BackgroundAdhesion molecules are involved in the development of atherosclerosis. An increased level of the ICAM 1 molecule is associated with numerous inflammatory diseases including atherosclerosis of carotid arteries. The rs5498 (K469E) polymorphism of the ICAM-1 gene leads to an increase in the level of serum ICAM. We investigated the association between the rs5498 (K469E) polymorphism of the ICAM-1 gene and the progression of carotid atherosclerosis in subjects with type 2 diabetes mellitus (T2DM). MethodsThe study included 595 patients with T2DM and 200 subjects in the control group without T2DM. The control examination was made 3.8 years after the initial examination. Indicators of atherosclerosis (carotid intima-media thickness (CIMT), total plaque sum and sum of the plaques thickness) were detected by ultrasound examination. Genetic analyses of the polymorphism rs5498 of the ICAM-1 gene were made by RT-PCR.ResultsThe distribution of genotypes and frequencies of rs5498 polymorphism was not significantly different between the group with type 2 diabetes ( T2DM) and the control group. Genotype EE K469E polymorphism is associated with a statistically significant annual plaques growth.ConclusionThe EE genotype of the rs5498 of the ICAM-1 gene was associated with a more rapid progression of carotid atherosclerosis in patients with T2DM in comparison with other genotypes.

The platelet endothelial cell adhesion molecule 1 (PECAM-1) plays an important role in many inflammatory processes, including the development of atherosclerosis. Polymorphism rs668 of the PECAM-1 gene (373C/G) is functional, and it was reported to be associated with increased serum levels of PECAM-1. We investigated the association between the rs668 polymorphism of PECAM-1 and subclinical markers of carotid atherosclerosis in subjects with type 2 diabetes mellitus (T2DM). Five hundred and ninety-five T2DM subjects and 200 control subjects were enrolled. The carotid intima-media thickness (CIMT) and plaque characteristics (presence and structure) were assessed ultrasonographically. Biochemical analyses were performed using standard biochemical methods. Geno-typing of the PECAM-1 gene polymorphism (rs668) was performed using KASPar assays. The control examinations were performed 3.8 ± 0.5 years after the initial examination. Higher CIMT was found in patients with T2DM in comparison with subjects without T2DM. Statistically sig-nificantly faster progression of the atherosclerotic markers was shown in subjects with T2DM in comparison with the control group. When adjusted to other risk factors, the rs668 GG genotype was associated with an increased risk of carotid plaques in subjects with T2DM. We concluded that our study demonstrated a minor effect of the rs668 PECAM-1 on markers of carotid atherosclerosis in subjects with T2DM.

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Many studies have investigated the association between the angiotensin-coverting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and carotid intima-media thickness (ITM). However, only a few reports so far have studied carotid artery disease by plaque score in non-insulin-dependent diabetes mellitus (NIDDM) patients. To investigate the impact of genetic polymorphisms of the ACE on carotid atherosclerosis in the Slovenian population with NIDDM, we searched for the association between the ACE I/D gene polymorphism and either ITM or plaque score in subjects with NIDDM. Study participants were 292 NIDDM patients, randomly selected from one centre, with diabetes duration ≥ 10 years. The ITM and plaque score of the carotid arteries was determinated by bilateral B-mode ultrasonography. Polymerase chain reaction was used to evaluated the ACE I/D polymorphism. The frequency of the allele D was 55.3 %, and the frequency of the allele I was 44.7 %. The mean ITM was 1.08, 1.09 and 1.07 in the ACE DD, ID, and II genotypes, respectively. The ITM and the prevalence of focal plaque assessed by plaque score were not significantly different among the three genotypes in NIDDM patients. We may conclude that the ACE I/D gene polymorphism is not associated with ITM and plaque score. Therefore it could not be used as a genetic marker of carotid atherosclerosis in NIDDM patients

Diabetično stopalo je najpogostejši vzrok netravmatske amputacije. Posledice sladkorne bolezni, kot so periferna nevropatija, slaba prekrvavitev, omejena gibljivost sklepov, deformacija stopala in posledično spremenjeni pritiski na podplatu stopala, predstavljajo dejavnike tveganja za nastanek diabetičnega stopala. Pri zdravljenju diabetičnega stopala se poslužujemo s preventivnimi kirurškimi posegi, s katerimi skušamo preprečiti amputacijo,  travmatskimi kirurškimi posegi, s katerimi odstranjujemo uničene dele stopala in korektivnimi, s katerimi poskušamo doseči celjenje ran.