3) (Fig 2a) Serum markers of endothelial function underwent the

3) (Fig. 2a). Serum markers of endothelial function underwent the same changes as FMD (Table 3). Baseline

vWF was higher in HIV-positive patients compared with controls (2.0 vs. 0.9 U/L, respectively; P < 0.001). Although treatment with both PI- and NNRTI-containing regimens reduced vWF levels, vWF remained significantly elevated compared with controls after 6 months click here (1.24 vs. 0.9 U/L, respectively; P < 0.01). sICAM-1 was higher in treatment-naïve patients than in controls (313 vs. 211 ng/L, respectively; P < 0.001). The value fell during the first treatment period with a PI (313 vs. 235 ng/L, respectively; P < 0.001), but no significant change was seen with efavirenz (Fig. 2b). Baseline E-selectin was similar in the two groups (29.4 vs. 28.4 ng/L, respectively; P = 0.7), but selleck kinase inhibitor in HIV-positive patients it dropped significantly during PI treatment (19.8 ng/L; P < 0.001). During the treatment period with efavirenz, the median value did not decrease any further. hs-CRP was almost three times higher in HIV-infected patients at baseline than in controls (24 vs. 8.6 mM, respectively; P < 0.05). During PI treatment, the level in HIV-positive patients decreased to 7.8 mM, (P = 0.004) similar to that in controls. Treatment with efavirenz

did not have any further impact on the results (Fig. 2c). Fibrinogen followed the same trend, and was higher in treatment-naïve patients than in controls (9.4 vs. 8.6 μM, respectively; P = 0.041); however, the decrease during therapy was only significant after 6 months (9.4 vs.

7.2 μM at baseline vs. 6 months, respectively; P = 0.002). In untreated HIV-positive patients, the median level of D-dimers was significantly higher than that found in healthy subjects (0.55 vs. 0.23 μg/mL, respectively; P < 0.001). Treatment for 6 months lowered D-dimer values to a level comparable to that of controls (0.35 vs. 0.23 μg/mL, respectively, P = 0.4) (Fig. 2d). Baseline APTT was marginally but not significantly lower in HIV-positive patients vs. controls (30 vs. 32 s, respectively; Baricitinib P < 0.07). With PI treatment, APTT decreased further (28.8 s), becoming significantly different from that in controls (P < 0.01). Changing treatment to efavirenz did not alter this value significantly (29.0 s). PT was similar in the two groups throughout the entire study period. Looking at the correlation between CD4 cell count and the vascular, inflammatory, and coagulation markers in treatment-naïve HIV-infected patients, only E-selectin was significantly associated with CD4 count (r = 0.5; P = 0.025) (for all others: r ≤ |0.36|; P ≥ 0.1). There was no significant correlation between VL and any of the parameters examined in the study (for all: r ≤ |0.4|; P ≥ 0.1). When the treatment-naïve patients were divided into groups according to CD4 count <200 cells/μL (n = 14) and ≥200 cells/μL (n = 6), only vWF was significantly different in the two groups (2.13 vs. 1.59 U/L, respectively; P = 0.048) (E-selectin 23.0 vs. 30.

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