CORRELATION BETWEEN THE WAIST CIRCUMFERENCE, DIASTOLIC BLOOD PRESSURE AND INSULIN RESISTANCE IN NON-OBESE YOUNG ADULTS.

CONTEXT: The metabolic syndrome is a profound, systemic impairment of the metabolism of lipids, carbohydrates and branched amino-acids, affecting specially obese people. Recently, many studies outlined the presence of the metabolic syndrome, also in non obese persons. OBJECTIVE AND DESIGN: To assess the relationship between insulin resistance and the cardiovascular component of the metabolic syndrome in a group of young, non obese subjects using a cross sectional study. SUBJECTS AND METHODS: We enrolled 103 subjects with body mass index < 30 Kg/m2, without metabolic syndrome to whom fasting glucose, triglycerides, high density lipoprotein cholesterol, insulinemia, waist circumference and arterial pressure were recorded in a cross-sectional approach. Insulin resistance was evaluated using the homeostasis model assessment for insulin (HOMA-IR) index. Statistic data processing included Pearson relation and multiple regression (backward method), using the SPSS version 21 software. RESULTS: A significant relationship between waist circumference, diastolic blood pressure and HOMA-IR is found. High value of HOMA-IR (>2.6) was more frequently in men (p=0.011). The incidence of the 2 metabolic components mentioned above was higher in the high value HOMA-IR group: 33% vs. 7% in women and 50% vs. 4% in men. Multiple regression showed a strong correlation between HOMA-IR and waist circumference (p<0.001) and diastolic blood pressure (p=0.008) that was maintained inside the women group (p=0.016 and p=0.032, respectively). In men, HOMA-IR correlated with waist circumference (p=0.031). CONCLUSION: We found a significant interdepen-dence between waist circumference, diastolic blood pressure and HOMA-IR. Based on our results, we consider that lifestyle intervention should start as soon as abnormal waist circumference is recorded.

Gene-environment interactions in parkinsonism and Parkinson's disease: the Geoparkinson study.

OBJECTIVES: To investigate associations of Parkinson's disease (PD) and parkinsonian syndromes with polymorphic genes that influence metabolism of either foreign chemical substances or dopamine and to seek evidence of gene-environment interaction effects that modify risk. METHODS: A case-control study of 959 prevalent cases of parkinsonism (767 with PD) and 1989 controls across five European centres. Occupational hygienists estimated the average annual intensity of exposure to solvents, pesticides and metals, (iron, copper, manganese), blind to disease status. CYP2D6, PON1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, CYP1B1, MAO-A, MAO-B, SOD 2, EPHX, DAT1, DRD2 and NAT2 were genotyped. Results were analysed using multiple logistic regression adjusting for key confounders. RESULTS: There was a modest but significant association between MAO-A polymorphism in males and disease risk (G vs T, OR 1.30, 95% CI 1.02 to 1.66, adjusted). The majority of gene-environment analyses did not show significant interaction effects. There were possible interaction effects between GSTM1 null genotype and solvent exposure (which were stronger when limited to PD cases only). CONCLUSIONS: Many small studies have reported associations between genetic polymorphisms and PD. Fewer have examined gene-environment interactions. This large study was sufficiently powered to examine these aspects. GSTM1 null subjects heavily exposed to solvents appear to be at increased risk of PD. There was insufficient evidence that the other gene-environment combinations investigated modified disease risk, suggesting they contribute little to the burden of PD.

Environmental risk factors for Parkinson's disease and parkinsonism: the Geoparkinson study.

OBJECTIVE: To investigate the associations between Parkinson's disease and other degenerative parkinsonian syndromes and environmental factors in five European countries. METHODS: A case-control study of 959 prevalent cases of parkinsonism (767 with Parkinson's disease) and 1989 controls in Scotland, Italy, Sweden, Romania and Malta was carried out. Cases were defined using the United Kingdom Parkinson's Disease Society Brain Bank criteria, and those with drug-induced or vascular parkinsonism or dementia were excluded. Subjects completed an interviewer-administered questionnaire about lifetime occupational and hobby exposure to solvents, pesticides, iron, copper and manganese. Lifetime and average annual exposures were estimated blind to disease status using a job-exposure matrix modified by subjective exposure modelling. Results were analysed using multiple logistic regression, adjusting for age, sex, country, tobacco use, ever knocked unconscious and family history of Parkinson's disease. RESULTS: Adjusted logistic regression analyses showed significantly increased odds ratios for Parkinson's disease/parkinsonism with an exposure-response relationship for pesticides (low vs no exposure, odds ratio (OR) = 1.13, 95% CI 0.82 to 1.57, high vs no exposure, OR = 1.41, 95% CI 1.06 to 1.88) and ever knocked unconscious (once vs never, OR = 1.35, 95% CI 1.09 to 1.68, more than once vs never, OR = 2.53, 95% CI 1.78 to 3.59). Hypnotic, anxiolytic or antidepressant drug use for more than 1 year and a family history of Parkinson's disease showed significantly increased odds ratios. Tobacco use was protective (OR = 0.50, 95% CI 0.42 to 0.60). Analyses confined to subjects with Parkinson's disease gave similar results. CONCLUSIONS: The association of pesticide exposure with Parkinson's disease suggests a causative role. Repeated traumatic loss of consciousness is associated with increased risk.

Study of fluticasone propionate efficacy in the treatment of patients with bronchial asthma not controlled by other inhaled corticosteroids.

The aim of the study was to test the fluticasone propionate (FP) efficacy in the treatment of patients with bronchial asthma (BA), not controlled by high doses (more than 1 mg) of other inhaled corticosteroids. Asthma symptoms (degree of dyspnea on Sadoul scale, percentage of symptom-free days and nights), and drug consumption were measured and lung function tests were performed in 20 patients (11 women and 9 men, mean age 47 years) for a 2 months period. Biochemical measurements were done referring to oxidant/antioxidant imbalance, which is characteristic to inflammatory diseases of respiratory system. We evaluated lipoperoxidation (LPO) in the plasma and the blood, before and after FP treatment, by determining malondialdehyde (MDA) status, superoxide-dismutase and ceruloplasmine activity and non-protein SH groups (essential glutathione) status. The biochemical measurements showed a significant decrease in lipid peroxides level in the plasma and the blood and a slight increase of glutathione after 2 months treatment with FP. Lung function tests were performed on a Flow Streen Jaeger and we determined: peak expiratory flow (PEF), vital capacity (VC), forced expiratory volume in 1 sec. (FEV1) and mid-expiratory flow at 50% VC (MEF50). The measurements were done before FP administration, after 3 days, 7 days, 1 month and 2 months. The dose of FP was equivalent to 50-75% of the daily dose of Beclomethasone dipropionate (BD) previously administered. The degree of dyspnea diminished from 3-4 to 0-1. The percentage of symptom-free days and nights improved from 12% to 78% and 25% to 95% respectively. The use of short acting beta agonists diminished with 75% and no patients required i.v. corticotherapy or theophylline. PEF increased with a mean of 25%, VC with a mean of 23%, FEV1 with a mean of 30% and MEF50 with a mean of 36%. Our results demonstrate improved efficacy of FP vs high doses of other inhaled corticosteroids in the treatment of moderate persistent and severe forms of BA.