Visfatin and 25-Hydroxyvitamin D3 Levels Affect Coronary Collateral Circulation Development in Patients with Chronic Coronary Total Occlusion

Background: Coronary collateral circulation (CCC) plays a vital role in the myocardial blood supply, especially forischemic myocardium. Evidence suggests that the visfatin and 25-hydroxyvitamin D3 [25(OH)D3] levels are related to the degree and incidence of vascular stenosis associated with coronary artery disease; however, few studies have evaluated the effect of visfatin and 25(OH)D3 on CCC development in patients with chronic total occlusion (CTO).This study aimed to evaluate the relationship between the serum visfatin and 25(OH)D3 levels and CCC in patients with CTO.Methods: A total of 189 patients with CTO confirmed by coronary angiography were included. CCC was graded from 0 to 3 according to the Rentrop-Cohen classification. Patients with grade 0 or grade 1 collateral development were included in the poor CCC group (n = 82), whereas patients with grade 2 or grade 3 collateral development were included in the good CCC group (n = 107). The serum visfatin and 25(OH)D3 levels were measured by ELISA.Results: The visfatin level was significantly higher in the poor CCC group than in the good CCC group, and the 25(OH)D3 level was significantly lower in the poor CCC group than in the good CCC group (P = 0.000). Correlation analysis showed that the Rentrop grade was negatively correlated with the visfatin level (r = − 0.692, P = 0.000) but positively correlated with the 25(OH)D3 level (r = 0.635, P = 0.000). Logistic regression analysis showed that the visfatin and 25(OH)D3 levels were independent risk factors for CCC (odds ratio 1.597, 95% confidence interval 1.300–1.961, P = 0.000 and odds ratio 0.566, 95% confidence interval 0.444–0.722, P = 0.000, respectively). The visfatin and25(OH)D3 levels can effectively predict the CCC status.Conclusion: Serum visfatin and 25(OH)D3 levels are related to CCC development and are independent predictors of poor CCC.

Visfatin and Rheumatoid Arthritis: Pathogenetic Implications and Clinical Utility

Objective: Analysis and generalization of data related to visfatin involvement in the pathogenesis of inflammation at various stages of rheumatoid arthritis. Data Synthesis: Visfatin is an adipocytokine which has also been identified in non-adipose tissues. It influences directly on the maturation of B cells, which are involved in autoantibody production and T cell activation. Visfatin can promote inflammation via regulation of pro-inflammatory cytokines including TNF, IL-1β and IL-6. The concentration of circulating visfatin in rheumatoid arthritis patients is higher compared to healthy individuals. Several studies suggest that visfatin level is associated with rheumatoid arthritis activity, and its elevation may precede clinical signs of the relapse. In murine collagen-induced arthritis, visfatin levels were also found to be elevated both in inflamed synovial cells and in joint vasculature. Visfatin blockers have been shown to confer fast and long-term attenuation of pathological processes; however, most of their effects are transient. Other factors responsible for hyperactivation of the immune system can participate in this process at a later stage. Treatment of rheumatoid arthritis with a combination of these blockers and inhibitors of other mediators of inflammation can potentially improve treatment outcomes compared to current therapeutic strategies. Recent advances in the treatment of experimental arthritis in mice as well as the application of emerging treatment strategies obtained from oncology for rheumatoid arthritis management could be a source of novel adipokine-mediated anti-rheumatic drugs. Conclusion: The ongoing surge of interest in anticytokine therapy makes further study of visfatin highly relevant as it may serve as a base for innovational RA treatment.

The The Circulating Visfatin Level Relation to the Severity of Chronic Kidney Disease

BACKGROUND: Adipokines have been associated with atherosclerotic heart disease, which has plenty of common risk factors with chronic kidney disease (CKD), but their association with CKD has not been well characterized. AIM: We investigated the association between the serum visfatin level and CKD. METHODS: The serum visfatin levels in 101 CKD patients and 101 controls were compared. CKD was defined as estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 or presence of albuminuria (≥30 mg/24 h). RESULTS: After adjustment for established CKD risk factors, the median (interquartile range) of the serum visfatin was 3.65 ng/ml (2.31–4.59) in patients with CKD and 1.66 ng/ml (0.90–2.45) in controls without CKD (p < 0.0001 for group difference). Serum visfatin was significantly and inversely correlated with eGFR (r = –0.79, p < 0.0001) and positively correlated with urine albumin (r = 0.71, p < 0.0001) in the study participants. There was a strong dose-response and the significant relationship between serum visfatin level and CKD severity, assessed by GFR and albuminuria, regardless of established risk factors for CKD, including hypertension, diabetes, and cardiovascular disease. CONCLUSION: Our results show that circulating visfatin is associated with the risk and severity of CKD. These results suggest that longitudinal studies and clinical trials should be conducted to investigate if adipocytokines play a role in the development and progression of CKD independent of body mass index or waist circumference. These important findings may advance our further understanding of CKD risk factors.

