A sub-analysis of the SAGE study in Italy indicates good glycemic control in type 1 diabetes.

BACKGROUND AND AIMS: Intensive glycemic control minimizes the risk of micro- and macrovascular complications in patients with type 1 diabetes (T1D). We report glycemic control in Italian participants (age groups: 26-44, 45-64, and ≥65 years) of the global SAGE study. METHODS AND RESULTS: The primary endpoint was proportion of participants who achieved an HbA1c <7% in predefined age groups. In the 523 patients with T1D, mean age was 44.6 years and mean body mass index (BMI) was 25 kg/m2. Mean HbA1c was 7.5% and 29.4% had HbA1c <7.0%, with the highest percentage in those 26-45 years (31.7%) and the lowest in those ≥65 years (20%). Altogether, 22.9% of patients achieved their physician-established individualized HbA1c target. Most patients had ≥1 symptomatic hypoglycemic episode in the previous 3 months (≤70 mg/dL 82.5%; ≤54 mg/dL 61%). Severe hypo- and hyperglycemia were experienced by 16.3% and 12% of patients, of which 7.1 and 9.5%, respectively, required hospitalization/emergency visits. More patients achieved HbA1c <7% with CSII (30%) than with multiple daily insulin injections (27.9%). In multivariate analysis, BMI (OR 0.94, 95% CI 0.89-0.99, p = 0.032) and adherence to diet (OR 0.36, 95% CI 0.18-0.70, p = 0.0028) were significantly associated with HbA1c <7.0%. CONCLUSIONS: Glycemic control can be considered good in the Italian SAGE cohort, especially in younger patients, who more frequently use pumps/continuous glucose monitoring. Greater patient education and use of technology may further support this achievement. Patients should be encouraged to maintain a low BMI and adhere to their diet.

The use of flash glucose monitoring significantly improves glycemic control in type 2 diabetes managed with basal bolus insulin therapy compared to self-monitoring of blood glucose: A prospective observational cohort study.

AIM: This prospective, observational cohort study aimed to measure HbA1c change over 3-6 months in type 2 diabetes managed with basal-bolus insulin and FreeStyle Libre® Flash Glucose Monitoring System (FSL) use compared to self-monitored blood glucose (SMBG). METHODS: Sixteen Italian hospitals enrolled patients with type 2 diabetes (n = 322, [109 FSL, 213 SMBG users]) using basal-bolus insulin therapy for ≥ 1 year, HbA1c 8.0-12.0% (64-108 mmol/mol), new to FSL use (<3 months) or continuing with SMBG (controls). Eligible FSL and SMBG users were matched (1:2 ratio) for baseline HbA1c (within ± 0.5%, recorded ≤ 3 months previously), study site and baseline data collection date. RESULTS: Overall, baseline HbA1c was 8.9 ± 0.8% (74 ± 9 mmol/mol), age 67.2 ± 10.0 years, BMI 30.5 ± 6.5 kg/m2 and insulin use duration 8.6 ± 6.6 years (mean ± SD), 56.2% were males. After 3-6 months, 234 complete cases (83 FSL, 151 SMBG users) demonstrated significantly reduced HbA1c for FSL use compared to SMBG (0.3% ± 0.12 [3 mmol/mol ± 1.3, (mean ± SE)], p = 0.0112). The difference remained statistically significant after adjusting for confounders. CONCLUSIONS: HbA1c significantly improved in basal-bolus treated type 2 diabetes after flash glucose monitoring use for 3-6 months compared to SMBG.

Difference in carotid artery elasticity in subjects with different brachial artery kinetic of vasodilatation.

