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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.eblue.org/?rss=yes"><title>Journal of the American Academy of Dermatology</title><description>Journal of the American Academy of Dermatology RSS feed: Current Issue. As the official publication of the American Academy of Dermatology, the Journal is dedicated to the clinical and continuing education 
needs of the entire dermatologic community and is internationally known as the leading journal in the field. Original, peer-reviewed 
articles cover clinical and investigative studies, treatments, new diagnostic techniques, and other topics relating to the prevention, 
diagnosis, and treatment of disorders of the skin. Included are CME articles based on the Core Curriculum of the American Academy of 
Dermatology. 
 
The  Journal  is ranked 3rd of 43 journals in the Dermatology category in the 2009 Journal Citation Reports®, 
published by Thomson Reuters, and has an Impact Factor of  4.081.

 The Journal of the American Academy of Dermatology  is also 
recommended for purchase in the Brandon-Hill study, Selected List of Books and Journals for the Small Medical Library.</description><link>http://www.eblue.org/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2009 American Academy of Dermatology, Inc. Published by Elsevier Inc All rights reserved. </dc:rights><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:issn>0190-9622</prism:issn><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:publicationDate>March 2010</prism:publicationDate><prism:copyright> © 2009 American Academy of Dermatology, Inc. Published by Elsevier Inc All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962209014492/abstract?rss=yes"/><rdf:li 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rdf:resource="http://www.eblue.org/article/PIIS019096221000071X/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.eblue.org/article/PIIS0190962209014492/abstract?rss=yes"><title>Treatment of cellulite: Part I. Pathophysiology</title><link>http://www.eblue.org/article/PIIS0190962209014492/abstract?rss=yes</link><description>Cellulite is a topographic skin change that is nearly ubiquitous in postpubertal women. Treatment remains elusive. The various treatments currently available are only partially or temporarily effective. Newer therapeutic modalities continue to evolve without much understanding of the complex nature of cellulite. The successful treatment of cellulite will ultimately depend upon our understanding of the pathophysiology of cellulite adipose tissue. Part I of this two-part series on cellulite reviews how the concept and perception of cellulite has evolved over time and its proposed etiologies. The article also focuses on the physiology of human adipose tissue, particularly regarding cellulite.Learning objectives: After completing this learning activity, participants should be able to differentiate adipocyte physiology between the cellulite-prone areas and other parts of the body, understand the spectrum of conventional and interventional treatment modalities available, including their modes of action and controversies that dominate and question their long-term efficacy based on published studies, and discuss newer horizons for the treatment of cellulite.</description><dc:title>Treatment of cellulite: Part I. Pathophysiology</dc:title><dc:creator>Misbah H. Khan, Frank Victor, Babar Rao, Neil S. Sadick</dc:creator><dc:identifier>10.1016/j.jaad.2009.10.042</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>361</prism:startingPage><prism:endingPage>370</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220901500X/abstract?rss=yes"><title>CME examination</title><link>http://www.eblue.org/article/PIIS019096220901500X/abstract?rss=yes</link><description></description><dc:title>CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2009.11.031</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>371</prism:startingPage><prism:endingPage>371</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209015072/abstract?rss=yes"><title>Answers to CME examination</title><link>http://www.eblue.org/article/PIIS0190962209015072/abstract?rss=yes</link><description></description><dc:title>Answers to CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2009.11.035</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>372</prism:startingPage><prism:endingPage>372</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000915/abstract?rss=yes"><title>Announcing a New Online E-Blue Feature</title><link>http://www.eblue.org/article/PIIS0190962210000915/abstract?rss=yes</link><description></description><dc:title>Announcing a New Online E-Blue Feature</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00091-5</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>372</prism:startingPage><prism:endingPage>372</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209014480/abstract?rss=yes"><title>Treatment of cellulite: Part II. Advances and controversies</title><link>http://www.eblue.org/article/PIIS0190962209014480/abstract?rss=yes</link><description>Treatments for localized adiposities range from topical creams to liposuction. Most treatments lack a substantial proof of efficacy. The unpredictable treatment outcome can be related to the fact that cellulite adipose tissue is physiologically and biochemically different from subcutaneous tissue found elsewhere in the body. Part II of this two-part series on cellulite reviews the various treatment options that are currently available for human adipose tissue including, but not limited to, cellulite. It also focuses on newer techniques that can be potentially useful in the future for the treatment of cellulite.Learning objectives: After completing this learning activity, participants should be able to understand the wide range of treatments available for localized adiposities including, but not limited to, cellulite-prone areas, know the differences in their mechanisms of action and be able to make the most appropriate decision for patient care, and discuss and understand newer treatments for cellulite that are still being investigated along with the physiologic and biochemical basis for their mechanisms of action.</description><dc:title>Treatment of cellulite: Part II. Advances and controversies</dc:title><dc:creator>Misbah H. Khan, Frank Victor, Babar Rao, Neil S. Sadick</dc:creator><dc:identifier>10.1016/j.jaad.2009.10.041</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>373</prism:startingPage><prism:endingPage>384</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209014972/abstract?rss=yes"><title>CME examination</title><link>http://www.eblue.org/article/PIIS0190962209014972/abstract?rss=yes</link><description></description><dc:title>CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2009.11.029</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>385</prism:startingPage><prism:endingPage>385</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209014984/abstract?rss=yes"><title>Answers to CME examination</title><link>http://www.eblue.org/article/PIIS0190962209014984/abstract?rss=yes</link><description></description><dc:title>Answers to CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2009.11.030</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>386</prism:startingPage><prism:endingPage>386</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000927/abstract?rss=yes"><title>American Board of Dermatology Examination Dates</title><link>http://www.eblue.org/article/PIIS0190962210000927/abstract?rss=yes</link><description></description><dc:title>American Board of Dermatology Examination Dates</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00092-7</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>386</prism:startingPage><prism:endingPage>386</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012110/abstract?rss=yes"><title>Hydroxychloroquine and lichen planopilaris: Efficacy and introduction of Lichen Planopilaris Activity Index scoring system</title><link>http://www.eblue.org/article/PIIS0190962209012110/abstract?rss=yes</link><description>Background: Lichen planopilaris (LPP) and its variant frontal fibrosing alopecia (FFA) are primary lymphocytic cicatricial alopecias for which there is no evidence-based therapy.Objective: We assessed the efficacy of hydroxychloroquine in active LPP and FFA using the LPP Activity Index (LPPAI), a numeric score that allows quantification of the symptoms and signs of the condition for statistical comparison. In addition, we determined with the LPPAI if any improvement (reduction) in the numeric score pretreatment and posttreatment reached statistical significance.Methods: This was a retrospective, single-center chart review of 40 adult patients with LPP, FFA, or both who were treated with hydroxychloroquine for up to 12 months from 2004 to 2007 at the University of California, San Francisco Hair Center. Symptoms, signs, activity, and spreading were scored at each visit in the standardized cicatricial alopecia flow chart. A numeric score was assigned to these markers of disease activity and a numeric score was calculated at each visit.Results: There was significant reduction (P &lt; .001) in the LPPAI at both 6 and 12 months. After 6 months, 69% had improved (reduced) symptoms and signs. At 12 months, 83% had improvement (reduction) in symptoms and signs.Limitations: Retrospective analysis and uncontrolled study are limitations.Conclusions: Hydroxychloroquine is effective in decreasing symptoms and signs in LPP and FFA as shown by significant reduction in the LPPAI in 69% and 83% of patients after 6 and 12 months of treatment, respectively.