<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_3155"
                     title="Targeted Therapy Shows Early Promise in Melanoma (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/HematologyOncology/SkinCancer/tb/21881?impressionId=1283457933563"
                     
      &lt;p&gt;A novel drug targeted to a common mutation behind melanoma appears effective in skin tumors that carry the mutation, according to early results.&lt;/p&gt;
&lt;p&gt;In a phase I trial, 10 of the 16 patients with melanoma tumors carrying the V600E mutation in the serine&amp;#8211;threonine protein kinase B-RAF (&lt;em&gt;BRAF&lt;/em&gt;) gene had a partial response when treated with at least 240 mg of the agent known as PLX4032, or RG7204.&lt;/p&gt;
&lt;p&gt;One of these patients had a complete response to the oral inhibitor of mutated BRAF, Keith T. Flaherty, MD, of the Massachusetts General Hospital Cancer Center in Boston, and colleagues found.&lt;/p&gt;
&lt;p&gt;The results looked even better in an extension phase of trial in BRAF-mutation metastatic melanoma, the researchers reported in the Aug. 26 issue of the &lt;em&gt;New England Journal of Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Altogether, 81% of melanoma patients with the mutation responded, noted co-author Jeffrey A. Sosman, MD, of Vanderbilt University in Nashville, Tenn.&lt;/p&gt;
&lt;p&gt;&quot;These responses occur rapidly, in organs where we infrequently see tumor regression, and patients can actually feel better overnight with this therapy,&quot; he said in an interview.&lt;/p&gt;
&lt;p&gt;The dramatic results were &quot;much beyond&quot; that expected from such an early phase study, Vernon K. Sondak, MD, of the Moffitt Cancer Center and Research Institute in Tampa, Fla., said in an interview.&lt;/p&gt;
&lt;p&gt;Even in phase III melanoma trials with standard drugs the typical response rate might be only 6% to 12%, he explained.&lt;/p&gt;
&lt;p&gt;&quot;Overall, I think this is quite significant,&quot; he said in the interview, particularly since about half of melanoma cases are associated with the mutation targeted by the drug in the study.&lt;/p&gt;
&lt;p&gt;In an accompanying editorial with Keiran S.M. Smalley, PhD, also of the Moffitt Cancer Center and Research Institute, he called the results a major breakthrough that provides proof of principle for individualized treatment of a substantial proportion of metastatic melanoma.&lt;/p&gt;
&lt;p&gt;A similar strategy of imatinib (Gleevec) has some evidence of efficacy against melanoma in which mutations in the &lt;em&gt;KIT&lt;/em&gt; gene are culprit, but these are found in only a small minority of melanomas, the editorialists pointed out.&lt;/p&gt;
&lt;p&gt;Pretreatment screening for mutations in &lt;em&gt;BRAF&lt;/em&gt;, &lt;em&gt;KIT&lt;/em&gt;, and probably other key genes is likely on the horizon, they suggested.&lt;/p&gt;
&lt;p&gt;In the case of BRAF, they recommended confirmation of mutation before giving an inhibitor of this pathway since these drugs paradoxically stimulate cell proliferation via another route in cell lines without the mutations.&lt;/p&gt;
&lt;p&gt;Indeed, the study showed an unexpectedly high rate of cutaneous squamous cell carcinomas, nearly all of the keratoacanthoma type, in patients treated with PLX4032  --  eight (15%) in the dose-escalation cohort and 10 (31%) in the extension cohort.&lt;/p&gt;
&lt;p&gt;All of these cancers were resected with none leading to treatment discontinuation.&lt;/p&gt;
&lt;p&gt;The multicenter study included 55 patients in the dose-escalation phase who had a variety of solid-tumor types refractory to therapy or for which standard or curative therapy was not available. Among them, 49 had melanoma.&lt;/p&gt;
&lt;p&gt;Patients received PLX4032 twice daily until disease progression. Doses started at 160 mg twice daily and escalated to 1,120 mg twice daily with progressive enrollment.&lt;/p&gt;
&lt;p&gt;The recommended dose going forward was 960 mg twice daily. Beyond that dose, grade 2 or 3 rash, fatigue, and arthralgia limited escalation.&lt;/p&gt;
&lt;p&gt;In the extension phase, 32 additional patients with metastatic melanoma with confirmed V600E &lt;em&gt;BRAF&lt;/em&gt; mutation got this recommended dose.&lt;/p&gt;
