Benign intestinal tumors are rare in children, however we describe an inflammatory myofibroblastic tumor (IMT) of the jejunum in a 2-year-old girl who presented with an intestinal obstruction. During laparotomy, an annular mass around the jejunum was resected, from which a histological diagnosis of IMT was made. A review of the literature for this rare entity emphasizes the importance of histological confirmation of its benign nature. Because of the risk of local recurrence, IMT cases should have a long-term follow up.
Nabumetone is a nonsteroidal anti-inflammatory (NSAI) drug which is known to cause less gastrointestinal damage than other NSAI drugs. This study was performed to evaluate whether nabumetone treatment might alter the vascular aberrations related to inflammation in a rat model of adjuvant-induced arthritis. Nabumetone treatment (120 or 240 mg·kg–1·day–1, orally) was initiated on the 15th day of adjuvant inoculation and continued for 14 days. Arthritic lesions, vascular contractile and relaxant responses and gastroduodenal histopathological preparations were evaluated 29 days after adjuvant inoculation. The contractile responses of aortic rings to phenylephrine and KCl were increased in grade 2 arthritic rats. In grade 3 arthritis only the phenylephrine contractility was decreased. The relaxant responses to acetylcholine and sodium nitroprusside were decreased in grades 2 and 3. In healthy rats, nabumetone did not change the vascular responses. After treatment of arthritic rats with nabumetone, both the contractile and relaxant response of the aortic rings returned to normal, and arthritic score and paw swelling were reduced. Gastroduodenal histopathology did not show erosions or ulcers in any of the groups. In conclusion, nabumetone improved the systemic signs and vascular alterations in experimental arthritis without showing any gastrointestinal side effects.
The limited efficacy of standard medical therapies for inflammatory bowel diseases has resulted in a continuing search for alternative treatments. Growth hormone (GH) has shown to have mutagenic and proliferative effects on intestinal cells. This study was designed to identify the effect of growth hormone on trinitrobenzene slfonic acid-induced colitis (TNBSIC) in rats. This study was carried out on 30 rats, divided in 3 groups: group 1: TNBSIC+ GH, group 2: TNBSIC, group 3: saline enema. Colitis was induced in male Sprague-Dawley rats (200 g-250 g) by intracolonic installation of 2, 4, 6-trinitrobenzene sulphonic acid in 50% ethanol. GH treatment has been started and continued throughout the study after inducing colitis. All rats were killed after 5 weeks and colonic segments were examined histopathologically. Microscopic and macroscopic damage scores were caulculated. Intestinal damage scores were found higher in Goups II when compared with treatment group (P < 0.05). There was no damage in group 3 as expected. Both macroscopic and microscopic scores were highest in group 2 (P < 0.05). The myloperoxidase activity was found lower comparing to group 2 (P < 0.05). In conclusion, growth hormone replacement had protective effects against colonic inflammation while reducing intestinal damage on TNB-induced colitis.
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