New prognostic score based on galectin-3 has similar performance to model for end-stage liver disease and sodium score in patients with stable decompensated cirrhosis.

BACKGROUND: Galectin-3 (gal-3) has been proposed as a marker of established renal impairment, with predictive value in stable decompensated cirrhosis. METHODS: 150 stable decompensated patients were assessed in 2 transplant centers. Patients' renal function was assessed using 51Chromium-EDTA ("true" glomerular filtration rate). We measured basic laboratory variables and gal-3 in serum samples. Factors associated with patients' outcomes were determined. RESULTS: Our patients were followed up for 12 months (range 1-48, interquartile range [IQR] 6, 95% confidence interval [CI] 10-13.5) and their mean prognostic scores were Child-Turcotte-Pugh (CTP) 7±2 and model for end-stage liver disease and sodium (MELD-Na) 15±6. Median gal-3 levels were 22 ng/mL. In a multivariate analysis of 94 patients (training group), gal-3 (hazard ratio [HR] 1.026, 95% confidence interval [CI] 1.011-1.041; P=0.003) and serum sodium (HR 1.032, 95%CI 1.006-1.062; P=0.05) were the only factors independently associated with patients' outcomes. Kaplan-Meier analysis using the median gal-3 values revealed different times of survival (log-rank P=0.006). We derived a new prognostic score, (0.026) × serum gal-3+ (-0.079) × serum sodium, with very good discriminative accuracy for the outcome (area under the curve [AUC] 0.71, 95%CI 0.63-0.88), similar to that of the MELD-Na score (AUC 0.69, 95%CI 0.67-0.89; P=0.73), while its diagnostic accuracy was validated in the remaining 56 decompensated patients (AUC 0.81, 95%CI 0.65-0.97). CONCLUSIONS: Gal-3 proved to be an accurate and plausible biomarker of renal dysfunction in patients with decompensated cirrhosis. A new prognostic model incorporating gal-3 and sodium was derived, with very good discriminative accuracy for the outcome.

Galectin-3 is associated with glomerular filtration rate and outcome in patients with stable decompensated cirrhosis.

BACKGROUND: Newly introduced galectin-3 (gal-3) has been associated to impaired renal function. Gal-3 may become prognostic biomarker in hepatic diseases. AIM: To investigate the association of gal-3 with prognosis and renal function in patients with stable decompensated cirrhosis. METHOD: We studied prospectively 100 stable decompensated patients in our Department between 2010 and 2017. We measured gal-3 in serum samples. Patients' renal function was assessed using 51Chromium-EDTA ("true GFR"). RESULTS: Seventy patients (70%) survived and 30 died (n = 16) or underwent LT (n = 14). Twenty nine patients (29%) had normal gal-3, 71 (71%) had ≥11.7 ng/mL; they differed significantly regarding mean "true"-GFR: 90 ±â€¯20 mL/min vs. 76 ±â€¯26 mL/min, p = 0.03 and mean creatinine: 0.83 ±â€¯0.14 mg/dL vs. 0.97 ±â€¯0.4 mg/dL, p = 0.05. Median gal-3 levels were 17.5 ng/mL (range 4.9-76.5 ng/mL); 49 patients with gal-3 ≥17.5 ng/mL had significantly higher MELD score, (15 ±â€¯5 vs. 13 ±â€¯4, p = 0.02) and worse "true" GFR (74 vs. 85 mL/min, p = 0.04). Gal-3 had good performance in predicting "true"-GFR < 60 mL/min; AUC: 0.71, 95%CI [0.58-0.85], best cut off value 17.5 ng/mL. Kaplan-Meier analysis, using median gal-3 (17.5 ng/mL) revealed different survival time for our patients (log-rank p = 0.04). CONCLUSION: Gal-3 proved trustworthy marker of established chronic kidney disease, with predictive ability in stable decompensated cirrhosis. Gal-3 came also a significant factor for our patients' outcome.

