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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.amjmed.com//inpress?rss=yes"><title>The American Journal of Medicine - Articles in Press</title><description>The American Journal of Medicine RSS feed: Articles in Press.    
 The American Journal of Medicine  - "The Green Journal" -  publishes original clinical research of interest to physicians in internal 
medicine, both in academia and community-based practice.  The American Journal of Medicine  is the official journal of The Association 
of Professors of Medicine, a prestigious group comprised of chairs of departments of internal medicine at more than 125 medical schools 
across the country. Each issue carries useful reviews as well as seminal articles of immediate interest to the practicing physician, 
including peer-reviewed, original scientific studies that have direct clinical significance, and position papers on health care issues, 
medical education, and public policy.  The journal's ISI factor - the international measure of cited manuscripts and scientific impact 
- is fourteenth in the world among all general medical journals.
  
 The  AJM  publishes studies performed by multi-center groups 
in the various disciplines of medicine, including clinical trials and cohort studies from large patient populations, specifically: 

 
 Phase I, phase II, and phase III studies performed under the auspices of groups such as general clinical research centers, cooperative 
oncology groups, and the like.   
 Reports of patients with common presentations or diseases, especially studies that delineate 
the natural history and therapy of important conditions.  
 Reviews oriented to the practicing internist and  diagnostic puzzles, 
complete with images from a variety of specialties. 
 Careful physiological or pharmacological studies that explain normal function 
or the body's response to disease.  
 Analytic reviews such as meta-analyses and decision analyses that use a formal structure 
to summarize an important field.  
 
   </description><link>http://www.amjmed.com//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:issn>0002-9343</prism:issn><prism:publicationDate>2012-05-11</prism:publicationDate><prism:copyright> © 2012 Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000332/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312002513/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431200280X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311010278/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000782/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312002422/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312002501/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311010291/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000344/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000824/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000861/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312001180/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312001209/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311010266/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000812/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312001192/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000939/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000940/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312001234/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312001593/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312001775/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009909/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311010308/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000113/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000903/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431101028X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000034/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000733/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000800/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000071/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000721/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312001751/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000952/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009508/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311010710/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431200085X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000885/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000897/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934312000915/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS0002934311009016/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431100790X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.amjmed.com/article/PIIS000293431100581X/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000332/abstract?rss=yes"><title>Vascular Disease and Stroke Risk in Atrial Fibrillation: A Nationwide Cohort Study - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000332/abstract?rss=yes</link><description>Abstract: 
Background: 
Vascular disease (including myocardial infarction and peripheral artery disease) has been proposed as a less well-validated risk factor for stroke in patients with atrial fibrillation. We investigated whether vascular disease is an independent risk factor of stroke/thromboembolism in atrial fibrillation and whether adding vascular disease improves Congestive heart failure, Hypertension, Age75 years, Diabetes, previous Stroke (CHADS2) risk stratification.

Methods: 
By using nationwide Danish registers, we identified all patients discharged with atrial fibrillation and not treated with vitamin K antagonist or heparin between 1997 and 2008. The rate of stroke/thromboembolism in patients with atrial fibrillation with and without vascular disease was determined, and the risk associated with vascular disease was estimated in Cox regression analyses. The value of adding vascular disease to the CHADS2 score was evaluated by Net Reclassification Improvement and Integrated Discrimination Improvement.

Results: 
We included 87,202 patients with non-valvular atrial fibrillation; of these, 15,212 (17.4%) had vascular disease, 11,750 (77.2%) had myocardial infarction, 2503 (16.5%) had peripheral artery disease, and 959 (6.3%) had both. In patients with a CHADS2 score=0, the rate of stroke/thromboembolism at 1-year follow-up was 2.31 (1.63-3.26) and 1.52 (1.34-1.73) per 100 person-years in patients with and without vascular disease, respectively. Vascular disease increased the risk of stroke/thromboembolism in both univariate (hazard ratio [HR] 1.26; confidence interval [CI], 1.18-1.35) and multivariate (HR, 1.12; CI, 1.05-1.21) analyses. The risk of stroke/thromboembolism associated with peripheral artery disease alone (HR, 1.93; CI, 1.70-2.19) was greater than the risk with myocardial infarction alone (HR, 1.12; CI, 1.04-1.21), and vascular disease significantly improved the predictive ability of the CHADS2 score (Net Reclassification Improvement 0.032, P&lt;.001).

Conclusions: 
Vascular disease is an independent predictor of stroke/thromboembolism in atrial fibrillation and improves the predictive ability of the CHADS2 score.
</description><dc:title>Vascular Disease and Stroke Risk in Atrial Fibrillation: A Nationwide Cohort Study - Corrected Proof</dc:title><dc:creator>Jonas Bjerring Olesen, Gregory Y.H. Lip, Deirdre A. Lane, Lars Køber, Morten Lock Hansen, Deniz Karasoy, Carolina Malta Hansen, Gunnar Hilmar Gislason, Christian Torp-Pedersen</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.024</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-11</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-11</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312002513/abstract?rss=yes"><title>Research Leadership and Investigators: Gender Distribution in the Federal Government - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312002513/abstract?rss=yes</link><description>Abstract: 
Background: 
The National Academies reported in Beyond Bias and Barriers: Fulfilling the Potential of Women in Academic Science and Engineering (2006) that “women are very likely to face discrimination.” In academic medicine, gender distribution is becoming more balanced. In the federal government, women also have made progress, doubling their representation in professional positions to 44%. The Department of Veterans Affairs (VA) has a research program and a mission to train health care professionals; however, its gender distribution has not been described.

Methods: 
We conducted a descriptive study using public data for positions in the VA, National Institutes of Health (NIH), and Agency for Healthcare Research and Quality (AHRQ). We followed with a case-control analysis of predictors of receipt of grant funding in the VA. Participants were 224 leadership positions and 132 principal investigators.

Results: 
Women comprised 33% (AHRQ), 27% (NIH), and 0% (VA) of the top research leadership. Across all VA research levels, women comprised 45% to 0%, depending on the service. In the case-control analysis of principal investigators, men had greater odds (odds ratio 8.0) of a Cooperative Studies Program (CSP) trial award. History of first, last, or any authorship on a clinical trial publication in the 10 years before the index trial was only weakly associated with award of a CSP trial. The gender imbalance was not explained by publication history.

Conclusions: 
Marked gender disparities were seen in the VA, except in Health Services Research. Organizations must investigate their practices to reveal disparities, investigate underlying factors, and intervene as needed.
</description><dc:title>Research Leadership and Investigators: Gender Distribution in the Federal Government - Corrected Proof</dc:title><dc:creator>Madeline McCarren, Steven Goldman</dc:creator><dc:identifier>10.1016/j.amjmed.2012.03.006</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-11</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-11</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431200280X/abstract?rss=yes"><title>Advancing into the Community - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS000293431200280X/abstract?rss=yes</link><description>An infection once almost exclusively acquired in the hospital setting has made its way into a broader population—and for one 56-year-old woman, its course was devastating. She presented after 3 days of diffuse, cramping, abdominal pain, and 6-8 watery, nonbloody, bowel movements per day. Her illness began 4 days prior with the onset of generalized malaise and a low-grade fever that measured up to 100°F (37.8° C); she had no cough, chest pain, or shortness of breath. Employed as a department store cashier, the patient lived at home with her husband and had no history of hospitalization or travel within the preceding 5 years, no known sick contacts, and no history of antibiotic use in the previous 6 months. She was a cigarette smoker with a remote history of heroin addiction. Methadone, 100 mg, was administered daily at a substance abuse clinic, and she took alprazolam, 2 mg, and clonazepam, 1 mg, multiple times a day for chronic anxiety. She did not take any gastric acid suppressants.</description><dc:title>Advancing into the Community - Corrected Proof</dc:title><dc:creator>Darlene LeFrancois, Sharon Leung</dc:creator><dc:identifier>10.1016/j.amjmed.2012.04.001</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-11</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-11</prism:publicationDate><prism:section>IMAGES IN DERMATOLOGY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311010278/abstract?rss=yes"><title>Incident Gout in Women and Association with Obesity in the Atherosclerosis Risk in Communities (ARIC) Study - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934311010278/abstract?rss=yes</link><description>Abstract: 
Background: 
We hypothesized that women with early- and mid-adult life obesity, as well as high mid-adult life waist-to-hip ratios, and high weight gain during adulthood, experience a greater incidence of gout.

Methods: 
We examined the incidence of gout in the Atherosclerosis Risk in Communities Study, a population-based biracial cohort comprised of individuals aged 45-65 years at baseline (1987-1989). A total of 6263 women without prior history of gout were identified. We examined the association of body mass index (BMI) and obesity at cohort entry and at age 25 years, waist-to-hip ratio, and weight change with gout incidence (1996-1998).

