmentation, intestinal hamartomatous polyposis and a significantly increased risk of developing cancer. Mutations in the serine/threonine kinase (STK-)11 gene, also designated LKB1, are found in approximately 60% of cases of Peutz-Jeghers syndrome. There is evidence that genetic heterogeneity exists and gene(s) that have not yet been discovered may be responsible for the disease. Since most mutations in Peutz-Jeghers syndrome are null alleles and are dispersed throughout the entire STK11/LKB1 gene, the mutation screening strategies that combine approaches at both the DNA and RNA level are favored. Based upon the identification of novel mutational mechanisms, the impact of RNA-based screening for germinal STK11/LKB1 mutations in Peutz-Jeghers syndrome are specifically discussed.

AMP-Activated Protein Kinase Kinases↗
PubMed2001

[Gardner's syndrome. A case report].

Gardner's syndrome is a congenital condition characterised by diffuse intestinal adenomatous polyposis (IAP) associated with maxillary osteomas, odontomas, hypertrophy of the retinal epithelium and skin tumours. It may affect subjects of all ages with equal frequency in males and females. The fact that diffuse adenomatous polyposis, the most serious clinical aspect of the syndrome, is treated surgically, has led to improved survival in patients and, consequently, an increased incidence in associated lesions, particularly maxillary osteomas. A personal case observed at the Odontostoma-tological Clinic of the University of Rome La Sapienza is reported.

Adult↗
PubMed1993

[Turcot syndrome--a rare extra-intestinal manifestation of familial adenomatous polyposis?].

The case of a 15-year-old male with Turcot syndrome is presented. When the patient was aged 10 years a medulloblastoma was diagnosed. Five years later he developed multiple adenomatous polyps of the colon and multiple "congenital hypertrophy of the retina" (CHRPE), the most common extraintestinal manifestation of FAP, were described. Family history revealed familial adenomatous polyposis with 12 family members exhibiting a FAP. The mode of inheritance of Turcot syndrome is controverted. Our case strengthens the hypothesis that the syndrome is a further extraintestinal (rare) manifestation of the FAP gene.

Adenomatous Polyposis Coli↗
PubMed2004

Liposome-mediated adenomatous polyposis coli gene therapy: a novel anti-adenoma strategy in multiple intestinal neoplasia mouse model.

PURPOSE: Familial adenomatous polyposis is a highly penetrant, autosomal dominant disease resulting from a germline mutation of the adenomatous polyposis coli gene. Besides colorectal polyps and cancer, more than 90 percent of familial adenomatous polyposis patients also develop duodenal polyposis with an approximately 5 percent lifetime risk of malignant transformation. Because adenomatous polyposis coli protein has a "gatekeeper role" in the adenoma-carcinoma sequence, replacing its function may reduce polyp formation. We studied the functional outcome of per-oral, liposome-mediated adenomatous polyposis coli gene replacement therapy in a multiple intestinal neoplasia mouse model. METHODS: Twenty multiple intestinal neoplasia mice, heterozygous for the human homologue adenomatous polyposis coli gene, were randomly assigned to three groups: no treatment (n = 8); control plasmid containing green fluorescence protein reporter gene (n = 6); and plasmid containing the full-length adenomatous polyposis coli gene (n = 6). For the adenomatous polyposis coli-treated and green fluorescence protein reporter gene-treated groups, each mouse received the appropriate plasmid complexed with liposome, administered twice per week by oral gavage regime. Treatment lasted four weeks and all animals were killed at the end of treatment period with harvesting of intestinal tissue for polyp number estimation. RESULTS: There was a statistically significant 25 percent reduction in the total number of polyps in the adenomatous polyposis coli-treated (73.1 +/- 1.4) group compared with untreated control (97.8 +/- 5.3, P < 0.01, Tukey test) and multiple intestinal neoplasia mice treated with control green fluorescence protein gene (103.3 +/- 1.7, P < 0.01, Tukey test). CONCLUSION: Adenomatous polyposis coli gene dysfunction underlies tumorigenesis in familial adenomatous polyposis patients and multiple intestinal neoplasia mice. This in vivo study provides evidence to support a novel anti-adenoma strategy using enteral adenomatous polyposis coli gene replacement therapy.

