Plasma Visfatin Levels In Patients Research Articles

Elevated plasma visfatin concentrations in patients with community-acquired pneumonia

Visfatin has been associated with some inflammatory disease. This study aimed to compare plasma visfatin levels in patients with community-acquired pneumonia and healthy controls and to furthermore investigate the relationship between their concentrations and 30-day mortality in patients. Plasma visfatin concentrations were measured in 176 patients and 95 healthy controls. The admission visfatin levels were significantly increased in all patients, survivals and non-survivals with community-acquired pneumonia compared with healthy control individuals, associated with pneumonia severity index score, Acute Physiology and Chronic Health Evaluation II score, white blood cell count, and plasma C-reactive protein level, and identified as an independent predictor for 30-day mortality. Its predictive value was similar to those of pneumonia severity index score and Acute Physiology and Chronic Health Evaluation II score. However, visfatin did not statistically significantly improve the predictive values of pneumonia severity index score and Acute Physiology and Chronic Health Evaluation II score. Thus, higher plasma visfatin level correlates with disease severity and markers of system inflammation and represent a novel biomarker for predicting 30-day mortality in patients with community-acquired pneumonia.

Prognostic significance of plasma visfatin levels in patients with ischemic stroke

Plasma visfatin concentration has been enhanced in ischemic stroke. The aim of the current investigation was to test whether determination of visfatin in plasma is associated with 6-month clinical outcomes including mortality and unfavorable outcome (modified Rankin Scale score>2) in the patients with ischemic stroke. Between July 2009 and January 2012, plasma visfatin concentrations of 186 patients and 100 healthy individuals were quantified by enzyme-linked immunosorbent assay. Plasma visfatin concentrations were higher in patients than in healthy individuals (108.5±41.1ng/mL vs. 13.8±3.9ng/mL, P<0.001). A logistic regression analysis selected plasma visfatin concentration as an independent predictor for 6-month clinical outcomes (both P<0.01). Using receiver operating characteristic curve analysis, plasma visfatin concentration was found to predict 6-month clinical outcomes with the high predictive performance. The predictive value of visfatin was in the range of National Institutes of Health Stroke Scale score (both P>0.05). Combined use of visfatin and National Institutes of Health Stroke Scale score did not improve the predictive significance (both P>0.05). Thus, visfatin may help in the prediction of long-term clinical outcomes in patients with ischemic stroke.

Visfatin plasma concentrations in patients with hyperthyroidism and hypothyroidism before and after control of thyroid function

Alterations in thyroid function are associated with changes in body weight, metabolism, and low-grade inflammation. In several studies, plasma levels of visfatin were found to be associated with body mass index, diabetes, and metabolic syndrome. In our study we aimed to evaluate visfatin levels according to thyroid dysfunction. The study cohort comprised 56 Hashimoto thyroiditis patients with hypothyroidism (43.94+/-14.27 yr), 56 Graves patients with hyperthyroidism (45.87+/-13.28 yr), and 56 euthyroid healthy subjects (45.23+/-7.11 yr) as a control group. In addition, we evaluated the effect of therapy on plasma visfatin levels in 16 hypothyroid and in 25 hyperthyroid patients. Markedly low visfatin levels were found in hyperthyroid patients [9.44 (8.07- 10.8) ng/ml] compared with the hypothyroid [49.93 (40.72- 59.1) ng/ml] and control groups [38.6 (30.6-46.6) ng/ml] (p<0.001, p<0.001). Plasma visfatin levels in patients with hypothyroidism decreased significantly following treatment [58.58 (10.21-190.7) ng/ml vs 40.00 (10.01-102.6) ng/ml; p=0.001]. Plasma visfatin levels increased significantly after antithyroid therapy in patients with hyperthyroidism [7.86 (1.02-19.23) ng/ml vs 12.63 (3.48-110.9) ng/ml; p<0.001]. There were negative correlations between visfatin levels with free T3 (r=-0.719, p<0.001), and free T4 (r=-0.716, p<0.001) levels. There was a positive correlation between visfatin and TSH levels (r=0.701, p<0.001). There was a negative correlation between delta visfatin levels with delta free T3, delta free T4 (r=-0.686, p<0.001; r=-0.624, p<0.001). Visfatin thus seems to be regulated by thyroid hormones. While the influence of thyroid dysfunction on adipocytokine production and release is still poorly understood, the results of our study suggest that the effects of hyper- and hypothyroidism on various metabolic parameters may be partly mediated by visfatin.

