Ileo-ileal intussusception in a girl with solitary intestinal polyp and malrotation: Waugh Syndrome

Mesalazine is the gold standard drug for treatment of ulcerative colitis (UC). Here, we describe 4 cases of familial adenomatous polyposis (FAP) patients with UC that showed reduction of intestinal polyp diameter by mesalazine treatment. Of note, the effects of mesalazine on the development of intestinal polyps in FAP patients have not been reported, and we further investigated whether the short-term use of high-dose mesalazine (4 g/day) has harmful effects on FAP patients or not. The authors found that the treatment showed slightly adverse events in FAP patients. However, mesalazine tended to reduce the number of colon polyps in male subjects with FAP. This report provides basic information for planning a double-blind, randomized, clinical trial that aims to show mesalazine’s potential to suppress intestinal polyp development in FAP.

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Intestinal polyp recognition in capsule endoscopy images using color and shape features

2009 IEEE International Conference on Robotics and Biomimetics (ROBIO) ◽

10.1109/robio.2009.5420969 ◽

2009 ◽

Cited By ~ 10

Author(s):

Baopu Li ◽

Yichen Fan ◽

Max Q.-H. Meng ◽

Lin Qi

Keyword(s):

Capsule Endoscopy ◽

Shape Features ◽

Intestinal Polyp

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Inhibition of intestinal polyp growth by oral ingestion of bovine lactoferrin and immune cells in the large intestine

BioMetals ◽

10.1007/s10534-014-9747-2 ◽

2014 ◽

Vol 27 (5) ◽

pp. 1017-1029 ◽

Cited By ~ 15

Author(s):

Masaaki Iigo ◽

David B. Alexander ◽

Jiegou Xu ◽

Mitsuru Futakuchi ◽

Masumi Suzui ◽

...

Keyword(s):

Large Intestine ◽

Immune Cells ◽

Bovine Lactoferrin ◽

Oral Ingestion ◽

Intestinal Polyp

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Phase I study of ursodeoxycholic acid in combination with 5-fluorouracil, leucovorin, oxaliplatin, and bevacizumab for metastatic colorectal cancer.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.15_suppl.e14182 ◽

2012 ◽

Vol 30 (15_suppl) ◽

pp. e14182-e14182

Author(s):

Lily L. Lai ◽

Ken Chiu ◽

Vincent M. Chung ◽

Dean Lim ◽

Joseph Chao ◽

...

Keyword(s):

Colorectal Cancer ◽

Metastatic Colorectal Cancer ◽

Ursodeoxycholic Acid ◽

Bile Acids ◽

Mouse Models ◽

Body Weight Loss ◽

Eligibility Criteria ◽

Significant Treatment ◽

Intestinal Polyp ◽

Study Results

e14182 Background: Significant treatment advances have doubled the median survival in patients with metastatic colorectal cancer (mCRC). An emerging body of literature links cancer with aberrant metabolism. These findings suggest that treatment directed against CRC metabolism may add to improved survival outcomes. The bile acid, ursodeoxycholic acid (UDCA), lowers cholesterol and improves insulin sensitivity when used clinically. Moreover, UDCA protects against intestinal polyp development in animal and human studies. UDCA effects may be mediated through activation of FXR, since bile acids are the endogenous ligands for this nuclear receptor. FXR is a tumor suppressor in mouse models of colon cancer and a prognostic biomarker in patients with CRC. Activation of FXR with bile acids in mouse models suppresses intestinal tumorigenesis. We propose to determine the dose and safety of UDCA when added to standard therapy for mCRC. Methods: Trial Design: UDCA doses will be escalated using a 3+3 design which will stop at the MTD or at two levels above an Active Dose (AD), whichever is the lowest. The AD is defined as the dose that will activate FXR. After a 7 day run-in period of UDCA only, cytotoxic combination chemotherapy and antiangiogenic agent for mCRC will be given along with the UDCA. The use of a run-in period allows for metabolic studies to identify serum biomarkers of FXR activation and to determine an AD. Treatment or intervention planned: UDCA is given during a run-in period of 7 days. At the end of the run-in period, standard doses of 5-fluorouracil, leucovorin, oxaliplatin, and bevacizumab are added. Patients are treated until excessive toxicity, progression of disease, or surgical resection. Major eligibility criteria: Patients with mCRC are eligible. Patients with greater than 10% body weight loss within 6 months of entering the protocol, a diagnosis of diabetes and active diabetes treatment are excluded from the study. Results: Current enrollment: Cohorts 1, 2, 3 have been completed without DLT. Enrollment to Cohort 4 began in 12/2011. Conclusions: Continue dose escalation until MTD or 2 levels above AD.Clinical trial registry number: NCT00873275.

