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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> © 2010 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>63</prism:volume><prism:number>2</prism:number><prism:publicationDate>August 2010</prism:publicationDate><prism:copyright> © 2010 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/PIIS0190962210000198/abstract?rss=yes"/><rdf:li 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rdf:resource="http://www.eblue.org/article/PIIS0190962209014820/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962209014935/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962209021136/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962209023068/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962210002136/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962209002710/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962209001388/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962210007140/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962210007085/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962210007097/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962210007103/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962210007115/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.eblue.org/article/PIIS0190962210000198/abstract?rss=yes"><title>Photodynamic therapy for acne vulgaris: A critical review from basics to clinical practice: Part I. Acne vulgaris: When and why consider photodynamic therapy?</title><link>http://www.eblue.org/article/PIIS0190962210000198/abstract?rss=yes</link><description>The first-line treatments for acne vulgaris are conventional topical and/or oral medications. However, many patients have contraindications, only partial response, significant adverse effects, or recurrence. Light-based treatments and photodynamic therapy (PDT) using topical precursors of porphyrins are off-label alternative treatments for acne vulgaris, with their own advantages and disadvantages. To date, there is no consensus on PDT methodology and parameters. An understanding of pathophysiology of acne, light–tissue interactions, and PDT mechanisms of action is helpful whenever PDT is considered as an alternative treatment. In general, blue light alone improves acne because of its antiinflammatory effects. PDT using 5-aminolevulenic acid (ALA) or ALA derivatives induces transient antimicrobial and antiinflammatory effects. At high doses, red light PDT may induce inhibition or destruction of sebaceous glands, resulting in clinical improvement.Learning objectives: After completing this learning activity, participants should be able to compare different treatments of acne, recognize when photodynamic therapy may be a useful off-label treatment for acne vulgaris, and identify variables that may affect the efficacy of photodynamic therapy.</description><dc:title>Photodynamic therapy for acne vulgaris: A critical review from basics to clinical practice: Part I. Acne vulgaris: When and why consider photodynamic therapy?</dc:title><dc:creator>Fernanda H. Sakamoto, José Daniel Lopes, R. Rox Anderson</dc:creator><dc:identifier>10.1016/j.jaad.2009.09.056</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>183</prism:startingPage><prism:endingPage>193</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000241/abstract?rss=yes"><title>Answers to CME examination</title><link>http://www.eblue.org/article/PIIS0190962210000241/abstract?rss=yes</link><description></description><dc:title>Answers to CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2010.01.007</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>193</prism:startingPage><prism:endingPage>193</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096221000023X/abstract?rss=yes"><title>CME examination</title><link>http://www.eblue.org/article/PIIS019096221000023X/abstract?rss=yes</link><description></description><dc:title>CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2010.01.006</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>194</prism:startingPage><prism:endingPage>194</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000204/abstract?rss=yes"><title>Photodynamic therapy for acne vulgaris: A critical review from basics to clinical practice: Part II. Understanding parameters for acne treatment with photodynamic therapy</title><link>http://www.eblue.org/article/PIIS0190962210000204/abstract?rss=yes</link><description>Photodynamic therapy requires a photosensitizer, oxygen, and activating light. For acne, pilosebaceous units are “target” structures. Porphyrins are synthesized in vivo from 5-aminolevulinic acid (ALA), particularly in pilosebaceous units. Different photosensitizers and drug delivery methods have been reported for acne treatment. There are a variety of porphyrin precursors with different pharmacokinetic properties. Among them, ALA and methyl-ester of ALA (MAL) are available for possible off-label treatment of acne vulgaris. In addition, various light sources, light dosimetry, drug incubation time, and pre- and posttreatment care also change efficacy and side effects. None of these variables has been optimized for acne treatment, but a number of clinical trials provide helpful guidance. In this paper, we critically analyze clinical trials, case reports, and series of cases published through 2009.Learning objectives: After completing this learning activity, participants should be able to analyze photodynamic therapy using 5-aminolevulinic acid and its derivates for acne treatment, predict the effectiveness and outcomes of photodynamic therapy using different parameters and/or different porphyrin-related photosensitizers, and assess and manage the side effects of porphyrin-based photodynamic therapy for acne.</description><dc:title>Photodynamic therapy for acne vulgaris: A critical review from basics to clinical practice: Part II. Understanding parameters for acne treatment with photodynamic therapy</dc:title><dc:creator>Fernanda H. Sakamoto, Luis Torezan, R. Rox Anderson</dc:creator><dc:identifier>10.1016/j.jaad.2009.09.057</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>195</prism:startingPage><prism:endingPage>211</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000265/abstract?rss=yes"><title>Answers to CME examination</title><link>http://www.eblue.org/article/PIIS0190962210000265/abstract?rss=yes</link><description></description><dc:title>Answers to CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2010.01.009</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>211</prism:startingPage><prism:endingPage>211</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000253/abstract?rss=yes"><title>CME examination</title><link>http://www.eblue.org/article/PIIS0190962210000253/abstract?rss=yes</link><description></description><dc:title>CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2010.01.008</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>212</prism:startingPage><prism:endingPage>212</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012523/abstract?rss=yes"><title>Factors