The effects of pioglitazone and metformin on plasma visfatin levels in patients with treatment naive type 2 diabetes mellitus

Aims Circulating visfatin levels are altered in insulin resistant states. We evaluated the effects of two insulin-sensitizing hypoglycemic agents on plasma visfatin and adiponectin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM). Methods Forty-four patients with T2DM were randomized to treatment either with pioglitazone (15–45 mg/day) or metformin (1000–2000 mg/day). Plasma visfatin and adiponectin levels and homeostasis model assessment of insulin resistance (HOMA-IR) scores were determined at baseline and at 12th week of treatment. Results By the end of the 12th week, fasting plasma glucose, HbA1c, HOMA-IR scores and waist circumferences improved equally in both treatment arms. HDL cholesterol and adiponectin levels increased only in the pioglitazone group ( p = 0.01 and p = 0.003, respectively). On the other hand, metformin treatment had additional regulatory effects on BMI, blood pressure and total and LDL-cholesterol levels ( p = 0.002, p = 0.01, p = 0.004, p = 0.001 and p < 0.001, respectively). Neither pioglitazone nor metformin displayed a significant effect on circulating visfatin concentration. Conclusions Despite improvements in insulin sensitivity and glycemic regulation, either pioglitazone or metformin treatment did not result in any effect on blood visfatin levels in patients with treatment naïve T2DM.

Intensive Glycemic Control Lowers Plasma Visfatin Levels in Patients with Type 2 Diabetes

Visfatin is an independent association factor for type 2 diabetes mellitus (T2DM). In order to evaluate the plasma visfatin levels and investigate whether plasma visfatin concentrations are altered by intensive glycemic control in patients with diabetes, we determined plasma visfatin concentrations and metabolic parameters in 53 newly diagnosed type 2 diabetic patients and 35 healthy controls. Visfatin levels were also investigated before and after intensive glycemic control for three months in subgroup of patients with T2DM. Plasma visfatin levels were significantly elevated in diabetic patients compared with healthy controls (p<0.001). Circulating visfatin concentration was associated with fasting plasma glucose (FPG), 2-hour OGTT plasma glucose (2hPG), HOMA-beta indexes (r=0.338, p=0.001; r=0.340, p=0.002; r=-0.296, p=0.006, respectively), but not with insulin sensitivity (HOMA-IR) or other metabolic or anthropometric parameters in all subjects. In addition, visfatin levels were also correlated with HbA1c levels in diabetic patients. Furthermore, visfatin concentrations reduced from 25.0+/-6.5 ng/ml at baseline to 20.3+/-4.7 ng/ml (p<0.01) after 3 months of intensive glycemic control, while HbA1c levels decreased from 9.0+/-1.8% to 6.2+/-0.7% (p<0.01). We conclude that the change of visfatin concentration may be a compensatory mechanism to ameliorate insulin deficiency due to pancreatic beta-cell dysfunction.

Effect of rosuvastatin treatment on plasma visfatin levels in patients with primary hyperlipidemia

Visfatin is a novel adipokine involved in the process of atherosclerosis. We assessed the effect of rosuvastatin on plasma visfatin levels in patients with primary hyperlipidemia. Eighty hyperlipidemic patients without evidence of cardiovascular disease were randomized to receive either rosuvastatin 10 mg/day or therapeutic lifestyle changes intervention. Plasma visfatin levels were determined at baseline and after 12-weeks post-randomization. Rosuvastatin induced a significant decrease in plasma visfatin levels (17.1 ± 2.1 versus 15.5 ± 2.0 ng/ml, P = 0.03). This effect correlated with baseline visfatin levels ( r = 0.51, P < 0.01) and was independent of any lipid-lowering actions of rosuvastatin.

Plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance

Visfatin, a new adipokine, facilitates adipogenesis and has insulin-mimetic properties. We aimed to investigate the plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM) and impaired glucose tolerance (IGT), who had no obesity or hypertension. Twenty-two patients with T2DM, 18 subjects with IGT and 40 healthy controls were enrolled. Visfatin levels were measured along with the BMI, blood pressure, lipids, glucose, insulin, adiponectin and hsCRP levels, and HOMA-IR indexes. Age, sex and BMI were similar in all groups. Visfatin levels were higher in the diabetic group than the controls ( p = 0.01). There was no significant difference in the visfatin levels between the T2DM and IGT groups as well as IGT group and healthy controls. Plasma visfatin concentrations did not differ between men and women. Visfatin levels did not correlate with BMI, blood pressure, plasma adiponectin, insulin, hsCRP, glucose and lipid levels or HOMA-IR indexes in the three groups. These results indicate that hyperglycemia causes an increase in plasma visfatin levels and, as in people with T2DM but not with IGT, this increase gets more prominent as the glucose intolerance worsens.