Increased carotid stiffness and impaired brachial artery flow-mediated dilatation (FMD) associate with cardiovascular events. We have previously reported three FMD patterns based on the time of maximal dilatation. The aim of the present study was to verify whether different FMD patterns associate with carotid artery stiffness. In all, 133 subjects were enrolled. All participants underwent complete clinical examination, blood sampling and ultrasound study. FMD was used as a measure of endothelial function. Based on the maximal brachial artery FMD, subjects were divided into Early dilators (peak FMD at 50 s), Late dilators (peak FMD over 50 s) and No dilators. Echo-Doppler evaluation of carotid arteries was performed in order to calculate elastic indexes (strain, ß-stiffness index and distensibility). In all, 64 subjects were classified as Early FMD, 36 as Late FMD and 33 as No dilators. Age, gender and cardiovascular risk factors were comparable among three groups. Early FMD had higher values of strain compared with both Late and no Dilators (P<0.001). Furthermore, Early dilators showed a significantly lower stiffness and higher distensibility compared with Late and No dilators. No significant differences between Late FMD and No Dilators were detected. Our results demonstrate that common carotid artery elasticity indexes significantly differ among Early, Late and No dilators. Subjects with delayed or absent brachial artery dilatation have stiffer common carotid arteries compared with subjects with early dilatation. In conclusion, our research suggests that the assessment of the kinetics of FMD in a clinical setting might represent a useful screening tool to improve the cardiovascular risk stratification.

Blood urea impairs brachial artery flow mediated dilation.

AIM: Urea, the main product of protein catabolism, is a biochemical marker of renal function. Though it is known that serum urea impairs vascular health, the relationship between its concentration and vascular reactivity in vivo has not been explored. Our study was undertaken to investigate possible association between serum urea and endothelial function in subjects without chronic kidney disease (CKD). METHODS: Eighty free-living subjects with serum creatinine ≤1 mg/dL and without CKD were enrolled for the present study. Serum analyses and evaluation of endothelial function were performed in all subjects. Endothelial function was measured using the flow-mediated dilation (FMD) technique. Simple and multiple regression analyses were used to test the association between FMD and considered variables. RESULTS: In correlation analyses FMD was found directly associated with HDL cholesterol (r=0.21; P=0.05) and eGFR (r=0.25; P=0.02) and inversely associated with age (r=-0.26; P=0.02), serum urea (r=-0.37; P<0.01), serum creatinine (r=-0.31; P<0.01) and brachial artery baseline diameter (r=-0.41; P<0.01). In multiple regression analysis only baseline artery diameter and serum urea predicted FMD; age, gender and cardiovascular risk factors did not relate with FMD. CONCLUSION: Our study demonstrates the association between serum urea and FMD, suggesting that the accumulation of waste products of protein metabolism may impair vascular health in subjects without CKD.

[Topical pharmacologic approach with 5% lidocaine medicated plaster in the treatment of localized neuropathic pain]. / Approccio farmacologico topico con lidocaina cerotto 5% nel trattamento del dolore neuropatico localizzato.

The treatment of neuropathic pain is a medical challenge. The responsiveness to the different classes of drugs is often unsatisfactory and frequently associated to a wide range of side effects. International guidelines suggest for the "localized" neuropathic pain the topical treatment with 5% lidocaine medicated plaster, alone or associated to systemic drugs, as the first choice since its favorable efficacy and tolerability profile. Many clinical experiences support the rationale for using 5% lidocaine medicated plaster in different kinds of localized neuropathic pain, such as postherpetic and trigeminal neuralgia, compressive syndromes, painful diabetic polyneuropathy and pain secondary to trauma or surgical interventions. This paper reports a series of clinical cases whose heterogeneity suggests the wide burden of applicability of the topical 5% lidocaine, either alone and associated to systemic drugs. All the described conditions were characterized by a highly intense pain, not adequately controlled by actual medications, which improved after the use of topical lidocaine. The good response to lidocaine allowed the reduction, of even the withdrawal, of concurrent drugs and improved the patients' quality of life.

Time course analysis of brachial artery flow mediated dilatation in subjects with gingival inflammation.