influencing pain intensity during topical photodynamic therapy of complete cosmetic units for actinic keratoses</title><link>http://www.eblue.org/article/PIIS0190962209012523/abstract?rss=yes</link><description>Background: Topical photodynamic therapy is a good treatment option for extensively photodamaged skin with multiple actinic keratoses. Pain is one of the major adverse effects during and after the treatment.Objective: We sought to determine the pain intensity and its influencing factors during the extensive photodynamic treatment of complete cosmetic units.Methods: In total, 104 patients with 411 treated fields were enrolled in this retrospective monocentric study. All patients had multiple actinic keratoses on the face, scalp, or back of hands and received an extensive treatment of the complete photodamaged area in our dermatologic outpatient department between February and May 2009. Pain was rated using a visual analog scale directly and 8 hours after photodynamic therapy.Results: Multifactorial analysis of the data shows that pain intensity is dependent on sex of the patient (P = .030) and location of the treated field (P &lt; .001). Visual analog scale scores were independent of the age and skin type of the patient. No significant difference in pain between the use of 5-amino-4-oxo-pentanoate (methylaminolevulinate) and 5-aminolevulinic acid was noticed. During treatment, mean visual analog scale scores ± SEM of the different locations were 2.5 ± 0.36 (hand), 3.6 ± 0.35 (occiput), 5.2 ± 0.19 (forehead), 5.9 ± 0.20 (cheeks), and 7.4 ± 0.48 (lips). Eight hours after treatment the mean pain ± SEM in all locations was reduced significantly (P &lt; .001) from 5.2 ± 0.14 to 3.0 ± 0.14. The rate of therapy interruptions showed a significant correlation (P = .044) with the location of the treated field. In all, 71% of the patients showed a good and 29% a poor clinical outcome.Limitations: Because of the retrospective study design not all factors that may influence pain (eg, protoporphyrin IX fluorescence) were recorded.Conclusion: These results show that pain intensity is dependent on the location of the treated field. Pain intensity is higher in male patients. After 8 hours pain decreases significantly.</description><dc:title>Factors influencing pain intensity during topical photodynamic therapy of complete cosmetic units for actinic keratoses</dc:title><dc:creator>Patrick Gholam, Katharina Denk, Tanja Sehr, Alexander Enk, Martin Hartmann</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.062</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-06-10</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-06-10</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>213</prism:startingPage><prism:endingPage>218</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210007322/abstract?rss=yes"><title>American Board of Dermatology Examination Dates</title><link>http://www.eblue.org/article/PIIS0190962210007322/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)00732-2</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>218</prism:startingPage><prism:endingPage>218</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012067/abstract?rss=yes"><title>Retrospective analysis of drug-induced hypersensitivity syndrome: A study of 27 patients</title><link>http://www.eblue.org/article/PIIS0190962209012067/abstract?rss=yes</link><description>Background: Previous reports regarding the characteristics of patients with drug-induced hypersensitivity syndrome (DIHS) are mostly limited to small case reports and drug-specific case series, mainly involving Caucasian patients.Objective: We describe the trends in the clinical presentation and laboratory findings of our patients with DIHS and their response to therapy.Methods: This is a retrospective case series. Clinical records of patients treated in the Department of Dermatology, Changi General Hospital, Singapore, with a diagnosis of DIHS from January 2003 to January 2008 were retrieved and analyzed.Results: In all, 27 patients were analyzed. The 3 most consistent features in our patients were 1) history of drug exposure (100%); 2) a morbilliform cutaneous eruption in 81.5% of the patients; and 3) systemic involvement with hepatitis (96.3%), hematologic abnormalities (81.5%), and fever (77.8%) being most common. Superficial perivascular dermatitis was the most common skin biopsy specimen findings, with tissue eosinophilia occurring in half the biopsy specimens. Severe complications included renal failure requiring dialysis in two patients and hyperthyroidism and myocarditis occurring in one patient.Limitations: This is a retrospective study with a small number of patients during a 5-year period. We did not routinely document the presence of lymphadenopathy and hepatosplenomegaly in our patient's records. We do not measure viral serologies routinely as part of the workup for DIHS.Conclusion: DIHS is not uncommon. The presentation in an Asian population is similar to published studies. Treatment includes discontinuation of the offending drug, monitoring for organ involvement, and using systemic steroids.</description><dc:title>Retrospective analysis of drug-induced hypersensitivity syndrome: A study of 27 patients</dc:title><dc:creator>Chia-Chun Ang, Yi-Shi Wang, Eva-Leina M. Yoosuff, Yong-Kwang Tay</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.050</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-06-04</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-06-04</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>219</prism:startingPage><prism:endingPage>227</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210007334/abstract?rss=yes"><title>Announcing a New Online Feature</title><link>http://www.eblue.org/article/PIIS0190962210007334/abstract?rss=yes</link><description></description><dc:title>Announcing a New Online Feature</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00733-4</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>227</prism:startingPage><prism:endingPage>227</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209011505/abstract?rss=yes"><title>Efficacy and safety of adalimumab in patients with plaque psoriasis who have shown an unsatisfactory response to etanercept</title><link>http://www.eblue.org/article/PIIS0190962209011505/abstract?rss=yes</link><description>Background: The safety and efficacy of adalimumab in patients who have shown an unsatisfactory response to etanercept are unknown.Objective: We sought to evaluate the safety and efficacy of adalimumab in patients who failed to show a satisfactory response or lost their satisfactory response to etanercept.Methods: This multicenter study enrolled patients who