Fecal pancreatic elastase-1 and erythrocyte magnesium levels in diabetes type 1 and type 2.

In both types of diabetes mellitus (DM), type 1 and type 2 (T1DM and T2DM), there are both endocrine and exocrine dysfunctions of the pancreas (PED), as well as disturbances in serum magnesium levels. The aim of this study was to examine the frequency of PED according to the level of fecal elastase-1 (FE-1) in patients with T1DM and T2DM, determining the correlation of the level of FE-1 with certain anthropometric parameters, certain indicators of metabolic regulation of diabetes, and certain nutritive markers of PED. MATERIALS AND METHODS: In the examinees, (56 with T1DM (F = 35 and M = 21), 62 with T2DM (F = 30 and M = 32), and 40 in the control group (F = 19 and M = 21)), we examined anthropometric parameters, and using standard biochemical methods, we measured the level of FE-1, magnesium concentration in blood and erythrocytes, and selected blood parameters. RESULTS: FE-1 concentration < 200 µg/g was present in 14.2% of the examinees with T1DM, 20.9% with T2DM, and 2.5% in the control group. In all examinees with DM, there was a statistically significant correlation (P < 0.05) between the level of FE-1 and Mg concentration in the erythrocytes (R = 0.40). CONCLUSIONS: Prevalence of pancreatic exocrine insufficiency (PEI), according to the level of FE-1, is significantly higher in patients with DM than in the control group, while it is a bit higher in patients with T2DM than the ones with T1DM. In both types of DM, Mg concentration in erythrocytes is in a significant correlation with the level of FE-1.

Influence of decreased fibrinolytic activity and plasminogen activator inhibitor-1 4G/5G polymorphism on the risk of venous thrombosis.

: Objective of our study is to determine whether decreased fibrinolytic activity or plasminogen activator inhibitor (PAI)-1 4G/5G polymorphism influence the risk of venous thrombosis.Our case-control study included 100 patients with venous thrombosis, and 100 random controls. When patients were compared with random controls, unconditional logistic regression was used to calculate odds ratios (ORs) with 95% confidence intervals (CIs).Decreased fibrinolytic activity yielded a 2.7-fold increase in risk for venous thrombosis than physiological fibrinolytic activity (OR 2.70; 95% CI 1.22-5.98), when comparing patients with random controls. Adjustment for several putative confounders did not change the estimate (OR 3.02; 95% CI 1.26-7.22). Analysis of venous thrombotic risk influenced by PAI-1 genotype, showed no influence of PAI-1 4G/5G gene variant in comparison with 5G/5G genotype (OR 0.57 95% CI; 0.27-1.20).Decreased fibrinolytic activity increased, whereas PAI-1 4G/5G polymorphism did not influence venous thrombosis risk in this study.

Interrelated cathepsin S-lowering and LDL subclass profile improvements induced by atorvastatin in the plasma of stable angina patients.

AIM: We hypothesized that, in stable angina patients, atorvastatin therapy lowers the cathepsin S (CTSS) concentrations, as assessed non-invasively according to a plasma analysis. In addition, the low-density lipoprotein (LDL) and high-density lipoprotein (HDL) size and subclasses in the plasma were analysed to establish the association between CTSS and lipoprotein metabolism and determine whether this association is atorvastatin-sensitive. METHODS: A total of 43 patients with stable angina received atorvastatin therapy (20 mg/day, 10 weeks). The plasma CTSS mRNA levels, CTSS protein concentrations and CTSS activity, as well as LDL and HDL size and subclasses, were analysed before and after treatment. RESULTS: Atorvastatin treatment did not change the plasma CTSS mRNA levels, although it lowered the plasma CTSS concentrations and activity. An increased plasma CTSS concentration and activity were found to be associated with a more atherogenic LDL subclass profile (a decreased dominant LDL size and increased percentage of small, dense LDL particles). The atorvastatin-induced CTSS-loweringeffect was concomitant with an improvement in the LDL subclass profile, and the changes were found to be interrelated. Concomitant, interrelated changes in the CTSS levels and LDL subclass profiles were found in the LDL phenotype B patients only (a dominant LDL diameter of ≤ 25.5 nm at the start of the study). In this subgroup, lowering of the plasma CTSS mRNA level also correlated with lowering of the proportion of small, dense LDL particles. CONCLUSIONS: Atorvastatin-induced CTSS-lowering and LDL subclass profile improvements in the plasma of LDL phenotype B patients with stable angina are concomitant and interrelated.

Evaluation of lipid parameters and bioindices in patients with different stages of chronic renal failure.