AIM: Several investigations report an inverse association between periodontal disease and endothelial function measured by brachial artery Flow-Mediated-Dilatation (FMD) technique. These studies examined endothelial function by using the traditional approach to FMD calculation, that is from diameters assessed at 60 seconds after deflation. Nevertheless, possible relationship between gingival inflammation and endothelial dysfunction observed over this temporal threshold remains still unexplored. The purpose of our study was to explore the relationship between gingival inflammation and endothelial function, by considering the time course of brachial FMD. METHODS: Forty-six free-living white subjects, participating in a cardiovascular disease prevention campaign, were enrolled. FMD was measured at 60s and at 2 and 3 min after forearm ischemia. Maximal FMD was calculated (Peak FMD), for each patient. Gingival Index (GI) was evaluated as measure of gingival inflammation. RESULTS: In univariate analyses, GI was associated with both FMD at 60 sec (r=-0.30, P=0.038) and Peak FMD (r=-0.41, P=0.004). In multiple regression analyses including GI, age, gender, and known risk factors for atherosclerosis, only GI and age were independently and inversely associated with Peak FMD and FMD at 60 s, but this association was stronger with Peak FMD. Moreover, when we divided subjects on the basis of GI value, patients with GI > 1 presented lower Peak FMD and higher prevalence of absent FMD. CONCLUSION: The present study extends previous observations about the negative effects of periodontal disease on endothelial function, highlighting the importance of the evaluation of time course of vascular reactivity.

Markers of insulin resistance and carotid atherosclerosis. A comparison of the homeostasis model assessment and triglyceride glucose index.

AIMS: The present investigation was designed to test the association between carotid atherosclerosis and two simple markers of insulin resistance, i.e. HOMA-Index and TyG-Index. MATERIALS AND METHODS: The study was performed in two different cohorts. In the first cohort, 330 individuals were enrolled. Blood pressure, lipids, glucose, waist and cigarette smoking were evaluated. HOMA-IR and TyG-Index were calculated as markers of prevalent hepatic and muscular insulin resistance respectively. Carotid atherosclerosis was assessed by Doppler ultrasonography. The association between cardiovascular risk factors, markers of insulin resistance and carotid atherosclerosis was assessed by multiple logistic regression analyses. In the second cohort, limited to the evaluation of TyG-Index, 1432 subjects were studied. RESULTS: In the first cohort, TyG-Index was significantly associated with carotid atherosclerosis in a model including age, sex, diabetes, cigarette smoking and LDL cholesterol, while HOMA-IR was not. When components of metabolic syndrome were added to the model as dichotomous variables (absent/present), TyG-Index retained its predictive power. The same result was obtained when the metabolic syndrome was added to the model (absence/presence). The association between TyG-Index and carotid atherosclerosis was confirmed in the second cohort. CONCLUSIONS: The present findings suggest that TyG-Index is better associated with carotid atherosclerosis than HOMA-IR.

Thoracic spinal stenosis and myelopathy: report of two rare cases and review of the literature.

The authors report two cases of thoracic spinal canal stenosis (SCS) and myelopathy. One is extremely unusual because of degenerative changes occurred in the upper thoracic spine. The other because of its multiple etiology among which calcification and ossification of the ligamentum flavum (OLF) in a Caucasian man. Both patients presented with an history of slowly progressive spastic paraparesis. In the first case computed tomography (CT) scans and magnetic resonance (MR) images revealed hypertrophy of the legamentum flavum and laminae causing compression of the spinal cord at T2-T3. In the second case diagnostic imaging showed three levels of stenosis in the lower thoracic spine due to degenerative changes, calcification and OLF with cord damage at T9-T10. A decompressive laminectomy and medial facetectomy was performed in both patients. The ligamentum flavum, hypertrophied and infolded in the first case and calcified and ossified in the second, was removed with careful dissection of the dural adhesions. Both patients showed a rapid post-operative recovery and regained autonomous walking within 1 month of surgery. Thoracic spinal cord stenosis is a rare and complex disorder because of differential diagnosis, neuroimaging features and treatment options. Regardless of its cause, prompt surgical decompression plays a key role in improving the functional outcome of myelopathy.