Results: 
Over 9 years of follow-up, 106 women developed gout. The cumulative incidence of gout, by age 70 years, according to BMI category at baseline of &lt;25, 25-29.9, 30-34.9, and ≥35 kg/m2, was 1.9, 3.6, 7.9, and 11.8%, respectively (P &lt;.001). Obese women (BMI ≥30) at baseline had an adjusted 2.4-fold greater risk of developing gout than nonobese women (95% confidence interval [CI], 1.53-3.68). This association was attenuated after further adjustment for urate levels. Further, early adult obesity in women was associated with a 2.8-fold increased risk of gout compared with nonobese women (95% CI, 1.33-6.09), which remained statistically significant after baseline urate adjustment. There was a graded association between each anthropometric measure, including weight gain, with incident gout (each P for trend &lt;.001). The results were similar in black and white women.

Conclusions: 
In a large cohort of black and white women, obesity in early- and mid-adulthood, and weight gain during this interval, were each independent risk factors for incident gout in women.
</description><dc:title>Incident Gout in Women and Association with Obesity in the Atherosclerosis Risk in Communities (ARIC) Study - Corrected Proof</dc:title><dc:creator>Janet W. Maynard, Mara A. McAdams DeMarco, Alan N. Baer, Anna Köttgen, Aaron R. Folsom, Josef Coresh, Allan C. Gelber</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.018</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-09</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-09</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000782/abstract?rss=yes"><title>So, You Want to Live to 120? The Genie in the Bottle - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000782/abstract?rss=yes</link><description>Throughout human history, there has always been a keen interest in methods to prolong a healthy and active lifespan. Ponce de Leon's search for the fountain of youth in Florida in the 16th century is but one example of the fascination that anti-aging holds for human beings. Similar quests have been described in literature from ancient Rome and China. If one searches the Internet for anti-aging interventions, a vast array of techniques are offered, from starvation regimes to dietary supplements and growth hormones. All are for sale, but none so far have been proven as the magic bullet, despite exorbitant claims on many of the websites.</description><dc:title>So, You Want to Live to 120? The Genie in the Bottle - Corrected Proof</dc:title><dc:creator>Joseph S. Alpert, Qin M. Chen</dc:creator><dc:identifier>10.1016/j.amjmed.2012.02.002</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-09</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-09</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312002422/abstract?rss=yes"><title>Intramural Hematoma of the Aorta as a Presenting Sign of Accelerated Hypertension - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312002422/abstract?rss=yes</link><description>A 69-year-old woman with hypertension and poor adherence to antihypertensive therapy presented with sudden pain in the upper right flank that radiated anteriorly to the chest and posteriorly to the scapulae. Presenting blood pressure (BP) was 222/104 mm Hg, with a heart rate of 82 beats per minute. Physical examination and laboratory testing were otherwise unremarkable. Computed tomography (CT) angiography, including noncontrast imaging, demonstrated an intramural hematoma of the aorta, arising from the origin of the subclavian artery, traversing within the descending thoracic aorta and extending down to the level of the diaphragmatic crus. No dissection was present on postcontrast images (). The patient was admitted to the cardiac care unit and treated with an intravenous esmolol infusion followed by oral nifedipine 60 mg daily, hydrochlorothiazide 12.5 mg daily, metoprolol succinate 200 mg twice daily, and aliskiren 300 mg daily. Over the next 3 days, the systolic BP was reduced to 120-140 mm Hg. After 1 year of adherent therapy, CT imaging showed complete resolution of the intramural hematoma.</description><dc:title>Intramural Hematoma of the Aorta as a Presenting Sign of Accelerated Hypertension - Corrected Proof</dc:title><dc:creator>Ravi Marfatia, Electra Kaloudis, Beatriz E. Tendler, William B. White</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.035</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-09</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-09</prism:publicationDate><prism:section>CLINICAL COMMUNICATION TO THE EDITOR</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312002501/abstract?rss=yes"><title>Wegener's Granulomatosis in a Patient with Fever of Unknown Origin - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312002501/abstract?rss=yes</link><description>A 68-year-old woman presented with a several-month history of progressive fatigue, night sweats, and fevers. In addition, she reported onset of a nonproductive cough, sinus congestion, pleuritic chest pain, and significant weight loss.</description><dc:title>Wegener's Granulomatosis in a Patient with Fever of Unknown Origin - Corrected Proof</dc:title><dc:creator>Harsh C. Patel, Stephen D. Sisson, Naudia N. Lauder</dc:creator><dc:identifier>10.1016/j.amjmed.2012.02.012</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-09</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-09</prism:publicationDate><prism:section>CLINICAL COMMUNICATION TO THE EDITOR</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311010291/abstract?rss=yes"><title>Bullous Reactions to Bedbug Bites Reflect Cutaneous Vasculitis - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934311010291/abstract?rss=yes</link><description>Abstract: 
Background: 
There has been a worldwide resurgence of bedbug infestations. Bites by these insects may cause mild or severe cutaneous reactions, and anaphylaxis has been reported. Little is known about the most severe cutaneous reactions, termed bullous or complex reactions.

Objective: 
To study the time course and histopathologic findings of complex (bullous) cutaneous reactions to bedbugs in order to determine the optional treatment for them.

Design, Setting, and Participants: 
We prospectively photographed bullous reactions to observed bedbug bites at 30 minutes; 6, 12, 24, 36, 48, and 72 hours; 1, 2, 3, and 4 weeks, and biopsied reactions at 30 minutes, and 6, 12, and 24 hours. We also reviewed Internet postings and the available medical literature on bullous reactions after bedbug bites.

Main Outcomes and Measures: 
Correlations between clinical and histologic findings using both routine and immunofluorescent techniques.

Results: 
Bullous reactions to bedbugs are not rare. Of 357 photographs of bedbug bites posted on the Internet, 6% were bullous. In an individual with previous bullous reactions, experimental bedbug bites were associated with a progression of cutaneous responses at bite sites from immediate, pruritic, edematous lesions to a late-in-time macule, which evolved into bullous reactions by 24 hours. Bullous lesions eventually lysed but took weeks to heal. Histopathologic evaluation of bullous reactions showed a polymorphous picture with histologic evidence of an urticarial-like reaction early on that rapidly developed into a hybrid leukocytoclastic vasculitis. This vasculitis was initially neutrophilic but developed into a destructive, necrotizing, eosinophil-rich vasculitis with prominent infiltration of CD 68+ histiocytes and collagen necrobiosis. This histologic picture is similar to the dermal vasculitis in patients with Churg-Strauss vasculitis.

Conclusion: 
Historically, bedbug bite reactions have been considered to be of minor medical significance. However, the findings presented here demonstrate that the not-uncommon bullous reactions to bedbug bites reflect the presence of a local, highly destructive, cutaneous vasculitis. The histologic features of these reactions resemble those occurring in the Churg-Strauss syndrome. Therefore, efforts to prevent further bites and monitor for evidence of systemic vasculitis should be made in patients with bullous reactions to bedbug bites. Topical treatment with high potency corticosteroids may be useful in the treatment of bullous reactions.
</description><dc:title>Bullous Reactions to Bedbug Bites Reflect Cutaneous Vasculitis - Corrected Proof</dc:title><dc:creator>Richard D. deShazo, Mark F. Feldlaufer, Martin C. Mihm, Jerome Goddard</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.020</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000344/abstract?rss=yes"><title>Systolic Blood Pressure Reduction and Risk of Acute Renal Injury in Patients with Intracerebral Hemorrhage - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000344/abstract?rss=yes</link><description>Abstract: 
Background: 
Aggressive systolic blood pressure reduction may precipitate acute renal injury because of underlying hypertensive nephropathy in patients with intracerebral hemorrhage. The study's objective was to determine the rate and determinants of acute renal injury during acute hospitalization among subjects with intracerebral hemorrhage using a post hoc analysis of a multicenter prospective study.

Methods: 
Subjects with intracerebral hemorrhage and elevated systolic blood pressure of 170 mm Hg or greater who presented within 6 hours of symptom onset and underwent treatment of acute hypertensive response and fluid management as per study and local protocols, respectively. Acute renal injury was defined post hoc using the criteria used in Acute Kidney Injury Network classifications within 72 hours of admission. Descriptive statistics and standard statistical tests were used to characterize and evaluate the effect of systolic blood pressure reduction parameters (relative to initial systolic blood pressure) and average maximum hourly dose of nicardipine on the occurrence of acute renal injury.

Results: 
A total of 60 subjects were recruited (57% were men; mean age of 62.0±15.1 years). Five subjects (9%) had stage I acute renal injury according to the Acute Kidney Injury Network criteria. None of the subjects had stage II or III acute renal injury. The serum creatinine course for the first 3 days suggested that the peak elevation of creatinine was seen at 18, 30, 57, 58, and 71 hours after baseline measurements in these 5 subjects, all of which except for the first one were beyond the protocol-specified treatment period. The incidences of neurologic deterioration and symptomatic hematoma expansion were significantly greater in the subjects with stage I renal impairment. The systolic blood pressure reduction parameters (in particular, the area under the curve depicting the 24-hour systolic blood pressure summary statistic) and the higher average maximum hourly nicardipine dose were strongly associated with stage I renal impairment.

