title: The assessment of carotid intima media thickness and serum paraoxonase-1 activity in Helicobacter pylori positive subjects.
abstract: BACKGROUND
  The role of inflammation in the pathogenesis and progression of atherosclerosis has been increasingly discussed. Although the seroepidemiological studies have suggested a relationship between Helicobacter pylori (H. pylori) infection and atherosclerosis; the issue is still controversial. It is well known that abnormal lipid profil is related to atherosclerosis and the measurement of carotid-intima media thickness (CIMT) is one of the surrogate marker of atherosclerosis. The serum concentration of high-density lipoprotein (HDL-C) has been known to have an inverse correlation with the development of atherosclerosis. Paraoxonase-1 (PON1) is a major anti-atherosclerotic component of HDL-C. PON1 activity is related to lipid peroxidation and prospective cardiovascular risk. The aim of this study was to investigate CIMT and serum PON1 activities along with lipid parameters in H. pylori positive and negative subjects.
  
  
  METHODS
  Thirty H. pylori positive subjects and thirty-one negative subjects were enrolled. H. pylori infection was diagnosed by the presence of positivity of stool H. pylori antigen test or Carbon 14 labeled urea breath test. Serum PON1 activity was measured spectrophotometrically. Traditional cardiovascular risk factors were investigated and laboratory analysis included measurement of serum triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL-C) and low-density lipoprotein cholesterol (LDL-C). We assessed CIMT by high-resolution ultrasound of both common carotid arteries.
  
  
  RESULTS
  We found that the mean and maximum values of right and overall CIMT in H. pylori positive subjects were significantly thicker than those of H. pylori negative subjects. There was no significant differences in serum HDL-C, LDL-C, TC levels and TC/HDL-C ratios between two groups. Serum TG levels of H. pylori positive subjects were significantly higher than those of H. pylori negative subjects (p = 0.014). We found that PON1 activities were significantly lower in H. pylori positive subjects compared with negative subjects. No significantly correlation was observed between PON1 and CIMT values.
  
  
  CONCLUSIONS
  There is an increase in CIMT values in patients with H. pylori positive compared to H. pylori negative subjects. PON1 activity decrease significantly in H. pylori positive subjects. However, an association between PON1 and CIMT was not found. These data indicated that H. pylori may have a role in atherosclerotic processes, however, further studies are needed to evaluate the exact mechanisms.
authors.affiliation: Akdeniz University Faculty of Medicine, Department of Biochemistry, Antalya, Turkey. halideakbas@akdeniz.edu.tr
authors.forename: Halide S
authors.initials: HS
authors.lastname: Akbas
authors.forename: Sebahat
authors.initials: S
authors.lastname: Basyigit
authors.forename: Inci
authors.initials: I
authors.lastname: Suleymanlar
authors.forename: Didem
authors.initials: D
authors.lastname: Kemaloglu
authors.forename: Serkan
authors.initials: S
authors.lastname: Koc
authors.forename: Fatih
authors.initials: F
authors.lastname: Davran
authors.forename: Ibrahim
authors.initials: I
authors.lastname: Demir
authors.forename: Gultekin
authors.initials: G
authors.lastname: Suleymanlar
mesh_terms: D000328:Adult; D043303:Aryldialkylphosphatase / Q000097:blood*; D050197:Atherosclerosis / Q000097:blood / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000473:pathology; D015415:Biomarkers / Q000097:blood; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000473:pathology; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging / Q000473:pathology*; D042241:Early Diagnosis; D005260:Female; D016481:Helicobacter Infections / Q000097:blood / Q000150:complications* / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood / Q000150:complications; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012720:Severity of Illness Index; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology*; D018608:Ultrasonography, Doppler
chemical_list: D015415:Biomarkers; D008055:Lipids; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human
references.citation: Eur J Clin Invest. 2000 Jan;30(1):4-10
references.pmid: 10619995
references.citation: Circulation. 2002 Jul 9;106(2):184-90
references.pmid: 12105156
references.citation: Lancet. 1994 Jul 16;344(8916):146
references.pmid: 7912762
references.citation: Atherosclerosis. 2007 Sep;194(1):175-81
references.pmid: 16942773
references.citation: Ann Rheum Dis. 2003 Sep;62(9):842-5
references.pmid: 12922956
references.citation: Atheroscler Suppl. 2003 Mar;4(1):31-6
references.pmid: 12714035
references.citation: Atherosclerosis. 1995 Jun;115(2):243-53
references.pmid: 7661883
references.citation: Clin Chem. 1972 Jun;18(6):499-502
references.pmid: 4337382
references.citation: Circulation. 1998 Sep 1;98(9):845-50
references.pmid: 9738638
references.citation: Clin Biochem. 2009 Sep;42(13-14):1394-400
references.pmid: 19538950
references.citation: N Engl J Med. 1994 May 5;330(18):1267-71
references.pmid: 8145781
references.citation: Lipids Health Dis. 2009 Dec 23;8:59
references.pmid: 20030806
references.citation: Atherosclerosis. 2008 Jan;196(1):270-274
references.pmid: 17125774
references.citation: J Stroke Cerebrovasc Dis. 2008 Mar-Apr;17(2):86-94
references.pmid: 18346651
references.citation: Free Radic Biol Med. 2003 Mar 15;34(6):774-84
references.pmid: 12633754
references.citation: Curr Opin Lipidol. 2004 Aug;15(4):399-404
references.pmid: 15243212
references.citation: Br Heart J. 1994 May;71(5):437-9
references.pmid: 8011406
references.citation: Clin Biochem. 2004 May;37(5):388-94
references.pmid: 15087255
references.citation: J Cardiovasc Risk. 2002 Feb;9(1):1-6
references.pmid: 11984211
references.citation: N Engl J Med. 1999 Jan 7;340(1):14-22
references.pmid: 9878640
references.citation: Clin Rev Allergy Immunol. 2009 Aug;37(1):44-8
references.pmid: 18985284
references.citation: Atherosclerosis. 1999 Jan;142(1):207-10
references.pmid: 9920523
references.citation: Curr Opin Lipidol. 2004 Jun;15(3):261-7
references.pmid: 15166781
references.citation: Eur J Gastroenterol Hepatol. 1999 Nov;11(11):1335-7
references.pmid: 10563551
references.citation: Lancet. 1997 Aug 9;350(9075):430-6
references.pmid: 9259669
references.citation: Angiology. 2005 Jul-Aug;56(4):451-8
references.pmid: 16079929
references.citation: JAMA. 1995 Oct 4;274(13):1064-6
references.pmid: 7563460
references.citation: Clin Exp Hypertens. 2010 Jan;32(1):13-20
references.pmid: 20144068
references.citation: Int J Clin Pract. 2007 May;61(5):810-4
references.pmid: 17343667
references.citation: BMJ. 1998 Apr 11;316(7138):1130-2
references.pmid: 9552950
references.citation: Arterioscler Thromb Vasc Biol. 2001 Mar;21(3):427-32
references.pmid: 11231924
references.citation: Indian J Med Res. 2009 Oct;130(4):361-8
references.pmid: 19942738
references.citation: Circulation. 1997 Sep 2;96(5):1432-7
references.pmid: 9315528