Effects of competitive physical activity on serum irisin levels and bone turnover markers.

BACKGROUND: Irisin, a myokine, is a polypeptide derived from the cleavage of the extracellular domain of fibronectin domain-containing protein 5, a receptor that is present on different tissues (skeletal muscle, pericardium, myocardium, and brain), whose functions are not yet fully defined. PURPOSE: The main aim of our study was to evaluate the effect of competitive physical activity on serum irisin levels and bone turnover markers. METHODS: Fifteen male footballers and an equal number of subjects of the same age and gender, but with a predominantly sedentary lifestyle, had their serum levels of irisin and bone turnover markers measured. Bone mineral status was evaluated in both groups by quantitative bone ultrasound of the calcaneus. In addition, only in footballers, biochemical analyses were repeated after 3 months. RESULTS: We did not observe significant differences in the serum levels of calcium, phosphorus, and parathyroid hormone between the two groups. The footballers had significantly higher quantitative bone ultrasound, 25-OH vitamin D, and creatinine values than the controls. There were also no significant differences in the bone alkaline phosphatase, carboxy-terminal telopeptide of type I collagen, osteoprotegerin, sclerostin or Dkk-1 values, while the irisin levels (+ 89%, p < 0.001) and RANKL were significantly higher in the footballers compared to those in the controls. CONCLUSION: Our study shows that footballers have significantly higher serum irisin values than the general population. Irisin could be the "trait d'union" between bone health and physical activity.

Decreased bone cortical density at the forearm in subjects with subclinical peripheral arterial disease.

UNLABELLED: The association between peripheral arterial disease (PAD) and low bone mass is controversial. In our study, peripheral quantitative computed tomography shows a reduction of cortical but not trabecular, bone mineral density (BMD) at the forearm, in patients with subclinical PAD. INTRODUCTION: Some controversy exists regarding the association between peripheral arterial disease (PAD) and low bone mass. Previous studies have evaluated bone mineral density (BMD) in patients with subclinical PAD, with mixed results. Inconsistency of data may depend on the fact that most studies measured areal bone mineral density (aBMD) by Dual-energy-x ray absorptiometry (DXA). Because DXA cannot distinguish between cortical and trabecular compartments, we reasoned that a study aimed to establish whether these compartments were differentially affected by PAD status could give more information on the nature of this association. METHODS: In this cross-sectional study, we used peripheral quantitative computed tomography (pQCT) to examine volumetric cortical and trabecular mineral density at the radius (vBMD) in a cohort of subjects with subclinical PAD as defined by ABI ≤0.90 and compared them with healthy subjects with no evidence of PAD. RESULTS: Patients with subclinical PAD had significantly reduced cortical density (1101.0 ± 45.4 vs 1156.2 ± 51.3 mg/cm(3), p < 0.001) and cortical area (75.0 ± 20.9 vs 99.9 ± 18.2 mm(2), p < 0.001) than healthy subjects. Trabecular density (178.1 ± 47.9 vs 165.8 ± 29.6 mg/cm(3)) was not significantly different in the two groups. CONCLUSION: Subclinical PAD induces a selective bone loss at the radius compartment, not identified by standard DXA, which seems to occur primarily at the cortical level.

Effects of long-term hormone replacement therapy: results from a cohort study.

The positive effects of hormonal replacement therapy (HRT) in protecting the cardiovascular system in women have been supported by several observational studies, while also being questioned by other randomized controlled trials. Today, it is unclear whether HRT plays a crucial role, or even whether there is any role at all, for this therapy in preventing or in lowering cardiovascular disease (CVD). In the present study, we have evaluated the effectiveness of long-term HRT in post-menopausal women on the incidence of cardiovascular events and arterial remodeling, as well as on some metabolic factors. Eighty-four post-menopausal women (mean age: 46.3 ± 5.2; age range: 42-66 yr) underwent HRT for 10.9 ± 1.2 yr (range: 8-12 yr). None of these subjects showed new cardiovascular events, and we found a reduction of the intima-media thickness (baseline: 1.39 ± 0.2, 1.35 ± 0.2, 1.31 ± 0.2 mm) and total cholesterol, LDL and antithrombin III levels were lower, while HDL and fibrinogen levels increased. The study highlights a number of positive effects both on vascular conditions and metabolic and coagulative markers that are usually considered as generic and crucial risk factors for CVD. The relatively low number of patients is perhaps a limitation of this study, however, the long-term period of followup should be considered an interesting and important factor. Furthermore, this study underlines the real-life clinical experience of a Menopause Center.

