title: Peripheral vascular disease in Type 2 diabetic Chinese patients: associations with metabolic indices, concomitant vascular disease and genetic factors.
abstract: OBJECTIVE
  Conventional and genetic risk factors have been reported to play a role in the pathogenesis of vascular disease, but do not explain the lower burden of cardiac and peripheral vascular disease (PVD) in Chinese compared with Caucasians. The role of renin-angiotensin system (RAS) gene polymorphisms and conventional vascular risk factors has not been determined.
  
  
  METHODS
  A total of 3097 Chinese diabetic subjects were screened for PVD, which was identified in 194 of the 2967 patients with Type 2 diabetes. Biochemical parameters and the genotype and allele frequencies of three RAS gene polymorphisms, the angiotensin-converting enzyme (ACE) insertion/deletion, angiotensinogen (AGT) M235T and angiotensin II type 1 receptor (AT1R) A1166C polymorphisms were then compared between the PVD patients and 1046 age, gender and diabetes duration-matched patients without PVD.
  
  
  RESULTS
  PVD identified in 6.5% was associated with significantly worse glycaemic control, lipid profile and renal function. Smoking was more common, as were the other macro- and microvascular diseases. The prevalence of hypertension was similar between the groups, yet diastolic blood pressure was slightly lower in the PVD group. The ACE D allele was significantly more frequent in patients with PVD compared with the matched diabetic controls (38.1 vs. 29.8%, P = 0.039). No differences in the AT1R or AGT polymorphisms were observed.
  
  
  CONCLUSIONS
  PVD was associated with a worse metabolic profile and greater concomitant vascular disease than controls. The ACE I/D polymorphism was associated with PVD in these Type 2 diabetic patients.
authors: Department of Medicine and Therapeutics, The Chinese University of Hong Kong, The Prince of Wales Hospital, Shatin, Hong Kong SAR. gneilthomas@yahoo.co.uk
authors: G N
authors: GN
authors: Thomas
authors: J A J H
authors: JA
authors: Critchley
authors: B
authors: B
authors: Tomlinson
authors: C S
authors: CS
authors: Cockram
authors: J C N
authors: JC
authors: Chan
mesh_terms: D000368:Aged; D000418:Albumins / Q000032:analysis; D000808:Angiotensinogen / Q000235:genetics; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000150:complications; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003404:Creatinine / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000235:genetics / Q000378:metabolism; D003925:Diabetic Angiopathies / Q000208:ethnology / Q000235:genetics / Q000378:metabolism*; D005260:Female; D017353:Gene Deletion; D005787:Gene Frequency; D005838:Genotype; D006723:Hong Kong / Q000208:ethnology; D006801:Humans; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D016491:Peripheral Vascular Diseases / Q000150:complications* / Q000235:genetics / Q000378:metabolism; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D012084:Renin-Angiotensin System / Q000235:genetics; D014280:Triglycerides / Q000097:blood
chemical_list: D000418:Albumins; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D044140:Receptor, Angiotensin, Type 1; D014280:Triglycerides; D000808:Angiotensinogen; D002784:Cholesterol; D003404:Creatinine; D007703:Peptidyl-Dipeptidase A