<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_439"
                     title="Heart Often Affected in Churg-Strauss (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Rheumatology/GeneralRheumatology/tb/18353?impressionId=1265736556693"
                     
      &lt;p&gt;Cardiac involvement is common in patients with Churg-Strauss syndrome, even when their vasculitis is in clinical remission, a Dutch study found.&lt;/p&gt;
&lt;p&gt;Cardiac MRI detected abnormalities in 62% of patients with this rare, systemic disorder but in only 3% of matched controls (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001), according to Robert M. Dennert, MD, of Maastricht University in the Netherlands, and colleagues.&lt;/p&gt;
&lt;p&gt;Yet only 26% of the patients had clinical symptoms suggesting cardiac involvement, the researchers reported in February&apos;s &lt;em&gt;Arthritis &amp;amp; Rheumatism.&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;Cardiac involvement is an important predictor of poor outcome in Churg-Strauss syndrome, with approximately half of the associated mortality being heart-related. Myocardial damage typically results from eosinophilic infiltration and granuloma formation.&lt;/p&gt;
&lt;p&gt;However, the cardiac manifestations are often subclinical. They remain undiagnosed, and the exact incidence is unclear.&lt;/p&gt;
&lt;p&gt;So Dennert and colleagues enrolled 32 patients with confirmed Churg-Strauss syndrome who were in complete clinical remission, performing detailed imaging assessments to determine the frequency and extent of heart involvement.&lt;/p&gt;
&lt;p&gt;About two-thirds were men. The mean age was 61 years, and disease duration was slightly over six years.&lt;/p&gt;
&lt;p&gt;A total of 41% had antineutrophil cytoplasmic antibodies (ANCA), and most were on maintenance steroids or immunosuppressants.&lt;/p&gt;
&lt;p&gt;On EKG, major abnormalities (atrial fibrillation and conduction disturbances) were detected in only 13% of patients. Minor abnormalities such as T wave abnormalities were seen in 50% of patients and in one control subject.&lt;/p&gt;
&lt;p&gt;Echocardiography identified abnormalities in 50% of patients and in 3% of controls (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001). These included wall motion and valvular abnormalities, pericardial effusion, and pulmonary hypertension.&lt;/p&gt;
&lt;p&gt;In the 62% of patients whose MRIs revealed abnormalities, findings included fibrosis, inflammation, wall motion and valvular abnormalities, pericardial effusion, and obliterated right ventricle.&lt;/p&gt;
&lt;p&gt;Previous reports had suggested that ANCA positivity in Churg-Strauss syndrome was more often associated with renal disease and peripheral neuropathy, while ANCA negativity was associated with fever and heart involvement.&lt;/p&gt;
&lt;p&gt;In this cohort, 74% of ANCA-negative patients had cardiac involvement, and in 64%, these were wall motion disturbances.&lt;/p&gt;
&lt;p&gt;In comparison, only 23% of ANCA-positive patients had heart involvement.&lt;/p&gt;
&lt;p&gt;Defects were identified with echocardiography or MRI in 88% of patients who had clinical symptoms, and in all who had major EKG abnormalities.&lt;/p&gt;
&lt;p&gt;But in the absence of symptoms and even with a normal EKG, abnormalities could still be detected on echocardiography or MRI in almost 40% of patients, according to the investigators.&lt;/p&gt;
&lt;p&gt;&quot;We therefore recommend that the evaluation for cardiac involvement in patients with [Churg-Strauss syndrome] should include not only detailed history of cardiac symptoms and EKG, but also imaging with echocardiography or cardiac MRI,&quot; they stated.&lt;/p&gt;
&lt;p&gt;The high prevalence of heart abnormalities could not be attributed to concomitant heart disease such as coronary artery disease or hypertension, because the prevalence of these diseases among patients was comparable to that in controls.&lt;/p&gt;
&lt;p&gt;Churg-Strauss syndrome typically develops in three phases, beginning with asthma, followed by peripheral and tissue eosinophilia accompanied by pulmonary infiltrates, and finally the systemic small-vessel vasculitis.&lt;/p&gt;
&lt;p&gt;During this late phase the vasculitic lesions in the coronary vessels and myocardium can lead to myocardial infarction, heart failure, and cardiac tamponade.&lt;/p&gt;
&lt;p&gt;Studies have shown that long-term treatment with immunosuppressive drugs can improve survival and resolve the cardiac abnormalities, so early diagnosis is needed.&lt;/p&gt;