Carotid intima-media thickness and liver histology in hemodialysis patients with nonalcoholic Fatty liver disease.

The prevalence of atherosclerotic cardiovascular disease in chronic hemodialysis (HD) patients has been demonstrated to be higher than in healthy people. Severe liver fibrosis is strongly associated with early carotid atherosclerosis and it might reduce the survival of patients who undergo both renal replacement therapy and transplantation. We wanted to assess whether nonalcoholic fatty liver disease (NAFLD) was associated with altered intima-media thickness (IMT) in HD patients as an independent marker of subclinical atherosclerosis. We enrolled 42 patients undergoing HD and 48 patients with normal renal function, all of them with high levels of aminotransferases and an ultrasonographic diagnosis of liver steatosis. The control group consisted of 60 healthy subjects. Laboratory tests for inflammatory and oxidative markers, ultrasonographic liver evaluation, carotid IMT measurement, and liver biopsy were performed. Different degrees of fibrosis were detected in our study cohort. Worse liver histopathological scores and higher plasmatic levels of C-reactive protein, reactive oxygen species, and vascular cell adhesion molecule-1 were found in HD patients. Carotid IMT was significantly higher (p < 0.005) in patients with histological steatosis. HD patients may develop active and progressive chronic hepatitis faster than patients with normal renal function and the thickness of their carotid intima-media might be markedly increased. These two conditions seem to be independent on classical risk factors and on metabolic syndrome. They might be related to the high levels of oxidants and to the inflammatory state, which are typical of patients undergoing HD. Independently related with the traditional risk factors for cardiovascular disease, nonspecific inflammation and oxide-reductive imbalance may play an important role in the progression of NAFLD and atherosclerotic disease in HD patients.

The association between carotid or femoral atherosclerosis and low bone mass in postmenopausal women referred for osteoporosis screening. Does osteoprotegerin play a role?

Atherosclerosis and osteoporosis appear to be epidemiologically correlated. Most (but not all) animal and clinical studies suggest that osteoprotegerin (OPG) may represent a possible molecular link between bone loss and vascular calcification. The aim of this study was to investigate the association of OPG with bone mineral density (BMD) and vascular plaques, in order to contribute to a better understanding of the link between atherosclerosis and osteoporosis. The study population consisted of 100 consecutive postmenopausal women referred for routine osteoporosis screening. BMD was evaluated by dual-energy X-ray absorptiometry. Presence of carotid or femoral plaques was examined by ultrasonography. OPG was measured by enzyme immunoassay. Seventy-two subjects had low bone mass and were categorized as osteopenic (32) or osteoporotic (40). Fifty-two subjects had one or more atherosclerotic plaques at carotid or femoral level. Both lumbar spine and femoral BMD were associated with the number of plaques (r=-0.5370; p<0.0001, and r=-0.4423; p=0.0012, respectively), however only spine BMD remained significantly associated with the number of plaques after adjustment. OPG serum values showed a significant association with age (r(2)=0.057; p=0.042). The association between OPG and the number of plaques was significant only in patients with concomitant involvement of carotid and femoral districts (r(2)=0.758; p<0.0001).

Effects of antioxidants on postprandial oxidative stress and endothelial dysfunction in subjects with impaired glucose tolerance and type 2 diabetes.

