Could the performance of oral glucose tolerance test contribute to the brain health-focused care in multiple sclerosis?

BACKGROUND: It has not been clarified yet if persons with multiple sclerosis (MS) are at increased risk to develop glucose metabolism dysregulation. The aims of the present study were to evaluate glucose metabolism characteristics in persons with MS and to compare it to the healthy individuals; to examine the association of glucose metabolism with the level of disability and its progression. METHODS: The study enrolled 78 patients with MS and 26, comparable for age, gender and body mass index (BMI), healthy controls (HC). Disability and its progression were evaluated by the Expanded Disability Status Scale (EDSS) score, progression index (PI) and multiple sclerosis severity score (MSSS). All participants performed an oral glucose tolerance test (OGTT). Insulin and lipid parameters were analyzed. RESULTS: Fasting glucose concentrations (5.3±0.7 in MS patients vs. 4.5±0.9 mmol/L in HC, p=0.001) and 2 hour post-load glucose concentrations were statistically significantly higher in MS patients compared with controls. Glucose levels at all different time points during OGTT, baseline insulin, Homeostasis model assessment of insulin resistance (HOMA-IR), total cholesterol and LDL were statistically significantly (p<0.05) associated with MS, in univariable logistic regression analysis. Glucose level at 120' was independently associated with MS (OR=3.937, 95% CI 1.178-13.159, p=0.026), in the multivariable model. The prevalence of IR was 64.1% in the MS group compared to 30.8% in the control group (p=0.008), based on HOMA-IR. EDSS and Multiple sclerosis severity score (MSSS) were associated with glucose levels at different time points (p<0.05). According to the ROC analysis, best cut-off value for HOMA-IR is 2.3, providing both sensitivity and specificity of 66.7% in discriminating persons with MS and HC. CONCLUSION: Our results demonstrate the presence of higher prevalence of IR in MS patients compared to healthy individuals, and strong association between impaired glucose metabolism and disability. Finally, it has to be emphasized that further studies are warranted to confirm our findings implicating that MS patients have significantly higher risk of impaired glucose metabolism, which could suggest the potential importance of the performance of OGTT in patients with this disorder.

Impact of acute hyperglycemia on layer-specific left ventricular strain in asymptomatic diabetic patients: an analysis based on two-dimensional speckle tracking echocardiography.

BACKGROUND: Hyperglycemia has detrimental effect on ischemic myocardium, but the impact of acute hyperglycemia on the myocardium in asymptomatic diabetic patients has not been fully elucidated. Thus, this follow-up study was aimed to investigate the effects and reversibility of acute hyperglycemia on regional contractile function of left ventricle (LV) in diabetic patients without cardiovascular disease. METHODS: The two-dimensional speckle tracking echocardiography (2D-STE), including multilayer strain analysis, was used for evaluation of global and regional LV function in asymptomatic, normotensive patients with uncomplicated diabetes, with acute hyperglycemia ( ≥ 11.1 mmol/l) (Group A, n = 67), or with optimal metabolic control (fasting plasma glucose < 7 mmol/l and HbA1c < 7%) (Group B, n = 20), while 20 healthy individuals served as controls (Group C). In group A, after 72 h of i.v. continuous insulin treatment (at the time euglycemia was achieved) (second examination) and after 3 months following acute hyperglycemia (third examination) 2D-STE was repeated. RESULTS: Global longitudinal strain (GLS) (- 19.6 ± 0.4%) in Group A was significantly lower in comparison to both groups B (- 21.3 ± 0.4%; p < 0.05) and C (- 21.9 ± 0.4%; p < 0.01) at baseline, while we could not detect the differences between groups B and C. Peak systolic longitudinal endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) layer strain were significantly lower in group A at baseline compared to both groups B and C. Deterioration in peak systolic circumferential strain was observed at basal LV level, in all three layers (Endo, Mid and Epi) and in mid-cavity LV level in Epi layer in group A in comparison to group C. Moreover, in group A, after euglycemia was achieved (at second and third examination) GLS, as well as peak longitudinal and circumferential strain remain the same. CONCLUSION: Acute hyperglycemia in asymptomatic diabetic patients has significant negative effects on systolic LV myocardial mechanics primarily by reducing GLS and multilayer peak systolic longitudinal and circumferential strain which was not reversible after three months of good glycemic control.