Comparison of creatinine and cystatin formulae with 51 Chromium-ethylenediaminetetraacetic acid glomerular filtration rate in patients with decompensated cirrhosis.

BACKGROUND AND AIM: Evaluation of renal function, that is, glomerular filtration rate (GFR), has become very important, but conventional mathematical formulae for GFR assessment are inaccurate in patients with cirrhosis. The aim of the present study was to compare serum creatinine (sCr)-based and serum cystatin C (cysC)-based estimated GFR (eGFR) formulae with 51 Chromium-ethylenediaminetetraacetic acid GFR (51 Chr-GFR) in patients with stable decompensated cirrhosis. METHODS: In 129 Caucasian patients with decompensated cirrhosis, we assessed sCr-based GFRs [Modification of Diet in Renal Disease and chronic kidney disease-epidemiology (CKD-EPI)-sCr formulae], cysC-based GFRs [Hoek, Larsson, and CKD-EPI-cysC equations], and the mathematical formulae, which combined both sCr and cysC [i.e. CKD-EPI-sCr-cysC and the specific for cirrhotics formula recently proposed by Mindikoglu et al. (Mindikoglu-eGFR)]. Multivariate linear regression analysis was used for GFR predictors in our cohort. RESULTS: The correlations between 51 Chr-GFR and all mathematical formulae were good (Spearman r2 > 0.68, P < 0.001). Modification of Diet in Renal Disease and CKD-EPI-sCr had lower bias (6.6 and -4.8, respectively), compared with the other eGFRs, while Mindikoglu-eGFR and CKD-EPI-sCr-cysC formulae had greater precision (17.1 and 17.3, respectively), compared with the other eGFRs. CKD-EPI-sCr and Mindikoglu-eGFR had higher accuracy (39% and 41%, respectively), compared with the other eGFRs. The factors independently associated with the 51 Chr-GFR were age, cysC, and sCr, and the new derived formula had lower bias (0.89) and similar precision (17.2) and accuracy (41%) with Mindikoglu-eGFR formula. CONCLUSION: The specific mathematical formulae derived from patients with cirrhosis seem to provide superior assessment of renal function, compared with the conventional used sCr-based and cysC-based formulae.

The effects of resistance training on ApoB/ApoA-I ratio, Lp(a) and inflammatory markers in patients with type 2 diabetes.

The purpose of this study was to investigate the effects of resistance training (RT) on novel cardiovascular risk factors in patients with type 2 diabetes mellitus (T2DM). We enrolled 52 overweight/obese, type 2 diabetic patients, with inadequate glycemic control (HbA1c > 6.5 %), but without overt diabetic vascular complications. Participants were randomly assigned into two equivalent groups (n = 26): (1) Resistance exercise group: subjects underwent a supervised RT program (3-times/week, 60 min/session, 2-3 sets of 8 machine-weight exercises, 60-80 % of one-repetition maximum). (2) Control group (CG): at study entrance, they received a structured exercise counseling to increase daily physical activity. Clinical parameters, cardiorespiratory capacity, glycemic and lipid profile, apolipoprotein A-I (ApoA-I), apolipoprotein B (ApoB), Lipoprotein(a) [Lp(a)], insulin resistance (HOMA-IR), high-sensitivity CRP (hsCRP), fibrinogen were measured before and after 3 months. RT significantly reduced glycemic indexes, insulin resistance and systolic blood pressure, compared to CG (p < 0.05). Moreover, exercise-treated patients conferred a remarkable downregulation in ApoB levels (from 135.92 ± 30.97 mg/dL to 85.9 ± 26.46 mg/dL, p < 0.001) as compared to CG (from 126.33 ± 36.59 mg/dL to 116.23 ± 27.52 mg/dL, p = 0.872) (p < 0.001). Similarly, ApoB/ApoA-I ratio was considerably decreased in REG rather than CG (-0.32 ± 0.09 vs 0.02 ± 0.01, p < 0.001). Notably, ApoA-I, Lp(a), hsCRP, fibrinogen, the rest of lipid parameters, body weight and exercise capacity remained unaltered in both groups (p > 0.05). Among variables, HOMA-IR reduction was found to be an independent predictor of changes in ApoB/ApoA-I ratio (R (2) = 0.406, p = 0.041) in REG. Long-term RT ameliorated glycemic control, insulin sensitivity and ApoB/ApoA-I ratio in individuals with T2DM. Although we did not observe significant benefits in the rest of cardiovascular risk factors, our results indicate a merely beneficial impact of RT.