AIM: To compare changes in the oxidation-reduction balance and endothelial function before and after meal in patients with type 2 diabetes or impaired glucose tolerance and determine the effects of standard antioxidant supplementation. METHODS: Forty diabetics and 40 subjects with impaired glucose tolerance were compared with a control group. We assessed before and after a test meal (homogenized milkshake containing 80 g of saturated fat, amounting to 1,480 kcal), some reactive oxygen species, inflammation markers and flow-mediated vascular dilatation. These parameters were then reassessed after standard antioxidant treatment. RESULTS: After the meal, diabetics, subjects with impaired glucose tolerance and controls had higher levels of oxidant compounds compared to fasting levels. In subjects with diabetes and impaired glucose tolerance (IGT), Vascular Adhesion Molecule-1 and CRP were higher after the meal--diabetic subjects exhibited lower fasting flow-mediated dilatation, which deteriorated significantly after the meal. Antioxidant administration significantly improved the parameters investigated in all subjects. CONCLUSIONS: In diabetic subjects, altered glycaemia and lipaemia are closely correlated with markers of systemic oxidative stress. Our results show that the abnormal changes in oxidative-reductive balance parameters are paralleled by similar changes in markers of endothelial dysfunction and inflammation at 4 h after ingestion of a fatty meal. Supplementation with a pool of antioxidants can reduce oxidative stress and inflammation in healthy subjects and, more importantly, in IGT patients. This previous aspect suggests that the timing of antioxidant supplementation has an important role in endothelium protection in healthy and pre-diabetic subjects, and along with prompt antioxidant treatment before irreversible endothelial damage has occurred, may have an important protective role in subjects with IGT-patients who require administration of adequate dietary antioxidants.

High frequency of Chlamydophila pneumoniae infections: patients with peripheral arterial disease and those with risk factors for cardiovascular diseases compared to normal subjects.

The role of bacterial infections, mainly Chlamydophila pneumoniae, on atherosclerotic processes as well as the therapeutic utility of additional antibiotic treatment is still an open question. In this study we compared the serological profiles of 160 patients (80 with peripheral arterial disease (PAD), diagnosed with an ankle/brachial index (ABI) ≤ 0.9 and 80 with risk factors for cardiovascular disease - CVD) with those of 80 healthy subjects, serum levels of specific C. pneumoniae antibodies using the microimmunofluorescence test. Our results show that PAD patients had a higher frequency of C. pneumoniae infection than those with risk factors for cardiovascular disease. This frequency was lower if compared to the previous two groups in controls. 44 out of the 80 (55%) patients with PAD and 34 out of the 80 (42.58%) subjects with risk factors for cardiovascular disease were seropositive while only 24 of the 80 (30%) healthy subjects showed seropositivity to C. pneumoniae. Furthermore, higher anticorpal titers were also found in patients with peripheral arterial disease and in patients with cardiovascular risk factors if compared to healthy subjects. On the basis of these results, we confirm that C. pneumoniae infection is frequent in peripheral arterial disease patients and we believe that it could be considered as an additional risk factor involved in the pathogenesis of this disease.

Polymorphisms of steroid 5-alpha-reductase type I (SRD5A1) gene are associated to peripheral arterial disease.

Although animal studies support the hypothesis that androgenic biological actions may affect experimental atherosclerosis progression, evidence for a relationship between androgen effects and peripheral arterial disease (PAD), a common clinical form of atherosclerosis, is weak or contradictory. Testosterone, the main androgen hormone, is converted in a 5alpha-reduced form by enzymatic activities in the target cells and some specific actions are mediated by such metabolites. Steroid 5-alpha reductase isoenzymes (SRD5A1 and SRD5A2) catalyze the conversion to the bioactive potent androgen dihydrotestosterone and other reduced metabolites and represent relevant regulators of local hormonal actions. In the present study we tested for the association of selected single nucleotide polymorphisms (SNP) of SRD5A1 and SRD5A2 with symptomatic PAD patients. Two different SNP in the SRD5A1 were significantly associated which the PAD phenotype (p<0.03, odds ratio 1.73), while no association was found between PAD phenotypes and SRD5A2. Since the examined SRDA1 gene variant was previously associated with a low enzymatic activity, we suggest that a decreased local enzymatic conversion of testosterone may contribute to PAD genetic susceptibility.

Chronic peripheral arteriopathy is associated with seropositivity to Chlamydia pneumoniae.

