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<recommendedContent xmlns="http://api.mspoke.com">
    <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=1265752119677"
                     
      &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_261"
                     title="Scrubbing Away Germs Can Backfire on Backsides (CME/CE)"
                     score="0.001"
                     href="http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/tb/18121?impressionId=1265752119677"
                     
      Rashes from toilet seats are once again afflicting American children, and the rare condition is often misdiagnosed, which may delay proper treatment.&lt;br&gt;
&lt;br&gt;That&apos;s the conclusion from a report based of five-cases of toilet-seat contact dermatitis investigated by researchers at Johns Hopkins University School of Medicine and reported in the Jan. 25 issue of &lt;em&gt;Pediatrics&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;While toilet-seat dermatitis is commonly thought to result from allergies to wooden seats, the report concludes that another source is plastic toilet seats cleaned with harsh detergents.&lt;/p&gt;
&lt;p&gt;&quot;This case series and previous reports have documented that toilet-seat dermatitis is much more common than previously recognized in the U.S. and around the world,&quot; Bernard A. Cohen, MD, and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;Furthermore, the incidence of this condition is rising in North America because of a resurgent popularity of exotic-wood toilet seats and frequent use of detergents that contain highly irritant/sensitizing compounds such as quaternary ammonium compounds, phenol, formaldehyde, etc. in public restrooms.&quot;&lt;/p&gt;
&lt;p&gt;Of the cases analyzed by the authors, two occurred in the U.S. and the other three occurred in India.&lt;/p&gt;
&lt;p&gt;Both U.S. cases were girls, a 6-year-old who had a rash for over two years before it was correctly diagnosed and a 10-year-old whose rash lasted for a year. In both cases, the rashes seemed to worsen during the school year when the girls were using school restrooms. The younger girl&apos;s dermatitis twice became infected with methicillin-resistant &lt;em&gt;Staphylococcus aureus &lt;/em&gt;and required treatment with antibiotics.&lt;/p&gt;
&lt;p&gt;After doctors determined the rashes were the result of contact with toilet seats and instructed the girls to use toilet-seat covers and apply moisturizers and topical steroids to the affected areas, the eruptions cleared up within a few weeks.&lt;/p&gt;
&lt;p&gt;The cases in India included a 14-month old boy and two girls, 12 and 10.&lt;/p&gt;
&lt;p&gt;The boy and the 12-year-old girl were both initially misdiagnosed with ringworm and unsuccessfully treated with clotrimazole cream. The other girl was unsuccessfully treated with ayurvedic and homeopathic topical medications before doctors diagnosed toilet-seat dermatitis. Two of the children were instructed to use soaps that only exacerbated the problem.&lt;/p&gt;
&lt;p&gt;In all three cases, the rashes cleared up with some combination of topical steroids, using toilet-seat covers, replacing the household toilet seat, and limiting time on the toilet.&lt;/p&gt;
&lt;p&gt;The authors distinguished between two types of toilet-seat dermatitis: allergic contact dermatitis, the better described form of the condition, in which a patient develops allergy to wooden toilet seats, and irritant contact dermatitis, in which the rashes result from contact with harsh detergents used on plastic toilet seats.&lt;/p&gt;
&lt;p&gt;They noted that detergents used in public restrooms and in hospitals are potentially more irritating to the skin than those used at home and that alkaline detergents are more likely to cause skin irritation than acidic detergents, because they perturb the body&apos;s natural acidic environment.&lt;/p&gt;
&lt;p&gt;Toilet-seat dermatitis was first identified as an external skin rash in 1927. Exposure to wooden toilet seats and associated varnish, lacquers, and paints led to sensitization and development of an allergic contact dermatitis.&lt;/p&gt;
&lt;p&gt;The condition nearly disappeared in the U.S. in 1980s and 1990s, after public facilities and homeowners in the U.S. changed from wooden to plastic toilet seats and sanitary seat covers became readily available.&lt;/p&gt;
&lt;p&gt;However, in recent years the number of cases has grown as a result of homeowners installing toilet seats made of exotic woods and the increased use of harsh toilet seat detergents.&lt;/p&gt;
&lt;p&gt;Most reports have focused on adults with rashes, but little previous attention has focused on the condition in children. &quot;In this case series we describe toilet-seat contact dermatitis in children and underscore a typical history and physical findings that we hope will aid clinicians in recognizing this disease,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;It is important to underscore that regular use of toilet-seat covers is the key to success in treatment,&quot; the authors wrote. &quot;Such seat covers can be purchased at any major retailer such as Walmart or online.&lt;/p&gt;
&lt;p&gt;As an alternative, newspaper cutouts could be used to provide barrier protection. Although it is possible to develop an allergy to toilet-seat covers, none have been reported thus far in the literature.&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 reported no sources of funding or financial 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_218"
                     title="Even Mild COPD Affects the Heart (CME/CE)"
                     score="-0.003"
                     href="http://www.medpagetoday.com/Pulmonology/SmokingCOPD/tb/18070?impressionId=1265752119677"
                     