</description><dc:title>Hydroxychloroquine and lichen planopilaris: Efficacy and introduction of Lichen Planopilaris Activity Index scoring system</dc:title><dc:creator>Charles Chiang, Deborah Sah, Bryan K. Cho, Blanca E. Ochoa, Vera H. Price</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.054</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-01-11</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-01-11</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>387</prism:startingPage><prism:endingPage>392</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006057/abstract?rss=yes"><title>Efficacy and safety of mycophenolate mofetil for lichen planopilaris</title><link>http://www.eblue.org/article/PIIS0190962209006057/abstract?rss=yes</link><description>Background: Lichen planopilaris (LPP) is a chronic inflammatory disorder that causes permanent scalp hair loss and significant patient discomfort.Objectives: We sought to determine the efficacy and safety of mycophenolate mofetil (MMF) for treatment of LPP in patients who had failed prior topical, intralesional, or oral anti-inflammatory medications such as hydroxychloroquine or cyclosporine.Methods: We conducted a retrospective chart review of 16 adult patients with LPP treated with at least 6 months of MMF in an open-label, single-center study from 2003 to 2007. Subjective and objective end points were quantified using the LPP Activity Index (LPPAI) and scores before and after treatment were assessed using a paired t test. Adverse events were monitored.Results: Patients who completed treatment with MMF had significantly decreased signs and symptoms of active LPP despite having failed multiple prior therapies (P &lt; .005). Five of 12 patients were complete responders (LPPAI score decreased&gt;85%), 5 of 12 patients were partial responders (LPPAI score decreased 25%-85%), and two of 12 patients were treatment failures (LPPAI score decreased&lt;25%). Four patients withdrew from the trial because of adverse events.Limitations: Retrospective analysis and small sample size were limitations.Conclusions: MMF was effective at reducing the signs and symptoms of active LPP in 83% of patients (10 of 12) who had failed multiple prior treatments after at least 6 months of treatment.</description><dc:title>Efficacy and safety of mycophenolate mofetil for lichen planopilaris</dc:title><dc:creator>Bryan K. Cho, Deborah Sah, Jennifer Chwalek, Ingrid Roseborough, Blanca Ochoa, Charles Chiang, Vera H. Price</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.018</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-01-11</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-01-11</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>393</prism:startingPage><prism:endingPage>397</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209013565/abstract?rss=yes"><title>Commentary: Treatment of lichen planopilaris: Some progress, but a long way to go</title><link>http://www.eblue.org/article/PIIS0190962209013565/abstract?rss=yes</link><description>See related articles on pages 387 and 393   For both patients and clinicians, lichen planopilaris (LPP) is a very challenging disease. Clinically and histologically, we observe active inflammation and disease progression, but our safe and simple anti-inflammatory medications often prove to be woefully inadequate. After topical and intralesional corticosteroids have been tried without good disease control, what are we to do?</description><dc:title>Commentary: Treatment of lichen planopilaris: Some progress, but a long way to go</dc:title><dc:creator>Leonard C. Sperling, Jennifer V. Nguyen</dc:creator><dc:identifier>10.1016/j.jaad.2009.10.025</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-01-11</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-01-11</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>398</prism:startingPage><prism:endingPage>401</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000939/abstract?rss=yes"><title>Change of Address</title><link>http://www.eblue.org/article/PIIS0190962210000939/abstract?rss=yes</link><description></description><dc:title>Change of Address</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00093-9</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>401</prism:startingPage><prism:endingPage>401</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209009360/abstract?rss=yes"><title>‘Relaxers’ damage hair: Evidence from amino acid analysis</title><link>http://www.eblue.org/article/PIIS0190962209009360/abstract?rss=yes</link><description>Background: ‘Relaxers’ are used by more than two thirds of African females to straighten hair, with easy grooming and increased length often cited as reasons. A recent study reported relaxed hair lengths much shorter than expected, suggesting increased fragility; the potential for scalp inflammation and scarring alopecia remains unclear.Objective: To investigate the biochemical effects of ‘relaxers’ on hair.Methods: With informed consent, included participants represented 3 groups: natural hair, asymptomatic relaxed hair, and symptomatic (brittle) relaxed hair. Biochemical analysis was performed by using a Biochrom 30 amino acid analyzer. Differences in amino acid levels were assessed using either Wilcoxon rank sum test or matched-pairs signed-rank test.Results: There was a decrease in cystine, citrulline, and arginine; however, an increase in glutamine was found in all relaxed compared to natural hair. Cystine levels (milligram per gram amino acid nitrogen) were similar in natural proximal and distal hair: 14 mg/g (range, 4-15 mg/g) versus 14 mg/g (range, 12-15 mg/g); P = .139. In asymptomatic relaxed hair, cystine levels were higher in less frequently relaxed samples proximal to scalp: 7.5 mg/g (5.6-12) versus 3.3 mg/g (1.3-9.2); P = .005. Cystine levels in distal asymptomatic relaxed and symptomatic relaxed hair were similar to each other and to those in the genetic hair fragility disease trichothiodystrophy.Limitations: It was not possible to analyze lye and no-lye ‘relaxers’ separately.Conclusions: ‘Relaxers’ are associated with reduced cystine consistent with fragile damaged hair. A decrease in citrulline and glutamine has been associated with inflammation; prospective studies are needed to investigate whether or how ‘relaxers’ induce inflammation.</description><dc:title>‘Relaxers’ damage hair: Evidence from amino acid analysis</dc:title><dc:creator>Nonhlanhla P. Khumalo, Janet Stone, Freedom Gumedze, Emily McGrath, Mzudumile R. Ngwanya, David de Berker</dc:creator><dc:identifier>10.1016/j.jaad.2009.04.061</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>402</prism:startingPage><prism:endingPage>408</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209009359/abstract?rss=yes"><title>Commentary: Healthy hair and protein loss</title><link>http://www.eblue.org/article/PIIS0190962209009359/abstract?rss=yes</link><description>See related article on page 402   Hair is a complex protein-based fiber of significant value for the perception of human beauty. All ancient civilizations and modern societies appreciate the appearance of “healthy” hair, yet defining the chemical structure that correlates with the image of hair health has proved challenging for the cosmetic chemist. Khumalo et al investigated the effect of hair straightening on hair chemistry as compared to virgin black tightly curled hair.</description><dc:title>Commentary: Healthy hair and protein loss</dc:title><dc:creator>Zoe Diana Draelos</dc:creator><dc:identifier>10.1016/j.jaad.2009.07.020</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>409</prism:startingPage><prism:endingPage>410</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209011608/abstract?rss=yes"><title>Long-term follow-up of toenail onychomycosis caused by dermatophytes after successful treatment with systemic antifungal agents</title><link>http://www.eblue.org/article/PIIS0190962209011608/abstract?rss=yes</link><description>Background: Recurrences (relapse or reinfection) of onychomycosis are not uncommon, with percentages reported in various studies ranging from 10% to 53%.Objective: We sought to determine the prevalence of long-term recurrences of toenail onychomycosis caused by dermatophytes cured after systemic antifungal treatment with terbinafine (T) or itraconazole (I) and identify risk factors for recurrences.Methods: This 7-year prospective study, started in 2000 and ended in 2007, included 73 patients periodically followed after successful treatment of toenail onychomycosis using either T, 250 mg daily (59 patients), or I, 400 mg daily, for 1 week per month (14 patients). Patients were evaluated every 6 months, with clinical and mycological evaluations being performed.Results: Twelve of 73 patients (16.4%) developed a recurrence of onychomycosis a mean time of 36 months after successful treatment. These included 5 of the 14 patients (35.7%) who had taken I and 7 of the 59 (11.9%) who had taken T (P = .046).Limitations: The number of patients treated with T (59 patients) was more than that for I (14 patients).Conclusion: The administration of systemic T to treat the first episode of onychomycosis may provide better long-term success than I in those patients with a complete response. Other factors including the presence of predisposing factors, use of nail lacquer as a prophylactic treatment, and the dermatophyte strain isolated were not significantly related to relapse.