The study was carried out to clarify the correlation between Chlamydia pneumoniae infection and peripheral arterial disease (PAD). The level of specific antibodies of the 133 consecutive patients suffering from PAD at 2nd stage of Leriche's classification were compared with 60 healthy controls by using a commercial Micro-IF Test. A higher incidence of serological evidence of C. pneumoniae infection was found in the patients (106/133) than in controls (6/60). These results are in agreement with other findings that measured the infection in atheromasic plaques. A strong cause-effect relationship between bacterial infection and peripheral arterial disease was not found, but the raised seropositivity level could be considered as a target for medical therapy of PAD.

Analysis of G(-174)C IL-6 polymorphism and plasma concentrations of inflammatory markers in patients with type 2 diabetes and peripheral arterial disease.

AIMS: To determine whether the G(-174)C interleukin 6 (IL-6) polymorphism influences the development of peripheral arterial disease (PAD) in individuals with type 2 diabetes. This was investigated by comparing the distribution of G(-174)C genotypes between patients with type 2 diabetes and PAD (PAD+) and those with type 2 diabetes but without PAD (PAD-). Plasma concentrations of IL-6, fibrinogen, C reactive protein (CRP), and vascular endothelial growth factor (VEGF) were also compared in PAD+ and PAD- patients. METHODS: Blood samples were collected from 146 PAD+ and 144 PAD- patients. SfaNI was used to determine the G(-174)C genotype. Plasma concentrations of IL-6, fibrinogen, CRP, and VEGF were measured by an enzyme linked immunosorbent assay. RESULTS: The GG genotype was more common in PAD+ patients than in PAD- patients. PAD+ patients also had increased mean plasma concentrations of IL-6, fibrinogen, CRP, and VEGF compared with PAD- patients. Mean plasma concentrations of IL-6, fibrinogen, and CRP in both PAD+ and PAD- patients were higher in those with the GG genotype than in those with the GC or CC genotypes. In contrast, mean plasma concentrations of VEGF in PAD+ and PAD- patients were not significantly different between those with different G(-174)C genotypes. CONCLUSIONS: These results support a model in which the GG genotype promotes PAD development among individuals with type 2 diabetes by inducing increased release of IL-6. Higher concentrations of IL-6 among those with the GG genotype is associated with increased plasma concentrations of fibrinogen and CRP.

Ultrasound imaging in diagnosis of superior mesenteric artery syndrome.

OBJECTIVES: We screened a cohort of subjects affected by various degree of dyspepsia to reveal if they presented a reduction of the aorto-mesenteric angle and to diagnose suspected cases of superior mesenteric artery (SMA) syndrome. DESIGN: Controlled, prospective, study. SETTING: Subjects were studied as outpatients. SUBJECTS: The study investigated a total of 3622 subjects referred to our department by their general practitioners for dyspepsia and/or abdominal pain. Interventions. Abdominal ultrasonography with power colour Doppler, gastroduodenoscopy, hypotonic duodenography, contrast-enhanced spiral computerized tomography were performed. MAIN OUTCOME MEASUREMENT AND RESULTS: Color Doppler revealed a significant reduction of the SMA angle in 29 of 950 subjects; gastroscopy showed duodenal compressive pulsation in 14 of 29 patients and X-ray revealed compression of the third segment of the duodenum in 28 of 29 patients. CT confirmed the presence of a reduced angle and various degrees of duodenal compression in all patients. Ultrasonography and CT examinations gave overlapping results (P > 0.05) in diagnosing pathological aorto-mesenteric angle. CONCLUSION: The authors believe that the incidence of reduced aorto-mesenteric angle and SMA syndrome might be underrated. Ultrasound power colour Doppler imaging is useful in epidemiological screening of reduced aorto-mesenteric angle to diagnose suspected cases of SMA syndrome.

Low bone density and abnormal bone turnover in patients with atherosclerosis of peripheral vessels.

