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    <recommendedItem id="20100101_19_406"
                     title="AAPM: Opioid Gains Long-Term Control of Neuropathic Cancer Pain (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/MeetingCoverage/AAPM/tb/18316?impressionId=1265750519467"
                     
      &lt;p&gt;SAN ANTONIO  --  Patients with neuropathic cancer pain obtained consistent, long-term pain control with extended-release oxymorphone (Opana), according to results of a one-year, open-label extension study.&lt;/p&gt;
&lt;p&gt;Patients reported pain in the mild range throughout most of the follow-up, and only 11% discontinued because of lack of efficacy, Errol Gould, PhD, of Endo Pharmaceuticals in Chadds Ford, Pa., reported here at the American Academy of Pain Medicine meeting. The company manufactures Opana.&lt;/p&gt;
&lt;p&gt;No unexpected adverse events occurred.&lt;/p&gt;
&lt;p&gt;&quot;Current clinical guidelines recommend opioids as second- or third-line treatment for chronic neuropathic pain,&quot; Gould said in an interview. &quot;These results suggest that oxymorphone extended release may be a viable long-term option for patients with neuropathic pain.&quot;&lt;/p&gt;
&lt;p&gt;The findings came from a one-year extension of a multicenter, open-label, noncontrolled short-term study of patients with cancer-related chronic pain.&lt;/p&gt;
&lt;p&gt;Of 44 patients who entered the extension phase, 27 had pain that was primarily neuropathic in origin. The diagnosis of neuropathic pain was based on clinician judgment, with no prespecified diagnostic criteria for guidance.&lt;/p&gt;
&lt;p&gt;Patients began treatment in the extension phase with their ending dose from the short-term study. Dose adjustments to improve pain control or tolerability were allowed throughout the 52-week extension phase.&lt;/p&gt;
&lt;p&gt;Ten of the 27 patients completed the extension study. Principal reasons for withdrawal were adverse events, patient request, loss of effectiveness, and nonadherence.&lt;/p&gt;
&lt;p&gt;The median duration from initiation of long-term maintenance to final visit was 22 weeks. Baseline pain intensity averaged 32.9 on a 100-point scale and 32.6 at final visit. Mean least pain intensity was 13.8 at baseline and 16.2 at final visit, and worst pain intensity averaged 76.3 at baseline and 66.5 at final visit.&lt;/p&gt;
&lt;p&gt;&quot;Regression analysis showed that pain intensity changed very little throughout follow-up,&quot; Gould said.&lt;/p&gt;
&lt;p&gt;The median oxymorphone dose increased from 80 mg at baseline to 160 mg at 52 weeks.&lt;/p&gt;
&lt;p&gt;Eleven (41%) patients reported at least one treatment-related adverse event. The most common events were dry mouth, constipation, and fatigue. The only serious adverse event was an episode of depressed consciousness.&lt;/p&gt;
&lt;p&gt;&quot;Patients required some gradual increases in dosage over time, but that&apos;s consistent with the nature of the disease,&quot; said Gould.&lt;/p&gt;
&lt;p&gt;Not long ago opioids were considered ineffective for neuropathic pain, he added. This study provided additional evidence in support of opioids&apos; effectiveness in controlling neuropathic pain.&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 Endo Pharmaceuticals, which manufactures Opana.&lt;/p&gt;&lt;p&gt;Gould and another co-author are employees of Endo Pharmaceuticals.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_298"
                     title="FDA Updates Myeloma Drug Label for New Risks"
                     score="0.004"
                     href="http://www.medpagetoday.com/ProductAlert/DevicesandVaccines/tb/18158?impressionId=1265750519467"
                     
      &lt;p&gt;WASHINGTON  --  The FDA has revised dosage and safety information for bortezomib (Velcade), the myeloma and mantle cell lymphoma drug, to reflect an increased toxicity risk.&lt;/p&gt;
&lt;p&gt;The new labeling includes a warning for patients with moderate-to-severe hepatic impairment and now recommends at-risk patients start at a lower dosage of 0.7 mg for the first cycle of treatment and escalate to 1.0 mg, or reduce further to 0.5 mg, in subsequent cycles.&lt;/p&gt;
&lt;p&gt;The label has also been updated to include clinical study data showing a higher median survival rate in patients using a combination of bortezomib, melphalan, and prednisone versus a regiment of just melphalan and prednisone (&lt;em&gt;P&lt;/em&gt;=0.00084).&lt;/p&gt;
&lt;p&gt;The drug is contraindicated in patients with hypersensitivity to bortezomib, boron, or mannitol. The FDA also warns that women should avoid becoming pregnant while undergoing treatment with bortezomib.&lt;/p&gt;
&lt;p&gt;The drug is manufactured by Millennium: The Takeda Oncology Company of Cambridge, Mass.&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20090101_19_2323"
                     title="Mutations Linked to Hemolytic-Uremic Syndrome"
                     score="-0.005"
                     href="http://www.medpagetoday.com/HematologyOncology/Hematology/tb/15203?impressionId=1265750519467"
                     