&lt;p&gt;Among them, 24 had a partial response and two had a complete response. These responses occurred in visceral organs and bone metastases as well as sites where responses are common with other drugs, such as the lungs and lymph nodes.&lt;/p&gt;
&lt;p&gt;Symptom improvement occurred within one to two weeks, including reduced need for narcotics in three patients.&lt;/p&gt;
&lt;p&gt;In the entire treated cohort, the estimated median progression-free survival extended more than seven months with a substantial proportion still on study.&lt;/p&gt;
&lt;p&gt;So the novel agent isn&apos;t a cure for melanoma, Sosman noted.&lt;/p&gt;
&lt;p&gt;But there are good prospects for combining this targeted therapy with others, such as the novel immune-stimulating drug &lt;a href=&quot;http://www.medpagetoday.com/MeetingCoverage/ASCO/20490&quot; mce_href=&quot;http://www.medpagetoday.com/MeetingCoverage/ASCO/20490&quot; target=&quot;_blank&quot;&gt;ipilimumab&lt;/a&gt; which recently showed the first ever overall survival impact in metastatic melanoma, Sosman and the editorialists agreed.&lt;/p&gt;
&lt;p&gt;The mechanisms for the primary and secondary resistance seen to PLX4032 aren&apos;t known but warrant study, the researchers concluded.&lt;/p&gt;
&lt;p&gt;A phase III trial with the BRAF inhibitor is underway to determine whether it can improve overall survival similar to ipilimumab.&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 Plexxikon and Roche Pharmaceuticals.&lt;/p&gt;&lt;p&gt;Flaherty, Sosman, and several co-authors report the receipt by their institutions of grant support from Plexxikon to conduct this clinical trial. Flaherty, Sosman, and several co-authors also reported receiving consulting fees or reimbursement for travel expenses from Roche Pharmaceuticals.&lt;/p&gt;&lt;p&gt;Sosman reported pending receipt of grant support from Roche Pharmaceuticals.&lt;/p&gt;&lt;p&gt;Two co-authors reported being employees of Roche Pharmaceuticals; one reported being an employee of Plexxikon, holding equity in the company, and receiving reimbursement for travel expenses from the company.&lt;/p&gt;&lt;p&gt;Sondak reported having received honoraria and travel expenses from Hoffman-LaRoche, Genentech/Hoffman-LaRoche, and GlaxoSmithKline.&lt;/p&gt;&lt;p&gt;Smalley reported having received grants from the Melanoma Research Foundation, the State of Florida, the Harry Lloyd Trust, and the National Cancer Institute.&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_3144"
                     title="ESC: Statins Cleared of Causing Cancer (CME/CE)"
                     score="0.008"
                     href="http://www.medpagetoday.com/MeetingCoverage/ESCCongress/tb/21866?impressionId=1283457933563"
                     
      &lt;p&gt;STOCKHOLM  --  In what may be the final word on the issue, an international team of researchers report that statins neither cause nor prevent cancer.&lt;/p&gt;
&lt;p&gt;The finding comes from a meta-analysis of 25 randomized controlled trials of the lipid-lowering medications, according to Jonathan Emberson, PhD, of the University of Oxford, and colleagues in the international Cholesterol Treatment Trialists&apos; Collaboration.&lt;/p&gt;
&lt;p&gt;In those trials, which included more than 166,000 participants, there were no differences between treatment and control arms in terms of the incidence of cancer or the rate of cancer mortality, Emberson said in a telephone interview.&lt;/p&gt;
&lt;p&gt;He will report the results next week in a presentation at the annual congress of the European Society of Cardiology here.&lt;/p&gt;
&lt;p&gt;&quot;Randomization to statin therapy for at least five years had no effect on the incidence of cancer or of cancer mortality in any group of individuals,&quot; Emberson told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The main goal of the trials was to establish the effect of statins on lipid levels, and especially how changes in lipids affected the risk of major cardiovascular events. But Emberson said the collaborative group planned from the beginning to get data on cancer mortality, based on individual patient-level data from all the studies.&lt;/p&gt;