Patients with vascular calcifications often have low bone mineral density (BMD), but it is still uncertain if osteoporosis and peripheral vascular disease (VD) are interrelated and linked by a common pathomechanism. Moreover, data on bone turnover in patients with advanced atherosclerosis are lacking. We measured BMD by dual-energy X-ray absorptiometry (DXA) and quantitative bone ultrasound (QUS), as well as the serum levels of osteocalcin (OC), bone-specific alkaline phosphatase (BAP), osteoprotegerin (OPG) and its ligand RANKL, and the urinary concentration of the C-terminal telopeptides of type I collagen (CrossLaps), in 36 patient (20 male and 16 female) with serious atherosclerotic involvement of the carotid and/or femoral artery to investigate the underlying mechanism of vascular and osseous disorders. Thirty age-matched and gender matched healthy individuals served as controls. After adjustment for age, BMD was significantly reduced at the lumbar spine in 23/36 (63%) patients (mean T score -1.71+/-1.42) and at the proximal femur in 34/36 (93%) patients (neck mean T score -2.5+/-0.88). Ten patients (27%) had abnormal QUS parameters. Gender and diabetes had no effect on the relationship between vascular calcification and bone density at any site measured. VD subjects had OC and BAP serum levels lower than controls (13.3+/-3.1 vs 27.7+/-3.3 ng/ml, P<0.01, and 8.4+/-2.3 vs 12.5+/-1.4 microg/l, P<0.01, respectively). Urinary CrossLaps excretion was not significantly different in patients with VD and in controls (257.9+/-138.9 vs 272.2+/-79.4 micro g/mmol Cr, respectively). Serum OPG and RANKL levels were similar in patients and in controls (3.5+/-1.07 vs 3.4+/-1.05 pmol/l, and 0.37+/-0.07 vs 0.36+/-0.06 pmol/l, respectively). We proved high occurrence of osteoporosis in VD, with evidence of age and gender independence. Negative bone remodelling balance would be a consequence of reduced bone formation, with no apparent increased activation of the OPG-RANKL system.

Effects of long-term hormone replacement therapy on arterial wall thickness, lipids and lipoproteins, fibrinogen and antithrombin III.

We aimed to study the effects of hormone replacement therapy (HRT) in menopausal women on lipoproteins, blood coagulation, arterial blood pressure and markers of atherosclerosis. A total of 186 postmenopausal women were studied; 98 used HRT (0.625 mg 17 beta-estradiol plus 10 mg progestin) and were followed for 48 months, and were matched with 98 women without therapy. Low-density lipoproteins, high-density lipoproteins, triglycerides, antithrombin III, systolic and diastolic arterial pressure and intima-media thickness were measured at 6, 12, 24, 38 and 48 months. In users of HRT, we found a significant reduction of the lipoproteins, triglycerides, systolic and diastolic pressures and intima-media thickness; however, we found an increase in high-density lipoproteins and anthitrombin III in comparison with non-users. This study has shown a protective effect of HRT on such risk factors and on certain markers of atherosclerosis.

Circulating natriuretic peptide concentrations in patients with end-stage renal disease: role of brain natriuretic peptide as a biomarker for ventricular remodeling.

OBJECTIVES: To determine levels of natriuretic peptides (NPs) in patients with end-stage renal disease (ESRD) and to examine the relationship of these cardiovascular peptides to left ventricular hypertrophy (LVH) and to cardiac mortality. PATIENTS AND METHODS: One hundred twelve dialysis patients without clinical evidence of congestive heart failure underwent plasma measurement of NP concentrations and echocardiographic investigation for left ventricular mass index (LVMI). RESULTS: Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations correlated positively with LVMI and inversely with left ventricular ejection fraction, whereas C-type NP and Dendroaspis NP levels did not correlate with LVMI. In dialysis patients with LVH (LVMI >125 g/m2), plasma ANP and BNP concentrations were increased compared with those in dialysis patients without LVH (both P<001). In a subset of 15 dialysis patients without LVH or other concomitant diseases, plasma BNP concentrations were not significantly increased compared with those in 35 controls (mean +/- SD, 20.1+/-13.4 vs 13.5+/-9.6 pg/mL; P=.06), demonstrating that the BNP concentration was not increased by renal dysfunction alone. Furthermore, the BNP level was significantly higher in the 16 patients who died from cardiovascular causes compared with survivors (mean +/- SD, 129+/-13 vs 57+/-7 pg/mL; P<.003) and was significantly associated with greater risk of cardiovascular death in Cox regression analysis (P<.001), as was the ANP level (P=.002). CONCLUSIONS: Elevation of the plasma BNP concentration is more specifically related to LVH compared with the other NP levels in patients with ESRD independent of congestive heart failure. Thus, BNP serves as an important plasma biomarker for ventricular hypertrophy in dialysis patients with ESRD.