      HOUSTON, July 22 -- Mutations affecting thrombomodulin function account for a small portion of cases of atypical hemolytic-uremic syndrome, a multinational research team found. 
              &lt;p&gt;
              &lt;p&gt;About 5% of a group of patients with the syndrome had missense mutations in the thrombomodulin gene, Edward M. Conway, MD, PhD, of the University of British Columbia in Vancouver, and colleagues reported in the July 23 issue of the &lt;em&gt;New England Journal of Medicine&lt;/em&gt;. 
              &lt;p&gt;
              &lt;p&gt;The observation might point toward an effective therapy for at least some patients with atypical hemolytic-uremic syndrome. 
              &lt;p&gt;
              &lt;p&gt;&quot;Effective therapies are lacking, and in most patients, end-stage renal failure requiring dialysis develops,&quot; the authors said. &quot;Since thrombomudulin simultaneously suppresses the complement and coagulation systems, its administration may have therapeutic value for some patients with the atypical hemolytic-uremic syndrome.&quot; 
              &lt;p&gt;
              &lt;p&gt;The common form of the syndrome is caused by infection with Shiga toxin-producing bacteria and has a favorable prognosis. About 10% of patients have the poor-prognosis atypical form of the syndrome, which is of unknown etiology. 
              &lt;p&gt;
              &lt;p&gt;About half of patients with atypical presentation have mutations in genes involved in the regulation of the complement system, the authors said. The genetics of the remaining cases had not been determined. 
              &lt;p&gt;
              &lt;p&gt;In an attempt to fill in some missing pieces of the syndrome etiology, Dr. Conway and colleagues examined the role of thrombomodulin, an endothelial glycoprotein that has anticoagulant, anti-inflammatory, and cytoprotective properties. 
              &lt;p&gt;
              &lt;p&gt;Investigators sequenced the entire thrombomodulin gene (&lt;em&gt;THBD&lt;/em&gt;) in 152 patients with atypical hemolytic-uremic syndrome and in 380 controls. 
              &lt;p&gt;
              &lt;p&gt;By use of purified proteins and cell-expression system, they explored thrombomodulin&apos;s role in regulation of the complement system and characterized the mechanisms. 
              &lt;p&gt;
              &lt;p&gt;The investigators expressed thrombomodulin variants in cultured cells and evaluated the effects of thrombomodulin missense mutations in atypical hemolytic-uremic syndrome. 
              &lt;p&gt;
              &lt;p&gt;The work revealed seven unrelated patients who had six different heterozygous &lt;em&gt;THBD&lt;/em&gt; mutations. 
              &lt;p&gt;
              &lt;p&gt;In vitro thrombomodulin binds to complement factor C3b (a promoter of complement activation and opsonization) and negatively regulates complement by accelerating factor I-mediated inactivation of C3b, the authors said. 
              &lt;p&gt;
              &lt;p&gt;Thrombomodulin also promotes activation of plasma procarboxypeptidase B to accelerate inactivation of the anaphylatoxins C3a and C5a. 
              &lt;p&gt;
              &lt;p&gt;Cultured cells expressing thrombomodulin variants had a diminished capacity to inactivate C3b and to promote inactivation of the anaphylatoxins, thereby diminishing protection against activated complement.  
              &lt;p&gt;
              &lt;p&gt;&lt;table cellspacing=&quot;0&quot; hspace=&quot;1&quot; style=&quot;border-style:solid; border-width:1px; border-color:#8dabbc; font-family:arial; font-size:12px; background-color:#DBE9F2; padding:5px 5px 5px 5px;&quot;&gt;
&lt;tr&gt;&lt;td&gt;The study was supported by grants from the National Institutes of Health, the Istituto Superiore della Sanita, Fonds voor Wetenschappeljik Onderzoek, and Fondation Leducq to various members of the research team.
              &lt;p&gt;
              &lt;p&gt;Dr. Conway disclosed that he holds a patent for the use of the lectinlike domain of thrombomodulin as an anti-inflammatory agent. Coauthors Charles T. Esmon and Naomi L. Esmon hold licenses and patents related to protein C and activated protein C, unrelated to the article.&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        
    </recommendedItem>
    <recommendedItem id="20090101_1_167"
                     title="Off-Label Use of Hemophilia Drug May Be Risky"
                     score="-0.007"
                     href="