Exercise training ameliorates the effects of rosiglitazone on traditional and novel cardiovascular risk factors in patients with type 2 diabetes mellitus.

The aim of the study was to investigate the effects of rosiglitazone and/or exercise training on novel cardiovascular risk factors in patients with type 2 diabetes mellitus. One hundred overweight/obese type 2 diabetes mellitus patients, with inadequate glycemic control (hemoglobin A(1c) >7%) despite combined treatment with gliclazide plus metformin, were randomized using a 2 x 2 factorial design to 4 equivalent (n = 25) groups, as follows: (1) CO: maintenance of habitual activities, (2) RSG: add-on therapy with rosiglitazone (8 mg/d), (3) EX: adjunctive exercise training, and (4) RSG + EX: supplementary administration of rosiglitazone (8 mg/d) plus exercise training. No participant had diabetic vascular complications or was receiving lipid-lowering therapy. Anthropometric parameters, cardiorespiratory capacity, glycemic and lipid profile, apolipoprotein (apo) A-I, apo B, interleukin (IL)-10, IL-18, insulin resistance, and blood pressure were measured before and after 12 months of intervention (P < .05). Both RSG and EX groups significantly reduced glycemic indexes, insulin resistance, blood pressure, and IL-18, whereas they significantly increased high-density lipoprotein, cardiorespiratory capacity, and IL-10, compared with CO group (P < .05). Besides this, exercise-treated patients conferred a remarkable down-regulation in the rest of lipid parameters (total cholesterol, low-density lipoprotein cholesterol, triglycerides, apo B) and body fat content (P < .05) in comparison with CO group. On the other hand, RSG group rather than CO group considerably increased apo A-I levels and body mass index (P < .05). Notably, the combined treatment group yielded pronounced beneficial changes in glycemic indexes, lipid profile, insulin resistance, blood pressure, IL-10, IL-18, apo A-I, and apo B (vs CO group, P < .05). Furthermore, the addition of exercise to rosiglitazone treatment counteracted the drug-related negative effects on body weight, low-density lipoprotein, and total cholesterol. Rosiglitazone plus exercise training elicited additive effects on body composition, glycemic control, and traditional and novel cardiovascular risk factors in type 2 diabetes mellitus patients, indicating complementary effects.

The effect of capecitabine on the healing of colonic anastomoses in rats.

PURPOSE: Capecitabine is a fluoropyrimidine carbamate with antineoplasmatic activity, recommended for the treatment of colorectal cancer. This study was designed to assess the effectiveness of the perioperative administration of capecitabine on the healing process of colonic anastomosis. METHODS: Sixty Wistar rats were used, which were randomized in 2 groups of 30 each. The study group was subjected to colonic anastomosis and treated with therapeutic doses of capecitabine (359 mg/kg, or 2/3 of the mean toxic dose) by mouth one week before anastomosis and throughout the study. The control group received only placebo medication. Both groups were further divided into three subgroups, each of ten animals. In both study and control groups, ten animals were killed in each session on postoperative Days 3, 7, and 14. RESULTS: We found no negative impact on the healing of colonic anastomosis on capecitabine administration. The rate of anastomotic leakage and septic complications were not found to be significantly different between the study and control groups. The median bursting pressure was found to be significantly higher in the study subgroup killed on the third day (68 vs. 46 mmHg of the control group). CONCLUSIONS: Perioperative administration of capecitabine does not have a negative impact on colonic anastomosis in rats.