The effect of aging on blood and plasma viscosity. An 11.6 years follow-up study.

OBJECTIVE: Alterations of blood and plasma viscosity can promote atherosclerosis. The relationship between viscosity and aging is still controversial. The present study evaluated the influence of aging on blood and plasma viscosity in a group of subjects followed for 11.6 years. METHODS: Forty-five subjects have been evaluated twice 11.6 years apart for hemorheological parameters and coronary heart disease (CHD) risk factors. Plasma viscosity and blood viscosity have been measured with a cone-plate viscometer. Tk has been calculated as index of red blood cell rigidity. CHD risk factors, i.e. obesity, hypertension, hyperlipidemia and diabetes, have been evaluated by routine methods. RESULTS: Hematocrit and plasma viscosity did not change during the study, whereas blood viscosity (shear rate 225/sec: 4.46 ± 0.49 vs. 4.81 ± 0.54 cP, p < 0.0001; shear rate 45/sec: 6.19 ± 0.67 vs. 6.65 ± 0.79 cP, p < 0.0001) and Tk (0.80 ± 0.05 vs. 0.83 ± 0.06, p < 0.005) significantly increased. The percent variation in blood viscosity was not associated with the percent variation in any of the CHD risk factors. Furthermore, the increase in blood viscosity was similar in males and females and in subjects with CHD risk profile worsening or not. CONCLUSION: The present findings demonstrate that blood viscosity increases with age. This increase seems independent of classical CHD risk factors and is disjoined from haematocrit and plasma viscosity, suggesting a possible direct effect of aging on red blood cells.

Association among low whole blood viscosity, haematocrit, haemoglobin and diabetic retinopathy in subjects with type 2 diabetes.

OBJECTIVES: Haemorheological variables influence endothelial function through the release of several factors. Clinical studies have described an association among blood viscosity, haematocrit, haemoglobin and macro-angiopathy. Few data are reported about the association between haemorheological variables and micro-angiopathy. The aim of the present study was to evaluate the association between these variables and retinopathy in subjects with type 2 diabetes. METHODS: 111 men, 79 postmenopausal women, and 95 healthy age- and sex-matched controls were recruited. Haematocrit and haemoglobin were measured by standard methods. Blood viscosity was calculated according to the formula (0.12× haematocrit)+(0.17× (plasma proteins-2.07)). Subjects were grouped according to the presence or absence of diabetic retinopathy, while the severity of retinopathy was classified according to the Early Treatment Diabetic Retinopathy Study scale. RESULTS: Haemoglobin, haematocrit and whole blood viscosity were significantly lower in subjects with retinopathy compared to subjects without retinopathy in both sexes. These variables significantly decreased with increasing severity of retinopathy. A multiple logistic regression analysis confirmed the independent inverse association among viscosity, haematocrit, haemoglobin and retinopathy (p<0.01). CONCLUSION: Results demonstrate the association among low viscosity, haemoglobin, haematocrit and diabetic retinopathy. The mechanisms responsible for this association can be hypothesised. Reduced haemoglobin might cause direct organ damage. Low blood viscosity, through the reduction of shear stress, might inhibit the anti-atherogenic functions of endothelial cells.

Plasma and blood viscosity in metabolic syndrome.

