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Serum ,-glutamyltransferase within its normal concentration range is related to the presence of diabetes and cardiovascular risk factors

DIABETIC MEDICINE, Issue 9 2005
D.-J. Kim
Abstract Aims Although many studies have reported an association between serum ,-glutamyltransferase (GGT) and cardiovascular risk factors, the mechanism of this relationship has not been clarified. Methods The medical records of 29 959 subjects (age, median 48, range 14,90 years; 16 706 men, 13 253 women) who visited the Center for Health Promotion at Samsung Medical Center for a medical check-up between January 2001 and December 2003, were investigated. Subjects with hepatic enzyme/GGT concentrations higher than three times the upper limit of the reference range, a positive test for hepatitis C virus antibody, a positive test for hepatitis B virus surface antigen, currently taking anti-diabetic/anti-hypertensive/anti-lipid medication, or a white blood cell (WBC) count higher than 10 000 cells/ml, were excluded. The subjects of each gender were classified into five groups according to their serum GGT concentrations, into quartiles of the normal range of GGT (groups 1, 2, 3 and 4) and into a group with elevated GGT (group 5). Results As the group number increased (group 1 , 5), the frequencies of all of the following increased: (i) diabetes and impaired fasting glucose (IFG); (ii) hypertension, obesity (body mass index , 27 kg/m2), dyslipidaemia (LDL-cholesterol , 4.1 mmol/l and/or triglyceride , 2.46 mmol/l, or HDL-cholesterol < 1.16 mmol/l); (iii) metabolic syndrome. Moreover, these significant relationships between GGT concentrations within its normal range and the presence of diabetes/IFG, hypertension, obesity, dyslipidaemia, and metabolic syndrome persisted after adjusting for several clinical and biochemical variables and for the presence of fatty liver based on ultrasonographic findings. Odds ratios (95% CI) for group 4 (highest quartile of normal range of GGT) vs. group 1 (lowest quartile of normal range of GGT); the referent group, were 3.16 (2.15,4.65) for diabetes, 2.24 (1.73,2.90) for IFG, 1.93 (1.59,2.33) for obesity, 1.38 (1.23,1.55) for dyslipidaemia and 2.88 (2.28,3.65) for metabolic syndrome in men. In women, the odds ratios were 2.72 (1.34,5.52), 3.67 (2.26,5.97), 2.10 (1.61,2.74), 1.80 (1.58,2.04) and 3.57 (2.52,5.07), respectively. Conclusions Our data show that, even within its normal range, serum GGT concentrations are closely associated with the presence of diabetes and cardiovascular risk factors, and that these associations are independent of a fatty liver by ultrasonography. [source]

A Model of Ischemically Induced Ventricular Fibrillation for Comparison of Fixed-dose and Escalating-dose Defibrillation Strategies

ACADEMIC EMERGENCY MEDICINE, Issue 6 2004
James T. Niemann MD
Abstract Objectives: Fixed- and escalating-dose defibrillation protocols are both in clinical use. Clinical observations suggest that the probability of successful defibrillation is not constant across a population of patients with ventricular fibrillation (VF). Common animal models of electrically induced VF do not represent a clinical VF etiology or reproduce clinical heterogeneity in defibrillation probability. The authors hypothesized that a model of ischemically induced VF would exhibit heterogeneous defibrillation shock strength requirements and that an escalating-dose strategy would more effectively achieve prompt defibrillation. Methods:Forty-six swine were randomized to fixed, lower-energy (150 J) transthoracic shocks (group 1) or escalating, higher-energy (200 J,300 J,360 J) shocks (group 2). VF was induced by balloon occlusion of a coronary artery. After 1 or 5 minutes of VF, countershocks with a biphasic waveform were administered. The primary endpoint was successful defibrillation (termination of VF for 5 seconds) with ,3 shocks. Results: VF was induced with occlusion or after reperfusion in 35 animals. Only five of 17 group 1 animals (29%, 95% CI = 10 to 56) could be defibrillated with ,3 shocks; 15 of 18 group 2 animals (83%, 95% CI = 59 to 96) were defibrillated with ,3 shocks (p < 0.002 vs. group 1). Nine of the group 1 animals (75%) that could not be defibrillated with 150-J shocks were rescued with ,3 shocks ranging from 200 to 360 J. Conclusions: In this ischemic VF animal model, defibrillation shock strength requirements varied among individuals, and when defibrillation was difficult, an escalating-dose strategy was more effective for prompt defibrillation than fixed, lower-energy shocks. [source]

A randomized 4-arm multicenter study of interferon alfa,2b plus ribavirin in the treatment of patients with chronic hepatitis C not responding to interferon alone