Conclusions: 
Although acute renal injury is infrequent and mild among subjects with intracerebral hemorrhage undergoing systolic blood pressure reduction, a trend in association between systolic blood pressure reduction and renal impairment was observed in this small study. Therefore, it is important to carefully monitor the renal function when administering treatment to reduce systolic blood pressure in patients with intracerebral hemorrhage.
</description><dc:title>Systolic Blood Pressure Reduction and Risk of Acute Renal Injury in Patients with Intracerebral Hemorrhage - Corrected Proof</dc:title><dc:creator>Adnan I. Qureshi, Yuko Y. Palesch, Renee Martin, Jill Novitzke, Salvador Cruz Flores, Asad Ehtisham, Joshua N. Goldstein, Jawad F. Kirmani, Haitham M. Hussein, M. Fareed K. Suri, Nauman Tariq, Antihypertensive Treatment of Acute Cerebral Hemorrhage Investigators</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.031</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000824/abstract?rss=yes"><title>Late Effects in Adult Survivors of Pediatric Cancer: A Guide for the Primary Care Physician - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000824/abstract?rss=yes</link><description>Abstract: 
Because of significant medical advances in the past 50 years, the number of adult survivors of childhood/adolescent cancer has increased dramatically. Unfortunately, more than 60% of these survivors will have at least 1 long-term side effect from treatment. This growing population requires dedicated care by their primary physicians because they have specific risk factors depending on their initial cancer diagnosis and the treatment modalities they received. Internists and family physicians play an integral role in providing appropriate screening, treatment, and counseling to prevent morbidity and mortality in these patients.
</description><dc:title>Late Effects in Adult Survivors of Pediatric Cancer: A Guide for the Primary Care Physician - Corrected Proof</dc:title><dc:creator>Lisa M. Kopp, Puja Gupta, Luz Pelayo-Katsanis, Brenda Wittman, Emmanuel Katsanis</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.013</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate><prism:section>REVIEW</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000861/abstract?rss=yes"><title>High Risk of Transfusion-induced Alloimmunization of Patients with Inflammatory Bowel Disease - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000861/abstract?rss=yes</link><description>Abstract: 
Background: 
Anemia is highly prevalent in inflammatory bowel disease patients, and red blood cell transfusion is often indicated already at reproductive age. Both transfusion and pregnancy may induce red cell alloantibodies, potentially complicating further transfusions and pregnancies. As recent evidence suggests that inflammation may promote red cell antibody induction, the alloimmunization risk of these patients after allogenic erythrocyte exposure was investigated.

Methods: 
Red cell alloantibody status and clinical data were analyzed in 193 inflammatory bowel disease patients with a history of transfusion or pregnancy, and compared with transfused controls with noninflammatory diseases (n=357).

Results: 
In transfused patients with inflammatory bowel disease, a 2.5-fold-increased red cell antibody prevalence was found (10/119, 8.4%), compared with transfused sex-matched controls with noninflammatory diseases (12/357, 3.4%; P=.023). Patients with inflammatory bowel disease had fewer transfusions (mean 3.0 vs 4.2, P=.003) but higher C-reactive protein levels during transfusion than controls (mean 8.4 vs 5.4 mg/dL, P &lt;.001). The red cell antibodies of inflammatory bowel disease patients were clinically significant, directed against different Rh, Kell, Duffy, or Lutheran blood group antigens, and associated with higher number of transfusions (odds ratio 1.57; 95% confidence interval, 1.03-2.39). Conversely, immunomodulatory therapy during transfusion showed negative association (odds ratio 0.12; 95% confidence interval, 0.02-0.61). Only 1.4% of inflammatory bowel disease patients with pregnancy alone had antibodies.

Conclusions: 
Patients with inflammatory bowel disease exhibited a very high risk of transfusion-induced red cell alloimmunization, possibly potentiated by inflammation. Aside from a restrictive transfusion strategy, the implementation of prophylactic blood group phenotype matching of red cell concentrates (not only for ABO and RhD but also RhCcEe, Kell, Kidd, Duffy) could prevent antibody induction and associated complications in these patients.
</description><dc:title>High Risk of Transfusion-induced Alloimmunization of Patients with Inflammatory Bowel Disease - Corrected Proof</dc:title><dc:creator>Pavol Papay, Klaus Hackner, Harald Vogelsang, Gottfried Novacek, Christian Primas, Walter Reinisch, Alexander Eser, Andrea Mikulits, Wolfgang R. Mayr, Günther F. Körmöczi</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.028</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312001180/abstract?rss=yes"><title>Accidental Thyrotoxicosis Caused by Inadvertent Ingestion of Levothyroxine “Dog-Tabs” by a Veterinarian with Hypothyroidism - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312001180/abstract?rss=yes</link><description>A 33-year-old veterinarian with Hashimoto's thyroiditis and hypothyroidism, stable with a levothyroxine replacement dosage (thyroid-stimulating hormone, 0.9; normal, 0.4-5.0 mIU/L) of levothyroxine 50 μg/d, presented with mild anxiety, jitteriness, and insomnia. Repeat thyroid-stimulating hormone was undetectable. Serum total T4 was 15.4 μg/dL (normal, 6.0-10.0 μg/dL), and free thyroxine index was 14.9 (normal, 6-10). On further questioning, the patient realized she had recently run out of her prescribed levothyroxine tablets and had been taking levothyroxine “dog tabs” 0.5 mg/d, thinking that would be the same as the 50-μg tablets she had been prescribed, inadvertently taking 10 times the prescribed dose. Her levothyroxine therapy was discontinued, and repeat thyroid function studies 2 months later revealed a thyroid-stimulating hormone level of 5.1 mIU/L. The patient was restarted on levothyroxine 50 μg/d, and repeat thyroid-stimulating hormone level 2 months later was 1.0 mIU/L. The patient was instructed to take her prescribed levothyroxine tablets and not use her levothyroxine “dog tabs” in the future.</description><dc:title>Accidental Thyrotoxicosis Caused by Inadvertent Ingestion of Levothyroxine “Dog-Tabs” by a Veterinarian with Hypothyroidism - Corrected Proof</dc:title><dc:creator>Harmeet Singh Narula</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.020</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate><prism:section>CLINICAL COMMUNICATION TO THE EDITOR</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312001209/abstract?rss=yes"><title>Enhancing Quality of Trainee-written Consultation Notes - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312001209/abstract?rss=yes</link><description>Inpatient consultations between generalists and specialty care providers represent a specific situation where poor information exchange between physicians could result in delayed diagnoses, inadequate follow-up, or duplication of services. Unfortunately, subspecialty trainees do not receive formal instruction in how to provide an effective consultation. As a result, consultation notes are variable in quality and often do not meet the needs of referring providers or patients.</description><dc:title>Enhancing Quality of Trainee-written Consultation Notes - Corrected Proof</dc:title><dc:creator>Delphine S. Tuot, Niraj L. Sehgal, Naama Neeman, Andrew Auerbach</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.021</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate><prism:section>CLINICAL EFFECTIVENESS</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311010266/abstract?rss=yes"><title>Venous Thromboembolism in Patients with Diabetes Mellitus - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934311010266/abstract?rss=yes</link><description>Abstract: 
Purpose: 
The majority of epidemiological studies demonstrate an increased risk of venous thromboembolism among diabetic patients. Our aim was to compare clinical characteristics, prophylaxis, treatment, and outcomes of venous thromboembolism in patients with and without previously diagnosed diabetes.

Methods: 
We studied diabetic patients in the population-based Worcester Venous Thromboembolism Study of 2488 consecutive patients with validated venous thromboembolism.

Results: 
Of 2488 venous thromboembolism patients, 476 (19.1%) had a clinical history of diabetes. Thromboprophylaxis was omitted in more than one third of diabetic patients who had been hospitalized for non-venous-thromboembolism-related illness or had undergone major surgery within 3 months before diagnosis. Patients with diabetes were more likely than nondiabetic patients to have a complicated course after venous thromboembolism. Patients with diabetes were more likely than patients without diabetes to suffer recurrent deep vein thrombosis (14.9% vs 10.7%) and long-term major bleeding complications (16.4% vs 11.7%) (all P=.01). Diabetes was associated with a significant increase in the risk of recurrent deep vein thrombosis (adjusted odds ratio [AOR] 1.74; 95% confidence interval [CI], 1.21-2.51). Aspirin therapy at discharge (AOR 1.59; 95% CI, 1.1-2.3) and chronic kidney disease (AOR 2.19; 95% CI, 1.44-3.35) were independent predictors of long-term major bleeding.

Conclusion: 
Patients with diabetes who developed venous thromboembolism were more likely to suffer a complicated clinical course. Diabetes was an independent predictor of recurrent deep vein thrombosis. We observed a low rate of thromboprophylaxis in diabetic patients. Further studies should focus on venous thromboembolism prevention in this vulnerable population.
</description><dc:title>Venous Thromboembolism in Patients with Diabetes Mellitus - Corrected Proof</dc:title><dc:creator>Gregory Piazza, Samuel Z. Goldhaber, Aimee Kroll, Robert J. Goldberg, Catherine Emery, Frederick A. Spencer</dc:creator><dc:identifier>10.1016/j.amjmed.2011.12.004</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-04</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-04</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000812/abstract?rss=yes"><title>Safety of Symptom-limited Cardiopulmonary Exercise Testing in Patients with Aortic Stenosis - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000812/abstract?rss=yes</link><description>Abstract: 
Background: 
There are no published data on the safety of cardiopulmonary exercise testing in patients with aortic stenosis.