&lt;p&gt;The authors acknowledged that their study was cross-sectional, and that a longitudinal study could have provided more detailed data.&lt;/p&gt;
&lt;p&gt;Nonetheless, the study revealed a high incidence of cardiac involvement, which was often unrecognized, and they concluded that a multidisciplinary approach to management therefore should include a cardiologist.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the Netherlands Heart Foundation and the Dutch Organization for Scientific Research.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_438"
                     title="Rituximab Shows Promise in Scleroderma (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Rheumatology/GeneralRheumatology/tb/18352?impressionId=1265736556693"
                     
      &lt;p&gt;Rituximab (Rituxan) improved lung function in patients with scleroderma, a small proof-of-principle study found.&lt;/p&gt;
&lt;p&gt;At one year, patients randomized to receive rituximab had a median 10.25% increase in forced vital capacity (FVC) compared with baseline, while those who received standard treatment had a deterioration of 5.04% (&lt;em&gt;P&lt;/em&gt;=0.002), according to Dimitrios Daoussis, MD, and colleagues from the University of Patras in Greece.&lt;/p&gt;
&lt;p&gt;There also was a significant 19.46% increase in diffusing capacity of carbon monoxide (DL&lt;sub&gt;co&lt;/sub&gt;) in the rituximab-treated patients, while the controls showed deterioration of 7.5% (&lt;em&gt;P&lt;/em&gt;=0.023), the researchers reported in the February issue of &lt;em&gt;Rheumatology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Interstitial lung disease is a common manifestation of diffuse scleroderma and represents the disease component that dictates prognosis because it can be progressive and typically responds poorly to treatment. Animal and human studies have suggested a possible pathogenic role for B cells in the disease.&lt;/p&gt;
&lt;p&gt;There have been a few reports of clinical and histologic improvements in scleroderma and in graft-versus-host disease (which shares some features with scleroderma) after treatment with the B-cell depleting monoclonal antibody rituximab.&lt;/p&gt;
&lt;p&gt;These encouraging early findings led Daoussis and colleagues to undertake an open-label, controlled study that included 14 patients with diffuse disease.&lt;/p&gt;
&lt;p&gt;Median age was 55 and mean disease duration was seven years.&lt;/p&gt;
&lt;p&gt;All patients continued their standard medications, which included various agents such as prednisone, bosentan (Tracleer), mycophenolate mofetil (CellCept), and cyclophosphamide.&lt;/p&gt;
&lt;p&gt;Those randomized to rituximab treatment also underwent four weekly pulses of the drug (375 mg/m&lt;sup&gt;2&lt;/sup&gt;) at baseline and six months later.&lt;/p&gt;
&lt;p&gt;By one year, the mean FVC in the rituximab group had risen from 68.13% of normal predicted value based on age, sex, and height, to 75.63% (&lt;em&gt;P&lt;/em&gt;=0.0018), while FVC in the control group fell nonsignificantly from 86% of normal to 81.67%.&lt;/p&gt;
&lt;p&gt;In the rituximab group, DL&lt;sub&gt;co&lt;/sub&gt; increased from a mean of 52.25% of normal at baseline to 62% (&lt;em&gt;P&lt;/em&gt;=0.017) at one year, while the controls decreased nonsignificantly from 65.33% to 60.17%.&lt;/p&gt;
&lt;p&gt;None of the patients treated with rituximab experienced worsening of FVC or DL&lt;sub&gt;co&lt;/sub&gt;, whereas lung function deteriorated in five controls.&lt;/p&gt;
&lt;p&gt;&quot;We should note, however, that patients in the control group tended to have more early disease and better lung function parameters (although not statistically different from the [rituximab] group) making them more likely to deteriorate over the time of the study,&quot; the investigators commented.&lt;/p&gt;
&lt;p&gt;Skin manifestations of the disease also showed improvements in the rituximab group. Skin thickening, as measured by the Modified Rodnan Skin Score, improved by 39.25% in the rituximab group and by 20.80% in the control group, a difference that was not statistically significant.&lt;/p&gt;
&lt;p&gt;Skin fibrosis also improved by a median of 38.33%, while it worsened by 5.23% in controls.&lt;/p&gt;
&lt;p&gt;Histologic improvement was seen in four of the rituximab-treated patients, corresponding with clinical benefits. One patient in the active treatment group had a significant reduction of fibrosis in both the papillary and reticular dermis, accompanied by an almost complete resolution of skin lesions.&lt;/p&gt;