either failed to reach a physician global assessment (PGA) score of 0 or 1 after 12 weeks of etanercept (group A; 50 patients) or who lost their PGA score of 0 or 1 at any time after etanercept dose decrease from 50 mg twice a week to 50 mg every week (group B; 35 patients). Patients received adalimumab 40 mg every other week without loading dose for 12 weeks followed by 40 mg every week for an additional 12 weeks if they did not reach a PGA score of 0 or 1.Results: After 12 weeks of adalimumab, 34.0% (n = 17; 95% confidence interval [CI] 20.4-47.6) and 31.4% (n = 11; 95% CI 15.2-47.6) of patients from groups A and B, respectively, reached a PGA score of 0 or 1. A total of 46.0% (n = 23; 95% CI 31.7-60.3) and 45.7% (n = 16; 95% CI 28.4-63.1) of patients from group A and B, respectively, achieved a PGA score of 0 or 1 after 24 weeks of adalimumab. Adalimumab was well tolerated and no serious adverse events were reported.Limitations: This was an open-label uncontrolled study.Conclusions: Adalimumab should be considered as an alternative in patients with psoriasis who have not shown an adequate response or who lost their response to etanercept after a dose decrease.</description><dc:title>Efficacy and safety of adalimumab in patients with plaque psoriasis who have shown an unsatisfactory response to etanercept</dc:title><dc:creator>Robert Bissonnette, Chantal Bolduc, Yves Poulin, Lyn Guenther, Charles W. Lynde, Catherine Maari</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.040</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-05-24</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-05-24</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>228</prism:startingPage><prism:endingPage>234</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012109/abstract?rss=yes"><title>Body dysmorphic disorder among dermatologic patients: Prevalence and clinical features</title><link>http://www.eblue.org/article/PIIS0190962209012109/abstract?rss=yes</link><description>Background: An impairing preoccupation with a nonexistent or slight defect in appearance is the core symptom of body dysmorphic disorder (BDD), a psychiatric condition common in dermatology settings.Objective: We sought to determine the prevalence of BDD in dermatologic patients, comparing general and cosmetic settings, and describing some demographic and clinical characteristics.Methods: In all, 300 patients were consecutively assessed. Screening and diagnoses were performed with validated instruments plus a best estimate diagnosis procedure. The final sample comprised 150 patients in the cosmetic group, 150 patients in the general dermatology group, and 50 control subjects. Standard statistical analyses were performed (χ2, nonparametric tests, logistic regression).Results: The current prevalence was higher in the cosmetic group (14.0%) compared with general (6.7%) and control (2.0%) groups. No patient had a previous diagnosis. Frequently the reason for seeking dermatologic treatment was not the main BDD preoccupation. Patients with BDD from the cosmetic group were in general unsatisfied with the results of dermatologic treatments.Limitations: Cross-sectional study conducted in a university hospital is a limitation. It is uncertain if the findings can be generalized. Retrospective data regarding previous treatments are not free from bias.Conclusions: BDD is relatively common in a dermatologic setting, especially among patients seeking cosmetic treatments. These patients have some different features compared with general dermatology patients. Dermatologists should be aware of the clinical characteristics of BDD to identify and refer these patients to mental health professionals.</description><dc:title>Body dysmorphic disorder among dermatologic patients: Prevalence and clinical features</dc:title><dc:creator>Luciana Archetti Conrado, Ana Gabriela Hounie, Juliana Belo Diniz, Victor Fossaluza, Albina Rodrigues Torres, Euripedes Constantino Miguel, Evandro Ararigboia Rivitti</dc:creator><dc:identifier>10.1016/j.jaad.2009.09.017</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-06-21</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-06-21</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>235</prism:startingPage><prism:endingPage>243</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210007346/abstract?rss=yes"><title>Volunteers Needed</title><link>http://www.eblue.org/article/PIIS0190962210007346/abstract?rss=yes</link><description></description><dc:title>Volunteers Needed</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00734-6</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>243</prism:startingPage><prism:endingPage>243</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209011542/abstract?rss=yes"><title>Acral lesions in tuberous sclerosis complex: Insights into pathogenesis</title><link>http://www.eblue.org/article/PIIS0190962209011542/abstract?rss=yes</link><description>Background: Patients with tuberous sclerosis complex (TSC) are predisposed to developing ungual fibromas and other acral lesions.Objective: We sought to determine the numbers, types, and locations of acral skin lesions in TSC.Methods: We examined and photographed 76 adult women with TSC.Results: The age of the patients ranged from 20 to 69 years, with a mean age of 39 ± 11 years. Ungual fibromas were observed in 61 of 76 patients (80%). Periungual fibromas were more common than subungual fibromas, were more common on the feet than the hands, and showed the greatest frequency on the fifth toe. Longitudinal grooves in the nails occurred with or without a visible fibroma. Longitudinal short red streaks–lesions that we term “red comets”–were observed in 22 patients (29%). Longitudinal leukonychia was observed in 14 patients (18%). One patient had isolated digital overgrowth and one patient had pachydermodactyly.Limitations: No men or children were included in this study.Conclusions: Examination of patients for skin lesions of TSC could be improved by including inspection for longitudinal nail grooves, red comets, longitudinal leukonychia, and splinter hemorrhages in addition to ungual fibromas. The anatomic distribution of TSC ungual fibromas is not random and appears consistent with trauma-promoted tumor formation.