Methods: 
In this retrospective descriptive study, we examined 347 consecutive patients with aortic stenosis who underwent cardiopulmonary exercise testing at a tertiary referral center. We recorded major events including death, nonfatal major events (cardiac arrest, symptomatic or sustained ventricular or supraventricular tachycardia, myocardial infarction, and syncope), and minor events such as hypotension, nonsustained supraventricular and ventricular arrhythmias, positive electrocardiographic changes, and angina.

Results: 
Of 347 patients, 65 (19%) had mild, 145 (42%) had moderate, and 137 (40%) had severe aortic stenosis by echocardiographic criteria. No major events occurred during the tests. Minor events occurred in a total of 97 patients (28%), including 10 patients who developed supraventricular arrhythmias without hypotension; and one who had asymptomatic nonsustained ventricular tachycardia.

Conclusion: 
Symptom-limited cardiopulmonary exercise testing in cardiology-referred patients with aortic stenosis with preserved systolic function appears to be associated with very low risk of major adverse cardiovascular events during testing.
</description><dc:title>Safety of Symptom-limited Cardiopulmonary Exercise Testing in Patients with Aortic Stenosis - Corrected Proof</dc:title><dc:creator>Abhijeet Dhoble, Maurice E. Sarano, Stephen L. Kopecky, Randal J. Thomas, Courtney L. Hayes, Thomas G. Allison</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.012</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-04</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-04</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312001192/abstract?rss=yes"><title>Detection of Alpha-1 Antitrypsin Deficiency in the US - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312001192/abstract?rss=yes</link><description>Alpha-1 antitrypsin deficiency affects approximately 1 in 3000-5000 persons in the US, representing around 200,000 individuals with severe deficiency (genotypes ZZ, SZ, SS, and others) without considering carriers of one abnormal gene (genotypes MS, MZ). Unfortunately, less than 10% of affected individuals have been diagnosed properly. Current guidelines endorsed by major respiratory societies recommend targeted detection of individuals at risk, such as all subjects diagnosed with chronic obstructive pulmonary disease (COPD) or those with unexplained liver cirrhosis. The positive testing yield of alpha-1 antitrypsin deficiency screening following these recommendations is not known.</description><dc:title>Detection of Alpha-1 Antitrypsin Deficiency in the US - Corrected Proof</dc:title><dc:creator>Michael Campos, Diego Shmuels, John Walsh</dc:creator><dc:identifier>10.1016/j.amjmed.2011.12.014</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-05-04</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-05-04</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000939/abstract?rss=yes"><title>Risk of Chronic Dialysis and Death Following Acute Kidney Injury - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000939/abstract?rss=yes</link><description>Abstract: 
Background: 
Acute kidney injury frequently arises within an acute care hospitalization. Outcomes among acute kidney injury survivors following hospital discharge are poorly documented.

Methods: 
We conducted a population-based cohort study between 1996 and 2006 of all adult patients in Ontario with acute kidney injury who did not require in-hospital dialysis, and who survived free of dialysis ≥30 days after discharge. Those with acute kidney injury (n=41,327) were matched 1:1 to patients without acute kidney injury during their index hospitalization. Matching was by age (±1 year), sex, history of chronic kidney disease, receipt of mechanical ventilation during the index hospitalization, and a propensity score for developing acute kidney injury. The primary outcome was subsequent need for chronic dialysis. The secondary outcomes were all-cause mortality and rehospitalization.

Results: 
Mean age was 70 years, and median follow-up was 2 years (maximum 10 years). The incidence of chronic dialysis was 1.78 per 100 person-years among those with acute kidney injury and 0.74 per 100 person-years among unaffected controls (adjusted hazard ratio [HR]; 2.70, 95% confidence interval [CI], 2.42-3.00). Rates also were higher for all-cause mortality (15.34 vs 14.51 per-100 person-years; adjusted HR 1.10; 95% CI, 1.07-1.13) and rehospitalization (44.93 vs 37.18 per 100 person-years; adjusted HR 1.21; 95% CI, 1.18-1.24).

Conclusion: 
Even when acute dialysis is not required, survivors of acute kidney injury remain at higher risk of receipt of chronic dialysis thereafter. The absolute risk of death was more than 8 times the rate of chronic dialysis.
</description><dc:title>Risk of Chronic Dialysis and Death Following Acute Kidney Injury - Corrected Proof</dc:title><dc:creator>Ron Wald, Robert R. Quinn, Neill K. Adhikari, Karen E. Burns, Jan O. Friedrich, Amit X. Garg, Ziv Harel, Michelle A. Hladunewich, Jin Luo, Muhammad Mamdani, Jeffrey Perl, Joel G. Ray, University of Toronto Acute Kidney Injury Research Group</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.016</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-19</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-19</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000940/abstract?rss=yes"><title>Low-dose Aspirin and Cancer Mortality: A Meta-analysis of Randomized Trials - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000940/abstract?rss=yes</link><description>Abstract: 
Objective: 
Low-dose aspirin is a common strategy for preventing cardiovascular disease and associated mortality. A recent individual patient data meta-analysis of 8 trials of low- and high-dose aspirin, with long-term follow-up, found important reductions in cancer mortality. We aimed to determine whether cancer mortality also is reduced by low-dose aspirin in the shorter term.

Methods: 
We conducted a comprehensive search of 10 electronic databases up to December 2011. We conducted a meta-analysis using data from all randomized clinical trials evaluating low-dose (75-325 mg) daily aspirin. We extracted data on non-cardiovascular disease mortality and cancer mortality. We pooled studies using a random-effects model and conducted a meta-regression. We supplemented this with a cumulative meta-analysis and trial sequential monitoring analysis.

Results: 
Twenty-three randomized studies reported on nonvascular death. There were 944 nonvascular deaths of 41,398 (2.28%) patients receiving low-dose aspirin and 1074 nonvascular deaths of 41,470 (2.58%) patients not receiving aspirin therapy. The relative risk of nonvascular death was 0.88 (95% confidence interval [CI], 0.81-0.96, I2 = 0%). Eleven trials included data evaluating cancer mortality involving 16,066 patients. There were 162 of 7998 (2.02%) and 210 of 8068 (2.60%) cancer deaths among low-dose aspirin users versus non-aspirin users, respectively, reported over an average follow-up of 2.8 years. The relative risk of cancer mortality was 0.77 (95% CI, 0.63-0.95, I2 = 0%). Studies demonstrated a significant treatment effect after approximately 4 years of follow-up. The optimal information size analysis showed that a sufficient number of patients had been randomized to provide convincing evidence of a preventive role of low-dose aspirin in nonvascular deaths.

Conclusion: 
Nonvascular deaths, including cancer deaths, are reduced with low-dose aspirin.
</description><dc:title>Low-dose Aspirin and Cancer Mortality: A Meta-analysis of Randomized Trials - Corrected Proof</dc:title><dc:creator>Edward J. Mills, Ping Wu, Mark Alberton, Steve Kanters, Angel Lanas, Richard Lester</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.017</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-18</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-18</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312001234/abstract?rss=yes"><title>Fish Consumption and Colorectal Cancer Risk in Humans: A Systematic Review and Meta-analysis - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312001234/abstract?rss=yes</link><description>Abstract: 
Background: 
Fish consumption may protect against colorectal cancer, but results from observational studies are inconsistent; therefore, a systematic review with a meta-analysis was conducted.

Methods: 
Relevant studies were identified by a search of MEDLINE and EMBASE databases to May 2011, with no restrictions. Reference lists from retrieved articles also were reviewed. Studies that reported odds ratio (OR) or relative risk estimates with 95% confidence intervals (CIs) for the association between the consumption of fish and the risk of colorectal, colon, or rectal cancer were included. Two authors independently extracted data and assessed study quality. The risk estimate (hazard ratio, relative risk, or OR) of the highest and lowest reported categories of fish intake were extracted from each study and analyzed using a random-effects model.

Results: 
Twenty-two prospective cohort and 19 case-control studies on fish consumption and colorectal cancer risk met the inclusion criteria and were included in the meta-analysis. Our analysis found that fish consumption decreased the risk of colorectal cancer by 12% (summary OR, 0.88; 95% CI, 0.80-0.95). The pooled ORs of colorectal cancer for the highest versus lowest fish consumption in case-control studies and cohort studies were 0.83 (95% CI, 0.72-0.95) and 0.93 (95% CI, 0.86-1.01), respectively. There was heterogeneity among case-control studies (P&lt;.001) but not among cohort studies. A significant inverse association was found between fish intake and rectal cancer (summary OR, 0.79; 95% CI, 0.65-0.97), and there was a modest trend seen between fish consumption and colon cancer (summary OR, 0.96; 95% CI, 0.81-1.14). This study had no publication bias.