</description><dc:title>Long-term follow-up of toenail onychomycosis caused by dermatophytes after successful treatment with systemic antifungal agents</dc:title><dc:creator>Bianca Maria Piraccini, Andrea Sisti, Antonella Tosti</dc:creator><dc:identifier>10.1016/j.jaad.2009.04.062</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>411</prism:startingPage><prism:endingPage>414</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209011451/abstract?rss=yes"><title>Commentary: The illusory tinea unguium cure</title><link>http://www.eblue.org/article/PIIS0190962209011451/abstract?rss=yes</link><description>See related article on page 411   Onychomycosis is a common disorder and makes up approximately half of the nail disorders and 30% of the dermatophytoses we see as dermatologists. In older individuals the prevalence is high and likely approaches 60% or more in those older than 70 years. During the 1990s, onychomycosis was “hot,” not in any small part because of the onychomycosis treatment battles between orally administered terbinafine and itraconazole. Since 1996, however, no new Food and Drug Administration–approved systemic drugs for onychomycosis have come to market. During this time, the use of griseofulvin for tinea unguium has greatly diminished because of the greater efficacy of terbinafine and itraconazole. Topical ciclopirox lacquer is the latest onychomycosis drug to be approved in the United States, but its efficacy in providing a complete cure as a monotherapy is unacceptably low. This situation is compounded as long-term follow-up of patients treated for tinea unguium has been lacking. Indeed, the article by Piraccini et al is a welcome addition to the literature.</description><dc:title>Commentary: The illusory tinea unguium cure</dc:title><dc:creator>C. Ralph Daniel, Nathaniel J. Jellinek</dc:creator><dc:identifier>10.1016/j.jaad.2009.09.001</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>415</prism:startingPage><prism:endingPage>417</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000940/abstract?rss=yes"><title>Volunteers Needed</title><link>http://www.eblue.org/article/PIIS0190962210000940/abstract?rss=yes</link><description></description><dc:title>Volunteers Needed</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00094-0</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>417</prism:startingPage><prism:endingPage>417</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209003569/abstract?rss=yes"><title>Folliculotropic mycosis fungoides: Clinicopathological features and outcome in a series of 20 cases</title><link>http://www.eblue.org/article/PIIS0190962209003569/abstract?rss=yes</link><description>Background: Folliculotropic mycosis fungoides (MF) is a rare variant of cutaneous T-cell lymphoma in which the neoplastic T lymphocytes display tropism for the follicular epithelium.Objectives: To better categorize this rare form of cutaneous T-cell lymphoma we evaluated the clinical, pathological, and immunophenotypic findings, and the response to therapy and course of the disease.Methods: Folliculotropic MF cases were selected from the registry of the Thematic Network of Cutaneous Lymphoma of Barcelona (Spain) from 1988 to 2007.Results: Twenty patients (11 male, 9 female) with a mean age of 54 years were included. Mean follow-up time was 43 months. The most common sites of involvement were the head and neck (80%), upper extremities, and thorax. Infiltrated plaques (55%), acneiform lesions (comedo-like and epidermal cysts) (45%), and follicular keratosis-pilaris–like lesions (45%) were the more prominent features. Histopathological findings included selective infiltration of the follicular epithelium by atypical lymphocytes in all cases. Mucinous degeneration of the follicular epithelium occurred in 60% of cases. Psoralen plus ultraviolet A therapy was the treatment of choice in the majority of patients, but these patients did not respond as well as patients with classic MF. Radiotherapy (local or total skin electron beam) was found to be the most effective treatment. A good response to bexarotene was seen in some patients.Limitation: This was a case series descriptive study.Conclusions: Folliculotropic MF is a rare but well-defined clinicopathological variant of MF. Although refractory to standard therapies used in classic MF, most of our patients showed only slow disease progression.</description><dc:title>Folliculotropic mycosis fungoides: Clinicopathological features and outcome in a series of 20 cases</dc:title><dc:creator>Cristina Muniesa, Teresa Estrach, Ramon M. Pujol, Fernando Gallardo, Pilar Garcia-Muret, Josefina Climent, Octavio Servitje</dc:creator><dc:identifier>10.1016/j.jaad.2009.03.014</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-01-18</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-01-18</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>418</prism:startingPage><prism:endingPage>426</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006860/abstract?rss=yes"><title>A randomized, double-blind, placebo-controlled, phase I study of MEDI-545, an anti–interferon-alfa monoclonal antibody, in subjects with chronic psoriasis</title><link>http://www.eblue.org/article/PIIS0190962209006860/abstract?rss=yes</link><description>Background: Interferon-alfa (IFN-α) has been implicated in the pathogenesis of psoriasis.Objective: To evaluate the safety profile of MEDI-545, a fully human anti–IFN-α monoclonal antibody and to explore its effect on the involvement of type I IFN-α activity in the maintenance of established plaque psoriasis.Methods: We conducted an 18-week, randomized, double-blind, placebo-controlled, dose-escalating study in 36 subjects with chronic plaque psoriasis. Subjects received one intravenous dose of MEDI-545 (0.3-30.0 mg/kg) or placebo. Study outcomes were safety profile, pharmacokinetics, immunogenicity, and clinical effects.Results: There was no difference in adverse events between MEDI-545 and placebo. Two serious adverse events were reported; one drug-related hypotensive infusion reaction occurred in one subject in the 30.0 mg/kg MEDI-545 dose group, causing discontinuation of study drug in that subject and study dismissal of the other subjects in the same cohort; and a myocardial infarction occurred in one subject in the 10 mg/kg MEDI-545 dose group, which was considered to be unrelated to treatment. MEDI-545 was nonimmunogenic, had a half-life of 21 days, showed no significant inhibition of the type I IFN gene signature, and had no clinical activity.Limitations: The study addressed only IFN-α and chronic psoriatic lesions.Conclusion: The safety profile of MEDI-545 supports further clinical development. IFN-α does not appear to be significantly involved in the maintenance of established plaque psoriasis.</description><dc:title>A randomized, double-blind, placebo-controlled, phase I study of MEDI-545, an anti–interferon-alfa monoclonal antibody, in subjects with chronic psoriasis</dc:title><dc:creator>Robert Bissonnette, Kim Papp, Catherine Maari, Yihong Yao, Gabriel Robbie, Wendy I. White, Chenxiong Le, Barbara White</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.042</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>427</prism:startingPage><prism:endingPage>436</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000952/abstract?rss=yes"><title>What's New Online?</title><link>http://www.eblue.org/article/PIIS0190962210000952/abstract?rss=yes</link><description></description><dc:title>What's New Online?</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00095-2</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>436</prism:startingPage><prism:endingPage>436</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007105/abstract?rss=yes"><title>Human eyelid meibomian glands and tarsal muscle are recognized by autoantibodies from patients affected by a new variant of endemic pemphigus foliaceus in El-Bagre, Colombia, South America</title><link>http://www.eblue.org/article/PIIS0190962209007105/abstract?rss=yes</link><description>Background: Previously, we described a new variant of endemic pemphigus foliaceus (EPF) in Colombia, South America (El Bagre-EPF).Objective: Continuing our characterization of this variant of EPF, we now focus on one of our previously reported clinical findings: the presence of ocular lesions. These ocular lesions are seen in patients having extensive skin involvement, as measured by the Lund and Browder scale, which is generally used for patients with skin burns.Methods: We specifically searched for evidence of autoreactivity to various eyelid structures in these patients and correlated our immunologic data with the clinical findings. We performed indirect immunofluorescence studies using normal-appearing human eyelid skin from routine blepharoplasties as substrate tissue. We tested sera from 12 patients with El Bagre-EPF and ocular lesions, 5 patients with sporadic (nonendemic) pemphigus foliaceus, and 20 healthy control subjects (10 from the El Bagre-EPF endemic area and 10 from nonendemic areas). We used fluorescein isothiocyanate conjugated goat antiserum to human total IgG/IgA/IgM as a secondary antibody. In addition, we used fluorescein isothiocyanate conjugated antibodies to human fibrinogen, albumin, IgG, IgE, C1q, and C3, Texas Red (Rockland Immunochemicals, Inc, Gilbertsville, PA), Alexa Fluor 555, or Alexa Fluor 594 (Invitrogen, Carlsbad, CA). Ki-67 (a cell proliferation marker) was used to determine the cell proliferation rate, and nuclear counterstaining was performed with either 4′, 6-diamidino-2-phenylindole or Topro III (Invitrogen, Carlsbad, CA).Results: We observed autoreactivity to multiple eyelid structures, including meibomian glands and tarsal muscle bundles at different levels, and some areas of the epidermis and the dermis close to the isthmus of the eyelids. Tarsal plate autoreactivity was seen in 10 of 12 of the El Bagre-EPF sera and in one control with pemphigus erythematosus. Furthermore, immunoprecipitation using an eyelid sample as a substrate with 1 mmol/L of sodium orthovanodate showed autoreactivity to several antigens, including some of possible lipid origin.Limitations: The main limitation of this study is the fact that the antigen or antigens remain unknown.Conclusion: We identified for the first time to our knowledge autoantibodies to meibomian glands and tarsal muscle in El Bagre-EPF. Our findings suggest that the autoantibodies to the ocular structures cause the clinical and histopathological findings in the ocular lesions in El Bagre-EPF.