Circulating pentraxin 3 is positively associated with chronic hyperglycemia but negatively associated with plasma aldosterone concentration

<div><p>Pentraxin 3 (PTX3) is reported to be a vascular inflammation marker providing prognostic information of vasculopathy. Until today, however, the effect of aldosterone or oxidative stress on the regulation of PTX3 is unknown. In present study, we investigated to find regulative factors, especially aldosterone and oxidative stress, on PTX3. Serum PTX3 levels were measured in 75 patients (45 male and 30 women, aged 55.1±13.4 year-old (mean±SD)) with various endocrine disorders including 47 with diabetes, 24 with primary aldosteronism (PA). All participants were free from cardio vascular diseases and diabetic retinopathy. Serum PTX3 level was significantly lower in patients with PA than without PA and was significantly higher in patients with diabetes than without diabetes. PTX3 was significantly correlated with glycated hemoglobin (HbA1c), urinary albumin excretion (UAE) and plasma aldosterone concentration (PAC) (r = 0.431, P<0.001; r = 0.313, P = 0.009; r = -0.375, P = 0.004). A stepwise multiple regression analysis chose HbA1c and UAE as independent determinants of PTX3 (β = 0.282, P<0.001; β = 0.783, P<0.001). On the other hand, PTX3 was not significantly correlated with HbA1c and UAE but significantly negatively correlated with PAC in patients with diabetes. Therefore, it might be suggested that PTX3 is positively regulated by chronic hyperglycemia but negatively regulated by aldosterone, and is associated with urinary albumin excretion as a micro vasculopathy.</p></div

Stepwise multiple regression analysis between PTX3 and each parameter.

<p>Stepwise multiple regression analysis between PTX3 and each parameter.</p

Correlations between PTX3 and each parameter.

<p>Correlations between PTX3 and each parameter.</p

The clinical characteristics of participants.

<p>The clinical characteristics of participants.</p

Changes in LDL cholesterol (box plots).

<p><b>A. Percentage reduction of LDL-C after 12 weeks of treatment:</b> The solid bar represents the percent change in DST and the dotted bar represents the percent change in EST. B. <b>LDL-C values before and after 12 weeks of treatment:</b> The white bars represent basal values before treatment and the black bars represent values after treatment. The dotted textile indicates EAT therapy and the solid bar indicates DST therapy. n.s., not significant; *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001.</p

Demographic profiles of treatment groups.

<p>Demographic profiles of treatment groups.</p

Achievement rates in each treatment group.

<p>The bars representing the DST group are white and the bars representing the EAT group are black.</p

The changes in atherogenic lipid profiles (box plots).

<p>A, C: The percent changes in sd-LDL-C and RLP-C, respectively. B, D: sd-LDL-C and RLP-C values before and after the 12 weeks of treatment, respectively. The ‘before treatment’ values are shown as white bars and the ‘after treatment’ values are shown as black bars. n.s., not significant; *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001.</p

Baseline Characteristics of treatment groups.

<p>Baseline Characteristics of treatment groups.</p

Flow of Patients in the RESEARCH Study.

<p>One hundred and nine patients were randomized. Fifty-six patients were assigned to the double intensified dose statin therapy (DST) group and 53 patients were assigned to the ezetimibe-add-on therapy (EAT) group. The analysis was performed on 51 patients in the EAT group and 56 patients in the DST group. T2DM: type 2 diabetes mellitus.</p