Cost-utility analysis of a national project to reduce hypertension in Israel

<p>Abstract</p> <p>Background</p> <p>This study aims to calculate the health effects and costs of a proposed national hypertension prevention and control program.</p> <p>Methods</p> <p>Interventions are based on experience from our two programs: 10-year period of Ashkelon Hypertension Detection and Control Program (AHDC Program) and the Israel Blood Pressure Control (IBPC) program. The costs of a nationwide program were calculated based on economic data, training staff levels, course frequency and unit costs.</p> <p>Results</p> <p>Over the next 20 years, the program should decrease the risk in one-half of the treated hypertensive cases of the following ailments: cardiovascular events such as Acute Myocardial Infarction (AMI) and Unstable Angina Pectoris (UAP) by 16.0%, stroke by 41.2%, End stage renal disease (ESRD) by 50.0% and peripheral vascular disease (PVD) by 42.6%. In total, around 2,242 lives, 35,117 years of life or 24,433 disability adjusted life years will be saved due to decreased mortality.</p> <p>Program costs amount to $352.7 million. However savings ($537.6 million), from reduced medical treatment ($444.3 million) and reduced pharmaceutical use ($93.3 million) as a result of morbidity decreases, exceed costs by $185.0 million.</p> <p>Conclusion</p> <p>The project which saves both lives and resources should be extended nation-wide to reach as wide a population as possible.</p

Relation between augmentation index and adiponectin during one-year metformin treatment for nonalcoholic steatohepatosis: effects beyond glucose lowering?

<p>Abstract</p> <p>Background</p> <p>Insulin resistance (IR) is the major driving force behind development and progression of atherosclerosis in patients with nonalcoholic fatty liver disease (NAFLD). Therefore, correction of IR is a relevant therapeutic target.</p> <p>We performed the current trial to evaluate whether 12- month metformin therapy improves vascular stiffness in patients with NAFLD and to assess if this improvement is associated with change in glucose control, insulin resistance or circulating adiponectin.</p> <p>Methods</p> <p>In randomized, placebo controlled study, 63 patients with NAFLD were assigned to one of two groups: Group 1 received daily metformin; Group 2 received placebo. Central aortic augmentation index (AI) was performed using SphygmoCor (version 7.1, AtCor Medical, Sydney, Australia) at baseline, at 4-and 12-month treatment period. Metabolic parameters, insulin resistance markers and serum adiponectin levels were determined.</p> <p>Results</p> <p>In placebo group: AI did not improve during the treatment period. Liver function and adiponectin levels did not change during the study.</p> <p>In multiple linear regression analysis, the independent predictors of arterial stiffness improvement were metformin treatment and increase in circulating adiponectin levels.</p> <p>Among metformin treated patients: AI decreased significantly during the study. ALP and ALT decreased during initial 4-month treatment period, however raised to the pretreatment levels after 12 months. Serum adiponectin level tended to increase during treatment period with metformin.</p> <p>Conclusions</p> <p>Metformin treatment was associated with significant decrease in AI during one year treatment in NAFLD patients. These beneficial vascular effects was associated with exposure to metformin per se as well as change in adiponectin levels suggesting that metformin may mediate its vascular effects via glicemic control-independent mechanisms.</p> <p>Trial registry</p> <p>no: NCT01084486</p

Defective metabolism of hypertriglyceridemic low by guest on M ay 16, 2016 D ow nloaded from Treating mixed hyperlipidaemia 427 density lipoprotein in cultured human skin fibroblasts. Normalization with bezafibrate therapy

Abstract The metabolism of hypertriglyceridemic low density lipoprotein (HTG-LDL) was investigated in upregulated cultured human skin fibroblasts. Low density lipoprotein (LDL) was isolated by zonal centrifugation from the plasma of seven HTG subjects, before and 2 wk after the initiation of bezafibrate (BZ) therapy. HTG-LDL is a cholesterol-poor, triglyceride-rich lipoprotein of smaller diameter than BZ-LDL or normal LDL (N-LDL). Binding, cell association, and proteolytic degradation of HTG-LDL were compared with that of BZ-LDL and N-LDL and were found to be significantly lower by a paired t test analysis (P &lt; 0.001). After 6 h preincubation with unlabeled HTG-LDL, the incorporation of [14Clacetate to sterols was significantly higher than with BZ-LDL or N-LDL (577±43.7; 330±41.5; 262±47, mean±SE, picomoles sterols per milligram cell protein per 2 h, respectively; P &lt; 0.001 by paired t test). To determine the effectiveness of HTG-LDL and BZ-LDL on the down-regulation of LDL receptor activity, up-regulated cells were incubated for 48 h with HTG-LDL and BZ-LDL. LDL receptor activity was significantly higher after preincubation with HTG-LDL compared with BZ-LDL, and the rates of sterol synthesis were similarly increased. These results demonstrate that HTG-LDL does not down-regulate the LDL receptor activity as efficiently as BZ-LDL and that its cholesterol content is not enough to adequately suppress cellular sterol synthesis. Significant correlation between LDL composition and cholesterol synthesis by cultured cells was found with all LDL preparations over a wide range of cholesteryl ester to protein ratio (0.8-2.2). This correlation indicates that the compositional and structural abnormalities of HTG-LDL, and especially the low cholesterol content of the lipoprotein, alter LDL metabolism and cellular cholesterol formation