</description><dc:title>Human eyelid meibomian glands and tarsal muscle are recognized by autoantibodies from patients affected by a new variant of endemic pemphigus foliaceus in El-Bagre, Colombia, South America</dc:title><dc:creator>Ana Maria Abreu-Velez, Michael S. Howard, Takashi Hashimoto, Hans E. Grossniklaus</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.007</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-01-11</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-01-11</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>437</prism:startingPage><prism:endingPage>447</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209009621/abstract?rss=yes"><title>A randomized study of the efficacy and safety of injectable poly-L-lactic acid versus human-based collagen implant in the treatment of nasolabial fold wrinkles</title><link>http://www.eblue.org/article/PIIS0190962209009621/abstract?rss=yes</link><description>Background: Injectable poly-L-lactic acid (PLLA) is a synthetic, biodegradable, biocompatible polymer device.Objective: We sought to compare the efficacy and safety of injectable PLLA with human-derived collagen in treating nasolabial fold wrinkles.Methods: In this randomized, evaluator-blinded, parallel-group, multicenter study, subjects received injectable PLLA (n = 116) or collagen (n = 117) injections (1-4 visits, 3-week intervals). Wrinkle Assessment Scale scores were calculated at screening; posttreatment week 3; months 3, 6, 9, and 13 (injectable PLLA or collagen groups); and months 19 and 25 (injectable PLLA group). Safety data were obtained from subject interviews and case report forms.Results: Injectable PLLA significantly improved mean Wrinkle Assessment Scale scores (all time points, P &lt; .001). Improvements (up to 25 months after last treatment) were significantly greater (P &lt; .001) than with collagen for posttreatment months 3 to 13.Limitations: Mostly white women and subjects with Fitzpatrick skin types II and III were included.Conclusion: Injectable PLLA provides well-tolerated, effective, and long-lasting (up to 25 months) nasolabial fold wrinkle correction.</description><dc:title>A randomized study of the efficacy and safety of injectable poly-L-lactic acid versus human-based collagen implant in the treatment of nasolabial fold wrinkles</dc:title><dc:creator>Rhoda S. Narins, Leslie Baumann, Fredric S. Brandt, Steven Fagien, Scott Glazer, Nicholas J. Lowe, Gary D. Monheit, Marta I. Rendon, Rod J. Rohrich, Wm. Philip Werschler</dc:creator><dc:identifier>10.1016/j.jaad.2009.07.040</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Dermatologic Surgery</prism:section><prism:startingPage>448</prism:startingPage><prism:endingPage>462</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006963/abstract?rss=yes"><title>Epidermotropic Merkel cell carcinoma: A case series with histopathologic examination</title><link>http://www.eblue.org/article/PIIS0190962209006963/abstract?rss=yes</link><description>Background: Merkel cell carcinoma (MCC), an aggressive malignancy that has been increasing in incidence, rarely presents with an epidermotropic pattern.Objective: We conducted an immunohistochemical evaluation of 6 previously unpublished cases of epidermotropic MCC, focusing particularly on the staining characteristics of epithelial membrane antigen and cytokeratin-20 in the hope of providing insight into the mechanism of epidermotropism in MCC.Methods: This study is a retrospective evaluation using light microscopy and immunohistochemistry.Results: Forty cases of MCC with pathology at Rhode Island Hospital and the Miriam Hospital in Providence, RI, from 1983 through 2009 were reviewed. Following exclusion criteria, 6 patients (5 men, 1 woman) with a mean age of 82.5 years (range, 72-92) demonstrated epidermotropism. Three of 6 patients had MCC of the eyelid. In cases 1, 3, and 6, the perinuclear dot pattern observed with cytokeratin-20 in the epidermotropic MCC cells was less pronounced than the pattern observed in the dermis, and in all 6 of the tumors, the epidermal staining pattern observed with epithelial membrane antigen was not more or less prominent than the staining observed in the dermis.Limitations: The small total number of cases of epidermotropic MCC is a limitation.Conclusion: The data presented reinforce the differential diagnosis of tumors with an epidermotropic growth pattern and the importance of immunohistochemical staining in the histologic workup of such tumors: squamous cell carcinoma in situ, melanoma, mycosis fungoides, eccrine porocarcinoma, sebaceous carcinoma of the eyelid, mammary and extramammary Paget disease, MCC, and epidermotropic metastases. It is notable that 3 of 6 identified tumors were located on the eyelid; further study of epidermotropic MCC may shed more light on this finding, either as an unusual coincidence or a finding with unexplained significance.</description><dc:title>Epidermotropic Merkel cell carcinoma: A case series with histopathologic examination</dc:title><dc:creator>Mark D'Agostino, Christina Cinelli, Robert Willard, Jeffrey Hofmann, Nathaniel Jellinek, Leslie Robinson-Bostom</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.023</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Dermatopathology</prism:section><prism:startingPage>463</prism:startingPage><prism:endingPage>468</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007737/abstract?rss=yes"><title>The dermal-based borderline melanocytic tumor: A categorical approach</title><link>http://www.eblue.org/article/PIIS0190962209007737/abstract?rss=yes</link><description>Background: The borderline melanocytic tumor (BMT) is a morphologically and biologically indeterminate melanocytic proliferation manifesting worrisome architectural features and cytologic atypia exceeding that encountered in melanocytic nevi yet insufficient to warrant designation as melanoma. The criteria that define the BMT are not well defined nor is the concept widely recognized.Objective: The purpose of this study is to provide a practical framework for the approach to the dermal BMT.Methods: Thirty-two patients with BMTs extending into the reticular dermis and at a depth of 0.75 mm or more underwent local excision and sentinel lymph node biopsy between 2000 and 2006. Four categories of BMT were recognized: (1) nevoid BMT (BNM); (2) the atypical Spitz tumor (AST); (3) pigmented epithelioid melanocytoma (PEM); and (4) BMT arising in a deep penetrating nevus (B-DPN).Results: Four patients were in the BNM category (male/female ratio [M:F] = 1:3; mean age = 27 years, range = 15-36), 14 in the AST category (M:F = 7:7; mean age = 20.9, range = 3-58), 7 in the PEM category (M:F = 4:3; mean age = 23.5, range = 3-39), and 7 in the B-DPN category (M:F = 5:2; mean age = 22.3, range = 14-36). The percentages of patients with positive sentinel nodes in each category were 25% (1/4), 35% (5/14), 14% (1/7), and 57% (4/7), respectively. The average time of follow-up was approximately 4.2 years. One patient, a 36-year-old man, died of disease, while the others are alive and well. In the one death attributable to widespread metastatic disease, the lesion was initially interpreted as a deep penetrating nevus; however, retrospective review revealed features compatible with a B-DPN; the review was prompted by a recurrence that was morphologically compatible with a Clark level V malignant melanoma, reflecting clinical and morphologic progression.Limitations: The mean follow-up was less than 5 years. Molecular studies to further explore the biologic commonality with melanoma were not performed.Conclusion: The dermal variant of BMT is a tumor of younger adults and children that can be associated with lymph node disease and a potential for morphologic and biologic progression when inadequately treated.