Effects of major adipokines and the -420 C > G resistin gene polymorphism on the long-term outcome of patients with acute ischemic stroke.

Aim: The association between adiponectin, leptin, and resistin and the long-term outcome of ischemic stroke are controversial. We aimed to evaluate this relationship. Methods: We prospectively studied 83 patients consecutively hospitalized for acute ischemic stroke (38.6% males, age 79.7 ± 6.3 years). Serum adiponectin, leptin, and resistin levels and the -420C > G polymorphism of the resistin gene were determined at admission. Stroke severity at admission was evaluated with the National Institutes of Health Stroke Scale (NIHSS). One year after discharge, functional status, incidence of cardiovascular events and all-cause mortality were recorded. Functional status was evaluated with the modified Rankin scale (mRS). Results: Patients with the G allele had lower mRS (p < .05) and patients with adverse outcome had higher serum resistin levels (p < .05). The only independent predictor of adverse outcome was mRS at discharge (risk ratio (RR) 2.78, 95% confidence interval (CI) 1.54-5.00; p < .001). Higher adiponectin levels were an independent predictor of cardiovascular morbidity (RR 1.07, 95% CI 1.01-1.14; p < .05). Patients who died had higher serum adiponectin levels than those who survived (p < .05). The only independent predictor of all-cause mortality was NIHSS at admission (RR 1.19, 95% CI 1.04-1.35; p < .01). Conclusions: In patients with acute ischemic stroke, the G allele of the -420C > G polymorphism of the resistin gene promoter is more frequent in those with a more favorable functional outcome at one year after discharge. Patients with higher serum resistin levels appear to have worse long-term functional outcome, while higher serum adiponectin levels are associated with higher incidence of cardiovascular events.

Major Adipokines and the -420C>G Resistin Gene Polymorphism as Predictors of Acute Ischemic Stroke Severity and In-Hospital Outcome.

BACKGROUND: The role of adiponectin, leptin, and resistin and the -420C>G polymorphism of the resistin gene promoter in the pathogenesis of ischemic stroke are controversial. We aimed to evaluate whether serum levels of these adipokines and the -420C>G polymorphism are associated with ischemic stroke severity and in-hospital outcome. METHODS: We prospectively studied 93 patients who were consecutively hospitalized for acute ischemic stroke (39.8% males, age 79.7 ± 6.3 years). Stroke severity was evaluated at admission by the National Institutes of Health Stroke Scale (NIHSS). In-hospital outcome was evaluated by dependency rates at discharge and in-hospital mortality. RESULTS: The G allele was more prevalent in patients with severe stroke (P < .05). Independent predictors of severe stroke were high-sensitivity C-reactive protein levels (relative risk [RR] 1.43, 95% confidence interval [CI] 1.08-1.91, P < .05). Patients with dependency at discharge had lower serum leptin levels (P < .05). Independent predictors of functional dependence were prior ischemic stroke (RR 7.55, 95% CI 1.69-33.58, P < .01), serum triglyceride levels (RR .98, 95% CI .96-0.99, P < .05), and NIHSS at admission (RR 1.47, 95% CI 1.17-1.84, P < .001). The G allele was more prevalent in patients who died (P < .05). Independent predictors of in-hospital mortality were systolic blood pressure (RR 1.09, 95% CI 1.01-1.19, P < .05) and NIHSS at admission (RR 1.26, 95% CI 1.08-1.48, P < .005). CONCLUSIONS: The G allele of the -420C>G polymorphism of the resistin gene promoter appears to be associated with more severe stroke and higher in-hospital mortality in patients with acute ischemic stroke. Higher leptin levels appear to be related to favorable functional outcome.

Adefovir plus lamivudine are more effective than adefovir alone in lamivudine-resistant HBeAg- chronic hepatitis B patients: a 4-year study.

BACKGROUND AND AIM: Adefovir dipivoxil (ADV) is effective in lamivudine (LAM)-resistant hepatitis B e antigen-negative (HBeAg(-)) chronic hepatitis B (CHB). However, it is unclear whether LAM treatment should be continued in these patients. We aimed to compare the long-term efficacy of adding ADV to ongoing LAM treatment versus switching to ADV monotherapy in LAM-resistant HBeAg(-) CHB. METHODS: Sixty LAM-resistant patients with HBeAg(-) CHB were randomly assigned (3:1) to combination therapy (10 mg ADV once daily plus ongoing LAM at 100 mg once daily [n = 45]) or 10 mg ADV monotherapy once daily (n = 15). Virological and biochemical responses were defined as hepatitis B virus (HBV)-DNA <400 copies/mL and as normalization of alanine aminotransferase levels, respectively. RESULTS: The median follow-up time was 53 months (range 20-60 months). A virological response was observed in 38/45 (84.4%) and 11/15 (73.3%) patients in the ADV/LAM and ADV monotherapy groups, respectively (P = 0.56). Biochemical response rates were higher in the ADV/LAM group than in the ADV monotherapy group (90.9% vs 57.1%, respectively; P = 0.01). In the ADV/LAM group, serum HBV-DNA remained undetectable in all patients who achieved a virological response (n = 38). In the ADV monotherapy group, virological breakthrough occurred in four of the 11 patients who achieved a virological response (36.4%; P < 0.001 vs the ADV/LAM group, log-rank test). In addition, two patients in each group who did not achieve a virological response eventually developed ADV resistance. CONCLUSIONS: Adding ADV to LAM is more effective than switching to ADV monotherapy in LAM-resistant patients with HBeAg(-) CHB.

Common ABCB1 polymorphisms in Greek patients with chronic hepatitis C infection: A comparison with hyperlipidemic patients and the general population.

BACKGROUND: Hepatitis C virus infectivity and replication efficiency appears to be dependent on the lipid content and organization of the plasma membrane of the host cell, as well as of the intracellular membranous web. As there is increasing awareness of a role played by the efflux pump ABCB1 (p-glycoprotein, P-gp) in lipid homeostasis, its function could be a determinant of chronic HCV infection. The aim of the present study was to examine and compare the distribution of common ABCB1 genotypes in patients with chronic HCV infection (n=168), hyperlipidemic patients (n=168) and a control group (n=173), all from Greece. METHODS: Participants were genotyped for the ABCB12677G>T/A and 3435C>T polymorphisms with previously reported PCR-RFLP methods. Genotype and allele frequency distributions were compared between the three groups with the χ(2) test of independence. RESULTS: The ABCB1 2677GG (ancestral) genotypes were significantly over-represented in patients with chronic hepatitis C compared to controls (39.3% vs. 26.6%, p=0.015 according to the dominant model). A similar result was obtained when hyperlipidemic patients were compared to controls (45.2% vs. 26.6%, p<0.001 according to the dominant model). Comparison of ABCB1 3435C>T genotype and allele distributions provided similar but not as significant differences. Genotype and allele distributions for both ABCB12677G>T/A and 3435C>T were very similar between HCV patients and hyperlipidemic patients. CONCLUSION: Our findings imply an influence of ABCB1 polymorphisms on HCV infectivity, possibly through an effect on lipid homeostasis.