The effects of 3-year statin therapy and the achievement of LDL cholesterol target values in familial hypercholesterolemia patients: An experience from Serbia.

BACKGROUND AND AIMS: Despite the use of statins, familial hypercholesterolemia (FH) patients often have increased LDL-cholesterol (Ch) and high risk for atherosclerotic cardiovascular disease (ASCVD). This study aimed to analyze the effect of statin therapy on attainment of LDL-Ch treatment targets and appearance of new ASCVD and diabetes in FH patients. METHODS: This study is a retrospective analysis of data from medical records of 302 FH patients treated continuously with statins during 3 years. At baseline and once yearly, anthropometric measurements, lipids (total Ch, LDL-Ch, HDL-Ch, triglycerides, apoliporotein A1 and B), fasting plasma glucose, and insulin were determined. RESULTS: In FH patients, high intensity statin was prescribed only in 17.9% of cases. LDL-Ch levels were significantly lower after 3 years of statin treatment (3.61 ±â€¯1.19 mmol/l) vs. baseline (4.51 ±â€¯1.69 mmol/l; p < 0.01), but only 6.9% of FH patients reached the recommended ≥50% LDL-Ch reduction and 16.2% attained the LDL-Ch <2.6 mmol/l target. Simultaneously, 9.6% of FH patients developed new ASCVD, with lower HDL-Ch after 3 years of statin treatment than in those who remained free of ASCVD. In addition, we observed new onset diabetes in 6.4% of FH patients who were more obese, older and with higher fasting glucose at baseline than FH patients free of diabetes, regardless of the type of statin. CONCLUSIONS: These results imply that only a small proportion of FH patients achieved the recommended LDL-Ch treatment targets, mostly due to the use of low statin dose and infrequent implementation of high-intensity statin treatment, which altogether could not prevent the increase in residual cardiovascular risk.

Endothelial dysfunction of coronary arteries in subjects without diabetes: An association with both insulin resistance and impaired insulin secretion response.

AIMS: This study was aimed to compare insulin sensitivity and secretion response, lipoprotein and plasminogen activator inhibitor 1 (PAI-1) levels between the subjects with and without coronary artery endothelial dysfunction (ED). METHODS: ED was detected by intracoronary injection of acetylcholine (ACh) in 47 nondiabetes subjects without stenotic coronary arteries, selected from 316 consecutive patients with coronary angiography performed for suspected coronary artery disease. The subjects were divided into two groups: presence of ACh-induced coronary spasm (group ED+, N = 30) and absence of ACh-induced coronary spasm (group ED-, N = 17). Insulin sensitivity (Si) was evaluated by frequently sampled intravenous glucose tolerance test (FSIGTT) with minimal model analysis and by HOMA-IR, insulin secretion by acute insulin response (AIR) (calculated from the first 8 min of FSIGTT) and by disposition index (DI) (Si × AIR). Lipids and PAI-1 levels were determined enzymatically, and LDL particle size by gradient gel electrophoresis. RESULTS: Si was significantly lower (4.22 ±â€¯0.62 vs 6.98 ±â€¯1.47 min-1/mU/l × 104; p < 0.05) while HOMA-IR was significantly higher in ED + group vs ED- group (2.8 ±â€¯0.3 vs 1.7 ±â€¯0.2; p < 0.05). Simultaneously, AIR and DI was significantly lower in ED + vs ED- groups (p < 0.05 and p < 0.01, respectively). Investigated groups did not differ in fasting lipid levels but ED+ group had significantly smaller LDL particles (p < 0.01) and higher PAI-1 levels (p < 0.05). Regression analysis shown that DI was a strong independent predictor of appearance of ED, together with PAI-1 and LDL particle size. CONCLUSIONS: Both insulin resistance and impairment in insulin secretion response strongly correlate with coronary ED in subjects without diabetes.