Serum Visfatin does not seem to be a Useful Marker to Guide Glucocorticoid Substitution in Adrenal Insufficiency

Primary adrenal insufficiency (Addison’s disease, AD) requires lifelong steroid substitution. Excess exogenous glucocorticoids promote abdominal obesity, insulin-glucose imbalance, and hypertension. Reliable markers of the adequate glucocorticoid replacement are lacking. Visfatin is a pro-inflammatory adipokine, with enzymatic activity of nicotinamide phosphoribosyltransferase. It enhances leukocyte function and synthesis of tumour necrosis factor α (TNFα) and interleukin-6 (IL-6). Serum visfatin is elevated in autoimmunity, but also in obesity, insulin resistance, and metabolic syndrome. This study was aimed to investigate whether serum visfatin could guide the glucocorticoid substitution in AD. Biochemical analyses were performed in 96 patients with AD (mean age 43.3±14.9 years) and 91 controls (43.5±12.5 years). Visfatin level was significantly elevated in patients with AD compared to controls (p<0.0001). Higher circulating IL-6 was also detected among subjects with AD (p=0.006). In AD, visfatin level was positively correlated with IL-6 (p=0.014), TNFα (p=0.001), body mass (p=0.015), fasting insulin (p=0.001) and HOMA-IR (p=0.001). No relationship was noticed with daily hydrocortisone (p=0.096) and urinary free cortisol excretion (p=0.499). Only the correlations with IL-6 and fasting insulin survived multiple regression analysis (p=0.049 and p=0.005, respectively). Additionally, positive correlation between visfatin and autoantibodies to 21-hydroxylase was noted (p=0.005). In the control group serum visfatin was correlated with IL-6 (p=0.009) and TNFα (p=0.0002). The current study reveals elevated serum visfatin in autoimmune AD. Visfatin does not seem a useful marker of the glucocorticoid replacement, although it correlates with fasting insulin and pro-inflammatory molecules. Further functional analyses are warranted to elucidate the role of visfatin in autoimmunity.

Assessment of serum visfatin level in beta thalassemia patients

Background Thalassemias are monogenetic hematologic disorders which are caused by faulty synthesis of one or more of the Hb chains which leads to imbalance in globin chains resulting in hemolysis and impaired erythropoiesis and chronic inflammatory condition. Visfatin is a pro-inflammatory adipocytokine which is mostly expressed in visceral adipose tissue and its testing may help in assessment of severity of the disease. Aim of the work This study aims at measuring serum visfatin level in Beta thalassemia patients and its possible correlation to disease severity (major andintermedia). Patients and methods Forty-one patients diagnosed as β-thalassemia (major, intermedia) and twenty age and sex-matched healthy individuals as the control group were tested for serum visfatin levels by enzyme-linked immunosorbent assay. Results Serum visfatin was higher in theß-thalassemia major(ß-TM) group than in the control group (P&lt;0.001). Serum visfatinand serum ferritin were higher inß-TM group than in ß-thalassemia intermediagroup (ß-TI)(p &lt; 0.001).Serum visfatin was found positively correlated with platelet count (P&lt; 0.001) in the ß-TM group.As per ROC curve analysis, measured serum visfatin level was found to discriminate ß-TM group from β-TI group and control group. Conclusion There is an association between serum visfatin and the degree of severity of β thalassemia disease. Recommendations Testing of the relationship between serum visfatin level and other vascular inflammatory markers in β-thalassemia disease (asadiponectin, resistin, intracellular adhesion molecule (ICAM)) to clarify the exact mechanism of the inflammatory process in the disease and its complications to alter the course of the disease.Also to study serum visfatin in complicated β-thalassemia patients to establish its possible role in cardiac, vascular, endocrine or any other complications and comparing it with non-complicated patients.