&lt;p&gt;&quot;Because we have individual patient data, we can really look at particular hypotheses and test them,&quot; he said  --  something that many meta-analyses can&apos;t do.&lt;/p&gt;
&lt;p&gt;The researchers conducting the trials were asked to track cancer, he said, because of observational studies that had suggested that lower cholesterol was linked to a higher risk of cancer. It now seems likely that those results arose from residual confounding or perhaps reverse causality, since it is known that the early stages of cancer can have the effect of lowering cholesterol, he said.&lt;/p&gt;
&lt;p&gt;There have also been observational studies suggesting the opposite effect  --  that statins prevent cancer.&lt;/p&gt;
&lt;p&gt;The 25 studies included 20 in which a statin was compared to placebo, involving 126,753 participants, and five in which higher and lower doses were compared, involving 39,612 participants. All the trials had at least 1,000 participants and lasted at least five years, Emberson said.&lt;/p&gt;
&lt;p&gt;The investigators calculated rate ratios for the effect on cancer incidence and cancer mortality of each 1.0 millimole per liter reduction in low-density lipoprotein cholesterol.&lt;/p&gt;
&lt;p&gt;All told, they reported, 9,954 participants developed cancer and 3,498 died from it.&lt;/p&gt;
&lt;p&gt;But reducing LDL cholesterol with a statin had no effect on the risk of developing cancer or on the risk of cancer death: &lt;ul&gt; &lt;li&gt;In the 20 statin versus control trials, cancer incidence in the treatment arms was 3,502 (or 1.4% a year) versus 3,514 cases in the control arms (also 1.4% a year), for a rate ratio of 0.99.&lt;/li&gt; &lt;li&gt;In those trials, there were 1,289 deaths among those taking statins versus 1,281 in those getting the placebo  --  0.5% a year for both  --  leading to a rate ratio of 1.00.&lt;/li&gt; &lt;li&gt;In the five trials of more versus less statin, cancer incidence was 1,466 versus 1,472 (1.6% a year for both arms) yielding a rate ratio of 1.02, while cancer mortality was 447 deaths versus 481 (0.5% a year for both arms) for a rate ratio of 0.88 and a 95% confidence interval from 0.67 to 1.15. &lt;/li&gt; &lt;li&gt;There was no evidence of any effect of statin therapy on cancer incidence or mortality at any particular site, with increasing years of treatment, or in any particular subgroup.&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;The only gap, Emberson said, is that the study only covers five years of treatment and it remains possible that an effect might be seen after longer therapy. But he said that some of the studies now have a decade of data and no evidence of a long-term effect has emerged.&lt;/p&gt;
&lt;p&gt;While statins are widely used, there has been &quot;an ongoing background worry&quot; among physicians that they might cause harm, according to Chris Cannon, MD, of Brigham and Women&apos;s Hospital in Boston.&lt;/p&gt;
&lt;p&gt;That fear has now been laid to rest, he told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;The key message is that statins are safe and there&apos;s no issue of increasing cancer,&quot; he said. &quot;And there&apos;s also no effect of reducing cancer, at least in a five-year time frame.&quot;&lt;/p&gt;
&lt;p&gt;The data, he said, meet the &quot;gold standard&quot; of randomized trials and &quot;trump the many observational analyses that have come out on both sides of the equation.&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;Emberson said he had no financial conflicts.&lt;/p&gt;
&lt;p&gt;Cannon reported research funding from Accumetrics, AstraZeneca, GlaxoSmithKline, InteKrin Therapeutics, Merck, Takeda; an advisory and ownership relationship with Bristol-Myers Squibb/Sanofi Partnership,  Novartis, and Alnylam; Honorarium for development of independent educational symposium from Pfizer; and clinical advisor and equity in Automedics Medical Systems.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3031"
                     title="Redheads Seem to Have Multiple BCCs (CME/CE)"
                     score="0.002"
                     href="http://www.medpagetoday.com/Dermatology/SkinCancer/tb/21695?impressionId=1283457933563"
                     