BACKGROUND AND AIM: The relationship between metabolic syndrome (MS) and blood and plasma viscosity has been scarcely investigated. In the present study we have evaluated the difference in blood and plasma viscosity between subjects with and without MS, in order to verify whether viscosity measurement can add more information on the overall cardiovascular risk connected with the presence of the MS. METHODS AND RESULTS: Two hundred and sixty nine women and 520 men have been enrolled. Blood and plasma viscosity have been measured with a cone-plate viscometer equipped with a cp-40 spindle. MS has been defined according to the third report of the National Cholesterol Education Program, Adult Treatment Panel III. Eighty four women and 154 men fulfilled the criteria for MS. Hematocrit adjusted blood viscosity was higher in subjects with MS compared to those without the syndrome, both in males (shear rate 225 s(-1): 4.60+/-0.38 vs. 4.52+/-0.33 cP, p<0.01) and females (4.57+/-0.28 vs. 4.46+/-0.31 P, p<0.01). Blood viscosity was correlated with all components of MS but glucose, and after adjustment for them the difference between subjects with or without MS was completely abolished. Plasma viscosity was significantly higher only in females with MS. CONCLUSIONS: These data demonstrate that blood viscosity is increased in subjects with MS, but the increase seems to depend on the metabolic alterations of the syndrome. The independent contribution of the rise in blood viscosity to the cardiovascular risk connected with the presence of MS seems therefore negligible. The increased plasma viscosity in females with MS needs further clarification.

Stromelysin gene promoter polymorphism and common carotid geometry in diabetic subjects.

AIM: Stromelysin (MMP3), through its action on collagen and other matrix metalloproteinases, influences arterial wall remodeling. In healthy subjects, the 5A/6A polymorphism located in the promoter of the MMP3 gene is associated with common carotid remodeling, 6A/6A subjects having increased arterial diameter, wall thickness (intima-media thickness, IMT) and decreased wall shear stress (WSS). In the present study, we have investigated the influence of the 5A/6A polymorphism on common carotid remodeling in subjects with diabetes mellitus. METHODS: Diabetic subjects (N.=136) and age-matched healthy male controls (N.=101) have been studied. Common carotid diameter, IMT and flow velocity have been measured by echo-Doppler. Blood viscosity has been measured by a cone/plate viscometer. WSS has been calculated. RESULTS: Diabetic patients had increased common carotid diameter, IMT, and decreased flow velocity and WSS (all P<0.05), compared with controls. In controls, subjects homozygous for the 6A allele had increased diameter, IMT and decreased WSS. In diabetics, no difference was observed in vascular parameters among the three genotypes. CONCLUSION: The 5A/6A polymorphism of the MMP3 gene influences arterial remodeling of the common carotid artery in healthy subjects, but not in patients with diabetes mellitus. Therefore, the significance of the 5A/6A polymorphism as a marker of risk in this high cardiovascular risk population seems to be somehow blunted.

Isolated intraorbital schwannoma arising from the abducens nerve.

CASE REPORT: A case of isolated schwannoma of the orbit, arising from the terminal branches of the abducens nerve to the lateral rectus muscle, is reported. The patient presented with a painless proptosis of the left eye. DISCUSSION: Preoperative diagnosis of benign intraorbital neoplasm was made by means of CT and MR scans; the mass was radically excised through a microsurgical lateral orbitotomy and the pathological examination revealed a schwannoma. Features of orbital schwannoma are described, together with some details concerning the surgical strategy and the history of the evolution of the lateral orbitotomy.

Beta-sitosterolaemia: a new nonsense mutation in the ABCG5 gene.

BACKGROUND: Sitosterolaemia is a rare autosomal recessive disorder characterised by elevated plasma levels of plant sterols and cholesterol. Sitosterolaemia is caused by gene mutations in either of two ATP-binding cassette (ABC) half transporters, ABCG5 and ABCG8. The plasma sterol profile and genetic analysis of a 10-year-old girl who had tuberous xanthomas is the subject of this report. MATERIALS AND METHODS: Genomic DNA was isolated from white blood cells from the proband, her family and a control group of healthy people. All exons of ABCG5 and ABCG8 were sequenced. Plasma cholesterol and triglycerides were measured by routine methods. All other plasma sterols were measured by Gas Chromatography coupled to Mass Spectrometry. RESULTS: The proband was found to be homozygous for a single nucleotide mutation in exon 10 of the ABCG5 gene, consisting of a C to T transition at nucleotide 1336 of the coding sequence, which results in the premature termination of the ABCG5 protein at amino acid 446 (Arg446X). Her mother and brother were also homozygous for the same mutation and all had elevated plasma beta-sitosterol levels. The father was heterozygous and showed normal beta-sitosterol levels. This mutation was not found in healthy normolipidaemic subjects. CONCLUSIONS: We describe a novel nonsense mutation in exon 10 of the ABCG5 gene in a 10-year-old girl showing clinical and biochemical features of sitosterolaemia. This family study broadens the spectrum of the ABCG5/ABCG8 mutations causing sitosterolaemia and helps highlight the correlations between such gene mutations, biochemical phenotype and the development of cardiovascular disease.