</description><dc:title>Acral lesions in tuberous sclerosis complex: Insights into pathogenesis</dc:title><dc:creator>Capt Shelley L. Aldrich, Chien-Hui Hong, Leslie Groves, Cara Olsen, Joel Moss, Thomas N. Darling</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.042</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-05-12</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-05-12</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>244</prism:startingPage><prism:endingPage>251</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012134/abstract?rss=yes"><title>Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male pattern hair loss: A randomized, double-blind, placebo-controlled, phase III study</title><link>http://www.eblue.org/article/PIIS0190962209012134/abstract?rss=yes</link><description>Background: Dutasteride (Avodart) is a dual inhibitor of both type I and type II 5 alpha reductases, and thus inhibits conversion of testosterone to dihydrotestosterone, a key mediator of male pattern hair loss.Objectives: The aim of this randomized double-blind phase III study was to compare the efficacy, safety, and tolerability of dutasteride (0.5 mg) and placebo for 6 months of treatment in male patients with male pattern hair loss.Methods: A total of 153 men, 18 to 49 years old, were randomized to receive 0.5 mg of dutasteride or placebo daily for 6 months. Efficacy was evaluated by the change of hair counts, subject assessment, and photographic assessment by investigators and panels.Results: Mean change of hair counts from baseline to 6 months after treatment start was an increase of 12.2/cm2 in dutasteride group and 4.7/cm2 in placebo group and this difference was statistically significant (P = .0319). Dutasteride showed significantly higher efficacy than placebo group by subject self-assessment and by investigator and panel photographic assessment. There was no major difference in adverse events between two groups.Limitations: The study was limited to 6 months.Conclusions: This study clearly showed that 0.5 mg of dutasteride improved hair growth and was relatively well tolerated for the treatment of male pattern hair loss.</description><dc:title>Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male pattern hair loss: A randomized, double-blind, placebo-controlled, phase III study</dc:title><dc:creator>Hee Chul Eun, Oh Sang Kwon, Je Ho Yeon, Hyo Seung Shin, Byung Yoon Kim, Byung In Ro, Han Kyong Cho, Woo Young Sim, Bark Lynn Lew, Won-Soo Lee, Hwa Young Park, Seung Phil Hong, Jae Hong Ji</dc:creator><dc:identifier>10.1016/j.jaad.2009.09.018</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-06-04</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-06-04</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>252</prism:startingPage><prism:endingPage>258</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209009840/abstract?rss=yes"><title>Leukocytoclastic vasculitis and necrolytic acral erythema in patients with hepatitis C infection: Do viral load and viral genotype play a role?</title><link>http://www.eblue.org/article/PIIS0190962209009840/abstract?rss=yes</link><description>Background: Leukocytoclastic vasculitis (LCV) and necrolytic acral erythema (NAE) are skin disorders associated with hepatitis C virus (HCV) infection. However, they have not been found to occur simultaneously in the same patient.Objective: We sought to analyze the role of serum HCV-RNA levels and HCV genotype in the pathogenesis of both LCV and NAE in an attempt to assess whether these two parameters play a role in mutual exclusivity of LCV and NAE in the same patient.Methods: The study included 11 patients with LCV and 13 with NAE, all of whom were infected with HCV. All 24 patients were evaluated for the quantitative levels of HCV-RNA, using real-time polymerase chain reaction. HCV genotyping was performed on 10 patients in each group (N = 20).Results: Patients with LCV had a higher prevalence of moderate and high levels of HCV-RNA viremia (P = .038) than those with NAE. However, there was no significant difference in HCV genotype between LCV and NAE groups (P = .211).Limitations: Small number of cases is a limitation.Conclusion: Viral load seems to play a role in determining the response of the skin to HCV infection. High levels of HCV viremia were found to be significantly associated with LCV but not with NAE. HCV viremia may play a role in the development of LCV in HCV-infected patients.</description><dc:title>Leukocytoclastic vasculitis and necrolytic acral erythema in patients with hepatitis C infection: Do viral load and viral genotype play a role?</dc:title><dc:creator>Mohammad A. El-Darouti, Heba M. Mashaly, Eman El-Nabarawy, Amal M. Eissa, Mona R.E. Abdel-Halim, Marwa M.T. Fawzi, Nermine H. El-Eishi, Sherine O. Tawfik, Naglaa S. Zaki, Anoud Z. Zidan, Marwa Fawzi, Mohammad Abdelaziz, Mai M.T. Fawzi, Olfat G. Shaker</dc:creator><dc:identifier>10.1016/j.jaad.2009.07.050</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-05-12</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-05-12</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>259</prism:startingPage><prism:endingPage>265</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012171/abstract?rss=yes"><title>Long-term follow-up study of clear cell papulosis</title><link>http://www.eblue.org/article/PIIS0190962209012171/abstract?rss=yes</link><description>Background: Clear cell papulosis (CCP) was described as a new entity in 1987. Since then, only case reports or small case series have appeared in the literature and the long-term outcome of CCP remains unknown.Objectives: The aim of this study was to review cases of CCP diagnosed at our institution and to investigate their outcome.Methods: Nineteen patients given a diagnosis of CCP more than 6 years previously were identified. Their medical records and histopathologic findings were reviewed.Results: With a median follow-up duration of 11.5 years, regression of skin lesions was observed in 85.7% of patients. Persistence of skin lesions 11.5 years after diagnosis was confirmed histopathologically in one case, with a reduction in clear cell density.Limitations: Retrospective nature of the study is a limitation.Conclusion: No treatment is necessary for CCP because the skin lesions are asymptomatic and most patients experience at least partial regression.</description><dc:title>Long-term follow-up study of clear cell papulosis</dc:title><dc:creator>Fang-Wen Tseng, Tseng-Tong Kuo, Pei-Hsuan Lu, Heng-Leong Chan, Ming-Jing Chan, Rosaline Chung-Yee Hui</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.056</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-06-04</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-06-04</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>266</prism:startingPage><prism:endingPage>273</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012079/abstract?rss=yes"><title>Efficacy and safety of a carbon-dioxide ablative fractional resurfacing device for treatment of atrophic acne scars in Asians</title><link>http://www.eblue.org/article/PIIS0190962209012079/abstract?rss=yes</link><description>Background: Treatment of atrophic scars with a fractional laser resurfacing technique has demonstrated favorable outcomes, although data on the efficacy and adverse effects of this procedure in persons with dark-skinned phototypes are limited.Objective: This study was conducted to evaluate the efficacy and safety of carbon-dioxide ablative fractional resurfacing on atrophic acne