</description><dc:title>The dermal-based borderline melanocytic tumor: A categorical approach</dc:title><dc:creator>Cynthia M. Magro, A. Neil Crowson, Martin C. Mihm, Kapil Gupta, Michael J. Walker, Garron Solomon</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.042</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Dermatopathology</prism:section><prism:startingPage>469</prism:startingPage><prism:endingPage>479</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209005027/abstract?rss=yes"><title>X-linked ichthyosis: An oculocutaneous genodermatosis</title><link>http://www.eblue.org/article/PIIS0190962209005027/abstract?rss=yes</link><description>X-linked ichthyosis (XLI) is an X-linked recessive disorder of cutaneous keratinization with possible extracutaneous manifestations. It was first described as a distinct type of ichthyosis in 1965. XLI is caused by a deficiency in steroid sulfatase activity, which results in abnormal desquamation and a retention hyperkeratosis. XLI is usually evident during the first few weeks of life as polygonal, loosely adherent translucent scales in a generalized distribution that desquamate widely. These are quickly replaced by large, dark brown, tightly adherent scales occurring primarily symmetrically on the extensor surfaces and the side of the trunk. In addition, extracutaneous manifestations such as corneal opacities, cryptorchidism, and abnormalities related to contiguous gene syndromes may be observed. Diagnosis of XLI is usually made clinically, as the histopathology is nonspecific, but confirmation may be obtained through either biochemical or genetic analysis. Treatment should focus on cutaneous hydration, lubrication, and keratolysis and includes topical moisturizers and topical retinoids</description><dc:title>X-linked ichthyosis: An oculocutaneous genodermatosis</dc:title><dc:creator>Neil F. Fernandes, Camila K. Janniger, Robert A. Schwartz</dc:creator><dc:identifier>10.1016/j.jaad.2009.04.028</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-01-18</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-01-18</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>480</prism:startingPage><prism:endingPage>485</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209022117/abstract?rss=yes"><title>Hormone therapy for acne</title><link>http://www.eblue.org/article/PIIS0190962209022117/abstract?rss=yes</link><description>Dialogues in Dermatology, a monthly audio program from the American Academy of Dermatology, contains discussions between dermatologists on timely topics. Commentaries from Dialogues Editor-in-Chief Jacqueline M. Junkins-Hopkins, MD, are provided after each discussion as a topic summary and are provided here as a special service to readers of the Journal of the American Academy of Dermatology.</description><dc:title>Hormone therapy for acne</dc:title><dc:creator>Jacqueline M. Junkins-Hopkins</dc:creator><dc:identifier>10.1016/j.jaad.2009.12.002</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Dialogues in Dermatology</prism:section><prism:startingPage>486</prism:startingPage><prism:endingPage>488</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209005441/abstract?rss=yes"><title>Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature (CANDLE) syndrome</title><link>http://www.eblue.org/article/PIIS0190962209005441/abstract?rss=yes</link><description>Several syndromes manifest as recurrent daily fevers, skin lesions, and multisystem inflammation. We describe 4 patients with early-onset recurrent fevers, annular violaceous plaques, persistent violaceous eyelid swelling, low weight and height, lipodystrophy, hepatomegaly, and a range of visceral inflammatory manifestations. Laboratory abnormalities included chronic anemia, elevated acute-phase reactants, and raised liver enzymes. Histopathologic examination of lesional skin showed atypical mononuclear infiltrates of myeloid lineage and mature neutrophils. Our patients have a distinctive early-onset, chronic inflammatory condition with atypical or immature myeloid infiltrates in the skin. We propose the acronym CANDLE (chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature) syndrome for this newly described disorder, which is probably genetic in origin.</description><dc:title>Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature (CANDLE) syndrome</dc:title><dc:creator>Antonio Torrelo, Sapna Patel, Isabel Colmenero, Dolores Gurbindo, Francisco Lendínez, Angela Hernández, Juan Carlos López-Robledillo, Ali Dadban, Luis Requena, Amy S. Paller</dc:creator><dc:identifier>10.1016/j.jaad.2009.04.046</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case &amp; Review</prism:section><prism:startingPage>489</prism:startingPage><prism:endingPage>495</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209002722/abstract?rss=yes"><title>Leg ulcer and thigh telangiectasia associated with natural killer cell CD56– large granular lymphocyte leukemia in a patient with pseudo-Felty syndrome</title><link>http://www.eblue.org/article/PIIS0190962209002722/abstract?rss=yes</link><description>Clonal disorders of large granular lymphocytes (LGL) represent a rare spectrum of biologically distinct lymphoproliferative diseases originating either from mature T cells or natural killer cells. Both subtypes can manifest as indolent or aggressive disorders. We report a 77-year-old woman with rheumatoid arthritis, splenomegaly, and neutropenia who developed a painful leg ulcer refractory to treatment and thigh telangiectatic lesions. Because of the association of rheumatoid arthritis, splenomegaly, and nonspecific neutropenia, the diagnosis of Felty syndrome was initially made. Further investigation allowed the diagnosis of a CD56– natural killer–cell LGL leukemia and documented skin infiltration by natural killer cells. Cutaneous manifestations of LGL leukemia have been rarely reported. This report of pseudo-Felty syndrome with CD56– LGL leukemia, presenting with a leg ulcer and telangiectasia, enhances the role of dermatology in the diagnosis of hematologic neoplasia.</description><dc:title>Leg ulcer and thigh telangiectasia associated with natural killer cell CD56– large granular lymphocyte leukemia in a patient with pseudo-Felty syndrome</dc:title><dc:creator>Ana Filipa Duarte, Ana Nogueira, Alberto Mota, Teresa Baudrier, Áurea Canelhas, Jorge Cancela, Margarida Lima, Filomena Azevedo</dc:creator><dc:identifier>10.1016/j.jaad.2009.03.001</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2009-12-04</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2009-12-04</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>496</prism:startingPage><prism:endingPage>501</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220900382X/abstract?rss=yes"><title>An outbreak of Mycobacterium chelonae infections in tattoos</title><link>http://www.eblue.org/article/PIIS019096220900382X/abstract?rss=yes</link><description>Nontuberculous mycobacteria infections may occur after cutaneous procedures. Review of the medical records of patients who developed a rash within a tattoo revealed 6 patients with skin infections caused by Mycobacterium chelonae after receiving tattoos by one artist at a single tattoo establishment. The interval between tattoo placement and the skin findings was 1 to 2 weeks. All patients received alternate diagnoses before mycobacterial infection was identified. Skin findings included pink, red, or purple papules; papules with scale; pustules; granulomatous papules; and lichenoid papules and plaques. Histopathologic examination revealed granuloma, lymphohistiocytic infiltrate, or mixed inflammation; acid-fast bacilli stains produced negative results. Diagnosis was made by culture in 3 patients, histopathology in two patients, and clinical/epidemiologic association in one patient. The M chelonae isolates were clarithromycin susceptible, and the infections responded to macrolide antibiotics. Physicians should consider mycobacterial infections in patients with skin findings within a new tattoo.</description><dc:title>An outbreak of Mycobacterium chelonae infections in tattoos</dc:title><dc:creator>Lisa A. Drage, Phillip M. Ecker, Robert Orenstein, P. Kim Phillips, Randall S. Edson</dc:creator><dc:identifier>10.1016/j.jaad.2009.03.034</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2009-09-07</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2009-09-07</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>501</prism:startingPage><prism:endingPage>506</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209009979/abstract?rss=yes"><title>Grooming and central centrifugal cicatricial alopecia</title><link>http://www.eblue.org/article/PIIS0190962209009979/abstract?rss=yes</link><description>To the Editor: I read with interest both the review and recent study by Gathers et al and would like to make a few comments as follows:   The author's statements on the lack of epidemiologic data suggest that they may not be aware of two published population studies that examine these very questions.</description><dc:title>Grooming and central centrifugal cicatricial alopecia</dc:title><dc:creator>Nonhlanhla P. Khumalo</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.012</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>507</prism:startingPage><prism:endingPage>508</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209010597/abstract?rss=yes"><title>Goeckerman treatment: Neglected in the consensus approach for critically challenging case scenarios in moderate to severe psoriasis</title><link>http://www.eblue.org/article/PIIS0190962209010597/abstract?rss=yes</link><description>To the Editor: We note that Goeckerman treatment (ultraviolet light phototherapy plus crude coal tar) was considered as one of the top 10 options for managing moderate to severe psoriasis for only six (including three that concerned its use in pregnancy) of the 32 critically challenging case scenarios in the consensus statement recently published in the Journal. In contrast, at Mayo Clinic, Goeckerman treatment is one of our top considerations (and often the top choice) for managing the vast majority of scenarios described in this article. Goeckerman treatment has been well documented for decades to be extraordinarily effective, safe, and associated with long-lasting remission; it is also cost effective (current cost, approximately $10000-12000) and is associated with a low incidence of adverse effects. There are no absolute contraindications. As a skin-directed therapy, it is particularly useful in the described critically challenging case scenarios. Although topical tar and ultraviolet B light are both known carcinogens, the risk of developing nonmelanoma skin cancer has been documented to be low.