The Effect of Natural-Based Formulation (NBF) on the Response of RAW264.7 Macrophages to LPS as an In Vitro Model of Inflammation

Macrophages are some of the most important immune cells in the organism and are responsible for creating an inflammatory immune response in order to inhibit the passage of microscopic foreign bodies into the blood stream. Sometimes, their activation can be responsible for chronic inflammatory diseases such as asthma, tuberculosis, hepatitis, sinusitis, inflammatory bowel disease, and viral infections. Prolonged inflammation can damage the organs or may lead to death in serious conditions. In the present study, RAW264.7 macrophages were exposed to lipopolysaccharide (LPS; 20 ng/mL) and simultaneously treated with 20 &micro;g/mL of natural-based formulation (NBF), mushroom&ndash;cannabidiol extract). Pro-inflammatory cytokines, chemokines, and other inflammatory markers were analyzed. The elevations in the presence of interleukin-6 (IL-6), cycloxygenase-2 (COX-2), C-C motif ligand-5 (CCL5), and nitrite response, following exposure to LPS, were completely inhibited by NBF administration. IL-1&beta; and tumor necrosis factor alpha (TNF-&alpha;) release were inhibited by 3.9-fold and 1.5-fold, respectively. No toxic effect of NBF, as assessed by lactate dehydrogenase (LDH) release, was observed. Treatment of the cells with NBF significantly increased the mRNA levels of TLR2, and TLR4, but not NF-&kappa;B. Thus, it appears that the NBF possesses anti-inflammatory and immunomodulatory effects which can attenuate the release of pro-inflammatory markers. NBF may be a candidate for the treatment of acute and chronic inflammatory diseases and deserves further investigation

Comparison of short-term renal effects and efficacy of rosuvastatin 40 mg and simvastatin 80 mg, followed by assessment of long-term renal effects of rosuvastatin 40 mg, in patients with dyslipidemia

Background: An open-label, randomized, multinational, parallel-group trial compared the short-term (6-week) renal effects of rosuvastatin 40 mg and simvastatin 80 mg in patients with hypercholesterolemia. Most patients (93%) then entered an optional open-label extension (OLE) to assess long-term (up to 72 weeks) renal effects of rosuvastatin. Methods: After dietary lead-in, 626 patients were randomized to rosuvastatin or simvastatin for 6 weeks, followed by an optional, single-arm OLE to assess longer-term effects of rosuvastatin on renal function, safety, and efficacy. Results: The primary endpoint, a shift in urine dipstick protein from "none" or "trace" at baseline to "+" or greater in the first 4 weeks, was observed in 6.4% of patients receiving rosuvastatin and 1.0% of those receiving simvastatin. The incidence of shifts in urine dipstick protein at any time from none or trace to "++" or greater (proteinuria), was low (1.3%, rosuvastatin; 0.3%, simvastatin), transient and urine protein was predominantly of tubular or mixed origin. More patients achieved Third Adult Treatment Panel of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (NCEP ATP III) low-density lipoprotein cholesterol (LDL-C) goals with rosuvastatin vs simvastatin after 6 weeks (77.9% vs 60.4%). Results from the OLE (median rosuvastatin treatment = 47 weeks) were consistent with the randomized period. Mean serum creatinine levels remained stable, indicating no decline in renal function. Conclusion: A small proportion of patients treated with rosuvastatin 40 mg may experience a transient proteinuria, predominantly of tubular origin and not associated with declining renal function. Rosuvastatin modified lipid levels effectively, enabled more patients to attain LDL-C goals, and demonstrated a favorable benefit/risk profile. © 2007 National Lipid Association.SCOPUS: ar.jinfo:eu-repo/semantics/publishe