scars in Asian individuals.Methods: Thirteen subjects (8 female and 5 male, aged 25-52 years) with skin phototype IV and atrophic acne scars were treated with 3 sessions of carbon-dioxide ablative fractional resurfacing laser on an average of 7-week interval. Objective (ultraviolet A-light video camera) and subjective (clinical evaluation by two blinded dermatologists) assessments were obtained at baseline and at 1, 3, and 6 months after the final treatment.Results: At the 6-month follow-up, 85% of the subjects were rated as having at least 25% to 50% improvement of scars. Improvement significantly progressed from the 1-month follow-up to the 6-month follow-up (P = .002). At 1 month after 3 treatments, surface smoothness (P = .03) and scar volume (P &lt; .001) significantly improved, compared with baseline measurements. Of the subjects, 62% rated themselves as having at least 50% improvement in their scars. Mild postinflammatory hyperpigmentation was the most common adverse effect observed in 92% of the subjects or 51% of treatment sessions, and was completely resolved in an average of 5 weeks.Limitation: The small sample size was a study limitation.Conclusions: Carbon-dioxide ablative fractional resurfacing appears to be effective and well tolerated for the treatment of atrophic acne scars in Asians.</description><dc:title>Efficacy and safety of a carbon-dioxide ablative fractional resurfacing device for treatment of atrophic acne scars in Asians</dc:title><dc:creator>Woraphong Manuskiatti, Daranporn Triwongwaranat, Supenya Varothai, Sasima Eimpunth, Rungsima Wanitphakdeedecha</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.051</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Dermatologic Surgery</prism:section><prism:startingPage>274</prism:startingPage><prism:endingPage>283</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209009967/abstract?rss=yes"><title>Combined Erdheim-Chester disease and Langerhans cell histiocytosis of skin are both monoclonal: A rare case with human androgen-receptor gene analysis</title><link>http://www.eblue.org/article/PIIS0190962209009967/abstract?rss=yes</link><description>Background: Erdheim-Chester disease (ECD) is a rare xanthogranulomatous histiocytic disorder. Langerhans cell histiocytosis (LCH) is a proliferative disorder of histiocytes with a phenotype similar to dendritic Langerhans cells. Both are derived from myeloid stem cells in the bone marrow and, thus, can overlap.Objective: We report a rare case of hybrid LCH and ECD of the skin with systemic ECD.Methods: Pathologic examinations and human androgen-receptor gene assay were used to study this case.Results: A 34-year-old woman presented with recurrent ulcerative skin lesions on both thighs associated with polydipsia and polyuria since childhood. Radiography revealed osteosclerosis of bilateral distal tibias and soft tissue masses of bilateral chest walls and ankles. Pathologically, the chest wall lesions showed dense aggregates of lipid-laden histiocytes, which were CD68+/CD163+/S100−/CD1a−. Combined with the clinical and radiographic findings, this xanthogranulomatous infiltrate was consistent with ECD. However, thigh skin showed discrete foci of a xanthogranulomatous infiltrate and S100+/CD1a+ Langerhans cells with eosinophils. In addition, Birbeck granules were found. Dissected tissues from both ECD and LCH were monoclonal, supporting their neoplastic nature.Limitations: Single case report is a limitation.Conclusion: ECD and LCH may have a close association with divergent differentiation from the same stem cells under different microenvironmental conditions.</description><dc:title>Combined Erdheim-Chester disease and Langerhans cell histiocytosis of skin are both monoclonal: A rare case with human androgen-receptor gene analysis</dc:title><dc:creator>Jen-Wei Tsai, Jen-Hui Tsou, Liang-Yi Hung, Hung-Bo Wu, Kung-Chao Chang</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.013</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Dermatopathology</prism:section><prism:startingPage>284</prism:startingPage><prism:endingPage>291</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209011980/abstract?rss=yes"><title>Cutaneous CD4+ CD56+ hematologic malignancies</title><link>http://www.eblue.org/article/PIIS0190962209011980/abstract?rss=yes</link><description>Background: Hematologic malignancies expressing CD4 and CD56 are most commonly associated with the recently described CD4+ CD56+ hematodermic neoplasm.Methods: Thirteen cases of CD4+ CD56+ hematologic malignancies were prospectively encountered in the routine and referral practices of the authors.Results: Patients 1 and 2 were elderly men exhibiting an acute onset of skin, bone-marrow, and peripheral blood involvement, both dying of their disease within less than 12 months. CD3+ phenotype and a clonal T-cell receptor β rearrangement indicated categorization as a CD4+ natural killer T-cell lymphoma. Patient 3 developed a CD56+ anaplastic large cell lymphoma and is without disease after excision and radiation. Indolent CD4+ CD56+ poikilodermatous mycosis fungoides defined case 4. There were 7 patients with CD123+ CD4+ CD56+ hematodermic neoplasm, 4 dying within 18 months of presentation with peripheral blood/marrow involvement in 6 of the 7 cases. Two patients with granulocytic sarcoma dying within 100 days of presentation defined the last two cases.Limitations: There were relatively small numbers in each of the categories and the follow-up was limited in those cases where death was not reported.Conclusion: Cutaneous malignancies composed of CD4+ CD56+ hematopoietic cells define a varied group and oftentimes have an aggressive clinical course although not in every case.</description><dc:title>Cutaneous CD4+ CD56+ hematologic malignancies</dc:title><dc:creator>Cynthia M. Magro, Pierluigi Porcu, Jochen Schaefer, Jack W. Erter, Richard R. Furman, Paul K. Shitabata, A. Neil Crowson</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.044</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-06-11</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-06-11</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Dermatopathology</prism:section><prism:startingPage>292</prism:startingPage><prism:endingPage>308</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209011487/abstract?rss=yes"><title>New World cutaneous leishmaniasis: Updated review of current and future diagnosis and treatment</title><link>http://www.eblue.org/article/PIIS0190962209011487/abstract?rss=yes</link><description>Background: Cutaneous leishmaniasis (CL) has traditionally been underrecognized and underreported. Improved awareness is warranted as the number of cases has increased as a result of increased travel to endemic countries, the HIV/AIDS pandemic, and the larger number of military and contract workers deployed overseas.Objective: We sought to present a