Flow-mediated vasodilatation of the brachial artery and intima-media thickness of carotid artery in never-treated subjects.

AIM: Data on the association between brachial artery flow-mediated dilatation (FMD) and common carotid intima-media thickness (IMT) are contrasting. The present study investigated the relationship between FMD and IMT and carotid atherosclerosis in never treated subjects. METHODS: Seventy-seven subjects were investigated: 46 had no coronary heart disease (CHD) risk factors, 21 had only one, and 10 had more than one risk factor. IMT of the common carotid was measured by ultrasonography and FMD was evaluated according to standardized methods. RESULTS: IMT increased with increasing number of risk factors (0.66+/-0.12, 0.69+/-0.12 and 0.8+/-0.17 mm, respectively, ANOVA P<0.05). FMD decreased with increasing number of risk factors (10.44+/-5.2, 6.52+/-7.11 and 7.35+/-4.42%, respectively, P<0.05). Endothelium-independent vasodilatation was similar in the 3 groups. IMT and FMD did not correlate neither in subjects without risk factors (r=-0.151, P=0.3), nor in those with 1 (r=-0.196, P=0.4) or with 2 or more risk factors (r=-0.387, P=0.2), while in the group as a whole the correlation was borderline significant (r=-0.217, P=0.058). Eleven subjects had carotid atherosclerosis and higher values of IMT, but not reduced FMD. In multiple regression analysis, diabetes and IMT, but not FMD, were associated with carotid atherosclerosis. CONCLUSIONS: The present findings indicate that, in never treated subjects, FMD is not strictly associated with IMT or atherosclerosis of the carotid arteries.

Effects of iodinated contrast media on common carotid and brachial artery blood flow and wall shear stress.

The aim of our study was to evaluate the effect of the intravenous contrast media iomeprol on wall shear stress, blood flow and vascular parameters in the common carotid and brachial artery. Thirty outpatients undergoing thoracic or abdominal spiral CT scans were studied. The internal diameter and flow velocity of the common carotid and brachial artery were evaluated by ultrasound, and blood viscosity was measured before and after low osmolality iomeprol (Iomeron 350) injection. The wall shear stress, blood flow and pulsatility index were calculated. To test the differences between groups, the Wilcoxon rank test and Mann Whitney U test were applied. Blood viscosity decreased slightly, but significantly after contrast media (4.6+/-0.7 vs. 4.5+/-0.7 mPa.s, P = 0.02). Contrarily, blood flow and wall shear stress did not change in the common carotid artery, but significantly decreased in the brachial artery (0.9+/-0.4 vs. 0.6+/-0.3 ml/s, P < 0.0001, and 41.5+/-13.9 vs. 35.3+/-11.0 dynes/cm2, P < 0.002, respectively), whereas the pulsatility index significantly increased in the brachial artery (5.0+/-3.3 vs. 7.5+/-5.3, P < 0.001). Iomeprol injection causes blood flow and wall shear stress reduction of the brachial artery; the rise in the pulsatility index suggests an increase in peripheral vascular resistance. Further investigation is needed to evaluate whether these modifications can be clinically relevant.

HIF-1alpha reveals a binding activity to the promoter of iNOS gene after permanent middle cerebral artery occlusion.