</description><dc:title>Goeckerman treatment: Neglected in the consensus approach for critically challenging case scenarios in moderate to severe psoriasis</dc:title><dc:creator>Mark D.P. Davis, Marian T. McEvoy, Michael Camilleri, Alina G. Bridges, Lawrence E. Gibson, Rokea A. el-Azhary</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.027</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>508</prism:startingPage><prism:endingPage>508</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209010950/abstract?rss=yes"><title>Cutaneous leishmaniasis in Texas</title><link>http://www.eblue.org/article/PIIS0190962209010950/abstract?rss=yes</link><description>To the Editor: Wright et al documented nine cases of cutaneous leishmaniasis acquired in Texas between 2005 and 2007 and offered suggestions for the apparent movement of the disease into northeast Texas. Their statement, however, that all 30 previously reported cases were in south-central Texas is incorrect. McHugh et al documented one case in Brown County in Central Texas with a date of onset of June 1988 and another in the same county with a date of onset of 1992. One in Albany, Shackelford County, Texas—approximately 132 miles due west of the Dallas–Fort Worth metroplex—had a date of onset of November 1994 (this case was incorrectly reported in Fig 1 of Wright et al as occurring with the other two cases in Brown County, 70 miles to south). So there are some historic data indicating a northward trend in the distribution of human cases in Texas, almost as far north as the cases in the present report, by the mid-1990s.</description><dc:title>Cutaneous leishmaniasis in Texas</dc:title><dc:creator>Chad P. McHugh</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.034</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>508</prism:startingPage><prism:endingPage>510</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006732/abstract?rss=yes"><title>Dermatitis herpetiformis exacerbated by cornstarch</title><link>http://www.eblue.org/article/PIIS0190962209006732/abstract?rss=yes</link><description>To the Editor: Dermatitis herpetiformis (DH) is related to gluten sensitivity, especially to gliadin protein. Wheat, rye, and barley, but not corn or rice, contain gluten.   We report the cases of two patients with DH who described significant flares after ingestion of cornstarch. Both followed a strict gluten-free diet with good symptom control, only requiring occasional dapsone after unavoidable gluten ingestion.</description><dc:title>Dermatitis herpetiformis exacerbated by cornstarch</dc:title><dc:creator>Firas Al-Niaimi, Neil H. Cox, Susan Lewis-Jones</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.002</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>510</prism:startingPage><prism:endingPage>511</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006938/abstract?rss=yes"><title>Decrease of ultraviolet A light–induced “common deletion” in healthy volunteers after oral Polypodium leucotomos extract supplement in a randomized clinical trial</title><link>http://www.eblue.org/article/PIIS0190962209006938/abstract?rss=yes</link><description>To the Editor: Ultraviolet (UV) radiation causes sunburn, immunosuppression, pigmentary changes, photoaging, and skin cancer in a wavelength-dependent fashion. More than 95% of the incident UV radiation is ultraviolet A (UVA; 320-400 nm), which penetrates into the dermis. It induces DNA damage through the formation of reactive oxygen species (ROS), which are involved in oxidative base damage. ROS also induce matrix metalloproteinase (MMP) upregulation, which is partially responsible for skin photoaging.</description><dc:title>Decrease of ultraviolet A light–induced “common deletion” in healthy volunteers after oral Polypodium leucotomos extract supplement in a randomized clinical trial</dc:title><dc:creator>Adriana Villa, Martha H. Viera, Sadegh Amini, Ran Huo, Oliver Perez, Phillip Ruiz, Alexandra Amador, George Elgart, Brian Berman</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.045</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>511</prism:startingPage><prism:endingPage>513</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220900704X/abstract?rss=yes"><title>Interobserver accuracy of store and forward teledermatology for skin neoplasms</title><link>http://www.eblue.org/article/PIIS019096220900704X/abstract?rss=yes</link><description>To the Editor: Few studies have compared diagnostic accuracy rates between teledermatologists (TDs) based on the gold standard of histopathology, and none have reported accuracy rates (histopathology as standard) between clinic dermatologists (CDs) viewing the same patients as TDs nor accuracy (histopathology as standard) of management plans.</description><dc:title>Interobserver accuracy of store and forward teledermatology for skin neoplasms</dc:title><dc:creator>Erin M. Warshaw, Amy A. Gravely, Kimberly A. Bohjanen, Karen Chen, Peter K. Lee, Harold S. Rabinovitz, Robert H. Johr, David B. Nelson</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.015</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>513</prism:startingPage><prism:endingPage>516</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007075/abstract?rss=yes"><title>Goeckerman therapy versus biologics in the treatment of psoriasis</title><link>http://www.eblue.org/article/PIIS0190962209007075/abstract?rss=yes</link><description>To the Editor: Re: Goeckerman treatment for remission of psoriasis refractory to biologic therapy. The letter of Serrao and Davis raises some interesting points and questions. In this study they showed that 20 of 23 patients had greater than 80% clearance over the 3-week duration of Goeckerman therapy. Yet, it is interesting to note that only 3 of these subjects, “refractory to biologic therapy”, had previously received infliximab or adalimumab, agents expected to give greater than 80% clearance in the majority of patients. Thus this comparison and statement concerning “resistance to biologics” is certainly not warranted.</description><dc:title>Goeckerman therapy versus biologics in the treatment of psoriasis</dc:title><dc:creator>Alan Menter</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.003</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>516</prism:startingPage><prism:endingPage>517</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007129/abstract?rss=yes"><title>Hypnosis in refractory alopecia areata significantly improves depression, anxiety, and life quality but not hair regrowth</title><link>http://www.eblue.org/article/PIIS0190962209007129/abstract?rss=yes</link><description>To the Editor: Our preliminary results on the use of hypnosis in alopecia areata (AA), previously published in the JAAD, have suggested the possible efficacy of hypnosis in refractory AA forms. However, from the research finding of our latest study, another message emerges. In this prospective cohort study, a hypnotherapeutic approach was used without any other treatment, to compare the evolution of anxiety, depression, and health-related quality of life (HRQOL) of patients with AA that was refractory to conventional treatment, with control patients receiving only treatment for AA as usual. Only patients and controls presenting more than 30% hair loss with a minimal duration of 3 months were included. For ethical reasons, a nonrandomized controlled study protocol was selected.</description><dc:title>Hypnosis in refractory alopecia areata significantly improves depression, anxiety, and life quality but not hair regrowth</dc:title><dc:creator>Ria Willemsen, Patrick Haentjens, Diane Roseeuw, Johan Vanderlinden</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.029</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>517</prism:startingPage><prism:endingPage>518</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007130/abstract?rss=yes"><title>Dermatology inpatient consultations: A retrospective study</title><link>http://www.eblue.org/article/PIIS0190962209007130/abstract?rss=yes</link><description>To the Editor: Inpatient dermatology consultation remains an essential component of residency training; with the decline in direct admissions to dermatology services, dermatology inpatient care is provided more often in the consultative setting and can directly impact accurate diagnosis and management of patients. In 1994, Falanga et al reviewed 591 dermatology consults to a teaching hospital, concluding that common diseases may not be recognized or diagnosed correctly by non-dermatologists; misdiagnosis occurred in 78%, and two thirds resulted in treatment change. Nahass et al offered skin exams to medical inpatients; 35.9% of 231 had cutaneous findings, with one third of these directly related to systemic disease and/or reason for hospitalization. Recently Helms, Helms, and Brodell discussed the increasing need for dermatologists in the consultative role, the recognition of few published studies looking at such consultations, and the possible unmet need for dermatology consultations and mechanisms to provide this service.