Clinical cornerstone最新文献

{"title":"Pathophysiology and Clinical Manifestations of Osteoporosis","authors":"Carolyn Becker MD","doi":"10.1016/S1098-3597(09)62038-X","DOIUrl":"10.1016/S1098-3597(09)62038-X","url":null,"abstract":"<div><p><span><span>Osteoporosis is a complex skeletal disorder in which compromised bone strength increases the risk of </span>fragility fractures<span>. Recent scientific advances in bone biology and </span></span>immunology<span> have greatly expanded our insights into the pathogenesis of osteoporosis. For those with osteoporotic fractures, however, the physical and psychological effects remain severe. Primary care<span> physicians need to understand the basic mechanisms of bone physiology and pathophysiology in order to both prevent and treat this devastating disorder.</span></span></p></div>","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 2","pages":"Pages 42-50"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(09)62038-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28147957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fundamentals of Cardipmetabolic Risk Factor Reduction: Achieving and Maintaining Weight Loss with Pharmacotherapy or Bariatric Surgery","authors":"Elisa Fabbrini MD ,&nbsp;Samuel Klein MD","doi":"10.1016/S1098-3597(08)60027-7","DOIUrl":"10.1016/S1098-3597(08)60027-7","url":null,"abstract":"<div><p><span><span>Obesity is a major health problem in the United States and many other countries because of its high prevalence and causal relationship with serious medical comorbidities. The therapeutic options currently available to help obese patients lose weight are: (1) therapeutic lifestyle change (behavioral, dietary, and physical activity modification); (2) pharmacotherapy; and (3) </span>bariatric surgery<span><span>. Lifestyle modification is the first therapeutic choice; however, achieving a successful long-term weight loss with lifestyle intervention alone is difficult. There is increasing interest, therefore, in the use of pharmacotherapy and surgery to treat obesity. Although there are a number of antiobesity medications available, the only medications approved in the United States for long-term treatment<span> of obesity are sibutramine and </span></span>orlistat<span>. Use of these medications results in 3% to 5% more weight loss compared with placebo after 1 year. Bariatric surgery is an effective weight loss option for obese patients, but it is restricted to patients who are considered morbidly obese (ie, with a body mass index [BMI] ≥40 kg/m</span></span></span>² or a BMI of 35-39.9 kg/m² with ≥1 severe obesity-related medical complication).</p></div>","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 1","pages":"Pages 41-51"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(08)60027-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27870644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obesity, Abdominal Obesity, and Insulin Resistance","authors":"Sydney A. Westphal MD","doi":"10.1016/S1098-3597(08)60025-3","DOIUrl":"10.1016/S1098-3597(08)60025-3","url":null,"abstract":"<div><p><span>The correlation of body mass index<span><span> (BMI) with both adiposity and risk for type 2 diabetes mellitus (DM) is positive. An elevated BMI is also associated with increased mortality from cardiovascular disease (CVD). However, for any given BMI measurement, some persons are at risk for type 2 DM and CVD, while others are not. This disparity of risk may relate to differences in age, fitness, and body composition, including body fat. Obesity— excess body fat— is associated with insulin resistance. </span>Abdominal obesity, in particular, places people at higher risk for developing insulin resistance and, consequently, is associated with an increased risk for type 2 DM and CVD. The association between obesity and insulin resistance is largely due to changes in the function of </span></span>adipose tissue<span><span>, specifically, increased release of free fatty acids and abnormalities in adipokine secretion. The properties of visceral adipose tissue may cause these dysfunctions to become magnified. Weight loss has the potential to improve </span>insulin sensitivity through alterations in adipose tissue function.</span></p></div>","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 1","pages":"Pages 23-31"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(08)60025-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27871249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular Disease and Modifiable Cardiometabolic Risk Factors","authors":"Christopher P. Cannon MD","doi":"10.1016/S1098-3597(09)62037-8","DOIUrl":"10.1016/S1098-3597(09)62037-8","url":null,"abstract":"<div><p>Cardiovascular disease (CVD) is the leading cause of death in the United States and many parts of the world. Potentially modifiable risk factors for CVD include tobacco use, physical inactivity<span>, hypertension, elevated low-density lipoprotein cholesterol, and a cluster of interrelated metabolic risk factors. Over the last several decades, efforts to prevent or treat CVD risk factors<span><span> have resulted in significantly lower rates of CVD-related mortality. However, many patients never achieve adequate control of CVD risk factors even when these factors