      &lt;p&gt;Redheads appear to be at the highest risk for developing multiple basal cell carcinomas (BCC), according to a Dutch population-based study.&lt;/p&gt;
&lt;p&gt;The prospective study of nearly 11,000 people followed for almost a decade found those with red hair who had one BCC were 40.3% more likely to have multiple subsequent lesions compared with those who had dark hair (adjusted HR 1.43, 95% CI 1.05 to 1.93), Ville Kiiski, MD, and colleagues from Erasmus Medical Center in Rotterdam, reported.&lt;/p&gt;
&lt;p&gt;Using Andersen-Gill multifailure survival models to analyze repeated events, Kiiski&apos;s team determined that a high educational level (reflecting higher socioeconomic status) also was associated with a greater likelihood for multiple BCCs (HR 1.42, 95% CI 1.12 to 1.81), they wrote in the August &lt;em&gt;Archives of Dermatology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Risk factors for developing a first BCC lesion include age, male sex, race, and genetic predisposition, factors that may interact with environmental exposures such as ultraviolet light, the researchers explained.&lt;/p&gt;
&lt;p&gt;However, risk factors for subsequent lesions are not well documented, so the team analyzed data from participants in the Rotterdam Study, a prospective, population-based cohort study designed to study diseases in elderly people.&lt;/p&gt;
&lt;p&gt;Data from two cohorts were examined  --  7,983 people ages 55 or older enrolled in 1990 and 3,011 participants added in 1999. The team then compared risk factors for multiple lesions with those associated with initial incident BCC lesions among a total of 10,820 participants.&lt;/p&gt;
&lt;p&gt;The mean age at study entry was 69.1 years. Two-thirds of the participants were women and almost all were white.&lt;/p&gt;
&lt;p&gt;A total of 4.8% of the cohort had at least one BCC, and there were 854 unique lesions (excluding BCC recurrences) during almost ten years of follow-up.&lt;/p&gt;
&lt;p&gt;Risk factors for a first BCC included older age (65 to 75 years) at the time of enrollment (adjusted OR 1.39, 95% CI 1.11 to 1.75) and red hair (adjusted OR 1.98, 95% CI 1.24 to 3.14), the researchers found.&lt;/p&gt;
&lt;p&gt;Among two-thirds of the cohort, the most common BCC lesion site was the head or neck; more than half were of the nodular subtype.&lt;/p&gt;
&lt;p&gt;The incidence rate for first BCC lesions was 513 per 100,000 person-years.&lt;/p&gt;
&lt;p&gt;The incidence of multiple BCC lesions was 161.5 per 100,000 person-years, and 85.9% developed their second lesion within five years after the first.&lt;/p&gt;
&lt;p&gt;In a multivariate analysis that adjusted for factors such as sex, hair color, and lesion histologic subtype, older age at the time of first BCC was associated with a lower risk for developing multiple lesions, with a hazard ratio of 0.58 (95% CI 0.47 to 0.71) for those who were 75 or older at the time of their index lesion.&lt;/p&gt;
&lt;p&gt;The investigators acknowledged that this finding might be explained in part by a shorter mean follow-up time  --  6.66 years  --  among the oldest patients, compared with 10.36 years in those ages 65 to 75, and 10.70 years for those under age 65.&lt;/p&gt;
&lt;p&gt;&quot;However, this theory does not clarify the decreased risk of developing multiple lesions in the 65.0 to 74.99 year age group,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;The hazard ratio for that intermediate age group was 0.65 (95% CI 0.53 to 0.81).&lt;/p&gt;
&lt;p&gt;After adjusting for confounders, the only lesion factor associated with high risk was site of the index lesion being on an upper extremity (HR 1.49, 95% CI 1.02 to 2.15).&lt;/p&gt;
&lt;p&gt;The study findings, that patients who were younger at the time of first diagnosis, had higher socioeconomic status, red hair at a younger age, and whose first BCC was located on an upper extremity, could allow physicians to focus most closely on these patients for more rigorous follow-up.&lt;/p&gt;
&lt;p&gt;In the Netherlands and the U.S., the usual recommendation is for annual skin examination for five years.&lt;/p&gt;
&lt;p&gt;The incidence of BCC is steadily rising  --  around one million Americans develop a BCC each year.&lt;/p&gt;