Effects of ischaemic stress on leukocyte activation processes in patients with chronic peripheral occlusive arterial disease: role of L-propionyl carnitine administration.

An open study was carried out to assess whether, in patients with occlusive peripheral arterial disease (PAD), ischaemic stress induced by maximal physical exercise is associated with leukocyte activation processes, and to evaluate the effects of L-propionyl carnitine (LPC) administration on such processes. Fifteen patients with occlusive PAD (stage II-A), with a mean pain-free walking distance (PWD) of 199 +/- 70.66 m were orally treated with 2000 mg/day LPC for 2 months. Serum levels of E-selectin, P-selectin, L-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-I (VCAM-1) were measured at rest and after the performance of a treadmill walking test (treadmill speed 3.5 km h(-1), inclination 12%) in the untreated condition, and again after treatment with LPC. Significant increases of these factors were observed after maximal exercise compared with resting values. Such increase was significantly reduced after LPC treatment compared with the untreated condition. This study shows that ischaemia induced by maximal stress is associated with leukocyte activation processes, and that LPC is capable of modulating these processes. LPC, therefore, may have a protecting role during ischaemia.

Duration of menopause and behavior of malondialdehyde, lipids, lipoproteins and carotid wall artery intima-media thickness.

AIM: our study assessed whether minor or major hormonal deficiency influenced oxidative status and vascular wall structure in menopausal women. METHODS: the study series was made up of 62 non hypertensive non diabetic menopausal women (mean age 52.3+/-4.7 years) divided into two groups depending on duration of menopause (group 1 duration 0-5 years; group 2 duration over 5 years). Total cholesterol (TC), LDL cholesterol (LDL-C), HDL-cholesterol (HDL-C), triglycerides (TG), malondialdehyde (MDA) and common carotid artery wall intima-media thickness (IMT) were determined in the entire series. RESULTS: mean TC, LDL-C, TG, MDA and IMT values were higher in group 2 than group 1. The intergroup difference between MDA (P<0.007) and IMT values (P<0.006) values was statistically significant. CONCLUSIONS: the study revealed a close temporal correlation between plasma oxidative stress and carotid wall IMT, jeopardizes vascular wall status as menopause proceeds.

Oxidative stress and endothelial damage in patients with asymptomatic carotid atherosclerosis.

It is known that oxidative stress can be able to induce cytotoxicity of blood cells, stimulate release of inflammatory cytokines, and induce the production of growth factors. The aim of this study was to investigate oxidative stress and endothelial dysfunction in patients with asymptomatic carotid artery disease and healthy controls. Native low-density lipoproteins, oxidised low-density lipoproteins, malondialdehyde, nitrates, glutathione peroxidase activity and endothelin-1 were determined in patients without severe (range between 30% and 50%) carotid artery stenosis. Native low-density lipoproteins, oxidized low-density lipoproteins, malondialdehyde, glutathione peroxydase, and endothelin-1 concentrations were higher in patients than in health controls (P<0.001). No difference was observed in nitrate values (P<0.8). Our results revealed oxidative stress in patients without severe carotid artery stenosis and clinical symptoms. This was shown by the elevated malondialdehyde and oxidized low-density lipoprotein levels.

Effects of dietary protein restriction on fibrinogen and albumin metabolism in nephrotic patients.