      Chronic lung disease begins to affect cardiac function at even mild levels of emphysema, data from a large prospective cohort study showed.&lt;br&gt;
&lt;br&gt;A 10-point increase in percent emphysema by lung CT had a linear inverse relationship with left ventricular end-diastolic volume (LVEDV), stroke volume, and cardiac output (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for all parameters), researchers reported in the Jan. 21 issue of the &lt;em&gt;New England Journal of Medicine&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;Current smoking status increased the magnitude of the association compared with former smokers and nonsmokers, the researchers found.&lt;br&gt;
&lt;br&gt;Left ventricular ejection fraction did not change with increasing percent of emphysema and airflow obstruction.&lt;br&gt;
&lt;br&gt;&quot;Previously, it has been well known that in very severe lung disease, the damage to the lungs affects heart function,&quot; lead author R. Graham Barr, MD, of Columbia University in New York, said in an interview.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;&quot;What we have shown is that a similar physiology, a similar relationship, would appear to extend up and down the spectrum of lung disease from mild, subclinical COPD and emphysema, all the way to moderately severe lung disease.&quot;&lt;/p&gt;
&lt;p&gt;Severe COPD can lead to cor pulmonale, characterized by increased vascular resistance and right heart failure, accompanied by reduced left ventricular filling, left ventricular stroke volume, and cardiac output.&lt;/p&gt;
&lt;p&gt;However, left ventricular ejection fraction (LVEF) usually is preserved. Whether similar changes occurred with less severe COPD had not been determined, and examining that question was the principal objective of the study by Barr and colleagues.&lt;/p&gt;
&lt;p&gt;The study population comprised a subgroup of patients enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA), which is exploring the prevalence, correlates, and progression of subclinical cardiovascular disease. The MESA Lung Study comprised 2,816 MESA participants who underwent cardiac MRI assessment of left ventricular structure and function.&lt;/p&gt;
&lt;p&gt;Investigators in the lung study excluded patients who had a restrictive pattern on spirometry, defined as a forced vital capacity (FVC) below the lower limit of normal and an FEV&lt;sub&gt;1&lt;/sub&gt;:FVC ratio &amp;gt;0.7.&lt;/p&gt;
&lt;p&gt;Information collected for the lung study included patient demographics, smoking history, medical history, level of physical activity, height, weight, resting blood pressure, serum glucose, C-reactive protein, and fibrinogen levels.&lt;/p&gt;
&lt;p&gt;Extent of emphysema was calculated from lung fields of cardiac CT scans, which included 70% of the lung volume from the carina to the base. Investigators defined extent of emphysema as the percentage of voxels below -910 Hounsfield units in the lung windows of cardiac CT scans.&lt;/p&gt;
&lt;p&gt;Participants who smoked at least one cigarette in the 30 days before CT or who had urinary cotinine levels &amp;gt;100 ng/mL were classified as current smokers.&lt;/p&gt;
&lt;p&gt;The mean age of the lung population was 61, and 51% were women. Current smokers accounted for 13% of the participants, former smokers for 38%, and nonsmokers for 49%. LVEF averaged about 70%.&lt;/p&gt;
&lt;p&gt;Mean spirometric measures were normal, as were measures of left ventricular structure and function. Median percent emphysema was 15%. Comparison of percent emphysema with left ventricular measures showed that a 10-point increase in percent emphysema was associated with a: &lt;ul&gt; &lt;li&gt;4.1 mL decrement in LVEDV&lt;/li&gt; &lt;li&gt;2.7 mL decrement in stroke volume&lt;/li&gt; &lt;li&gt;0.19 L/min decrement in cardiac output&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;The investigators observed no evidence of an association between percent emphysema and LVEF, reflected in a 0.02-point mean increase with each 10-point increase in extent of emphysema.&lt;/p&gt;
&lt;p&gt;Smoking status significantly influenced associations of percent emphysema with LVEDV (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for interaction) and stroke volume (&lt;em&gt;P&lt;/em&gt;=0.008 for interaction).&lt;/p&gt;
&lt;p&gt;The magnitude of the association was greater among smokers than former smokers, and greater among former smokers than nonsmokers. However, the associations were evident in smokers and nonsmokers alike.&lt;/p&gt;
&lt;p&gt;&quot;The apparent effect of emphysema on left ventricular end-diastolic volume and cardiac output was similar to that of traditional cardiac risk factors previously reported in MESA and, among smokers, was greater than that of traditional cardiac risk factors,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;The linearity of associations across the study population &quot;suggests that even early-stage COPD influences stroke volume and left ventricular size,&quot; Anton Vonk-Noordegraaf, MD, of Vrije University Medical Center in Amsterdam, wrote in an accompanying editorial.&lt;/p&gt;
&lt;p&gt;&quot;Since oxygen delivery is directly related to cardiac output, a lower cardiac output in patients with COPD leads to impaired oxygen delivery,&quot; Vonk-Noordegraaf continued.&lt;/p&gt;
&lt;p&gt;&quot;Although the effects on cardiac output were small in this study population, they may be more pronounced in severe cases of emphysema and during exercise, as has been shown previously. The question is whether the striking clinical resemblance between COPD and chronic heart failure can be explained in part by a factor both diseases have in common: decreased cardiac output.&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;Co-author Paul L. Enright disclosed relationships with Pfizer and Gilead.&lt;/p&gt;&lt;p&gt;Coauthor Eric A. Hoffman disclosed relationships with VIDA Diagnostics, sanofi-aventis, AstraZeneca, and Chiesi Pharmaceuticals.&lt;/p&gt;&lt;p&gt;Coauthor Kawut disclosed a relationship with Pfizer.&lt;/p&gt;&lt;p&gt;Co-author Jo&amp;#227;o A. C. Lima disclosed relationships with Toshiba Medical Systems and General Electric.&lt;/p&gt;&lt;p&gt;Co-author Lewis J. Smith disclosed relationships with Merck and KarmelSonix.&lt;/p&gt;&lt;p&gt;Vonk-Noordegraaf had no disclosures.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20090101_1_851"
                     title="Antibiotics for Acne Raises Respiratory Infection Risk"
                     score="-0.006"
                     href="