&lt;p&gt;Early-stage lesions can be easily removed and the cure rate is high with early detection and treatment. Although not the most deadly skin cancer (that distinction belongs to melanoma) the high incidence and risk of multiple lesions make it the fifth most expensive cancer to treat in the U.S., according to the authors.&lt;/p&gt;
&lt;p&gt;&quot;The risk profiles associated with incident and multiple lesions differed; this information requires physicians to alter their risk assessment after a first lesion has been diagnosed,&quot; they concluded.&lt;/p&gt;
&lt;p&gt;Given the aging of the population, the authors called for further research in this area to help limit costs for follow-up in this large population.&lt;/p&gt;
&lt;p&gt;A limitation of the study was the lack of information about ultraviolet light exposure early in life.&lt;/p&gt;
&lt;p&gt;And, since the most study participants were Dutch females, white, and over age 55, the findings may not be generalizable to people of different age, ethnicity, skin type, or location.&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 declared no financial conflicts.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3058"
                     title="Cell Therapy Tops Foot Ulcer Healing (CME/CE)"
                     score="0.001"
                     href="http://www.medpagetoday.com/Endocrinology/Diabetes/tb/21724?impressionId=1283457933563"
                     
      &lt;p&gt;Engineered skin significantly improved healing of diabetic foot ulcers compared with other advanced biologic therapies, according to an analysis of a larger wound care database.&lt;/p&gt;
&lt;p&gt;When used as the initial advanced biologic therapy, engineered skin  --  or bilayered living cell therapy (Apligraf)  --  reduced the time to wound healing by 31% compared with topical recombinant growth factor (becaplermin, Regranex) and by 40% compared with platelet releasate (Procuren).&lt;/p&gt;
&lt;p&gt;The data also showed that earlier initiation of advanced biologic therapy increased the chances of early healing. However, the most effective therapy often was delayed well beyond the recommended 28 days.&lt;/p&gt;
&lt;p&gt;&quot;Overall, we found that treatment with advanced biological therapy for nonhealing wounds occurred by day 28, consistent with the Wound Healing Society guidelines,&quot; Robert S. Kirsner, MD, PhD, of the University of Miami, and co-authors wrote in the August issue of &lt;em&gt;Archives of Dermatology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;However, the median time to use of bilayered living cell therapy was six weeks, compared with four weeks for platelet releasate and three weeks for recombinant growth factor therapy. Furthermore, 25% of wounds treated with bilayered living cell therapy were not treated until after 24 weeks.&quot;&lt;/p&gt;
&lt;p&gt;The reason for the delay is unclear but could involve the higher cost of engineered skin, they added.&lt;/p&gt;
&lt;p&gt;As many as 15% of diabetic patients develop foot ulcers, which are a leading cause of nontraumatic amputation in the U.S. Beyond the associated morbidity, amputation involves direct costs ranging as high as $60,000, the authors noted.&lt;/p&gt;
&lt;p&gt;Improved and more rapid healing of diabetic foot ulcers reduces the risk of amputation. Several randomized clinical trials have shown that using advanced biologic therapy in combination with standard treatment (off-loading, debridement, and restoration of skin perfusion) improves healing of diabetic foot ulcers compared with standard therapy alone, the authors continued.&lt;/p&gt;
&lt;p&gt;To assess current practices regarding using of advanced biologic therapies, investigators queried the Curative Health Services database, a validated repository for data related to wound care. They identified 2,517 patients with diabetic foot ulcers, all treated with advanced biologic therapy: &lt;ul&gt; &lt;li&gt;1,892 patients treated with recombinant growth factor therapy&lt;/li&gt; &lt;li&gt;446 treated with bilayered living cell therapy&lt;/li&gt; &lt;li&gt;125 treated with platelet releasate&lt;/li&gt; &lt;li&gt;54 treated with bilayered living cell therapy after initial treatment with one of the other advanced therapies&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Overall, the time from first visit to initiation of treatment with advanced biologic therapy averaged 28 days, including 25% of patients who started therapy by day eight. Three-fourths of patients had received advanced biologic therapy by day 60.&lt;/p&gt;
