Serotonin transporter gene polymorphism in slow transit constipation.
- Author:
	        		
		        		
		        		
			        		Jian-hua DING
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Chuan-gang FU
			        		
			        		;
		        		
		        		
		        		
			        		Rong-hua ZHAO
			        		
			        		;
		        		
		        		
		        		
			        		Rong-gui MENG
			        		
			        		
		        		
		        		
		        		
			        		
			        		Author Information
			        		
 - Publication Type:Journal Article
 - MeSH: Adolescent; Adult; Aged; Alleles; Chronic Disease; Constipation; genetics; Female; Gene Frequency; Genotype; Humans; Male; Middle Aged; Polymorphism, Genetic; Serotonin Plasma Membrane Transport Proteins; genetics; Young Adult
 - From: Chinese Journal of Gastrointestinal Surgery 2006;9(4):328-330
 - CountryChina
 - Language:Chinese
 - 
		        	Abstract:
			       	
			       		
				        
				        	
OBJECTIVETo investigate the association between the polymorphism of serotonin transporter gene-linked polymorphic region(5-HTTLPR) and slow transit constipation(STC).
METHODSPolymerase chain reaction was used to assess 5-HTTLPR polymorphism of SERT gene in 54 patients with STC and 100 healthy controls.
RESULTSThe frequencies of serotonin transporter short/short(S/S) and allele S genotypes were significantly higher in STC patients than those in controls(72.2% vs 50.0%; 83.3% vs 72.5%; both P< 0.05). There were no significant differences in 5-HTTLPR polymorphism respectively between the two groups according to gender and age(less than 45 and more than 45 years old). The frequency of S/S genotype was higher in the patients with less than 40% of the ingested markers evacuated within 72 h than those with more than 40% evacuated(71.7% vs 42.6%, P< 0.05).
CONCLUSIONThe presence of 5-HTTLPR allele S may contribute to the pathogenesis of STC.
 
            