BACKGROUND: Nephrotic syndrome (NS) is characterized by profound changes in albumin and fibrinogen levels. Dietary protein restriction has been advocated in the treatment of patients with NS, but its effects on albumin and fibrinogen metabolism have not been fully elucidated. METHODS: We evaluated the effects of dietary protein restriction on endogenous leucine flux (ELF), fibrinogen and albumin metabolism in seven patients with NS who consumed either a normal protein diet (NPD; 1.20 +/- 0.06 g/kg/day), or a low protein diet (LPS; 0.66 +/- 0.04 g/kg/day) for four weeks. Seven normal subjects served as controls. The postabsorptive ELF value, fractional synthesis rate (FSR) and absolute synthesis rate (ASR) of both albumin and fibrinogen were evaluated during the last 120 minutes of a five-hour 5,5,5-D3-L-leucine infusion. RESULTS: During the NPD regimen. ELF was increased, serum albumin was reduced, plasma fibrinogen was increased, albumin FSR and ASR were both increased, fibrinogen FSR was normal, and fibrinogen ASR was greater in patients with NS compared to controls. In patients with NS the LPD regimen reduced proteinuria, ELF, albumin FSR and ASR, plasma fibrinogen levels, fibrinogen ASR, and increased serum ulbumin levels. Dietary-induced changes in albumin and fibrinogen synthesis were significantly correlated (r = 0.719, P < 0.05). CONCLUSIONS: Patients with NS treated with LPD show: (1) a reduction of proteinuria, albumin ASR and FSR, with an increase in serum albumin levels and its intravascular pool; (2) a decrease of fibrinogen ASR, with a reduction in both plasma fibrinogen levels and intravascular pool; and (3) a reduced rate of whole body proteolysis.

Venous stasis causes release of interleukin 1beta (IL-1beta), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNFalpha) by monocyte-macrophage.

BACKGROUND: many studies have investigated between venous stasis, functions of the vascular and perivascular anastomotic structure, venous endothelium and circulating leukocytes. SETTING: patients with varicose veins (n = 15) and a healthy control group (n = 15). METHODS: the authors investigated some soluble mediators of monocytes-macrophages, which induce inflammation. They determined interleukin 1beta (IL-1beta) and interleukin 6 (IL-6) and tumor necrosis factor alpha (TNFalpha) levels at rest and after induced venous occlusion (using an inflated cuff to 60 mmHg for 25 minutes). RESULTS: their results revealed elevated baseline production in the former and that induced venous occlusion further augmented the levels of all cytokines in the study series, especially in patients with varicose veins. CONCLUSION: The authors believe that the study shows functional activation of monocyte-macrophages related to venous stasis as a consequence of venous hypertension. Cell response damages the endothelial structure and may represent an important element in the pathophysiology of chronic venous insufficiency.

Behaviour of the carotid wall in menopausal women with and without arterial hypertension.

OBJECTIVE: A study was conducted on the carotid vascular wall to evaluate its behaviour in postmenopausal women suffering from arterial hypertension compared to normotensive postmenopausal women. METHOD: Intima-media thickness(IMT) of carotid artery was determined by ecoduplex scanner in 182 postmenopausal women (age range 40-60 years) divided in four age classes (40-45, 46-50, 51-55, 55-60 years). Ninety-one women presented normal arterial blood pressure (SBP 136.6+/-11.7 and DBP 82.3+/-8.9 mmHg) and 91 were hypertensive (SBP 172.6+/-11.7 and DBP 97.4+/-6.6 mmHg). RESULTS: The normotensive women presented the following IMT values: 1.19+/-0.21 mm (40-45 years), 1.21+/-0.25 mm (46-50 years), 1.25+/-0.20 mm (51-55 years), 1.25+/-0.20 mm (55-60 years). IMT values in hypertensive women were: 1.75+/-0.25 mm (40-45 years), 1.77+/-0.30 mm (45-50 years), 1.91+/-0.28 mm (51-55 years), 2.02+/-0.33 mm (55-60 years). ANOVA test was performed in both groups of women and did not show any significant difference in the four age classes of normotensive women. On the other hand it revealed a statistical significance between 40-45 and 46-50-year-old hypertensive classes (P<0.001) and between 51-55 and 55-60-year-old hypertensive clases (P<0.02). CONCLUSIONS: There was a correlation between age and IMT in the arterial hypertensives, especially in two older classes, and between the duration of menopause and IMT values. The results indicated that carotid wall thickening was constantly higher in hypertensive women compared with normotensive ones.