P 2: CRP as a possible predictor for peripheral arterial disease in patients with type 2 diabetes

Previous epidemiological studies have established a link between diabetes and increased prevalence of peripheral artery disease (PAD). C-reactive protein is indicated as a marker for the PAD, but also as a factor that probably participate in the development and progression of the illness. to evaluate predictive significance of CRP for PAD in patients with diabetes type 2. eighty patients with diabetes type 2 aged 45–70, treated with oral anti diabetic drugs were divided into two groups (with and without PAD), based on the value of ankle brachial index (ABI). After five years, all patents were reexamined and divided into subgroups depending on whether they developed PAD or whether the initially diagnosed PAD progressed according to ABI values also. We defined ABI decline from one category to another as a marker of PAD progression. during this period, 8 patients (21.1%) from group A showed a decrease in ABI and progression of PAD (subgroup A1) and 30 patients (79.9%) had no change in ABI (subgroup A2). At the same time in Group B in 22 patients (52.4%) there was a decrease in ABI (subgroup B1), which meant that they developed PAD and in 20 patients (47.6%) there was no ABI changes nor development of PAB (subgroup B2). Analysis of the studied parameters showed that patients in subgroup A1 had the highest and patients in subgroup B2 the lowest levels of hs-CRP. Using one-way analysis of variance, ANOVA, difference in hs-CRP levels was found between subgroups A1, A2, B1 and B2 at the first examination (4.69 ± 0.95 vs. 3.934 ± 0.42 vs. 4.034 ± 0.55 vs. 2.05 ± 0.24, p = 0.005), as well as at the control exam (5.046 ± 1.79 vs. 4.37 ± 1.95 vs. 5.16 ± 2.39 vs. 2.43 ± 0.85, p<0.001). Subgroups of subjects with PAB (A1, A2 and B1) were compared to subjects without PAB subgroup (B2). High sensitive CRP was the only parameter that differed between subjects with and without the PAB (4.09 ± 2.36 vs. 3.09±2.21, p<0.001) at the beginning and five years later (4.75± 2.11 vs. 2.43± 0.85, p<0.000). An analysis of ROC curves was made and the cut-off point for hs-CRP was 2.5 mg/dL, with specificity of 75% and sensitivity of 73.3% (χ2 = 14.76, p < 0.001). The cut-off for hs-CRP tested by Cochran Mantel-Haenszel method was useful for differentiating patients with PAB and those without PAD. Odds Ratio for the obtained cut-off point for hs-CRP was 8.25, (95% CI = 2.58–2.64, p < 0.001). Relative risk for PAB was 2.93 times higher if the value of hs-CRP is greater than or equal to 2.5 mg / L. Our data showed that the level of hs-CRP of 2.5 mg/L was that discriminative value that indicates the risk for development and/or progression of PAD in patients with diabetes type 2. Furthermore, our investigation has found that the hs-CRP value greater than 2.5 mg / L increase the risk for PAD approximately three times.