HEPATOLOGY, Issue 1 2001
Giorgio Saracco
To determine whether a higher dosage of interferon (IFN) associated with ribavirin and/or prolonged time of administration may improve therapeutic efficacy, we conducted a 4-arm randomized trial on patients with chronic hepatitis C not responding to one or more previous treatment courses with IFN monotherapy. Group 1 (n = 139) received 3 million units (MU) IFN-,2b 3 times a week (t.i.w.) plus ribavirin 1,000 mg/d for 12 months; group 2 (n = 162) received 5 MU t.i.w. plus ribavirin for 12 months; group 3 (n = 142) received 3 MU t.i.w. plus ribavirin for 6 months; and group 4 (n = 151) received 5 MU t.i.w. plus ribavirin for 6 months. The primary end point was hepatitis C virus (HCV)-RNA clearance at the end of 6-month follow-up. HCV-RNA was negative in 15% of group 1, 23% of group 2, 11% of group 3, 16% of group 4 (group 2 vs. group 3, P = .04). Among patients with genotypes 1 and 4, sustained response was significantly higher in group 2 vs. group 3 (18% vs. 7%, P = .03; group 1 = 9%, group 4 = 12%, P = not significant [NS]). In patients with genotypes 2 and 3, sustained virologic response was not affected by the different regimens (group 1 = 32%, group 2 = 30%, group 3 = 30%, group 4 = 35%, P = NS). In conclusion, about 23% of nonresponders to IFN monotherapy may achieve a sustained response if re-treated by 5 MU t.i.w. IFN plus ribavirin 1,000 mg/d for 1 year. Patients with genotype 1 should receive a high dosage of IFN plus ribavirin for 12 months, whereas therapy for patients with genotype 2 or 3 should be less aggressive. [source]

Atazanavir and lopinavir with ritonavir alone or in combination: analysis of pharmacokinetic interaction and predictors of drug exposure

HIV MEDICINE, Issue 4 2008
S Di Giambenedetto
Objectives Studies on the pharmacokinetic interaction between atazanavir and lopinavir with ritonavir (lopinavir/ritonavir) report contradictory results. We aimed to establish the in vivo interaction between these two protease inhibitors as well as the variables influencing drug exposure. Methods Pharmacokinetic parameters were investigated in HIV-infected patients treated with atazanavir 300 mg with ritonavir 100 mg q24h (group A) or lopinavir/ritonavir 400/100 mg q12h (group B) or atazanavir 300 mg q24h with lopinavir/ritonavir 400/100 mg q12h (group C). Patients receiving other concomitant protease inhibitors or non-nucleoside reverse transcriptase inhibitors were excluded. Results In group A (n=10), mean ± standard deviation atazanavir Cmin was 390 ± 460 ng/mL, Cmax 3051 ± 1996 ng/mL and AUC24 29 913 ± 17 686 ng/mL/h. In group B (n=9), lopinavir Cmin was 7562 ± 4292 ng/mL, Cmax 12 944 ± 4838 ng/mL and AUC0,12 122 313 ± 38 225 ng/mL/h. In group C (n=7), atazanavir Cmin was 876 ± 460 ng/mL (P=0.039 vs. group A), Cmax 3421 ± 3399 ng/mL and AUC0,24 65 055 ± 49 843 ng/mL/h (two-sided P>0.05 for each comparison with group A), lopinavir Cmin was 7471 ± 3745 ng/mL, Cmax 10 143 ± 5217 ng/mL and AUC0,12 104 501 ± 43 565 ng/mL/h (P>0.05 for each comparison with group B). When analysing all the groups, including controls from routine clinical practice, higher body mass index was associated with lower atazanavir Cmin and with lower lopinavir Cmax. Atazanavir Cmin showed a correlation with total bilirubin levels. Conclusions Combination with lopinavir/ritonavir provides higher atazanavir Cmin than combination with ritonavir alone, possibly because of an effect of the additional ritonavir dose. Low BMI may be associated with higher drug exposure. [source]

Endothelial progenitor cells and arterial functions in the late convalescence period of Kawasaki disease

ACTA PAEDIATRICA, Issue 8 2009
Xiao-qin Liu
Abstract Aim:, The relationship was investigated between endothelial progenitor cells (EPCs) level and arterial functions in the convalescence of Kawasaki disease (KD). Methods:, Sixty-three children were divided into coronary artery lesion (CAL) group (group 1, n = 21), non-CAL group (group 2, n = 20) and control group (group 3, n = 22). EPCs were examined by flow cytometry and arterial functions (flow-mediated dilation [FMD], carotid artery stiffness index [SI]) were measured by ultrasound. Results:, From group1 to group 3, FMD was 4.5%± 1.5%, 9.5%± 2.8% and 12.1%± 2.3% (p < 0.01 between any two groups); carotid artery SI was 4.10 ± 0.44, 3.81 ± 0.50 and 3.59 ± 0.46 (group 1 vs. group 2, p < 0.05; group 1 vs. group 3, p < 0.01; group 2 vs. group 3, p = 0.142) and the number of EPCs was 2.0 ± 0.6/,L, 4.2 ± 0.8/,L, 4.5 ± 0.7/,L (p < 0.01 for group1 vs. group 2 and group 1 vs. group 3; group 2 vs. group 3, p = 0.292). Multiple linear regressions analysis and correlation analysis identified that FMD and carotid artery SI were significant determinants of EPCs level and were all independently correlated with EPCs level. Conclusions:, Our results indicate decreased EPCs are associated with arterial dysfunction in patients with CAL in the convalescence of KD. Our findings suggest EPCs may have a role in alteration of arterial functions. [source]