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Physical Activity Decreases Intestinal Polyp Development in the APCmin+/ − Mouse

Medicine & Science in Sports & Exercise ◽

10.1249/00005768-200405001-00763 ◽

2004 ◽

Vol 36 (Supplement) ◽

pp. S160

Author(s):

Kristen Mehl ◽

Julie M. Clements ◽

J. Mark Davis ◽

James A. Carson

Keyword(s):

Physical Activity ◽

Intestinal Polyp

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Massive intussusception caused by a solitary Peutz–Jeghers type hamartomatous polyp

Annals of The Royal College of Surgeons of England ◽

10.1308/rcsann.2018.0019 ◽

2018 ◽

Vol 100 (4) ◽

pp. e91-e93 ◽

Cited By ~ 3

Author(s):

V Kalliakmanis ◽

I Perysinakis ◽

K Koutsouvas ◽

P Karras ◽

E Margaris ◽

...

Keyword(s):

Intestinal Obstruction ◽

Preoperative Diagnosis ◽

Rare Case ◽

Hamartomatous Polyp ◽

Genetic Investigation ◽

Diagnostic Challenge ◽

Postoperative Course ◽

Presenting Symptoms ◽

Intestinal Polyp ◽

Peutz Jeghers Syndrome

Intussusception is a rare cause of intestinal obstruction in adults and represents a diagnostic challenge for the surgeon. In the majority of cases, presenting symptoms are not specific, making preoperative diagnosis difficult. Several medical conditions may cause intestinal intussusception. We present the case of a 16-year-old female patient with intussusception due to a hamartomatous Peutz–Jeghers type polyp. This is an extremely rare case in which the first manifestation of the intestinal polyp was jejunojejunal intussusception very close to the duodenojejunal junction, with a necrotic intussusceptum about 50 cm long. The patient was treated successfully with enterectomy and end-to-end anastomosis. Postoperative course was uneventful and the patient is currently under gastroenterological and genetic investigation to exclude the diagnosis of Peutz–Jeghers syndrome.

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Interleukin-6 and cachexia inApcMin/+mice

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00716.2007 ◽

2008 ◽

Vol 294 (2) ◽

pp. R393-R401 ◽

Cited By ~ 139

Author(s):

Kristen A. Baltgalvis ◽

Franklin G. Berger ◽

Maria Marjorette O. Pena ◽

J. Mark Davis ◽

Stephanie J. Muga ◽

...

Keyword(s):

Muscle Mass ◽

Interleukin 6 ◽

Gastrocnemius Muscle ◽

Significant Loss ◽

Mouse Tumor ◽

Fat Pad ◽

Muscle Weight ◽

Intestinal Polyps ◽

Epididymal Fat ◽

Intestinal Polyp

The ApcMin/+mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 wk of age. This mouse develops cachexia by 6 mo, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating interleukin-6 (IL-6) and the polyp burden for the development of cachexia in ApcMin/+mice. At 26 wk of age, mice exhibiting severe cachectic symptoms had a 61% decrease in gastrocnemius muscle weight, complete loss of epididymal fat, a 10-fold increase in circulating IL-6 levels, and an 89% increase in intestinal polyps compared with mildly cachectic animals. ApcMin/+/IL-6−/−mice did not lose gastrocnemius muscle mass or epididymal fat pad mass while overall polyp number decreased by 32% compared with ApcMin/+mice. Plasmid-based IL-6 overexpression in ApcMin/+/IL-6−/−mice led to a decrease in gastrocnemius muscle mass and epididymal fat pad mass and increased intestinal polyp burden. IL-6 overexpression did not induce cachexia in non-tumor-bearing mice. These data demonstrate that IL-6 is necessary for the onset of adipose and skeletal muscle wasting in the ApcMin/+mouse and that circulating IL-6 can regulate ApcMin/+mouse tumor burden.

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