</description><dc:title>Dermatology inpatient consultations: A retrospective study</dc:title><dc:creator>Jacob Bauer, Michele Maroon</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.030</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>518</prism:startingPage><prism:endingPage>519</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007841/abstract?rss=yes"><title>Mineral make-up and its potential utility in patients with contact dermatitis</title><link>http://www.eblue.org/article/PIIS0190962209007841/abstract?rss=yes</link><description>To the Editor: Mineral make-up has become increasingly popular in recent years. While there is no legal definition, these products are typically loose powders. Marketed as containing mainly inert minerals, many claim to be “free of preservatives, talc, oil, fragrance, and other harmful chemicals” (http://bareescentuals.com/id/) or “specially formulated for sensitive skin” (http://www.physiciansformula.com/en-us/staticpage/mineralwear.html). In our contact dermatitis clinic, we have noted more patients using mineral make-up when they develop facial rashes.</description><dc:title>Mineral make-up and its potential utility in patients with contact dermatitis</dc:title><dc:creator>Ming Yang Bi, Rajani Katta</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.052</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>519</prism:startingPage><prism:endingPage>522</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209008342/abstract?rss=yes"><title>Where did current academic dermatologists train?</title><link>http://www.eblue.org/article/PIIS0190962209008342/abstract?rss=yes</link><description>To the Editor: There is a shortage of academic dermatologists in the United States. Although dermatology resident applicants have strong academic and research backgrounds, many lose interest in academic careers. We assessed how many academic dermatologists different residency programs produced.</description><dc:title>Where did current academic dermatologists train?</dc:title><dc:creator>Ali Alikhan, Dina Farshidi, Steven R. Feldman</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.071</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>522</prism:startingPage><prism:endingPage>523</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220900142X/abstract?rss=yes"><title>Xanthogranuloma on the penis of an adult: An unusual localization</title><link>http://www.eblue.org/article/PIIS019096220900142X/abstract?rss=yes</link><description>To the Editor: A 44-year-old man was referred to our department with a 1-month history of lesions on his glans penis. A clinical examination revealed two well defined, orange-yellow to skin-colored, dome-shaped, smooth, 5- to 7-mm asymptomatic papules (). General laboratory screening, including lipid levels, renal and liver function tests, and a complete blood count, were within normal limits. A biopsy specimen from one of the papules showed a dermal infiltrate composed of macrophages, neutrophils, lymphocytes, and fibroblasts, along with foam cells and Touton giant cells (). A diagnosis of xanthogranuloma (XG) was made. An ophthalmology examination revealed no abnormalities. Two months after the biopsy, the papules disappeared spontaneously and no obvious relapse has been noted.</description><dc:title>Xanthogranuloma on the penis of an adult: An unusual localization</dc:title><dc:creator>Verónica López, Inmaculada Molina, Carlos Monteagudo, Nuria Martí, Esperanza Jorda</dc:creator><dc:identifier>10.1016/j.jaad.2009.02.005</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>524</prism:startingPage><prism:endingPage>524</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209001431/abstract?rss=yes"><title>Concordance rate of alopecia areata in identical twins supports both genetic and environmental factors</title><link>http://www.eblue.org/article/PIIS0190962209001431/abstract?rss=yes</link><description>To the Editor: We previously reported that alopecia areata (AA), an autoimmune disease targeting the hair follicle causing hair loss, had a 55% concordance rate in monozygotic twins, suggesting both genetic and environmental triggers. Recently, we also reported a possible association between Epstein–Barr virus (EBV)-related mononucleosis and onset of AA in 12 young individuals. To further study the role of genes versus environment in the pathogenesis of AA, we examined concordance rates for AA and exposure to EBV by IgG serology in a new cohort of twins from the National Alopecia Areata Registry.</description><dc:title>Concordance rate of alopecia areata in identical twins supports both genetic and environmental factors</dc:title><dc:creator>Thomas A. Rodriguez, Kerri E. Fernandes, Kelly L. Dresser, Madeleine Duvic, National Alopecia Areata Registry</dc:creator><dc:identifier>10.1016/j.jaad.2009.02.006</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>525</prism:startingPage><prism:endingPage>527</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209002436/abstract?rss=yes"><title>Acanthosis nigricans in a patient with sarcoma of unknown origin</title><link>http://www.eblue.org/article/PIIS0190962209002436/abstract?rss=yes</link><description>To the Editor: A 66-year-old man presented with a 2-month history of a slowly enlarging right axillary lymph node. Four years earlier, symmetric papillomatosis and darkening of the axillae and neck had developed (). The patient did not have diabetes and had a history of melanoma excised from his back 17 years earlier. The node was resected (); a skin biopsy specimen showed acanthosis nigricans, with acanthosis, papillomatosis, hyperkeratosis, and increased dermal pigmentation (). Histologic () and immunohistochemical analyses of the axillary node were consistent only with an unspecified sarcoma. Melanoma was excluded by immunohistochemistry. Computed tomography scans revealed metastases in multiple lymph nodes, the liver, and the spleen; the primary tumor was not found.</description><dc:title>Acanthosis nigricans in a patient with sarcoma of unknown origin</dc:title><dc:creator>Kay Dietmar Brantsch, Matthias Moehrle</dc:creator><dc:identifier>10.1016/j.jaad.2009.02.010</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>527</prism:startingPage><prism:endingPage>528</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209002540/abstract?rss=yes"><title>Unilateral nevoid telangiectasia on the lower extremity of a pediatric patient</title><link>http://www.eblue.org/article/PIIS0190962209002540/abstract?rss=yes</link><description>To the Editor: Unilateral nevoid telangiectasia (UNT) is a vascular dermatosis of obscure etiology that is characterized by linearly arranged telangiectasias in a unilateral or Blaschkoid pattern. The disorder is frequently found in the upper extremities and/or shoulders. Its histopathology is characterized by dilated capillaries in the papillary dermis and mid-dermis.</description><dc:title>Unilateral nevoid telangiectasia on the lower extremity of a pediatric patient</dc:title><dc:creator>Tamihiro Kawakami, Satoko Kimura, Yoshinao Soma</dc:creator><dc:identifier>10.1016/j.jaad.2009.02.030</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>528</prism:startingPage><prism:endingPage>530</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220900259X/abstract?rss=yes"><title>Acral lymphomatoid papulosis</title><link>http://www.eblue.org/article/PIIS019096220900259X/abstract?rss=yes</link><description>To the Editor: A 31-year old healthy woman presented with a painful, 6-mm ulcerated subcutaneous nodule on the ventral surface of her left hand (). A similar lesion had developed at a different site on the left palm a few months previously. Histologic examination of the current lesion revealed acanthosis with focal epidermal and dermal necrosis extending into the reticular dermis. There was a dense, superficial and deep, perivascular, and band-like predominantly lymphocytic infiltrate with scattered, enlarged mononuclear cells characterized by hyperchromatic nuclei and prominent nucleoli (, A and B). The latter cells were reactive for CD30 by immunohistochemistry (, C), consistent with lymphomatoid papulosis. Over the next 2 years, the patient had recurrent episodes of similar lesions on the hands. The lesions were tender or painful, and if untreated would ulcerate and then resolve over a 6-week period. The lesions resulted in temporary postinflammatory hyperpigmentation that resolved within 4 to 8 weeks. Some lesions were treated with intralesional or topical corticosteroids, which would hasten resolution.