Conclusion: 
Our findings from this meta-analysis suggest that fish consumption is inversely associated with colorectal cancer.
</description><dc:title>Fish Consumption and Colorectal Cancer Risk in Humans: A Systematic Review and Meta-analysis - Corrected Proof</dc:title><dc:creator>Shengjun Wu, Bin Feng, Kai Li, Xia Zhu, Shuhui Liang, Xufeng Liu, Shuang Han, Biaoluo Wang, Kaichun Wu, Danmin Miao, Jie Liang, Daiming Fan</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.022</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-18</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-18</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312001593/abstract?rss=yes"><title>Increased Risk of Mortality and Readmission among Patients Discharged Against Medical Advice - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312001593/abstract?rss=yes</link><description>Abstract: 
Background: 
Approximately 500,000 patients are discharged from US hospitals against medical advice annually, but the associated risks are unknown.

Methods: 
We examined 148,810 discharges from an urban, academic health system between July 1, 2002 and June 30, 2008. Of these, 3544 (2.4%) were discharged against medical advice, and 80,536 (54.1%) were discharged home. We excluded inpatient deaths, transfers to other hospitals or nursing facilities or discharges with home care. Using adjusted and propensity score-matched analyses, we compared 30-day mortality, 30-day readmission, and length of stay between discharges against medical advice and planned discharges.

Results: 
Discharge against medical advice was associated with higher mortality than planned discharge, after adjustment (odds ratio [OR]adj 2.05; 95% confidence interval [CI], 1.48-2.86), and in propensity-matched analysis (ORmatched 2.46; 95% CI, 1.29-4.68). Discharge against medical advice also was associated with higher 30-day readmission after adjustment (ORadj 1.84; 95% CI, 1.69-2.01), and in propensity-matched analysis (ORmatched 1.65; 95% CI, 1.46-1.87). Finally, discharges against medical advice had shorter lengths of stay than matched planned discharges (3.37 vs 4.16 days, P &lt;.001).

Conclusions: 
Discharge against medical advice is associated with increased risk for mortality and readmission. In addition, discharges against medical advice have shorter lengths of stay than matched planned discharges, suggesting that the increased risks associated with discharge against medical advice are attributable to premature discharge.
</description><dc:title>Increased Risk of Mortality and Readmission among Patients Discharged Against Medical Advice - Corrected Proof</dc:title><dc:creator>William N. Southern, Shadi Nahvi, Julia H. Arnsten</dc:creator><dc:identifier>10.1016/j.amjmed.2011.12.017</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-18</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-18</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312001775/abstract?rss=yes"><title>The Physics of Geriatric Pharmacotherapy: Overcoming Therapeutic Inertia and Momentum - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312001775/abstract?rss=yes</link><description>


   SEE RELATED ARTICLE p. XXX</description><dc:title>The Physics of Geriatric Pharmacotherapy: Overcoming Therapeutic Inertia and Momentum - Corrected Proof</dc:title><dc:creator>Jerry H. Gurwitz</dc:creator><dc:identifier>10.1016/j.amjmed.2012.02.007</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-18</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-18</prism:publicationDate><prism:section>GERIATRICS AND GERONTOLOGY SPECIAL SECTION EDITORIAL</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009909/abstract?rss=yes"><title>Endothelial Progenitor Cells Are Suppressed in Anemic Patients with Acute Coronary Syndrome - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934311009909/abstract?rss=yes</link><description>Abstract: 
Objective: 
Anemia is an independent predictor of poor prognosis in acute coronary syndrome. Endothelial progenitor cells are bone marrow-derived cells that are mobilized into the circulation in response to ischemia. The number of circulating endothelial progenitor cells increases within days of acute coronary syndrome. There is no confirmation regarding the correlation between the occurrence of anemia and the deficiency in endothelial progenitor cells in patients with acute coronary syndrome. The correlation between chronic anemia and endothelial progenitor cells in patients with acute coronary syndrome was investigated.

Methods: 
Endothelial progenitor cells were examined in 26 patients with acute coronary syndrome. Fifteen patients had chronic nonprogressive anemia, and 11 patients had a normal blood count. Blood samples were drawn on the first day of admission and 4 to 7 days later. Mononuclear cells were separated and cultured on fibronectin-coated plates with EndoCult medium (StemCell Technologies, Vancouver, BC, Canada) for 5 days. Colony forming unit count and a migration assay were performed at each time point.

Results: 
Baseline colony forming unit in the non-anemic group was higher than in the anemic group (P&lt;.0001). There was a highly significant correlation between admission hemoglobin and colony forming unit count (R=0.83, P&lt;.0001). Colony forming units increased in both groups on the second measurement but to a lower extent in the anemic group (P = .0004). The migration assay in the non-anemic group was higher than in the anemic group at baseline (P = .017) and 4 to 7 days later (P = .0054).

Conclusion: 
Patients with acute coronary syndrome with anemia demonstrate a reduced number of peripheral endothelial progenitor cells with impaired function, possibly representing a lower capacity for vascular healing. These phenomena may partly explain the poor prognosis observed in patients with acute coronary syndrome and anemia.
</description><dc:title>Endothelial Progenitor Cells Are Suppressed in Anemic Patients with Acute Coronary Syndrome - Corrected Proof</dc:title><dc:creator>Aya Solomon, Arnon Blum, Aviva Peleg, Eli I. Lev, Dorit Leshem-Lev, Yonathan Hasin</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.025</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-16</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-16</prism:publicationDate><prism:section>BRIEF OBSERVATION</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311010308/abstract?rss=yes"><title>Mystery of Chronic Kidney Disease Awareness - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934311010308/abstract?rss=yes</link><description>


   SEE RELATED ARTICLE p. XXX.</description><dc:title>Mystery of Chronic Kidney Disease Awareness - Corrected Proof</dc:title><dc:creator>Yeong-Hau H. Lien</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.021</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-16</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-16</prism:publicationDate><prism:section>COMMENTARY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000113/abstract?rss=yes"><title>Angiotensin II Receptor Blocker-based Therapy in Japanese Elderly, High-risk, Hypertensive Patients - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000113/abstract?rss=yes</link><description>Abstract: 
Background: 
It is unknown whether high-dose angiotensin II receptor blocker therapy or angiotensin II receptor blocker + calcium channel blocker combination therapy is better in elderly hypertensive patients with high cardiovascular risk. The objective of the study was to compare the efficacy of these treatments in elderly, high-risk Japanese hypertensive patients.

Methods: 
The OlmeSartan and Calcium Antagonists Randomized (OSCAR) study was a multicenter, prospective, randomized, open-label, blinded-end point study of 1164 hypertensive patients aged 65 to 84 years with type 2 diabetes or cardiovascular disease. Patients with uncontrolled hypertension during treatment with olmesartan 20 mg/d were randomly assigned to receive 40 mg/d olmesartan (high-dose angiotensin II receptor blocker) or a calcium channel blocker + 20 mg/d olmesartan (angiotensin II receptor blocker + calcium channel blocker). The primary end point was a composite of cardiovascular events and noncardiovascular death.

Results: 
During a 3-year follow-up, blood pressure was significantly lower in the angiotensin II receptor blocker + calcium channel blocker group than in the high-dose angiotensin II receptor blocker group. Mean blood pressure at 36 months was 135.0/74.3 mm Hg in the high-dose angiotensin II receptor blocker group and 132.6/72.6 mm Hg in the angiotensin II receptor blocker + calcium channel blocker group. More primary end points occurred in the high-dose angiotensin II receptor blocker group than in the angiotensin II receptor blocker + calcium channel blocker group (58 vs 48 events, hazard ratio [HR], 1.31, 95% confidence interval, 0.89-1.92; P=.17). In patients with cardiovascular disease at baseline, more primary events occurred in the high-dose angiotensin II receptor blocker group (HR, 1.63, P=.03); in contrast, fewer events were observed in the subgroup without cardiovascular disease (HR, 0.52, P=.14). This treatment-by-subgroup interaction was significant (P=.02).