BACKGROUND/AIM: Cardiovascular morbidity and mortality are markedly increased in chronic renal failure (CRF). The aim of this study was to evaluate lipid parameters and bioindices in patients with different stages of CRF. METHODS: In 46 hemodialysed (HD), 50 CRF patients with II, III and IV stage of CRF (non-HD) and 48 control subjects triglycerides (TG), total cholesterol (C), HDL-C, urea, creatinine, creatinuria (standard biochemical methods), apolipoprotein (apo) AI, apo B, lipoprotein(a), cystatin C (immunoturbidimetric method) were evaluated, and LDL-C, non-HDL-C, LDLC/HDL-C, non-HDL-/HDL-C, TG/HDL-C, and new bioindices, LTI (lipid tetrad index), logLTI, LPI (lipid pentad index), logLPI, AIP (atherogenic index of plasma), and creatinine clearance were calculated. RESULTS: There were significant differences in the levels of TG, HDL-C, LDL-C, non-HDL-C, total C and apo A-I between the HD and non-HD patients, and the HD patients and the controls. LTI and LPI were significantly higher in the HD and non-HD patients compared to the controls (p < 0.05), without a good separation by the Box-Whisker plots. The values of TG/HDL-C ratio and AIP were significantly higher in the HD and nonHD-patients compared to the controls (p < 0.05), and significantly higher in the HD compared to non-HD patients (p < 0.05). AIP > 0.11 was found in 71.7% of the HD, 56% of non-HD and 31.3% of the controls. CONCLUSION: Among lipid parameters and indices, AIP and TG/HDL-C ratio are most suitable for evaluation of lipid disturbances in different stages of CRF. In addition to, non-HDL-/HDL-C, and apoB/A-I ratios, apo A-I, HDL-C and TG are important markers in HD patients. Non-HDL-C is not a suitable marker. LTI and LPI need to be further investigated.

Fibrinolytic parameters, lipid status and lipoprotein(a) in ischemic stroke patients.

INTRODUCTION: Ischemic stroke is the third leading cause of mortality and morbidity in most countries in the world. Impaired fibrinolysis, as well as disordered lipid metabolism have been recognized as risk factors for this disease. OBJECTIVE: To study some of fibrinolytic parameters, lipid status and lipoprotein(a) - Lp(a) in ischemic stroke patients in Serbia and to examine associations between Lp(a) and fibrinolytic parameters. METHODS: Sixty ischemic stroke patients (case group, mean age 63.48 +/- 9.62 years) and 30 age and sex matched healthy controls (control group, mean age 60.2 +/- 7.96 years) were studied. RESULTS: A significantly longer euglobulin clot lysis time (219.7 +/- 78,8 min. vs 183.5 +/- 58,22 min; p = 0.005) and higher levels of plasminogen activator inhibitor-1 (PAI-1) (48.5 +/- 17.1 ng/ml vs 27.1 +/- 10.1 ng/ml; p = 6.2 x 10(-11)), tissue-type plasminogen activator antigen (t-PA) (11.1 +/- 7.14 ng/ml vs 6.0 +/- 3.66 ng/ml; p = 5.2 x 10(-5)) and D-dimer (382.27 +/- 504.22 ng/ml vs 116.12 +/- 88.81 ng/ml; p = 0.0002) were found in cases compared to controls. There were no significant differences in fibrinogen levels (4.30 +/- 0.84 g/l vs 4.09 +/- 0.64 g/l; p = 0.23) or plasminogen activity (92.67 +/- 11.37% vs 96.87 +/- 9.48%; p = 0.085). There was no significant difference in Lp(a) concentration between cases and controls (0.15 +/- 0.11 g/l vs 0.12 +/- 0.11 g/l; p = 0.261). However, in the cases, but not in the controls, multivariate analysis of associations between fibrinolytic parameters and Lp(a) showed the highest correlation between t-PA and PAI-1, and the latent effect of Lp(a) on t-PA and PAI-1. CONCLUSIONS: Our results show that there are important differences in the characteristics of the fibrinolytic mechanism in ischemic stroke patients compared to healthy population. The major differences are prolonged euglobulin clot lysis time and elevated PAI-1 and t-PA antigen in ischemic stroke patients. In addition, Lp(a) appears to be involved in the inhibition offibrinolysis in ischemic disease through a mechanism unrelated to its serum concentrations.

Influence of sodium monoketocholate on the hypolipidemic activity of lovastatin in healthy and diabetic rats.

Recent findings regarding the physiological transport mechanisms and metabolism of bile acids have led to an increased interest in their synthetic derivatives, especially as transmucous transporters. The aim of this study was to examine the influence of the synthetic sodium salt of monoketocholic acid (Na-MKHA) on the hypolipidemic activity of lovastatin. The effects of a 7 days administration of lovastatin (20 mg/kg b.w.) (experimental group 1, n=5) and a combination of lovastatin (20 mg/kg b.w.) and Na-MKHA (2 mg/kg b.w.) (experimental group 2, n=5) in group of healthy and diabetic male Wistar rats were investigated. The animals in the control group of healthy (n=5) and diabetic (n=5) rats were treated with physiological saline (10 ml/kg b.w.) per os twice a day. In the healthy rats, lovastatin increased the low density lipoprotein (LDL) (32.14%) and non-high density lipoprotein (HDL) (15.38%) cholesterol and decreased HDL cholesterol levels (9.89%), and also increased the investigated atherogenic ratios. Na-MKHA significantly potentiated lovastatin activity, and its effects on the LDL (p<0.05; 102.70%), HDL (p<0.01; 32.93%) and non-HDL (p<0.05; 65%) cholesterol levels, as well as the LDL/HDL (p<0.02; 231.11%), total cholesterol/HDL (p<0.02; 70.52%) and non-HDU/HDL cholesterol ratios (p<0.02; 167.12%). In diabetic animals, the potentiating effect of Na-MKHA was not significant. The stimulatory effect of Na-MKHA is probably a consequence of the intensified transmembrane transport of lovastatin due to the direct action of bile acids on the cell membranes, as well as a result of their enhanced transport via specific bile acid transport systems.