have been identified. In addition, the growing prevalence of obesity and type 2 diabetes mellitus (DM) threatens to undermine the improvements in CVD that have been achieved. In the United States, approximately two thirds of adults are overweight or obese, and even modest excess body weight is associated with a significantly increased risk of CVD-related mortality. Lifestyle interventions to promote weight loss reduce the risk of CVD-related illness but are difficult for patients to sustain over long periods of time. The increased incidence of obesity has also contributed to significant increases in the prevalence of other important CVD risk factors, including hypertension, dyslipidemia<span>, insulin resistance, and type 2 DM. Pharmacologic therapies are currently available to address individual CVD risk factors, and others are being evaluated, including endocannabinoid </span></span>receptor antagonists, inhibitors of peroxisome proliferator-activated receptor subtypes alpha and gamma, and several agents that modulate the activity of glucagon-like peptide-1. The new agents have the potential to significantly improve several CVD risk factors with a single medication and may provide clinicians with several new strategies to reduce the long-term risk of CVD.</span></span></p></div>","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 2","pages":"Pages 24-41"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(09)62037-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28147506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improving Insulin Sensitivity: A Review of New Therapies","authors":"Mary K. Rhee MD ,&nbsp;Guillermo E. Umpierrez MD","doi":"10.1016/S1098-3597(09)60023-5","DOIUrl":"10.1016/S1098-3597(09)60023-5","url":null,"abstract":"<div><p><span><span><span><span><span>Insulin resistance is a state of impaired insulin action in insulin—dependent tissues-liver, muscle, and fat tissues. Impaired insulin action results in a reduction in insulin-stimulated glucose uptake<span> and impaired insulin-mediated suppression of hepatic glucose production and </span></span>adipocyte<span><span> lipolysis. Insulin resistance may result from a disruption in any step of the insulin-signaling cascade. Defects in </span>insulin signaling have been demonstrated in association with clinical predictors of insulin resistance, such as obesity, lack of physical activity, and a family history of type 2 diabetes mellitus. Weight loss and physical activity have been shown to improve </span></span>insulin sensitivity </span>in patients<span><span> with diabetes. For many years, metformin<span> and thiazolidinediones were the only pharmacologic </span></span>treatments available that targeted insulin resistance; however, new classes of </span></span>drugs<span><span><span><span><span>, including the incretin analogs, dipeptidylpeptidase (DPP)-4 inhibitors, and </span>endocannabinoid inhibitors, have been discovered. Incretins are </span>intestinal hormones<span> that are released in response to nutrient ingestion to stimulate </span></span>insulin secretion<span> by the β-cells of the pancreatic islets. Incretin analogs improve insulin secretion and insulin sensitivity and promote weight loss. DPP-4 inhibitors block DPP-4, an enzyme that degrades the endogenous incretin hormone glucagon-like peptide-1. DPP-4 inhibitors stimulate insulin secretion, inhibit </span></span>glucagon secretion, and increase postmeal insulin sensitivity, but they do not appear to promote weight loss. Pharmacologic blockade of CB</span></span>₁<span><span> receptors with endocannabinoid inhibitors has been shown to reduce food intake, promote weight loss, and increase adiponectin levels. These treatments may not only improve </span>glycemic control but also offer the potential for additional metabolic and cardiovascular benefits.</span></p></div>","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 ","pages":"Pages S28-S38"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(09)60023-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56553809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CME Test Answer Sheet and Evaluation Form for Managing Cardiovascular Risk Factors in Type 2 Diabetes Mellitus Volume 9, Supplement 2","authors":"","doi":"10.1016/S1098-3597(09)60025-9","DOIUrl":"https://doi.org/10.1016/S1098-3597(09)60025-9","url":null,"abstract":"","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 ","pages":"Pages S41-S44"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(09)60025-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137161280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Treatment of Prediabetes to Prevent Progression to Type 2 Diabetes","authors":"Vivian A. Fonseca MD","doi":"10.1016/S1098-3597(09)62039-1","DOIUrl":"10.1016/S1098-3597(09)62039-1","url":null,"abstract":"<div><p><span>Overt type 2 diabetes is usually preceded by a condition known as prediabetes<span><span><span>, which is characterized by impaired fasting glucose (IFG) and impaired glucose tolerance (IGT). Both IFG and IGT exhibit elevated glucose levels that are not sufficient to be classified as diabetes but that represent the development of insulin resistance. Achieving </span>glycemic control </span>in patients<span> with prediabetes through lifestyle and pharmacologic interventions can effectively prevent or delay the development of diabetes and its associated complications. The first step, however, is to identify patients at risk. Although patients can be identified with an oral glucose tolerance test<span><span> (OGTT) or a fasting plasma glucose (FPG) screening, a normal FPG does not preclude an elevated OGTT and, therefore, the presence of prediabetes. For patients who progress to type 2 diabetes, intensive therapy aimed at reducing and maintaining glycosylated hemoglobin (A1C) levels &lt; 7% has been shown to reduce the risk of complications. An A1C level ≥ 7% should signal the need to initiate or change therapy to achieve </span>glycemic goals. (</span></span></span></span><em>Clinical Cornerstone.