Conclusion: 
The angiotensin II receptor blocker and calcium channel blocker combination lowered blood pressure more than the high-dose angiotensin II receptor blocker and reduced the incidence of primary end points more than the high-dose angiotensin II receptor blocker in patients with cardiovascular disease. The addition of a second antihypertensive agent is more effective at lowering blood pressure than simply doubling the dose of an existing agent.
</description><dc:title>Angiotensin II Receptor Blocker-based Therapy in Japanese Elderly, High-risk, Hypertensive Patients - Corrected Proof</dc:title><dc:creator>Hisao Ogawa, Shokei Kim-Mitsuyama, Kunihiko Matsui, Tomio Jinnouchi, Hideaki Jinnouchi, Kikuo Arakawa, OlmeSartan and Calcium Antagonists Randomized (OSCAR) Study Group</dc:creator><dc:identifier>10.1016/j.amjmed.2011.12.010</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-16</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-16</prism:publicationDate><prism:section>GERIATRICS AND GERONTOLOGY SPECIAL SECTION</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000903/abstract?rss=yes"><title>The Missing Link - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000903/abstract?rss=yes</link><description>In this case, an extensive evaluation of a patient with chest symptoms identified an unusual etiology amenable to a simple treatment.   A 40-year-old man presented to our clinic in Bengaluru, India, because of 15 days of fever, breathlessness, and worsening productive cough. He had been treated for repeated episodes of productive cough with intermittent nebulization and expectorants since childhood. Over the 5 years prior to presentation, the cough had become persistent, with expectoration of about 50 mL of mucopurulent sputum per day. Worsening breathlessness during level walking had developed over the past 2 years.</description><dc:title>The Missing Link - Corrected Proof</dc:title><dc:creator>Srinivas Rajagopala, Uma Devaraj, Smrita Swamy, Pritilatha Rout</dc:creator><dc:identifier>10.1016/j.amjmed.2012.02.004</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-16</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-16</prism:publicationDate><prism:section>DIAGNOSTIC DILEMMA</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431101028X/abstract?rss=yes"><title>An Unusual Cause of Jaundice - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS000293431101028X/abstract?rss=yes</link><description>A 48-year-old man suffering from infectious endocarditis developed septic emboli in the left foot and the right hand. Furthermore, computed tomography (CT) showed several infarcts of the spleen. Consequently, an aortic valvuloplasty was performed. The liver was unremarkable (, A). Four weeks later, the patient presented with severe epigastric pain and jaundice. An arterial phase of an abdominal contrast-enhanced CT scan showed a new, strongly enhancing mass, 45 mm in diameter, with contact to the right hepatic artery (, B, asterisk). Furthermore, dilatation of the intrahepatic biliary ducts was seen.</description><dc:title>An Unusual Cause of Jaundice - Corrected Proof</dc:title><dc:creator>Andreas Gunter Bach, Jasmin Abbas, Dominik Schramm, Alexey Surov</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.019</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-13</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-13</prism:publicationDate><prism:section>CLINICAL COMMUNICATION TO THE EDITOR</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000034/abstract?rss=yes"><title>Alternative Smoking Cessation Aids: A Meta-analysis of Randomized Controlled Trials - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000034/abstract?rss=yes</link><description>Abstract: 
Background: 
Acupuncture, hypnotherapy, and aversive smoking are the most frequently studied alternative smoking cessation aids. These aids are often used as alternatives to pharmacotherapies for smoking cessation; however, their efficacy is unclear.

Methods: 
We carried out a random effect meta-analysis of randomized controlled trials to determine the efficacy of alternative smoking cessation aids. We systematically searched the Cochrane Library, EMBASE, Medline, and PsycINFO databases through December 2010. We only included trials that reported cessation outcomes as point prevalence or continuous abstinence at 6 or 12 months.

Results: 
Fourteen trials were identified; 6 investigated acupuncture (823 patients); 4 investigated hypnotherapy (273 patients); and 4 investigated aversive smoking (99 patients). The estimated mean treatment effects were acupuncture (odds ratio [OR], 3.53; 95% confidence interval [CI], 1.03-12.07), hypnotherapy (OR, 4.55; 95% CI, 0.98-21.01), and aversive smoking (OR, 4.26; 95% CI, 1.26-14.38).

Conclusion: 
Our results suggest that acupuncture and hypnotherapy may help smokers quit. Aversive smoking also may help smokers quit; however, there are no recent trials investigating this intervention. More evidence is needed to determine whether alternative interventions are as efficacious as pharmacotherapies.
</description><dc:title>Alternative Smoking Cessation Aids: A Meta-analysis of Randomized Controlled Trials - Corrected Proof</dc:title><dc:creator>Mehdi Tahiri, Salvatore Mottillo, Lawrence Joseph, Louise Pilote, Mark J. Eisenberg</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.028</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-13</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-13</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000733/abstract?rss=yes"><title>Transesophageal Echocardiograms in Patients with Catheter-derived Staphylococcus aureus Bacteremia - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000733/abstract?rss=yes</link><description>In the evaluation of a bacteremic patient, the clinician should determine the origin and possible destinations of the invading pathogen. As a result of medical progress, intravenous catheters have become a distressingly common portal of entry. Fortunately, most bacteria do not regularly seed endovascular structures, with the notable exception of Staphylococcus aureus, which has a predilection to settle on both normal and damaged tissues. Consequently, every patient developing a bloodstream infection with S. aureus is at risk for endocarditis and other metastatic infections, although the likelihood varies with the source and circumstances.</description><dc:title>Transesophageal Echocardiograms in Patients with Catheter-derived Staphylococcus aureus Bacteremia - Corrected Proof</dc:title><dc:creator>Mark J. DiNubile</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.032</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-13</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-13</prism:publicationDate><prism:section>COMMENTARY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000800/abstract?rss=yes"><title>Strange Case of Dr Jekyll and Mr Hyde—and John Hunter - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000800/abstract?rss=yes</link><description>John Hunter is a legendary figure in the history of medicine. This 18th-century Scotsman who lived and worked in London was an innovative surgeon, a pioneering human and comparative anatomist who, late in life, anticipated Charles Darwin's theory of evolution, and a groundbreaking medical educator. (Darwin was a regular visitor to Hunter's museum following his return from the voyage of H. M. S. Beagle.) Hunter challenged Galenic precepts and was an early proponent of direct observation and evidence-based medicine. Hunter also was the model used by Robert Louis Stevenson, another Scotsman who knew London well, for Dr Jekyll and Mr Hyde. How did this come about?</description><dc:title>Strange Case of Dr Jekyll and Mr Hyde—and John Hunter - Corrected Proof</dc:title><dc:creator>Lloyd Axelrod</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.011</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-13</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-13</prism:publicationDate><prism:section>MEDICAL HUMANITIES PERSPECTIVES</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000071/abstract?rss=yes"><title>Impact of the CHA2DS2-VASc Score on Anticoagulation Recommendations for Atrial Fibrillation - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000071/abstract?rss=yes</link><description>Abstract: 
Background: 
The Congestive heart failure, Hypertension, Age≥75 years, Diabetes mellitus, Stroke (CHADS2) score is used to predict the need for oral anticoagulation for stroke prophylaxis in patients with atrial fibrillation. The Congestive heart failure, Hypertension, Age≥75 years, Diabetes mellitus, Stroke, Vascular disease, Age 65-74 years, Sex category (CHA2DS2-VASc) schema has been proposed as an improvement. Our objective is to determine how adoption of the CHA2DS2-VASc score alters anticoagulation recommendations.

Methods: 
Between 2004 and 2008, 1664 patients were seen at the University of Virginia Atrial Fibrillation Center. We calculated the CHADS2 and CHA2DS2-VASc scores for each patient. The 2006 American College of Cardiology/American Heart Association/Heart Rhythm Society guidelines for atrial fibrillation management were used to determine anticoagulation recommendations based on the CHADS2 score, and the 2010 European Society of Cardiology guidelines were used to determine anticoagulation recommendations based on the CHA2DS2-VASc score.

Results: 
The average age was 62±13 years, and 34% were women. Average CHADS2 and CHA2DS2-VASc scores were 1.1±1.1 and 1.8±1.5, respectively (P&lt;.0001). The CHADS2 score classified 33% as requiring oral anticoagulation. The CHA2DS2-VASc score classified 53% as requiring oral anticoagulation. For women, 31% had a CHADS2 score≥2, but 81% had a CHA2DS2-VASc score≥2 (P.0001). Also, 32% of women with a CHADS2 score of zero had a CHA2DS2-VASc score≥2. For men, 25% had a CHADS2 score≥2, but 39% had a CHA2DS2-VASc score≥2 (P&lt;.0001).