&lt;p&gt;Improvement in skin fibrosis was most common in patients who had evidence of B-cell depletion in the skin.&lt;/p&gt;
&lt;p&gt;Overall function, as evaluated by the Health Assessment Questionnaire, improved from a median baseline score of 0.687 to 0.312 at one year (&lt;em&gt;P&lt;/em&gt;=0.03), while no change was seen in controls.&lt;/p&gt;
&lt;p&gt;The pathogenesis of scleroderma is poorly understood, according to the authors, but this study adds support to a possible role for B cells.&lt;/p&gt;
&lt;p&gt;In addition, rituximab indirectly targets T cells, which also are thought to be implicated.&lt;/p&gt;
&lt;p&gt;The authors noted potential limitations, including the study&apos;s small size and the fact that most patients had longstanding disease, had been treated with multiple immunosuppressive agents in the past, and were receiving concurrent therapies during the study.&lt;/p&gt;
&lt;p&gt;&quot;This is a proof-of-principle study that was performed in order to obtain preliminary data regarding the effect of [rituximab] on a limited number of patients,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;Our data could serve as a good starting point for the design of larger scale, multicenter studies with longer evaluation periods and especially in earlier stages of the disease,&quot; they concluded.&lt;/p&gt;
&lt;p&gt;In an accompanying editorial, Robert W. Simms, MD, and Robert Lafyatis, MD, of Boston University, echoed concerns about the small number of patients and the lack of blinding in the study.&lt;/p&gt;
&lt;p&gt;&quot;One cannot...on the basis of this study, recommend rituximab in the routine clinical care of patients with scleroderma,&quot; the editorialists wrote.&lt;/p&gt;
&lt;p&gt;The findings will need to be replicated in a multicenter randomized trial, but &quot;do provide some hope that B-cell depletion might enhance the currently restricted therapeutic armamentarium of this disease.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the Hellenic Rheumatology Society.&lt;/p&gt;&lt;p&gt;Funding to pay Open Access publication charges was provided by Roche Hellas.&lt;/p&gt;&lt;p&gt;Authors and editorialists declared to conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_431"
                     title="Down a Beer to Improve Bone Health? Not So Fast"
                     score="0.012"
                     href="http://www.medpagetoday.com/PrimaryCare/DietNutrition/tb/18347?impressionId=1265736556693"
                     
      &lt;p&gt;A flagon of ale may indeed be a good source of dietary silicon, a recent study showed, but experts say any attempt to link beer drinking to bone health is not based on scientific data.&lt;/p&gt;
&lt;p&gt;The study of 100 commercial beers in the February issue of the &lt;em&gt;Journal of the Science of Food and Agriculture&lt;/em&gt;, by Charles Bamforth, PhD, DSc, and Troy Casey, of the University of California Davis, examined the silicon content that results from different ingredients and brewing processes.&lt;/p&gt;
&lt;p&gt;Although a press release issued with the study prominently mentioned the link between silicon and bone health, the study itself did not look at bone mineral density or analyze any patient data at all, according to several researchers contacted by &lt;em&gt;MedPage Today&lt;/em&gt; and ABC News.&lt;/p&gt;
&lt;p&gt;The authors wrote that they explored the silicon content in beer because the popular beverage has been identified as one of the richest potential sources of dietary silicon in the Western diet. The average intake is 20 to 50 mg/day.&lt;/p&gt;
&lt;p&gt;The beers sampled contained an average of 29.4 mg/L of silicon, with a range of 6.4 to 56.4 mg/L. Beers made from a barley-based grist (as opposed to wheat-based beers ) and brews containing more hops had the highest silicon levels.&lt;/p&gt;
&lt;p&gt;The beer type with the overall highest silicon level was India Pale Ale, with an average of 41.2 mg/L. Other ales came in second with 32.8 mg/L.&lt;/p&gt;
&lt;p&gt;Nonalcoholic beers, light lagers, and wheat beers had the least silicon.&lt;/p&gt;
&lt;p&gt;In the end, the authors concluded that &quot;beer is a substantial source of silicon in the diet&quot; and that &quot;beers containing high levels of malted barley and hops are richest in silicon,&quot; but they did not attempt to establish a link between beer drinking and bone health.&lt;/p&gt;
&lt;p&gt;Experts contacted for comment on the study also cautioned the public against establishing any such connection.&lt;/p&gt;
&lt;p&gt;&quot;To conclude any bone health benefits from this study would require a great leap,&quot; Tim Byers, MD, MPH, deputy director of the University of Colorado Cancer Center in Aurora, wrote in an e-mail.&lt;/p&gt;