Hypoxia inducible factor (HIF-1)-1alpha is a specific, oxygen-sensitive protein that regulates the activity of HIF-1, a transcriptional factor that increases after cerebral ischemia and may either promote or prevent neuronal survival. In this study to determine whether the inducible nitric oxide synthase (iNOS) gene containing the sequence of the hypoxia-responsive enhancer (HRE) was an HIF-1 target after cerebral ischemia induced by permanent middle cerebral artery occlusion (pMCAO), electrophoretic mobility shift assay (EMSA) and iNOS western blot analysis were performed in the ischemic core, in the area surrounding the infarct and in the hippocampus ipsilateral and contralateral to the lesion. In addition, both HIF-1alpha mRNA and protein expression were examined in the ischemic core, in the area surrounding the ischemic core and in the hippocampus ipsilateral to the insult. Our results revealed that pMCAO up-regulates iNOS protein in the ischemic core, in the area surrounding the ischemic core and in the hippocampus ipsilateral to the lesion, and that the activation of iNOS expression is mediated by HIF-1. Moreover, HIF-1alpha mRNA and protein levels increased in the ischemic core and in the hippocampus ipsilateral to the lesion compared with the levels obtained in the corresponding areas of sham-operated controls or in the contralateral hemisphere. Particularly in the area surrounding the ischemic core, HIF-1alpha protein accumulated during pMCAO although mRNA did not increase. Our study suggests that the activation of HIF-1 might be involved in the mechanisms whereby iNOS promotes cell survival and/or death after cerebral ischemia.

A multiplex PCR-based DNA assay for the detection of paraoxonase gene cluster polymorphisms.

Paraoxonase (PON) is a high-density lipoprotein (HDL) associated protein which is supposed to protect low-density lipoprotein (LDL) against oxidation and to play a role in the development of atherosclerosis. Interindividual variability in serum PON activity is attributable to common variants in components of the PON gene cluster on chromosome 7. We describe experimental conditions that permit the simultaneous determination of three common PON polymorphisms (PON1-192, PON1-55 and PON2-311) that are tightly associated with an increased risk of atherosclerosis. We used a multiplex PCR-based DNA assay using mismatch primers that introduce a unique recognition site for the endonuclease HinfI in the PCR products in case of presence of the R allele of PON 1-192, of the L allele of PON1-55 and of the S allele of PON2-311. The restriction analysis with HinfI allows to identify an electrophoretic band pattern which is specific for the combination of the three polymorphisms. This technique could be applied in the association studies aimed at assessing the role of PON and their polymorphisms in many clinical settings. In a preliminary study on a small population sample from south Italy about 10% of chromosomes exhibited the presumed risk-related haplotype R(192)/L(55)/S(311).

Comparison of endothelial function evaluated by strain gauge plethysmography and brachial artery ultrasound.

Strain gauge plethysmography and brachial artery ultrasound are widely used to study endothelial function. No data on correlation between these two procedures are reported. The present study compared these two methods and investigated the correlation between vasodilation and brachial wall shear stress. In six healthy subjects and ten patients with hypertension or obesity, strain gauge plethysmography was performed in resting conditions and after infusion of 7.5,15 and 30 microg/min of acetylcholine, and brachial artery ultrasound in resting conditions and after 5 min hand ischemia. Wall shear stress was calculated as: blood viscosity x blood velocity/internal diameter. Forearm blood flow following acetylcholine infusion increased more in healthy subjects than in patients with hypertension or obesity. In addition, brachial artery dilated more in the former group. Change in brachial artery diameter correlated with change in forearm blood flow, calculated as area under the curve of acetylcholine infusion (r=0.739, P<0.001). Wall shear stress was higher in healthy subjects (67.8+/-20.0 dynes/cm(2)) than in patients with either hypertension or obesity (39.2+/-16.7, P<0.001), and correlated with variations of diameter (r=0.796, P<0.0002), and marginally of blood flow (r=0.516, P<0.05). The present findings demonstrate that there is a high correlation between endothelial function evaluated by strain gauge plethysmography and brachial artery ultrasound. Wall shear stress correlates with brachial artery diameter change following hand ischemia, and marginally with blood flow change following acetylcholine infusion.