Conclusion: 
Compared with the CHADS2 score, the CHA2DS2-VASc score more clearly defines anticoagulation recommendations. Many patients, particularly older women, are redistributed from the low- to high-risk categories.
</description><dc:title>Impact of the CHA2DS2-VASc Score on Anticoagulation Recommendations for Atrial Fibrillation - Corrected Proof</dc:title><dc:creator>Pamela K. Mason, Douglas E. Lake, John P. DiMarco, John D. Ferguson, J. Michael Mangrum, Kenneth Bilchick, Liza P. Moorman, J. Randall Moorman</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.030</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-12</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-12</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000721/abstract?rss=yes"><title>Rules of Engagement: The Principles of Underserved Global Health Volunteerism - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000721/abstract?rss=yes</link><description>The day begins at 7:00 am with a layer of mosquito repellent and boiled coffee in a tin cup. Our medical clinic in the small village of Rancho Pedro along the Dominican Republic-Haiti border is a small hut composed of dilapidated wooden planks fastened together under a thatched reed roof. Patients with a variety of ailments line up daily outside the clinic door in anticipation of seeing a physician, often for the first time. Most patients have been waiting for hours, usually after enduring an overnight mountainous trek from a neighboring Haitian or Dominican village. Many of the medical problems encountered can be treated effectively with simple measures of wound debridement, bandages, analgesics, or antibiotics; however, some are more complex with no referral options. The work is intense but inspiring, rewarding but often frustrating as the limitations of our abilities quickly become apparent.</description><dc:title>Rules of Engagement: The Principles of Underserved Global Health Volunteerism - Corrected Proof</dc:title><dc:creator>John W. Wilson, Stephen P. Merry, Walter B. Franz</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.008</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-12</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-12</prism:publicationDate><prism:section>APM PERSPECTIVES</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312001751/abstract?rss=yes"><title>Paradoxical Response to Tuberculosis Treatment in a Patient Receiving Tumor Necrosis Factor-Alpha Antagonist - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312001751/abstract?rss=yes</link><description>A 32-year-old man, treated for refractory psoriasis with adalimumab (Humira, Abbott Laboratories, Abbott Park, Ill), a tumor necrosis factor-alpha antagonist, for the last 5 months experienced protracted fever, nonproductive cough, progressive weakness, and weight loss. Chest computed tomography demonstrated diffuse mediastinal necrotic lymphadenopathy and disseminated micronodules in lung parenchyma. A right retroclavicular adenopathy also was identified (). A diagnosis of tuberculosis was readily established by polymerase chain reaction from a bronchoalveolar lavage fluid specimen, which was ultimately confirmed by culture of a Mycobacterium tuberculosis, fully susceptible to isoniazid, ethambutol, rifampicin, and pyrazinamide. Adalimumab was discontinued, and the 4 previously mentioned antimicrobials were administered. However, spiking fever and general discomfort worsened during the next 8 weeks. Moreover, a chest computed tomography performed after 2 months of antibiotherapy demonstrated additional enlargement of the mediastinal lymph nodes with increasing confluence and worsening necrosis. The retroclavicular adenopathy also had greatly increased in size (), whereas miliary lung disease was unchanged. A new culture obtained from the enlarging retroclavicular lymph node was negative. A drug-induced fever was discarded by temporary removal of isoniazid and rifampicin. After more than 10 weeks of antibiotherapy, fever finally abated and general improvement ensued.</description><dc:title>Paradoxical Response to Tuberculosis Treatment in a Patient Receiving Tumor Necrosis Factor-Alpha Antagonist - Corrected Proof</dc:title><dc:creator>Caroline Moureau, Lucie Pothen, Dunja Wilmes, Jean Cyr Yombi, Emmanuel Coche, Philippe Hainaut</dc:creator><dc:identifier>10.1016/j.amjmed.2012.02.006</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-12</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-12</prism:publicationDate><prism:section>CLINICAL COMMUNICATION TO THE EDITOR</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000952/abstract?rss=yes"><title>Body Mass Index and Mortality in Acute Myocardial Infarction Patients - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000952/abstract?rss=yes</link><description>Abstract: 
Background: 
Previous studies have described an “obesity paradox” with heart failure, whereby higher body mass index (BMI) is associated with lower mortality. However, little is known about the impact of obesity on survival after acute myocardial infarction.

Methods: 
Data from 2 registries of patients hospitalized in the US with acute myocardial infarction between 2003-2004 (PREMIER) and 2005-2008 (TRIUMPH) were used to examine the association of BMI with mortality. Patients (n=6359) were categorized into BMI groups (kg/m2) using baseline measurements. Two sets of analyses were performed using Cox proportional hazards regression with fractional polynomials to model BMI as categorical and continuous variables. To assess the independent association of BMI with mortality, analyses were repeated, adjusting for 7 domains of patient and clinical characteristics.

Results: 
Median BMI was 28.6. BMI was inversely associated with crude 1-year mortality (normal, 9.2%; overweight, 6.1%; obese, 4.7%; morbidly obese; 4.6%; P &lt;.001), which persisted after multivariable adjustment. When BMI was examined as a continuous variable, the hazards curve declined with increasing BMI and then increased above a BMI of 40. Compared with patients with a BMI of 18.5, patients with higher BMIs had a 20% to 68% lower mortality at 1 year. No interactions between age (P=.37), sex (P=.87), or diabetes mellitus (P=.55) were observed.

Conclusions: 
There appears to be an “obesity paradox” among patients after acute myocardial infarction such that higher BMI is associated with lower mortality, an effect that was not modified by patient characteristics and was comparable across age, sex, and diabetes subgroups.
</description><dc:title>Body Mass Index and Mortality in Acute Myocardial Infarction Patients - Corrected Proof</dc:title><dc:creator>Emily M. Bucholz, Saif S. Rathore, Kimberly J. Reid, Philip G. Jones, Paul S. Chan, Michael W. Rich, John A. Spertus, Harlan M. Krumholz</dc:creator><dc:identifier>10.1016/j.amjmed.2012.01.018</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-09</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-09</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009508/abstract?rss=yes"><title>Why P Is Not Perfect - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934311009508/abstract?rss=yes</link><description>In a recent meta-analysis regarding the effects of statins on mortality, Ray et al wrote “there is no evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention setup.” The author's conclusion (based on a risk ratio of 0.91; 95% confidence interval, 0.83-1.01; P≥.05) is emblematic of a growing trend: categorizing studies as positive or negative solely on the results of statistical testing.</description><dc:title>Why P Is Not Perfect - Corrected Proof</dc:title><dc:creator>Vineet Chopra, Rodney A. Hayward</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.024</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311010710/abstract?rss=yes"><title>Patient-centered Shared Decision-making: A Public Imperative - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934311010710/abstract?rss=yes</link><description>A 65-year-old primary care nurse presents with stable angina when quickly climbing a flight of stairs. She has a history of hyperlipidemia and hypertension treated with an aspirin, a statin, and a beta-blocker. An exercise treadmill test with normal exercise capacity shows ischemic changes on the electrocardiogram. Coronary angiography demonstrates 70% stenosis in both the mid-left anterior descending artery and the right coronary artery. Her cardiologist recommends stenting of both lesions, and the patient wonders whether stenting will prevent a heart attack.</description><dc:title>Patient-centered Shared Decision-making: A Public Imperative - Corrected Proof</dc:title><dc:creator>Megan Coylewright, Victor Montori, Henry H. Ting</dc:creator><dc:identifier>10.1016/j.amjmed.2011.12.007</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate><prism:section>CLINICAL EFFECTIVENESS</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431200085X/abstract?rss=yes"><title>Acute Cytomegalovirus Colitis Mimicking Exacerbation of Ulcerative Colitis: Precipitating or Coincidental? - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS000293431200085X/abstract?rss=yes</link><description>Cytomegalovirus colitis is an uncommon cause of diarrhea in older adults, despite the high seroprevalence of cytomegalovirus in the general population: 40%-70% of adults in higher socioeconomic groups, and up to 90% of adults in lower socioeconomic groups. The majority of primary cytomegalovirus infections in immunocompetent adults are asymptomatic or associated with mild mononucleosis-like syndrome. Cytomegalovirus produces characteristic cytopathic effects, consisting of a large 25- to 35-μm cell containing a basophilic intranuclear inclusion, which is sometimes surrounded by a clear halo. Immunohistochemistry of the biopsied tissue using monoclonal antibodies and in situ DNA hybridization enhances the sensitivity of the histologic analysis.</description><dc:title>Acute Cytomegalovirus Colitis Mimicking Exacerbation of Ulcerative Colitis: Precipitating or Coincidental? - Corrected Proof</dc:title><dc:creator>Owolabi Ogunneye, Jaime Hernandez</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.027</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate><prism:section>CLINICAL COMMUNICATION TO THE EDITOR</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000885/abstract?rss=yes"><title>Lead Poisoning Mimicking Amyotrophic Lateral Sclerosis: An Adverse Effect of Rituals - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000885/abstract?rss=yes</link><description>A 61-year-old Algerian woman was admitted for progressive loss of upper extremity strength and decline of cognitive functions evolving for 1 year. On admission, Mini Mental State Examination was scored at 13/28. A muscular atrophy of the upper limbs was present, with severe diffuse motor weakness preventing the patient from being able to feed herself. Deep tendon reflexes were normal. Magnetic resonance imaging of the spine was unremarkable. Electromyographic study was suggestive of a pure axonal motor neuropathy, with reduced compound motor action potentials in the upper limbs and chronic neurogenic changes in myotomes C5-C8. Therefore, diagnosis of amyotrophic lateral sclerosis associated with cognitive impairment was established. The patient also reported a marked weight loss (23 kg), assumed to be related to the neurological disorder, and diffuse abdominal tenderness. A blood cell count showed a hemoglobin level of 9.3 g/dL, a mean corpuscular volume of 80 fL, a reticulocyte count of 263×109/L, and normal platelet and leukocyte counts. Blood smear showed basophilic stippling in 3% of erythrocytes (). Liver function tests, serum creatinine, serum electrophoresis of proteins, level of iron, folate and vitamin B12, thyroid-stimulating hormone, haptoglobin, and hemoglobin electrophoresis were unremarkable. An abdominal ultrasonogram was normal. Two months after admission, although the patient had gained 10 kg of weight, decrease of strength and anemia with basophilic stippling were still present; an alternative diagnosis of lead intoxication was confirmed, with blood lead level of 3.02 μmol/L (normal&lt;0.5; exposure&lt;1.9), and urine level of 2.36 μmol/L (normal&lt;0.14). Four courses of calcium edetate were administered intravenously at a daily dose of 500 mg/m2 for 5 days, repeated after an interval of 7 days without treatment, but the blood lead was still elevated at 1.7 μmol/L. The patient admitted that, for several years, she would sometimes melt lead in a saucepan, then spread it into a metal container full of cold water, with respiratory exposure, in an unbewitching ritual. Four months after the cessation of lead exposure, a progressive improvement in strength in the upper limbs was observed; the patient was able to eat by herself and cognitive functions improved (Mini Mental State Examination score at 24/28). The patient was discharged and then lost to follow-up.</description><dc:title>Lead Poisoning Mimicking Amyotrophic Lateral Sclerosis: An Adverse Effect of Rituals - Corrected Proof</dc:title><dc:creator>Claude Bachmeyer, Elsa Bagur, Timothée Lenglet, Micheline Maier-Redelsperger, Isabelle Lecomte</dc:creator><dc:identifier>10.1016/j.amjmed.2011.11.030</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate><prism:section>CLINICAL COMMUNICATION TO THE EDITOR</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000897/abstract?rss=yes"><title>The Association of Tooth Scaling and Decreased Cardiovascular Disease: A Nationwide Population-based Study - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000897/abstract?rss=yes</link><description>Abstract: 
Objective: 
Poor oral hygiene has been associated with an increased risk for cardiovascular disease. However, the association between preventive dentistry and cardiovascular risk reduction has remained undetermined. The aim of this study is to investigate the association between tooth scaling and the risk of cardiovascular events by using a nationwide, population-based study and a prospective cohort design.

