A number of recent epidemiologic observations support the need for new and broader strategies to reduce serum cholesterol levels on a population-wide basis. First, the limited data available suggest a halt in the declining incidence of coronary artery disease (CAD) in the United States since 1990, raising concerns about our current strategies to promote primary prevention of CAD. Data from the 1970s and 1980s support a key role for population-wide cholesterol lowering as a strategy to reduce CAD. Second, large and carefully performed surveys support no further reductions in serum cholesterol levels in the US population since 1990. Is this observation and that of stagnating declines of CAD incidence a coincidence? Interestingly, the lack of cholesterol level reduction occurred in the setting of increased use of prescription cholesterol-lowering drugs, suggesting that drug treatment of the highest-risk persons alone will not shift the population curve. Third, the treatment gap persists, with recent population-wide data suggesting that half of all people with hypercholesterolemia (>/=200 mg/dL) are unaware of their condition, only half of those persons aware are treated, and only half of those treated are controlled. Finally, the moderate-risk population (10% to 20% risk of CAD over 10 years) is sizable in the ages recommended for over-the-counter statin use (>/=45 years in men, >/=55 years in women). Risk reduction in this group, which contributes a significant portion of CAD cases, should be part of any program to reduce the population burden of CAD.
"In diabetes, targeting glycosylated haemoglobin (HbA1c) levels of 7% and control of hypertension have led to better outcomes over the past decade  . Likewise, hypertensive treatment aiming for predefined levels of blood pressure and control of serum lipid levels according to established guidelines improve cardiovascular risk  . Treat-to-target strategies have recently been applied in rheumatology  , and an international panel of experts has formulated recommendations on how to implement this in RA, with a defined target of clinical remission . "
[Show abstract][Hide abstract] ABSTRACT: With recent improvements in the treatment of rheumatoid arthritis (RA), remission has become an achievable goal for a large proportion of RA patients, and remission is now a defined target in current RA guidelines. However, studies have shown that progression of radiographic joint damage may occur in clinical remission, regardless of the choice of remission definition. Sub-clinical inflammation detected by modern imaging techniques such as ultrasonography and magnetic resonance imaging is present in the majority of patients in clinical remission, and is associated with progressive joint damage and disease activity flare in these patients. This chapter aims to assess the importance of imaging findings in RA patients in clinical remission and to discuss the possible role of modern imaging in future remission criteria.
Best practice & research. Clinical rheumatology 12/2012; 26(6):767-85. DOI:10.1016/j.berh.2012.10.004 · 2.60 Impact Factor
"Residual analyses showed that the model in the table fit well. b The explored independent variables were antipsychotic type, baseline high BMI (≥30 kg/m 2 ), baseline high glucose levels (≥110 mg/dL), baseline high cholesterol levels (≥240 mg/dL), low HDL-C levels (males, b40; females, b 50 mg/dL), high triglyceride levels (≥150 mg/dL) (Ford et al., 2002; Pearson, 2004), age, gender, smoking and alcohol use. The variables reported in the table were obtained through a stepwise selection procedure. "
[Show abstract][Hide abstract] ABSTRACT: Antipsychotic effects on C-reactive protein (CRP) have received little attention. This randomized open-label study investigated the possible effects of antipsychotics on CRP levels after 3 and 12 months of treatment in a Spanish drug-naïve sample taking haloperidol (N=36 after 3 months), olanzapine (N=36 after 3 months) or risperidone (N=39 after 3 months). After 3 months and adjusting for differences in baseline CRP levels, baseline smoking and high baseline triglyceride levels, patients on haloperidol treatment had CRP levels that were 92.7% higher than those of patients on risperidone treatment (p=0.009). After 12 months, only smoking was associated with increased CRP levels. Future studies need to verify that different antipsychotics may have differential effects on CRP levels, particularly after 3 months of treatment.
Schizophrenia Research 08/2010; 121(1-3):207-12. DOI:10.1016/j.schres.2010.06.002 · 3.92 Impact Factor
"From these three obesity measures, linear regression analyses suggested that body fat percentage and waist circumference were the best predictors for cholesterol and triglyceride levels, respectively (de Leon et al., 2007). Hypertriglyceridemia was defined as having a triglyceride level ≥ 150 mg/dl (Ford et al., 2002) or undergoing current treatment for hyperlipidemia, and hypercholesterolemia as having a total cholesterol level ≥ 240 mg/dl (Pearson, 2004) or undergoing current treatment for hyperlipidemia. "
[Show abstract][Hide abstract] ABSTRACT: The goal of this study was to select some genes that may serve as good candidates for future studies of the direct effects (not explained by obesity) of some antipsychotics on hyperlipidemia. A search for single-nucleotide polymorphisms (SNPs) that may be associated with these direct effects was conducted. From a published cross-sectional sample, 357 patients on antipsychotics were genotyped using a DNA microarray with 384 SNPs. A total of 165 patients were taking olanzapine, quetiapine or chlorpromazine which may directly cause hypertriglyceridemia or hypercholesterolemia. Another 192 patients taking other antipsychotics were controls. A two-stage statistical analysis that included loglinear and logistic models was developed to select SNPs blindly. In a third stage, physiological knowledge was used to select promising SNPs. Known physiological mechanisms were supported for 3 associations found in patients taking olanzapine, quetiapine or chlorpromazine [acetyl-coenzyme A carboxylase alpha SNP (rs4072032) in the hypertriglyceridemia model, and for the neuropeptide Y (rs1468271) and ACCbeta, (rs2241220) in the hypercholesterolemia model]. These genes may be promising candidates for studies of the direct effects of some antipsychotics on hyperlipidemia.
Schizophrenia Research 02/2008; 98(1-3):40-6. DOI:10.1016/j.schres.2007.10.003 · 3.92 Impact Factor
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