&lt;p&gt;Other researchers noted that previous studies have shown an association between alcohol consumption and an increased risk of fracture.&lt;/p&gt;
&lt;p&gt;That&apos;s probably because of a greater chance of falling after drinking, according to Walter Willett, MD, DrPH, of the Harvard School of Public Health.&lt;/p&gt;
&lt;p&gt;In fact, Stephen Richardson, MD, an endocrinologist at NYU Langone Medical Center, noted that &quot;alcohol consumption is a risk factor for osteoporosis.&quot;&lt;/p&gt;
&lt;p&gt;Still, there is some evidence supporting a positive link between overall dietary silicon and bone health.&lt;/p&gt;
&lt;p&gt;A 2004 cross-sectional study in the &lt;em&gt;Journal of Bone and Mineral Research&lt;/em&gt; that used data from the Framingham Offspring cohort found a significant association between greater dietary silicon intake, including that from beer, and higher bone mineral density in the hip in men and premenopausal women.&lt;/p&gt;
&lt;p&gt;The researchers concluded: &quot;These findings suggest that higher dietary silicon intake in men and younger women may have salutary effects on skeletal health, especially cortical bone health, that has not been previously recognized.&quot;&lt;/p&gt;
&lt;p&gt;Another study by the same group published last year in the &lt;em&gt;American Journal of Clinical Nutrition&lt;/em&gt; found that moderate consumption of alcohol, including beer, wine, and liquor, was associated with higher bone mineral density in men and postmenopausal women.&lt;/p&gt;
&lt;p&gt;However, it also showed that men who drank too much liquor were more likely to have lower spine and hip bone mineral density.&lt;/p&gt;
&lt;p&gt;The relationship between beer and bone mineral density appeared to be mediated by silicon, the researchers concluded.&lt;/p&gt;
&lt;p&gt;Bottom line: considering the increased fracture risk and the various other problems associated with drinking too much alcohol, experts agree that guzzling beer is not strategy for improving bone health.&lt;/p&gt;
&lt;p&gt;&quot;In the absence of bone density values or preferably fracture incidence, it would be premature to tout beer as a preventative or treatment,&quot; Richardson said.&lt;/p&gt;
&lt;p&gt;David Katz, MD, MPH, of the Yale School of Public Health, agreed.&lt;/p&gt;
&lt;p&gt;&quot;This is NOT a reason to drink beer,&quot; he said in an e-mail. &quot;This is simply a bit of good news for those who do drink beer already  --  yours truly among them!&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The authors did not make any financial disclosures.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;&lt;p&gt;&lt;em&gt;This article was developed in collaboration with ABC News. &lt;/em&gt;&lt;img src=&quot;http://www.medpagetoday.com/upload/2009/10/1/14357_1.jpg&quot; mce_src=&quot;http://www.medpagetoday.com/upload/2009/10/1/14357_1.jpg&quot; alt=&quot;&quot;&gt;&lt;/p&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_428"
                     title="Blocking Serotonin in Gut Reverses Osteoporosis in Mice (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Endocrinology/Osteoporosis/tb/18346?impressionId=1265736556693"
                     
      &lt;p&gt;Blocking serotonin production in the intestine might help restore lost bone mass, rather than just preventing further loss like most current osteoporosis treatments, an animal study suggested.&lt;/p&gt;
&lt;p&gt;Once daily treatment with a novel serotonin inhibitor prevented development of osteoporosis and also fully reversed existing low bone mass in mice, according Gerard Karsenty, MD, PhD, of Columbia University in New York City, and colleagues.&lt;/p&gt;
&lt;p&gt;These proof-of-principle findings came without any impact on serotonin levels in the brain, the researchers reported in the Feb. 7 issue of &lt;em&gt;Nature Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Just two years ago, Karsenty&apos;s group discovered that the vast majority of serotonin in the body acts to regulate bone formation.&lt;/p&gt;
&lt;p&gt;Only 5% plays the chemical&apos;s better-known role as a brain neurotransmitter. The rest comes from the gut for circulation below the blood-brain barrier which, in this regard, Karsenty called &quot;more hermetic than the Berlin Wall was.&quot;&lt;/p&gt;
&lt;p&gt;So the gut treatment is unlikely to affect mood and other critical functions serotonin plays in the brain, he emphasized in an interview. But he acknowledged that much more proof is needed on the way to the clinic.&lt;/p&gt;