systematic review of evidence from a gamut of research trials on the treatment efficacy of different regimens and aggregate this knowledge for use as a guide for clinical practice decisions.Methods: We performed a comprehensive search of print and electronic sources to identify the accumulated research information on New World CL.Results: Topical treatment of New World CL lesions is generally not recommended. Findings support the systemic administration of pentavalent antimonials as first-line treatment. Exception to this is infection with L guyanensis in French Guiana where systemic pentamidine is suggested as first-line treatment.Limitations: The reliability of the findings of this review of research evidence is dependent on the individual quality and potential bias in its component principal trials. There was a conscious attempt to only include evidence derived from randomized controlled studies, with adequate randomization, adequate patient numbers, and complete follow-up information. However, because of the relatively small number of such studies on New World CL, evidence from nonrandomized studies and case series studies was also considered.Conclusions: The pentavalent antimony compounds remain the first-line treatment choice for the treatment of New World CL. Concerns with cost, availability, poor compliance, and systemic toxicity, however, may compel clinicians to opt for alternative treatment modalities. Some advances in the development of an antileishmanial vaccine have been made but none is yet available for clinic use. The increase, over recent years, in the incidence of CL warrants an enhanced effort to increase awareness of the disease, assure timely diagnosis, and implement effective management and treatment strategies.</description><dc:title>New World cutaneous leishmaniasis: Updated review of current and future diagnosis and treatment</dc:title><dc:creator>Panagiotis Mitropoulos, Pete Konidas, Mindy Durkin-Konidas</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.088</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-03-22</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-03-22</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>309</prism:startingPage><prism:endingPage>322</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096221000397X/abstract?rss=yes"><title>Brittle hair, developmental delay, neurologic abnormalities, and photosensitivity in a 4-year-old girl</title><link>http://www.eblue.org/article/PIIS019096221000397X/abstract?rss=yes</link><description>A 4-year-old Caucasian girl presented to the National Institutes of Health (NIH) for evaluation of sparse brittle hair, developmental delay, poor growth, recurrent infections, and photosensitivity ( and ). The patient was born preterm at 35 weeks after a pregnancy complicated by elevated maternal alpha-fetoprotein at 16 weeks and pregnancy-induced hypertension beginning at 26 weeks. At birth, her skin showed generalized erythroderma and she was described as having a collodion membrane (, A) that resolved over 2.5 weeks. By 1 month of age, the patient was reported to have congenital ichthyosis and mild scaling on her scalp, trunk, and lower extremities. By 23 months, she was reported to sunburn with minimal sun exposure and sweat very little in hot environments. Short brittle hair, nail spooning, head tremor (titubation), and asymmetric horizontal nystagmus were also noted. The patient did not sit unassisted until 12 months and did not crawl until 22 months. A magnetic resonance imaging (MRI) scan of her brain at 19 months was read as normal. By age 3 years she had ataxia and ambulated only with a reverse walker. The patient experienced multiple ear infections and pneumonias beginning at 6 months of age that did not require hospitalization, were not cultured, and responded to empiric antibiotic treatment. Her parents reported that when she experienced severe respiratory infections the patient had temporary developmental regression that improved when the infection resolved. Complement and immunoglobulin levels were within normal limits at 16 months.</description><dc:title>Brittle hair, developmental delay, neurologic abnormalities, and photosensitivity in a 4-year-old girl</dc:title><dc:creator>Xiaolong Zhou, Sikandar G. Khan, Deborah Tamura, Nicholas J. Patronas, Wadih M. Zein, Brian P. Brooks, Kenneth H. Kraemer, John J. DiGiovanna</dc:creator><dc:identifier>10.1016/j.jaad.2010.03.041</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Dermatology Grand Rounds at the NIH</prism:section><prism:startingPage>323</prism:startingPage><prism:endingPage>328</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210005542/abstract?rss=yes"><title>Malignant melanoma: Molecular cytogenetics and their implications in clinical medicine</title><link>http://www.eblue.org/article/PIIS0190962210005542/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>Malignant melanoma: Molecular cytogenetics and their implications in clinical medicine</dc:title><dc:creator>Jacqueline M. Junkins-Hopkins</dc:creator><dc:identifier>10.1016/j.jaad.2010.04.044</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Dialogues in Dermatology</prism:section><prism:startingPage>329</prism:startingPage><prism:endingPage>332</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210007358/abstract?rss=yes"><title>Change of Address</title><link>http://www.eblue.org/article/PIIS0190962210007358/abstract?rss=yes</link><description></description><dc:title>Change of Address</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00735-8</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Dialogues in Dermatology</prism:section><prism:startingPage>332</prism:startingPage><prism:endingPage>332</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209008238/abstract?rss=yes"><title>Permanent chemotherapy-induced alopecia: Case report and review of the literature</title><link>http://www.eblue.org/article/PIIS0190962209008238/abstract?rss=yes</link><description>Reversible alopecia following chemotherapy is well recognized and typically not evaluated by dermatologists. However, there are an increasing number of reports of permanent chemotherapy-induced alopecia, typically following high-dose chemotherapy and subsequent bone marrow transplantation. We describe an unusual case of permanent alopecia in a patient who received adjuvant chemotherapy for breast carcinoma, and not a conditioning regimen before bone marrow transplantation. A unique histologic finding of replacement of anagen hair follicles by linear columns of basaloid epithelium is reported. We review the clinical and histologic findings of permanent chemotherapy-induced alopecia and speculate on its pathogenesis.