The aim of this study was to assess vitamin D status in patients with type 2 diabetes and diabetic foot ulcers (DFU). A total of 242 participants with type 2 diabetes, mean age 59.1 ± 10 years, mean body mass index 31.4 ± 6.3 kg/m2, and estimated glomerular filtration rate ≥45 mL/min/1.73m2, were divided into 2 groups: 73 with DFU (35 with and 38 without active infection) and 169 without DFU (106 with diabetic peripheral neuropathy, 63 without complications). Neuropathy was assessed by 10 g monofilament, Rydel-Seiffer 128 Hz tuning fork, and temperature discrimination. Serum 25(OH)D (25-hydroxy vitamin D) was assessed by ECLIA (electro-chemiluminescence immunoassay) method. Median 25(OH)D level was 12.6 ng/mL (IQR [interquartile range] 9.3-17.6 ng/mL) in the studied cohort. The DFU group presented with lower 25(OH)D level as compared with diabetic patients without foot ulcers (non-DFU group): 11.6 ng/mL (IQR 8.5-15.8 ng/mL) versus 13.5 ng/mL (IQR 9.6-18.6 ng/mL), P = .001; the diabetic peripheral neuropathy subgroup demonstrated lower 25(OH)D level in comparison with participants without complications: 12.5 ng/mL (IQR 9-17.2 ng/mL) versus 15.9 ng/mL (IQR 10.4-20.8 ng/mL), P = .031. This remained significantly different even after correction for age and duration of diabetes. There was no difference in 25(OH)D level between the subgroups according to the presence of active infection. In conclusion, vitamin D deficiency may play a role in the development of diabetes complications.

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The aim of this study is to compare the efficacy of procalcitonin (PCT) and high-sensitive C-reactive protein (hsCRP) as diagnostic biomarkers in patients with diabetes and mild-to-moderate diabetic foot infections. A total of 119 patients (102 with type 2 diabetes and 17 with type 1 diabetes), of mean age 60.29 ± 10.05 years, divided into 3 groups—diabetic foot ulcer (DFU) with active infection (IDFU group, n = 41), DFU without clinical signs of infection (non-IDFU group, n = 35), and a control group with diabetes without DFU (n = 43). Infection severity was graded according to the International Working Group on the Diabetic Foot guideline—non-IDFU group as Grade 1, IDFU group as Grade 2 (n = 22), and Grade 3 (n = 19). Serum hsCRP was assessed by the immunoturbidimetric method and PCT by the enzyme chemiluminescence immunoassay (ECLIA) method. Levels of white blood cells (WBC) were assessed using the Medonic hematology analyzer and erythrocyte sedimentation rate (ESR) by the Westergren method. Serum hsCRP, WBC count, and ESR were significantly higher in the IDFU group as compared to non-IDFU and control groups, whereas PCT levels did not differ between the groups. hsCRP presented with higher sensitivity (80%), specificity (79%), area under the curve (AUC) 0.856, in comparison to PCT (sensitivity 63%, specificity 62%, AUC 0.617) for the presence of IDFU, as well as in the Grade 3 subgroup (84% sensitivity and specificity, AUC 0.911). The combined model of both markers did not present with better accuracy than using hsCRP alone. In conclusion, hsCRP appears to be a better diagnostic biomarker than PCT in the diagnosis of moderate foot ulcer infection. Both markers fail to distinguish mild infection.

The effects of endothelin 1 (ET-1; 300 pmol/rat intracarotid) on somatosensory evoked potential were investigated in rats. ET-1 led to an amplitude reduction, peak latency prolongations and waveform disturbances. There was a large interindividual variability. The late cortical components were more affected than the earlier potentials at a thalamic or cortical level. ET-1-induced SEP changes developed quickly after the drug injection and persisted for at least 30 min. It is assumed that the observed effects probably reflect the occurrence of a progressively developing ischemia subsequent to ET-1 administration. Moreover, the pattern of ET-1-induced changes suggests a greater sensitivity of the synaptic transmission to the ischemic influence than the axonal conduction.

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