&lt;p&gt;The tip-off to bone effects of serum serotonin came from a group of patients with a syndrome that produced high bone mass when they were into their 60s.&lt;/p&gt;
&lt;p&gt;Usually, bone destruction outpaces formation after menopause, eventually leading to osteoporosis. But something different was happening in these patients, who never developed the condition.&lt;/p&gt;
&lt;p&gt;&quot;The only cause we could find was that it was due to a decrease in the synthesis of serotonin in the gut,&quot; Karsenty told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;After their initial experiments showed serotonin did indeed boost the pace of bone formation, the researchers found that a biotech company had already developed a compound that would reduce gut synthesis of the hormone. It had been tested in women with irritable bowel syndrome.&lt;/p&gt;
&lt;p&gt;So Karsenty&apos;s group examined its effects on bone in mice and found a dose-dependent reduction in serum serotonin.&lt;/p&gt;
&lt;p&gt;Mice that got 250 mg/kg body weight per day of this compound  --  known as LP533401, a small molecule inhibitor of Tph1, the initial enzyme in gut serotonin synthesis  --  produced 30% less serotonin than controls, without a change in brain serotonin levels.&lt;/p&gt;
&lt;p&gt;Then the researchers tested the compound on mice whose ovaries had been excised to simulate the dramatic drop-off in hormones women experience after menopause. That condition, in turn, leads to an imbalance in bone resorption versus formation.&lt;/p&gt;
&lt;p&gt;Mice given the experimental drug at doses up to 10 mg/kg, starting the day after surgery, had elevated bone resorption but maintained higher bone mass than those that got placebo. The placebo group all developed osteopenia.&lt;/p&gt;
&lt;p&gt;Treated mice had a &quot;major&quot; increase in bone formation markers, including osteoblast numbers, bone formation rate, and osteocalcin serum levels. But again, brain serotonin remained unaffected.&lt;/p&gt;
&lt;p&gt;These benefits were achieved with a modest, roughly 30% reduction in serum serotonin  --  which appeared to be the threshold beyond which skeletal response increased only marginally.&lt;/p&gt;
&lt;p&gt;Some mice were left untreated for two weeks  --  &quot;a long time for a rodent,&quot; Karsenty noted  --  to develop osteopenia. Subsequently treated with a daily 250 mg/kg dose of LP533401, they had such an increase in bone formation over four weeks that it normalized their bone mass, the researchers noted.&lt;/p&gt;
&lt;p&gt;The same thing happened when researchers began treatment even longer after surgery, six or 12 weeks, when bone loss was already severe. Bone mass rose with serotonin inhibition in the vertebrae and long bones, but without a change in bone length or width.&lt;/p&gt;
&lt;p&gt;Nor were there effects on platelets, coagulation, or the GI tract with regard to the key measures of transit, colonic mobility, and gastric emptying.&lt;/p&gt;
&lt;p&gt;Serotonin inhibition in the gut as a potential anabolic treatment for osteopenia and osteoporosis appeared to work as well as the only currently available treatment that can increase bone formation sufficiently to compensate for the increased resorption caused by menopause  --  parathyroid hormone injections.&lt;/p&gt;
&lt;p&gt;Since serum serotonin inhibitors could be given in pill form, this pathway is much more attractive, Karsenty said.&lt;/p&gt;
&lt;p&gt;The specific agent used in this trial was designed for proof-of-principle and wouldn&apos;t necessarily be what is developed for clinical use, he cautioned.&lt;/p&gt;
&lt;p&gt;&quot;Although the data presented here are promising we remain fully aware that, since rodents do not remodel bones as much as humans do, our results will have to be confirmed in other species,&quot; the researchers also warned in the paper.&lt;/p&gt;
&lt;p&gt;Karsenty said the group plans to continue animal model studies for the time being, with no plans to move into clinical trials.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by grants from the National Institutes of Health and a Gideon and Sevgi Rodan fellowship from the International Bone and Mineral Society.&lt;/p&gt;&lt;p&gt;The researchers reported no conflicts of interest or industry involvement in the study.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_411"
                     title="Older Women with Gout at Risk of MI (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Cardiology/MyocardialInfarction/tb/18319?impressionId=1265736556693"
                     