</description><dc:title>Permanent chemotherapy-induced alopecia: Case report and review of the literature</dc:title><dc:creator>Ben Tallon, Elizabeth Blanchard, Lynne J. Goldberg</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.063</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-05-14</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-05-14</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Case &amp; Review</prism:section><prism:startingPage>333</prism:startingPage><prism:endingPage>336</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209009918/abstract?rss=yes"><title>Atypical vascular lesion of the breast</title><link>http://www.eblue.org/article/PIIS0190962209009918/abstract?rss=yes</link><description>Atypical vascular lesions (AVLs) are vascular proliferations that develop after surgery and radiation for breast carcinoma and may represent precursors to angiosarcoma. AVLs are not well-known entities and currently lack official prognostic factors and guidelines for surgical treatment. We report the case of a patient who developed an AVL, vascular type, 4 years after lumpectomy and radiation therapy for ductal carcinoma in situ of the breast. The patient underwent wide local excision with 1-cm margins with subsequent pathologic examination confirming complete excision of the residual atypical vascular proliferation. This case highlights the importance of close cutaneous surveillance in patients with a history of surgery and radiation for breast carcinoma, and a low threshold for biopsy. More studies are needed to further delineate the risk of AVLs progressing to angiosarcoma and to identify histologic features or immunophenotypic markers, which may be predictive of this risk. Furthermore, formal treatment recommendations for these enigmatic entities would be helpful.</description><dc:title>Atypical vascular lesion of the breast</dc:title><dc:creator>Joshua Mandrell, Sheetal Mehta, Stacy McClure</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.017</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-02-08</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-02-08</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Case Report</prism:section><prism:startingPage>337</prism:startingPage><prism:endingPage>340</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209021161/abstract?rss=yes"><title>Neurotic excoriations</title><link>http://www.eblue.org/article/PIIS0190962209021161/abstract?rss=yes</link><description>To the Editor: I enjoyed the article in the October 2009 issue of the Journal by Mutasim and Adams that called attention to the varied underlying psychiatric conditions associated with cutaneous excoriations, but I am not sure we ought to be so insistent upon abandoning the common and time-honored “neurotic excoriation” in favor of “psychogenic excoriation.” The authors give several reasons, but none seems valid enough to warrant the change.</description><dc:title>Neurotic excoriations</dc:title><dc:creator>Michael B. Brodin</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.592</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>341</prism:startingPage><prism:endingPage>342</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209021173/abstract?rss=yes"><title>Treatment of psoriasis with cyclosporine in patients with hepatitis C infection: Risk or opportunity?</title><link>http://www.eblue.org/article/PIIS0190962209021173/abstract?rss=yes</link><description>To the Editor: We appreciated the article by Frankel et al in the December 2009 issue of the Journal regarding the treatment of psoriasis in patients with hepatitis C virus (HCV) infection and the considerable efforts of the Frankel et al to develop practical therapeutic guidelines and arrive at a consensus on treating psoriasis in this particular cohort of patients. Indeed, as a consequence of the worldwide distribution of HCV, it is not infrequent to encounter in daily clinical practice patients with psoriasis also carrying HCV. In such cases, the treatment of psoriasis often raises a special challenge for physicians.</description><dc:title>Treatment of psoriasis with cyclosporine in patients with hepatitis C infection: Risk or opportunity?</dc:title><dc:creator>Vito Di Lernia, Giuseppe Albertini</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.593</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>342</prism:startingPage><prism:endingPage>343</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209022099/abstract?rss=yes"><title>Scalp necrosis in giant cell arteritis after initiation of therapeutic corticosteroids</title><link>http://www.eblue.org/article/PIIS0190962209022099/abstract?rss=yes</link><description>To the Editor: We read with interest the article by Tsianakas et al in the October 2009 issue of the Journal entitled “Scalp necrosis in giant cell arteritis: case report and review of the relevance of this cutaneous sign of large-vessel vasculitis,” in which the authors analyzed 78 case reports published between 1946 and 2007. Important findings of this article included an increased incidence of vision loss, an increased rate of mortality, and a delay of about 1 month in diagnosis of giant cell arteritis (GCA) with associated scalp necrosis compared with those of patients with GCA alone. The authors emphasized the need for early treatment with glucocorticoids to help prevent serious complications, and noted that scalp necrosis has never been reported after initiation of adequate treatment. Three case reports in the medical literature have detailed patients in whom scalp necrosis developed with low dose (range, 5-35 mg daily) prednisolone, whereas therapeutic doses are generally thought to be 40 mg to 60 mg or more.</description><dc:title>Scalp necrosis in giant cell arteritis after initiation of therapeutic corticosteroids</dc:title><dc:creator>Katherine E. Brick, Robert H. Cook-Norris, David A. Wetter, Kenneth J. Warrington</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.684</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>343</prism:startingPage><prism:endingPage>344</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210001210/abstract?rss=yes"><title>Methotrexate guidelines 2009?</title><link>http://www.eblue.org/article/PIIS0190962210001210/abstract?rss=yes</link><description>To the Editor: The article by Kalb et al in the May 2009 issue of the Journal was prepared as an update of previous methotrexate guidelines. Three of the original four authors (H.R., H.M., and R.A.) of previous methotrexate guidelines were not consulted in the 2009 update. Why have the guidelines changed from a function of the American Academy of Dermatology (AAD) to the National Psoriasis Foundation (NSF)? A recent member alert (June 22, 2009) from the AAD, requested “member review and comment on the fourth section of newly developed evidenced based Guidelines of Care for the Management and Treatment of Psoriasis.” The Psoriasis Expert Work Group of AAD includes some of the authors of the NSF Methotrexate and Psoriasis 2009 publication. The NSF is a patient advocacy organization, which may have funding conflicts from companies that make products to treat psoriasis. The AAD Guideline committee avoided these conflicts and tried to present sound scientific evidence. The AAD has a Guidelines Research Committee that reviews revised guidelines, and finally the AAD Board of Directors gives final approval. This structure, which was used for initial methotrexate guidelines, avoids conflicts of interest. Kalb et al quote Table III from the methotrexate guidelines written by the American College of Rheumatology (ACR) and not the Arthritis Foundation.