&lt;p&gt;Time to treatment averaged 23 days with becaplermin, 28 days with platelet releasate, and 43 days with bilayered living cell therapy (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001). Patients treated with becaplermin had significantly smaller median wound area (141 mm&lt;sup&gt;2&lt;/sup&gt;), compared with 311 mm&lt;sup&gt;2&lt;/sup&gt; for bilayered living cell therapy, 329 mm&lt;sup&gt;2&lt;/sup&gt; for platelet releasate, and 367 mm&lt;sup&gt;2&lt;/sup&gt; for combination advanced biologic therapy (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001). Patients treated with platelet releasate or more than one advanced biologic therapy had deeper wounds, 3 mm versus 2 mm for the other groups (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Longer time to healing after initial use of advanced biologic therapy was associated with larger wound area (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001), more severe wound grade (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001), longer duration prior to first visit (&lt;em&gt;P&lt;/em&gt;=0.003), and longer time from first visit to use of advanced biologic therapy (&lt;em&gt;P&lt;/em&gt;=0.001).&lt;/p&gt;
&lt;p&gt;The median time from first use of advanced biologic therapy to healing or last observation was 100 days. In a fully adjusted analysis, time to healing was significantly shorter with bilayered living cell therapy (84 days) compared with 100 days for becaplermin (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001), 133 days for platelet releasate (&lt;em&gt;P&lt;/em&gt;=0.01), and 175 days for use of bilayered living cell therapy after another advanced biologic therapy (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Acknowledging cost as a factor in the delay in using engineered skin, the authors noted that &quot;several studies have found that use of advanced biological therapies, in fact, does reduce costs.&quot;&lt;/p&gt;
&lt;p&gt;The authors cited several potential limitations of the study: its retrospective nature, lack of data on potential confounding factors, uncertainty about the rigorous nature of data collection, limited review of data quality, and potential confounding by the relationship between healing status and choice of therapy.&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 in part by Organogenesis.&lt;/p&gt;&lt;p&gt;Kirsner reported that he had no relevant disclosures. Co-author Laure Stasik was employed by Diversified Clinical Services during the study and currently is an employee of Organogenesis.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3044"
                     title="Psoriasis Phototherapy Increases Vitamin D, Too (CME/CE)"
                     score="0"
                     href="http://www.medpagetoday.com/Dermatology/Psoriasis/tb/21716?impressionId=1283457933563"
                     
      In patients with psoriasis, narrow-band ultraviolet-B light increased serum vitamin D levels while clearing the condition, researchers said.&lt;br&gt;
&lt;br&gt;In a prospective cohort study in Ireland, the median level of serum 25-hydroxyvitamin D [25(OH)D] had more than doubled at the end of successful phototherapy, compared with no change among untreated controls, according to Caitriona Ryan, MBBCh, of Baylor Research Institute in Dallas, and colleagues.&lt;br&gt;
&lt;br&gt;But the two changes  --  clearance of psoriasis and increased vitamin D  --  were not correlated, suggesting that any causal link is more indirect, the researchers wrote in the August issue of &lt;em&gt;Archives of Dermatology.&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;One possible explanation, indeed, is that the two changes are &quot;contemporaneous, but unrelated, consequences&quot; of the phototherapy, they wrote. But it is also possible, they contended, that the light increases production within the skin of other forms of the vitamin, such as calcitriol [1,25(OH)&lt;sub&gt;2&lt;/sub&gt;D].&lt;/p&gt;