</em><span> 2007;8[2]: 10–20) Copyright © 2007 Excerpta Medica, Inc.</span></p></div>","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 2","pages":"Pages 51-61"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(09)62039-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28147958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overcoming Patient Barriers to Initiating Insulin Therapy in Type 2 Diabetes Mellitus","authors":"David G. Marrero PhD","doi":"10.1016/S1098-3597(09)62041-X","DOIUrl":"10.1016/S1098-3597(09)62041-X","url":null,"abstract":"<div><p>Data from clinical trials underscore the fact that loss of β-cell function and insulin hyposecretion are progressive in type 2 diabetes. To achieve adequate glycemic control, most patients will eventually require insulin. Addition of insulin to sulfonylurea therapy, when maximal sulfonylurea does not adequately maintain fasting plasma glucose levels at &lt; 108 mg/dL, has been found to be more effective than initiating insulin therapy after oral agents have failed to maintain glycemic control. Nonetheless, both patients and providers are reluctant to begin insulin therapy. Research has shown that providers often delay modification of the diabetes treatment regimen because they believe their patients would be concerned about starting insulin therapy. In addition, they are concerned about patient nonadherence to nonpharmacologic and pharmacologic therapy. There are multiple reasons for patient nonadherence to insulin therapy; however, patients must be made to understand, early in the course of the disease, the progressive nature of type 2 diabetes and that exogenous insulin is an additional therapeutic option to help them achieve and maintain adequate glycemic control. (<em>Clinical Cornerstone.</em> 2007;8[2]:33–43) Copyright © 2007 Excerpta Medica, Inc.</p></div>","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 2","pages":"Pages 63-73"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(09)62041-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28147959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Natural history of asthma: Persistence versus progression — Does the beginning predict the end?","authors":"Panetteri RA,&nbsp;Covar R,&nbsp;Grant E,&nbsp;Richard A. Johnson MD","doi":"10.1016/S1098-3597(08)80015-4","DOIUrl":"10.1016/S1098-3597(08)80015-4","url":null,"abstract":"","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"8 4","pages":"Page 77"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(08)80015-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"100953869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abdominal adiposity: Early intervention and therapeutic options","authors":"André J. Scheen Md, Phd","doi":"10.1016/S1098-3597(08)80004-X","DOIUrl":"10.1016/S1098-3597(08)80004-X","url":null,"abstract":"<div><p>Abdominal obesity, especially visceral adipose tissue (VAT), increases the incidence of a cluster of metabolic disturbances (the so-called metabolic syndrome), type 2 diabetes, and associated cardiovascular risk. Not only is abdominal obesity a marker of a dysmetabolic profile, but VAT also appears to be a causal factor for morbidity and premature mortality, both by classic mechanisms (ie, dyslipidemia, hypertension, and glucose dysmetabolism), as well as less conventional mechanisms (ie, low adiponectin levels and high proinflammatory cytokine levels that promote insulin resistance and endothelial dysfunction). Because abdominal obesity is increasingly seen in young people, early intervention is mandatory to stop the cycle that leads to cardiometabolic risk. Obesity should be considered a chronic disease of multifactorial etiology,and treatment must be maintained for life —first with lifestyle interventions (energy-reduced diet and increased physical activity) and then with pharmacologic approaches (eg, orlistat, sibutramine, or rimonabant), when necessary. Beneficial metabolic effects may result from even moderate weight loss and are attributed primarily to a predominant reduction in VAT. Finally, special attention should be paid to possible additional positive effects beyond weight reduction, as especially demonstrated with the CB₁ antagonist rimonabant.</p></div>","PeriodicalId":80265,"journal":{"name":"Clinical cornerstone","volume":"9 ","pages":"Pages S20-S27"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1098-3597(08)80004-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56553764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}