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    <title>AMA Publishing Group: Phototherapy Topic Collection</title>
    <link>http://pubs.jamanetwork.com/</link>
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    <language>en-us</language>
    <pubDate>Thu, 01 Nov 2012 00:00:00 GMT</pubDate>
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      <title>The IgG “Lupus-Band” Deposition Pattern of Pemphigus Erythematosus Association With the Desmoglein 1 Ectodomain as Revealed by 3 Cases  Lupus-Band Deposition in Pemphigus Erythematosus </title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1216972</link>
      <pubDate>Mon, 01 Oct 2012 00:00:00 GMT</pubDate>
      <author>Oktarina DM, Poot AM, Kramer D, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;&lt;div class="boxTitle"&gt;Background&lt;/div&gt;Pemphigus foliaceus is an autoimmune skin disease characterized by subcorneal blistering and IgG antibodies directed against desmoglein 1. In the skin, these antibodies deposit intraepidermally. On rare occasions, an additional “lupus band” of granular depositions of IgG and complement is seen along the epidermal basement membrane zone. This combined pattern has been connected with a variant of pemphigus foliaceus named pemphigus erythematosus.&lt;div class="boxTitle"&gt;Observations&lt;/div&gt;We describe 3 pemphigus foliaceus cases in which phototherapy was administered after a misdiagnosis of psoriasis. This treatment resulted in a flare of skin lesions. Direct immunofluorescence of skin biopsy specimens that were obtained several weeks later demonstrated intraepidermal and granular basement membrane zone depositions. The basement membrane zone depositions consisted of IgG, complement, and the ectodomain of desmoglein 1 and were located below the lamina densa.&lt;div class="boxTitle"&gt;Conclusions&lt;/div&gt;High doses of UV light are likely to induce the cleaving of the desmoglein 1 ectodomain. In patients with pemphigus foliaceus, the circulating anti–desmoglein 1 antibodies precipitate this cleaved-off ectodomain along the basement membrane zone, resulting in a lupus band–like appearance. In pemphigus erythematosus, a similar mechanism may be active, which might explain the lupus-band phenomenon.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">148</prism:volume>
      <prism:number xmlns:prism="prism">10</prism:number>
      <prism:startingPage xmlns:prism="prism">1173</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">1178</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/archdermatol.2012.1896</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1216972</guid>
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    <item>
      <title>Association Between Tumor Necrosis Factor Inhibitor Therapy and Myocardial Infarction Risk in Patients With Psoriasis TNF Inhibitor Therapy and MI Risk </title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1352160</link>
      <pubDate>Thu, 01 Nov 2012 00:00:00 GMT</pubDate>
      <author>Wu JJ, Poon KT, Channual JC, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;&lt;div class="boxTitle"&gt;Objective&lt;/div&gt;To assess whether patients with psoriasis treated with tumor necrosis factor (TNF) inhibitors have a decreased risk of myocardial infarction (MI) compared with those not treated with TNF inhibitors.&lt;div class="boxTitle"&gt;Design&lt;/div&gt;Retrospective cohort study.&lt;div class="boxTitle"&gt;Setting&lt;/div&gt;Kaiser Permanente Southern California health plan.&lt;div class="boxTitle"&gt;Patients&lt;/div&gt;Patients with at least 3 International Classification of Diseases, Ninth Revision, Clinical Modification, codes for psoriasis (696.1) or psoriatic arthritis (696.0) (without antecedent MI) between January 1, 2004, and November 30, 2010.&lt;div class="boxTitle"&gt;Main Outcome Measure&lt;/div&gt;Incident MI.&lt;div class="boxTitle"&gt;Results&lt;/div&gt;Of 8845 patients included, 1673 received a TNF inhibitor for at least 2 months (TNF inhibitor cohort), 2097 were TNF inhibitor naive and received other systemic agents or phototherapy (oral/phototherapy cohort), and 5075 were not treated with TNF inhibitors, other systemic therapies, or phototherapy (topical cohort). The median duration of follow-up was 4.3 years (interquartile range, 2.9, 5.5 years), and the median duration of TNF inhibitor therapy was 685 days (interquartile range, 215, 1312 days). After adjusting for MI risk factors, the TNF inhibitor cohort had a significantly lower hazard of MI compared with the topical cohort (adjusted hazard ratio, 0.50; 95% CI, 0.32-0.79). The incidence of MI in the TNF inhibitor, oral/phototherapy, and topical cohorts were 3.05, 3.85, and 6.73 per 1000 patient-years, respectively.&lt;div class="boxTitle"&gt;Conclusions&lt;/div&gt;Use of TNF inhibitors for psoriasis was associated with a significant reduction in MI risk and incident rate compared with treatment with topical agents. Use of TNF inhibitors for psoriasis was associated with a non–statistically significant lower MI incident rate compared with treatment with oral agents/phototherapy.&lt;/span&gt;</description>
      <prism:volume xmlns:prism="prism">148</prism:volume>
      <prism:number xmlns:prism="prism">11</prism:number>
      <prism:startingPage xmlns:prism="prism">1244</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">1250</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/archdermatol.2012.2502</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1352160</guid>
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    <item>
      <title>The Efficacy of Afamelanotide and Narrowband UV-B Phototherapy for Repigmentation of Vitiligo Afamelanotide and UV-B for Vitiligo Repigmentation </title>
      <link>http://pubs.jamanetwork.com/article.aspx?articleID=1377949</link>
      <pubDate>Mon, 15 Oct 2012 00:00:00 GMT</pubDate>
      <author>Grimes PE, Hamzavi I, Lebwohl j, et al. </author>
      <description>&lt;span class="paragraphSection"&gt;&lt;div class="boxTitle"&gt;Background&lt;/div&gt;Vitiligo is characterized by depigmented patches of skin due to loss of cutaneous melanocytes. Many recent studies have demonstrated defects in the melanocortin system in patients with vitiligo, including decreased circulating and lesional skin levels of α–melanocyte-stimulating hormone (α-MSH). Afamelanotide is a potent and longer-lasting synthetic analogue of naturally occurring α-MSH.&lt;div class="boxTitle"&gt;Observations&lt;/div&gt;We describe the preliminary results of 4 patients with generalized vitiligo who developed repigmentation using afamelanotide in combination with narrowband UV-B (NB–UV-B) phototherapy. Patients were treated 3 times weekly with NB–UV-B and starting in the second month received a series of 4 monthly implants containing 16 mg of afamelanotide. Afamelanotide induced faster and deeper repigmentation in each case. All patients experienced follicular and confluent areas of repigmentation within 2 days to 4 weeks after the initial implant, which progressed significantly throughout treatment. All patients experienced diffuse hyperpigmentation.&lt;div class="boxTitle"&gt;Conclusions&lt;/div&gt;We propose that afamelanotide represents a novel and potentially effective treatment for vitiligo. The combined therapy of NB–UV-B and afamelanotide appears to promote melanoblast differentiation, proliferation, and eumelanogenesis. Further studies are necessary to confirm these observations.&lt;/span&gt;</description>
      <prism:startingPage xmlns:prism="prism">1</prism:startingPage>
      <prism:endingPage xmlns:prism="prism">6</prism:endingPage>
      <prism:doi xmlns:prism="prism">10.1001/2013.jamadermatol.386</prism:doi>
      <guid>http://pubs.jamanetwork.com/article.aspx?articleID=1377949</guid>
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