Adenomatous Polyposis Coli↗
PubMed2004

Comparison of capsule endoscopy and magnetic resonance imaging for the detection of polyps of the small intestine in patients with familial adenomatous polyposis or with Peutz-Jeghers' syndrome.

BACKGROUND AND STUDY AIMS: We have conducted a study to compare the diagnostic yields of magnetic resonance imaging (MRI) and capsule endoscopy for the detection of small-bowel polyps in patients with inherited polyposis syndromes. PATIENTS AND METHODS: MRI was performed in 20 patients, with either Peutz-Jeghers' syndrome (PJS; n = 4) or familial adenomatous polyposis (FAP; n = 16), and capsule endoscopy was done the next day. The number, size, and location of polyps were analyzed. RESULTS: Overall, 448 polyps ranging from about 1 mm to 30 mm in size were detected in eight patients by capsule endoscopy, whereas with MRI only 24 polyps all bigger than 5 mm could be seen in the four PJS patients. CONCLUSIONS: Polyps bigger than 15 mm were detected similarly with capsule endoscopy and MRI, whereas smaller polyps were seen much more often with capsule endoscopy. Polyps smaller than 5 mm were exclusively seen with capsule endoscopy. However, location of the detected polyps and determination of their exact sizes was more accurate by MRI.

Adenomatous Polyposis Coli↗
PubMed1993

[Results of preservation of distal parts of the large intestine in the surgical treatment of diffuse polyposis].

One hundred patients were examined in periods of one to 30 years after subtotal resection of the large intestine with the formation of an ileorectal or ileo-sigmoid anastomosis for diffuse polyposis with prevalence of proliferative processes. A malignant tumor developed in the preserved distal parts of the large intestine during this period in 19 (19%) persons. Such factors as the sex, age, duration of the postoperative follow-up period, the presence of a malignant tumor in the removed part, and the length of the functioning segment of the large intestine had no essential effect on the frequency of carcinoma. The presence of any number of polyps in the remaining part of the large intestine at the moment of the surgical intervention was the principal precondition for carcinoma development. The absence of polyps in it is a favorable factor for the survival of the operated on patients; in none of them did a malignant tumor develop in the preserved segment of the large intestine.

Adolescent↗
PubMed1976

[Clinical manifestations of polyposis and polyps of the large intestine and "risk groups"].

In processing of 1603 clinical observations, studied dynamically during 15 years, using the multifactor analysis of clinico-morphological, roentgenological and statistic parallels, there were registered 156 different possible variants in a combination of the forms and clinical manifestations of polyposis and polyps of the colon. The degree of the malignant transformation risk for various forms of polyposis and polyps of the colon is extremely variable.

Colonic Neoplasms↗
PubMed1985

Nodular lymphoid hyperplasia of the intestinal tract in infancy and childhood.

Over an 18-year period we have diagnosed nodular lymphoid polyposis of the intestinal tract in 6 patients. The site of the polyposis, which was due to prominent lymphoid hyperplasia, was ileal (3), colonic (2), and rectal (1). The diagnosis was made following complications arising from the polyps, which included recurrent intussusception (2), rectal prolapse (1), intestinal or pseudointestinal obstruction (2), and rectal bleeding (1). Immunoglobulin staining was performed on all the bowel specimens and in every case secretory IgA was present on the mucosal surfaces and IgG and IgA were seen in the lamina propria, thus excluding immunodeficiency in these patients. Viral studies were performed in 3 patients and all were positive. In one patient Echovirus II was seen in tissue homogenate from a mesenteric lymph node and in another, adenovirus type II was cultured from lymphoid polyps of the rectum. A further patient had positive serological tests for adenovirus. Thus it appears that nodular lymphoid hyperplasia is part of the generalized lymphoid hyperplasia associated with viral infections in infancy and childhood. Immunodeficiency states as a cause of the lymphoid hyperplasia should always be excluded by estimation of serum immunoglobulins.

Child↗