Biomedical subjects
Publications and source records attributed to Gianluca Bardini.
Explore the source record for details and available documents.
OBJECTIVES: The aim of this study was to determine the reference values for serum cystatin C (CysC) with a particular focus on the effect of aging. DESIGN AND METHODS: The study was performed on a consecutive series of subjects (258 men and 396 women). Laboratory parameters and a detailed personal and family medical history were collected. RESULTS: CysC showed a significant correlation with age in both sexes, which was confirmed with multivariate linear regression after adjustment for SCr (serum creatinine). Age-related reference intervals were established for cystatin C (<45 years, <0.95 mg/L and >45 years, <1.20 mg/L). CONCLUSIONS: The use of CysC reference values adjusted for age should be carefully taken into consideration.
Since oxidative stress is thought to play an important role in the pathogenesis and complications of diabetes, we used the comet assay (single cell alkaline gel electrophoresis) to evaluate DNA strand breaks and DNA base oxidation, measured as FPG (formamidopyrimidine DNA glycosylase)-sensitive sites, in peripheral blood cells (PBC) from type 2 diabetes patients and healthy controls. Oxidative DNA damage in leukocytes was increased in diabetic compared to normal subjects. However, no differences in the levels of DNA damage in isolated lymphocytes were found between the two groups. These data indicate a higher vulnerability to oxidative damage of polymorphonuclear as compared to mononuclear leukocytes in type 2 diabetes. Thus, the measurement of oxidative DNA damage in leukocytes by means of the comet assay is a suitable marker for the evaluation of systemic oxidative stress in diabetic patients.
INTRODUCTION: Low serum thyrotropin has been related to the presence of stroke as well as to a higher incidence of cardiovascular disease in the general population. Furthermore, abnormalities in serum thyrotropin have been observed in diabetic patients even if unaffected by known thyroid illness. On this basis we investigated whether stroke is associated with altered thyrotropin concentrations in a hospitalised population categorised for the presence of diabetes. PATIENTS AND METHODS: This study used a database concerning all patients consecutively admitted to hospital and discharged alive with a diagnosis of stroke or of transient ischemic attacks (TIA) confirmed by clinical and CT criteria during an 18-month period. The study group was composed of 698 (392 M/306 F) patients, aged 74+/-12(SD) years of whom 372 were affected with TIA and 326 with stroke. RESULTS: The median thyrotropin level was significantly lower in diabetic patients (0.91 mU/l) than in the non-diabetic group (1.3 mU/l; P=0.0001). Patients with stroke, compared to those with TIA, were older, had higher blood pressure, higher prevalence of diabetes and lower serum thyrotropin (median value in TIA group: 1.30 mU/l (95% CI 0.25-4.63) vs. 1.04 (95% CI 0.18-3.76) in the stroke group, P=0.03), stroke being significantly associated with reduced median thyrotropin only in diabetic patients (n=239; 0.82 mU/l, vs. 1.09 mU/l in diabetic group; P<0.05, and 1.21 mU/l vs. 1.37 mU/l in the non-diabetic group; P=NS). Stroke severity, as assessed by NIHSS, was weakly inversely related to thyrotropin levels. Finally, after adjusting for main confounders, the odds ratio for stroke in the first thyrotropin quartile was significantly higher only in diabetic patients (OR: 3.56; 95% CI: 1.55-8.19; P<0.01 by trend test). CONCLUSIONS: In conclusion, our findings suggest that stroke is significantly associated with low serum thyrotropin in patients with diabetes.
The insulin-sensitising adipose hormone adiponectin is reduced in type 2 diabetic patients. We assessed the relationships between plasma adiponectin and chronic hyperglycaemia. Adiponectin levels and glycated haemoglobin (HbA1c) were measured at enrolment and after 90 days in 16 patients with type 2 diabetes aged (mean +/- SEM) 63.0 +/- 0.6 years, with body mass index (BMI) 30.2 +/- 0.5 kg/m2 and HbA1c concentration 7.4 +/- 0.1%, who did not modify their hypoglycaemic treatment during the observation period. Furthermore, plasma adiponectin was measured in 29 adult patients with type 1 diabetes and compared with 29 control subjects matched for sex, age, BMI, waist circumference and bioimpedance-estimated fat mass. In type 2 diabetic patients at enrolment, adiponectin concentration correlated with BMI (r = -0.46; p < 0.05), but not with HbA1c. During the prospective observation, variations of adiponectin showed a significant correlation with variations of BMI (r = -0.47; p < 0.01), but not with variations of HbA1c concentration. These results were confirmed by multivariate analysis after adjustment for sex and age. Adiponectin levels in type 1 diabetic patients (380.8 +/- 13.7 ng/ml in women, 192.5 +/- 13.9 ng/ml in men) were significantly (p < 0.05) higher than in control subjects (277.6 +/- 11.0 ng/ml in women, 102.7 +/- 5.1 ng/ml in men); plasma adiponectin correlated significantly with BMI and waist circumference, but not with HbA1c. In conclusion, the reduction of plasma adiponectin levels in type 2 diabetic patients does not appear to be determined by chronic hyperglycaemia. Adiponectin levels are increased in type 1 diabetes, but this phenomenon is not attributable to differences in nutritional status or body composition.