Guest guest Posted September 2, 2001 Report Share Posted September 2, 2001 Can someone put this in a language the average dummy like myself can understand? Bottom line it.....will the study help find a cure or answers to get this monster into remission? (Mom of ...19yrs. old dx UC/PSC 3/2000) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 7, 2001 Report Share Posted September 7, 2001 This is Greek to me; what does it mean? **************************************************************** This e-mail and any documents accompanying this e-mail contain information which is confidential and/or legally privileged. The information is intended only for the use of the individual or entity named on this e-mail. If you are not the intended recipient, you are hereby notified that any disclosure, copying, distribution, or the taking of any action in reliance on the contents of this e-mail information, is strictly prohibited and that the documents should be returned to Saiber Schlesinger Satz & Goldstein, LLC immediately. In this regard, if you have received this e-mail in error, please notify us by return e-mail or telephone () immediately, delete the e-mail and all attachments and destroy all hard copies of same. >>> " Barb Henshaw " 09/02/01 02:14PM >>> 1: Gastroenterology 2001 Jul;121(1):124-130 <http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?http://www.gastrojournal ..org/cgi/pmidlookup?view=full & pmid=11438501> A functional polymorphism of the stromelysin gene (MMP-3) influences susceptibility to primary sclerosing cholangitis. Satsangi J, Chapman RW, Haldar N, son P, S, J, Norris S, Marshall SE, Bell JI, Jewell DP, Welsh KI. Oxford Radcliffe Hospitals, Oxford, England. BACKGROUND AND AIMS: We have investigated the influence of a biallelic polymorphism of the promoter region of stromelysin (matrix metalloproteinase 3) on susceptibility to primary sclerosing cholangitis (PSC). The 5A allele is associated with increased transcription, compared with wild-type (6A). METHODS: An allelic association study was performed: in stage 1, 52 PSC patients (43 with inflammatory bowel disease [iBD]) and 99 healthy subjects (HS) were genotyped. In stage 2, 59 PSC patients (49 IBD), 84 patients with uncomplicated ulcerative colitis, and 72 HS were genotyped. RESULTS: In stage 1, 5A carriage rate (90.4% vs. 72.7%; P = 0.012) and 5A allelic frequency (65.4% vs. 48.5%; P = 0.005) were increased, and 6A homozygosity was reduced in PSC (9.6% vs. 27.3%; P = 0.012). In stage 2, 5A allelic carriage was increased in PSC (93.2% vs. 76.4% in HS; P = 0.0092) and 6A homozygosity was reduced (6.8% vs. 23.8% in HS; P = 0.0092). Portal hypertension was associated with 5A homozygosity in PSC (P = 0.035; odds ratio [OR], 3.88). In the combined data set, 5A allelic frequencies (63.5% vs. 49.4%; P = 0.001; OR, 1.78) and 5A carriage rates (91.9% vs. 74.2%; P = 0.0002; OR, 3.92) were increased, and 6A homozygosity was reduced in PSC (8.1% vs. 25.7%; P = 0.0002; OR, 0.25). Overall, portal hypertension was associated with 5A homozygosity (P = 0.0192; OR, 3.12). CONCLUSIONS: Stromelysin polymorphism may influence susceptibility and disease progression in PSC. PMID: 11438501 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
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