&lt;p&gt;Psoriasis affects up to 3% of the population and abnormalities in vitamin D metabolism may be partly responsible. People get most of their vitamin D from skin production following exposure to solar ultraviolet-B, but less than 15% comes from dietary sources, Ryan (who was at St. Vincent&apos;s University Hospital in Dublin when the study was conducted) and colleagues wrote.&lt;/p&gt;
&lt;p&gt;Vitamin D deficiency is common in countries such as Ireland, where sun exposure is limited, especially in the winter. To examine the link between psoriasis and vitamin D, the researchers enrolled 30 consecutive patients and treated them with narrow-band ultraviolet-B  --  in wavelengths of 311 to 313 nanometers  --  three times a week until their condition cleared.&lt;/p&gt;
&lt;p&gt;Controls were psoriasis patients who had not had phototherapy within the previous six months. The study was conducted from late October 2008 to early February 2009 to control for seasonal variation in serum 25(OH)D levels.&lt;/p&gt;
&lt;p&gt;At baseline, the median psoriasis activity and severity index was 7.1 in the treatment group, which was significantly higher (at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) than the 3.6 median seen in the control group.&lt;/p&gt;
&lt;p&gt;At the same time, the treatment group had a higher median serum 25(OH)D level of 23 nanograms per milliliter, compared with 13 for the controls, a difference that was also significant at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001.&lt;/p&gt;
&lt;p&gt;A level of less than 20 nanograms per milliliter is regarded as vitamin D insufficiency, the researchers noted, so that the findings highlight low levels of vitamin D among Irish psoriasis patients.&lt;/p&gt;
&lt;p&gt;After treatment, the researchers found: &lt;ul&gt; &lt;li&gt;Levels of serum 25(OH)D increased significantly (at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) among the treated patients, to a median of 59 nanograms per milliliter, compared with no change in the controls. &lt;/li&gt; &lt;li&gt;The change in serum 25(OH)D levels correlated with the number of exposures to the ultraviolet-B light (at r=0.61 and &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) and cumulative dose (at r=0.47 and &lt;em&gt;P&lt;/em&gt;=0.01), but not with treatment response. &lt;/li&gt; &lt;li&gt;At the end of the study, all patients in the treatment group were vitamin D sufficient, but 75% of the controls still had serum 25(OH)D levels of less than 20 nanograms per milliliter.&lt;/li&gt; &lt;li&gt;In a multiple regression model, prior phototherapy was the sole predictor of baseline serum 25(OH)D levels while the number of exposures of to ultraviolet-B light during treatment predicted change in serum 25(OH)D level.&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Because the lack of association with response  --  those who needed more exposures to clear their condition had significantly higher serum 25(OH)D levels at the end of treatment  --  &quot;we cannot conclude, therefore, that narrowband UV-B mediates its therapeutic effects by increasing vitamin D levels,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;Nonetheless, the study &quot;provides further insight into the role of vitamin D specific to patients with psoriasis,&quot; argued Pranita Vemulapalli, BS, and Henry Lim, MD, both of the Henry Ford Medical Center in Detroit.&lt;/p&gt;
&lt;p&gt;In an accompanying editorial, they said that although the study could not establish a causal link, &quot;it did highlight the prevalence of hypovitaminosis D in the population of patients with psoriasis in northern latitudes.&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 report external support for the study.&lt;/p&gt;&lt;p&gt;Ryan reported financial links with Abbott Pharmaceuticals and Galderma. Other authors reported links with Janssen-Cilag, Wyeth, Schering Plough, and Merck-Serono.&lt;/p&gt;&lt;p&gt;Lim reported financial links with La Roche-Posay/L&apos;Oreal, Orfagen, and Dow Pharmaceutical Sciences.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
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