Methods: 
Our analyses were conducted using information from a random sample of 1 million persons enrolled in the nationally representative Taiwan National Health Insurance Research Database. Exposed individuals consisted of all subjects who were aged≥50 years and who received at least 1 tooth scaling in 2000. The comparison group of non-exposed persons consisted of persons who did not undergo tooth scaling and were matched to exposed individuals using propensity score matching by the time of enrollment, age, gender, history of coronary artery disease, diabetes, hypertension, and hyperlipidemia.

Results: 
During an average follow-up period of 7 years, 10,887 subjects who had ever received tooth scaling (exposed group) and 10,989 age-, gender-, and comorbidity-matched subjects who had not received tooth scaling (non-exposed group) were enrolled. The exposed group had a lower incidence of acute myocardial infarction (1.6% vs 2.2%, P&lt;.001), stroke (8.9% vs 10%, P=.03), and total cardiovascular events (10% vs 11.6%, P&lt;.001) when compared with the non-exposed group. After multivariate analysis, tooth scaling was an independent factor associated with less risk of developing future myocardial infarction (hazard ratio [HR], 0.69; 95% confidence interval [CI], 0.57-0.85), stroke (HR, 0.85; 95% CI, 0.78-0.93), and total cardiovascular events (HR, 0.84; 95% CI, 0.77-0.91). Furthermore, when compared with the non-exposed group, increasing frequency of tooth scaling correlated with a higher risk reduction of acute myocardial infarction, stroke, and total cardiovascular events (P for trend&lt;.001).

Conclusion: 
Tooth scaling was associated with a decreased risk for future cardiovascular events.
</description><dc:title>The Association of Tooth Scaling and Decreased Cardiovascular Disease: A Nationwide Population-based Study - Corrected Proof</dc:title><dc:creator>Zu-Yin Chen, Chia-Hung Chiang, Chin-Chou Huang, Chia-Min Chung, Wan-Leong Chan, Po-Hsun Huang, Shing-Jong Lin, Jaw-Wen Chen, Hsin-Bang Leu</dc:creator><dc:identifier>10.1016/j.amjmed.2011.10.034</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate><prism:section>CLINICAL RESEARCH STUDY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934312000915/abstract?rss=yes"><title>A Childlike Presentation? - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934312000915/abstract?rss=yes</link><description>“Age merely shows what children we remain,” observes Johann Wolfgang von Goethe in Faust, his celebrated 2-part play. The quote accurately captures the case of an adult who presented with a classic pediatric illness, the diagnosis of which was not initially considered.</description><dc:title>A Childlike Presentation? - Corrected Proof</dc:title><dc:creator>Gajarah B.B. Peterson, Lisa G. Criscione-Schreiber</dc:creator><dc:identifier>10.1016/j.amjmed.2012.02.005</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate><prism:section>DIAGNOSTIC DILEMMA</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS0002934311009016/abstract?rss=yes"><title>Minimizing Inappropriate Medications in Older Populations: A Ten-step Conceptual Framework - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS0002934311009016/abstract?rss=yes</link><description>Abstract: 
The increasing burden of harm resulting from the use of multiple drugs in older patient populations represents a major health problem in developed countries. Approximately 1 in 4 older patients admitted to hospitals are prescribed at least 1 inappropriate medication, and up to 20% of all inpatient deaths are attributable to potentially preventable adverse drug reactions. To minimize this drug-related iatrogenesis, we propose a quality use of medicine framework that comprises 10 sequential steps: 1) ascertain all current medications; 2) identify patients at high risk of or experiencing adverse drug reactions; 3) estimate life expectancy in high-risk patients; 4) define overall care goals in the context of life expectancy; 5) define and confirm current indications for ongoing treatment; 6) determine the time until benefit for disease-modifying medications; 7) estimate the magnitude of benefit versus harm in relation to each medication; 8) review the relative utility of different drugs; 9) identify drugs that may be discontinued; and 10) implement and monitor a drug minimization plan with ongoing reappraisal of drug utility and patient adherence by a single nominated clinician. The framework aims to reduce drug use in older patients to the minimum number of essential drugs, and its utility is demonstrated in reference to a hypothetic case study. Further studies are warranted in validating this framework as a means for assisting clinicians to make more appropriate prescribing decisions in at-risk older patients.
</description><dc:title>Minimizing Inappropriate Medications in Older Populations: A Ten-step Conceptual Framework - Corrected Proof</dc:title><dc:creator>Ian A. Scott, Leonard C. Gray, Jennifer H. Martin, Charles A. Mitchell</dc:creator><dc:identifier>10.1016/j.amjmed.2011.09.021</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-03-02</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-03-02</prism:publicationDate><prism:section>GERIATRICS SPECIAL SECTION REVIEW</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431100790X/abstract?rss=yes"><title>Semantic Confusion: The Case of Early Repolarization and the J Point - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS000293431100790X/abstract?rss=yes</link><description>Early repolarization and J point are classic electrocardiographic terms that have been co-opted. Although we agree with Surawicz and Macfarlane that these terms require standardization, the major commercial electrocardiography programs currently measure ST elevation at the traditional J point or QRS end and do not classify J waves or slurring for the statement of nonspecific ST elevation or “early repolarization.” Furthermore, although J waves or slurs have been noted to occur along with ST elevation as part of classic early repolarization, the clinical focus has been on ST elevation because it also can be confused with myocardial injury or ischemia and pericarditis ().</description><dc:title>Semantic Confusion: The Case of Early Repolarization and the J Point - Corrected Proof</dc:title><dc:creator>Marco V. Perez, Karen Friday, Victor Froelicher</dc:creator><dc:identifier>10.1016/j.amjmed.2011.08.024</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-02-15</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-02-15</prism:publicationDate><prism:section>COMMENTARY</prism:section></item><item rdf:about="http://www.amjmed.com/article/PIIS000293431100581X/abstract?rss=yes"><title>Canary in the Coal Mine: Cardiac Troponins in Noncoronary Diseases - Corrected Proof</title><link>http://www.amjmed.com/article/PIIS000293431100581X/abstract?rss=yes</link><description>The development and refinement of assays measuring serum concentrations of cardiac-specific troponins have added greatly to our ability to diagnosis and manage patients with signs and symptoms of acute coronary syndromes. Troponin samples also are frequently obtained to “rule out” myocardial infarction or ischemia in a host of different acute clinical settings and in less acute illness to determine if cardiac involvement might be present. The improved sensitivity of newer-generation assays has allowed detection of ever smaller elevations, often in patients with no evidence of clinical heart diseases.</description><dc:title>Canary in the Coal Mine: Cardiac Troponins in Noncoronary Diseases - Corrected Proof</dc:title><dc:creator>Stephen A. Geraci</dc:creator><dc:identifier>10.1016/j.amjmed.2011.07.014</dc:identifier><dc:source>The American Journal of Medicine (2012)</dc:source><dc:date>2012-02-10</dc:date><prism:publicationName>The American Journal of Medicine</prism:publicationName><prism:publicationDate>2012-02-10</prism:publicationDate><prism:section>COMMENTARY</prism:section></item></rdf:RDF>