</description><dc:title>Acral lymphomatoid papulosis</dc:title><dc:creator>Molly Yancovitz, Ruth F. Walters, Hideko Kamino, Lance H. Brown</dc:creator><dc:identifier>10.1016/j.jaad.2009.02.025</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>530</prism:startingPage><prism:endingPage>531</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209002618/abstract?rss=yes"><title>Cetuximab-induced hypertrichosis of the scalp and eyelashes</title><link>http://www.eblue.org/article/PIIS0190962209002618/abstract?rss=yes</link><description>To the Editor: Cetuximab is an epidermal growth factor receptor (EGFR)-inhibitor approved by the US Food and Drug Administration (FDA) and the European Medicines Agency (EMEA) for metastatic colorectal carcinoma and head and neck squamous cell carcinoma. More recently, a few authors have reported good responses with cetuximab in the treatment of recurrent squamous cell skin cancer in a palliative setting. The safety profile for these drugs is unique, with virtually no hematologic toxicity but frequent cutaneous side effects, which may cause serious discomfort and be disabling.</description><dc:title>Cetuximab-induced hypertrichosis of the scalp and eyelashes</dc:title><dc:creator>Sergio Vano-Galvan, Luis Ríos-Buceta, Dong-Lai Ma, Concepción Fernández-Chacón, Juan Carlos Viera, Pedro Jaén</dc:creator><dc:identifier>10.1016/j.jaad.2009.02.023</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>531</prism:startingPage><prism:endingPage>533</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209005301/abstract?rss=yes"><title>JAAD Grand Rounds quiz∗ Scalp abscesses, fluctuant nodules, and patchy alopecia in an African American male</title><link>http://www.eblue.org/article/PIIS0190962209005301/abstract?rss=yes</link><description>Learning objectives: At the conclusion of this learning activity, physician participants should be able to assess their own diagnostic and patient management skills and use the results of this exercise to help determine personal learning needs that can be addressed through subsequent CME involvement. Instructions for claiming CME credit appear in the front advertising section. See last page of Contents for page number.Instructions: In answering each question, refer to the specific directions provided. Because it is often necessary to provide information occurring later in a series that give away answers to earlier questions, please answer the questions in each series in sequence.</description><dc:title>JAAD Grand Rounds quiz∗ Scalp abscesses, fluctuant nodules, and patchy alopecia in an African American male</dc:title><dc:creator>Scott Paviol, Jennie T. Clarke</dc:creator><dc:identifier>10.1016/j.jaad.2009.04.042</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>JAAD Grand Rounds</prism:section><prism:startingPage>534</prism:startingPage><prism:endingPage>536</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209005295/abstract?rss=yes"><title>Patchy alopecia following chemotherapy</title><link>http://www.eblue.org/article/PIIS0190962209005295/abstract?rss=yes</link><description>A 57-year-old white female presented with small, scattered patches of alopecia. She had a history of metastatic ductal breast cancer, and 2 months before her visit had finished three cycles of adriamycin and cyclophosphamide followed by three cycles of docetaxol and cyclophosphamide. Her current medications included anastrazole and omeprazole. She denied any areas of alopecia before treatment, and she lost all of her hair during chemotherapy. Following chemotherapy, she noticed that some areas of her scalp remained bald. She denied pruritus, pain, and flaking. She had not attempted to treat the condition. She denied any personal or family history of autoimmune disorders. Her review of systems was negative. A physical examination revealed many scattered, 1- to 2-cm, white, atrophic patches of alopecia (). A biopsy specimen was taken and anticytokeratin (CAM 5.2) staining was performed ( ).</description><dc:title>Patchy alopecia following chemotherapy</dc:title><dc:creator>Joslyn S. Kirby, Mahsa Tehrani, Michael D. Ioffreda</dc:creator><dc:identifier>10.1016/j.jaad.2009.04.043</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>JAAD Grand Rounds</prism:section><prism:startingPage>536</prism:startingPage><prism:endingPage>538</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220900663X/abstract?rss=yes"><title>Linear scalp plaques</title><link>http://www.eblue.org/article/PIIS019096220900663X/abstract?rss=yes</link><description>An 88-year-old white man presented to our department for the evaluation of multiple scalp lesions of relatively recent onset. There was no pertinent family history. He denied trauma to the area, ever having been diagnosed with an infection of the area caused by herpes simplex virus (HSV) or varicella zoster virus (VZV), and ever having received radiation therapy. The physical examination revealed multiple indurated, red, and slightly violaceous plaques and nodules on the scalp in a strikingly linear pattern. The collection of tumors covered a 9 cm × 3 cm area on the right forehead, frontal scalp, and parietal scalp (). There was no clinical lymphadenopathy. Review by a dermatopathologist yielded a diagnosis of malignant epithelioid neoplasm, and additional special stains were performed. Immunohistochemical staining showed strong staining with CD31 and vimentin and negative staining with CD68, S-100 protein, HMB45, CK7, CK20, CD43, pancytokeratin, CK5/6, CD20, CD34, chromogranin, synaptophysin, mucicarmine, and carcinoembryonic antigen stains.</description><dc:title>Linear scalp plaques</dc:title><dc:creator>Mario L. Pinoli, Nathan W. Hanson, Michael J. Wells, Cloyce L. Stetson</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.036</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>JAAD Grand Rounds</prism:section><prism:startingPage>538</prism:startingPage><prism:endingPage>539</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000721/abstract?rss=yes"><title>Dermatology Calendar</title><link>http://www.eblue.org/article/PIIS0190962210000721/abstract?rss=yes</link><description></description><dc:title>Dermatology Calendar</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00072-1</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>540</prism:startingPage><prism:endingPage>540</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007282/abstract?rss=yes"><title>Hypopigmented macules</title><link>http://www.eblue.org/article/PIIS0190962209007282/abstract?rss=yes</link><description>A 15-year-old healthy black female presented with persistent white spots that had been present since the patient was 4 years of age. Her father had a similar condition. The physical examination revealed scattered circinate hypopigmented to pink macules across her forehead (), neck, and back (). She also had unrelated hyperpigmented scars from a previous chicken pox infection. Shave biopsy specimens revealed coarse hypergranulosis and enlarged keratinocytes with pale blue cytoplasm ().</description><dc:title>Hypopigmented macules</dc:title><dc:creator>Eric W. Hossler, Nektarios I. Lountzis, Dana R. Black</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.041</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Images in Dermatology</prism:section><prism:startingPage>e13</prism:startingPage><prism:endingPage>e14</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962208013157/abstract?rss=yes"><title>Iotaderma #194</title><link>http://www.eblue.org/article/PIIS0190962208013157/abstract?rss=yes</link><description></description><dc:title>Iotaderma #194</dc:title><dc:creator>Robert I. Rudolph</dc:creator><dc:identifier>10.1016/j.jaad.2008.10.021</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e15</prism:startingPage><prism:endingPage>e15</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962208011584/abstract?rss=yes"><title>February Iotaderma (#193)</title><link>http://www.eblue.org/article/PIIS0190962208011584/abstract?rss=yes</link><description></description><dc:title>February Iotaderma (#193)</dc:title><dc:creator>Robert I. Rudolph</dc:creator><dc:identifier>10.1016/j.jaad.2008.09.004</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e15</prism:startingPage><prism:endingPage>e15</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000691/abstract?rss=yes"><title>Editorial Board</title><link>http://www.eblue.org/article/PIIS0190962210000691/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00069-1</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A2</prism:startingPage><prism:endingPage>A2</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096221000068X/abstract?rss=yes"><title>Table of Contents</title><link>http://www.eblue.org/article/PIIS019096221000068X/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00068-X</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A5</prism:startingPage><prism:endingPage>A5</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000708/abstract?rss=yes"><title>Information for Readers</title><link>http://www.eblue.org/article/PIIS0190962210000708/abstract?rss=yes</link><description></description><dc:title>Information for Readers</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00070-8</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A23</prism:startingPage><prism:endingPage>A24</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096221000071X/abstract?rss=yes"><title>Instructions for Category 1 CME Credit</title><link>http://www.eblue.org/article/PIIS019096221000071X/abstract?rss=yes</link><description></description><dc:title>Instructions for Category 1 CME Credit</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00071-X</dc:identifier><dc:source>Journal of the American Academy of Dermatology 62, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>62</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0190-9622(10)X0002-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A30</prism:startingPage><prism:endingPage>A30</prism:endingPage></item></rdf:RDF>