      &lt;p&gt;Elderly women with gout are at increased risk of acute myocardial infarction (MI), even more so than men with this painful arthritis, a population-based study found.&lt;/p&gt;
&lt;p&gt;After adjusting for age, comorbidities such as hypertension and diabetes, and prescription drug use, the relative risk of MI among women ages 65 and older was 1.39 (95% CI 1.20 to 1.61), according to Mary A. De Vera of the Arthritis Research Centre of Canada in Vancouver, and colleagues.&lt;/p&gt;
&lt;p&gt;In comparison, the multivariate relative risk among men was 1.11 (95% CI 0.99 to 1.23, &lt;em&gt;P&lt;/em&gt;=0.003 for interaction), the researchers reported online in the &lt;em&gt;Annals of the Rheumatic Diseases&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Men with gout are known to be at higher risk for coronary heart disease and acute MI, but corresponding data for women were sparse.&lt;/p&gt;
&lt;p&gt;So De Vera and colleagues conducted a cohort study using the British Columbia Linked Health Database, comparing the incidence rates of MI between 9,642 patients with gout and 48,210 matched controls with no history of ischemic heart disease.&lt;/p&gt;
&lt;p&gt;A total of 3,890 of the cases were women, as were 19,450 of the controls.&lt;/p&gt;
&lt;p&gt;The gout incidence rate in women ages 65 to 85 years was 2.5 per 1,000 person-years, and 2.9 per 1,000 person-years in those ages 85 and higher.&lt;/p&gt;
&lt;p&gt;The rates in men of the corresponding ages were 5.7 and 6.5 per 1,000 person-years.&lt;/p&gt;
&lt;p&gt;Hospital records indicated that the incidence rates of acute MI among women and men were 6.7 and 10.7 per 1,000 person-years, respectively.&lt;/p&gt;
&lt;p&gt;During a median of seven years&apos; follow-up there were 3,268 incident cases of MI, including 996 in women.&lt;/p&gt;
&lt;p&gt;In unadjusted analysis, the relative risk of acute MI among women with gout was 1.67 (95% CI 1.45 to 1.93), while that for men with gout was 1.19 (95% CI 1.07 to 1.32).&lt;/p&gt;
&lt;p&gt;Multivariate analysis determined that the relative risk for nonfatal MI in women was 1.41 (95% CI 1.19 to 1.67), while that in men was 1.11 (95% CI 0.98 to 1.25, &lt;em&gt;P&lt;/em&gt;=0.005 for interaction).&lt;/p&gt;
&lt;p&gt;The gender difference did not show up in fatal events, however. The relative risk for fatal MI was 1.33 in women (95% CI 0.99 to 1.78) and 1.10 in men (95% CI 0.88 to 1.38, &lt;em&gt;P&lt;/em&gt;=0.30 for interaction).&lt;/p&gt;
&lt;p&gt;Overall, there was a 39% increased risk for MI among women with gout, an association that was independent of age, comorbidities, and use of prescription drugs including nonsteroidal anti-inflammatories, diuretics, statins, anticoagulants, and aspirin.&lt;/p&gt;
&lt;p&gt;The association was significantly stronger than for men, according to the researchers.&lt;/p&gt;
&lt;p&gt;These gender differences may relate to serum uric acid levels and metabolism. Levels in men are about 1 mg/dL higher, although levels do rise in women at menopause.&lt;/p&gt;
&lt;p&gt;&quot;Thus, the relative physiological impact of having gout or a certain level of hyperuricemia may be stronger among women than men,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;Possible mechanisms for the contribution of hyperuricemia to cardiovascular disease include vascular smooth muscle cell proliferation and inflammation, as well as platelet adhesiveness and aggregation.&lt;/p&gt;
&lt;p&gt;&quot;Inflammation associated with gout may also have a role in potential mechanisms, including promotion of atherogenesis and thrombogenesis, similar to other inflammatory arthritides associated with cardiovascular disease,&quot; the investigators noted.&lt;/p&gt;
&lt;p&gt;A strength of the study was its population-based design, which makes its findings generalizable. Limitations include the potential for misclassification of diagnosis because of the use of diagnostic codes, and the inability to adjust for lifestyle factors such as smoking.&lt;/p&gt;
&lt;p&gt;Nonetheless, according to the investigators, &quot;These findings provide support for the aggressive management of cardiovascular risk factors for male and female patients with gout.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was partly funded by the National Institute of Health.&lt;/p&gt;&lt;p&gt;The authors have received support from the Canadian Arthritis Network/The Arthritis Society, and one disclosed receiving research funding and honoraria from TAP Pharmaceuticals and Savient.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>