Leiden mutation (as genetic) and environmental (retinoids) sequences in the acute and chronic inflammatory and premalignant colon disease in human gastrointestinal tract

Citation
G. Mozsik et al., Leiden mutation (as genetic) and environmental (retinoids) sequences in the acute and chronic inflammatory and premalignant colon disease in human gastrointestinal tract, J PHYSL-PAR, 95(1-6), 2001, pp. 489-494
Citations number
28
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF PHYSIOLOGY-PARIS
ISSN journal
09284257 → ACNP
Volume
95
Issue
1-6
Year of publication
2001
Pages
489 - 494
Database
ISI
SICI code
0928-4257(200101/12)95:1-6<489:LM(GAE>2.0.ZU;2-V
Abstract
Background: Tumor, calor, dolor, pallor and functio laesa are together invo lved in the different acute and chronic inflammatory processes. The process es involved in the inflammation are determined by differently acquired and hereditary factors. Recently the presence of a new genetic marker (Leiden p oint mutation) was found in Crohn's disease and ulcerative colitis. On the other hand, the GI mucosal integrity was proven on gastrointestinal mucosal damage to be produced by different chemicals, xenobiotics, drugs. In human observations, the serum level of retinoids (vitamin A, lutein, zeaxanthin, alpha-, beta -carotene) was proven in patients with chronic gastrointestin al inflammatory bowel disease. The aims of this study were (1) to measure t he prevalence of Leiden mutation; (2) to identify the changes in the serum retinoid level in patients with Helicobacter pylori infection of the stomac h (n = 24), hepatitis C infection (n = 75), ileitis terminalis (Crohn's dis ease, n = 49), ulcerative colitis (n = 35), colon polyposis (n = 59) and ad enocarcinoma in colon polyps (n = 9), and 57 healthy persons were used in t he control group, (3) to compare the directions of the changes in the measu red parameters in the acute (H. pylori and hepatitis C infections), chronic (ileitis terminalis, ulcerative colitis) GI inflammatory diseases and in c olon polyposis without and with malignisation. Methods: The Leiden mutation was measured by the method of polimerase chain reaction, the retinoid leve l in the patient's serum was measured by high liquid cromathografic method (HPCL). Results: (1) It has been found that the prevalence of Leiden mutati on increased significantly in patients with ileitis terminalis (P < 0.001), ulcerative colitis (P < 0.001), colon polyposis (P < 0.001) and with colon polyps with malignisation (P < 0.01). (2) Serum level of vitamin A and zea xantin were decreased significantly in all group of patients except for the group with H. pylori infections. (3) alpha- and beta -carotenes were found to be practically at the same level as those in the control groups, except in patients of colon polyps with malignisation. (4) The vitamin A, lutein, zeaxantin, alpha- and beta -carotenes were decreased in patients with ilei tis terminalis. Conclusions: (1) The essential role of retinoids (carotenoi ds) as environmental factors are suggested for keeping GI mucosal integrity in human healthy subjects and patients. (2) Leiden mutation, as a genetic marker, can be used in the screening of patients with ileitis terminalis, u lcerative colitis and colon polyposis (without and with malignisation). (3) An opposite direction can be found between the increased prevalence of Lei den mutation and decrease of serum levels of retinoids in group of patients with ileitis terminalis, ulcerative colitis and colon polyposis (without a nd with malignisation). (C) 2001 Elsevier Science Ltd. All rights reserved.