</description><dc:title>Methotrexate guidelines 2009?</dc:title><dc:creator>Henry H. Roenigk, Robert Auerbach, Howard I. Maibach</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.068</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>344</prism:startingPage><prism:endingPage>345</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210003725/abstract?rss=yes"><title>Wound eversion caveats</title><link>http://www.eblue.org/article/PIIS0190962210003725/abstract?rss=yes</link><description>To the Editor: The achievement of a near imperceptible postsurgical scar is a somewhat elusive goal that all of us attempt to approach. The commentary by Kantor in the February 2010 issue of the Journal provides yet another tool towards that end. Historically, the concept of designing a dermal suture to exit lateral to the line of incision and below the undermined surface rather than at the leading dermal edge was introduced by Breuninger. His “intracutaneous butterfly suture” assumed more of a horizontal than a vertical orientation, but otherwise had characteristics similar to the “set-back” suture.</description><dc:title>Wound eversion caveats</dc:title><dc:creator>Leonard M. Dzubow</dc:creator><dc:identifier>10.1016/j.jaad.2010.03.022</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>345</prism:startingPage><prism:endingPage>345</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210003713/abstract?rss=yes"><title>Reply</title><link>http://www.eblue.org/article/PIIS0190962210003713/abstract?rss=yes</link><description>To the Editor: I am flattered by the interest taken in my short letter by Dr Dzubow, a lion of dermatologic surgery. I was unaware of the article by Breuninger, because it was published in a journal that is not indexed in Medline/PubMed. The intracutaneous butterfly suture, however, is fundamentally different from the set-back suture in that its orientation, as Dzubow notes, is horizontal. This increases the theoretical risk of tissue necrosis and results in less dramatic wound eversion. The butterfly suture is also predicated on incising the skin on an angle, which again would not be done with the set-back technique. Dzubow is absolutely correct in highlighting some of the limitations of this technique and the dangers of overeverting wound edges. My original manuscript included a more extensive discussion of these caveats, but unfortunately was edited for length. Figs 1 and 2 were meant to show the knot resting on the subcutaneous fat, rather than tacked down to it, and I appreciate Dzubow's clarification of this point. Fig 3, demonstrating a surgeon's eye view, clarifies that the knot is tied above the level of the subcutaneous fat. I thank Dzubow for his important clarifications and words of encouragement.</description><dc:title>Reply</dc:title><dc:creator>Jonathan Kantor</dc:creator><dc:identifier>10.1016/j.jaad.2010.03.021</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>345</prism:startingPage><prism:endingPage>346</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012390/abstract?rss=yes"><title>Global access to dermatopathology services: Physician survey of availability and needs in sub-Saharan Africa</title><link>http://www.eblue.org/article/PIIS0190962209012390/abstract?rss=yes</link><description>To the Editor: The availability of dermatopathology services varies across the world. Developing countries have limited to no access to dermatologists, pathologists, or histology and laboratory services. To address healthcare needs in underserved areas, medical specialists are increasingly providing patient care in remote areas, either through establishing local clinics or through telemedicine. Expanding clinical services creates a need for histologic assessment of diseases requiring clinicopathologic correlations for diagnosis. Proposed strategies include shipment of wet tissue for processing, or “virtual dermatopathology” through the electronic transfer of photomicrographs, scanned slides, or live interactive telepathology. We seek to characterize the presence of histology and dermatopathology services in sub-Saharan Africa, where many patients are evaluated clinically but laboratory services are scarce.</description><dc:title>Global access to dermatopathology services: Physician survey of availability and needs in sub-Saharan Africa</dc:title><dc:creator>Matthew W. Tsang, Carrie L. Kovarik</dc:creator><dc:identifier>10.1016/j.jaad.2009.09.038</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>346</prism:startingPage><prism:endingPage>348</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209013693/abstract?rss=yes"><title>Accuracy of teledermatology/teledermoscopy and clinic-based dermatology for specific categories of skin neoplasms</title><link>http://www.eblue.org/article/PIIS0190962209013693/abstract?rss=yes</link><description>To the Editor: Teledermatology (TD) may be less effective than clinic-based dermatology (CD) for certain conditions. Previously, we reported that diagnostic accuracy of store-and-forward TD for pigmented and nonpigmented skin neoplasms was inferior to CD. The analysis herein compares the accuracy of TD and CD for specific neoplasm categories and assesses the change in TD accuracy with the addition of polarized light dermatoscopy (TD + PLD) or contact immersion dermatoscopy (TD + CID).</description><dc:title>Accuracy of teledermatology/teledermoscopy and clinic-based dermatology for specific categories of skin neoplasms</dc:title><dc:creator>Erin M. Warshaw, Amy A. Gravely, David B. Nelson</dc:creator><dc:identifier>10.1016/j.jaad.2009.10.037</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>348</prism:startingPage><prism:endingPage>352</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220902204X/abstract?rss=yes"><title>The perceived influence of cosmetic dermatology on dermatology resident education</title><link>http://www.eblue.org/article/PIIS019096220902204X/abstract?rss=yes</link><description>To the Editor: Over the past decade, an increased focus on cosmetic products and procedures has increased the demand for cosmetic dermatology. Dermatology residents consistently report inadequate exposure to cosmetics. It is unknown if residency programs have increased training in cosmetics and, if so, if this change has compromised interest or expertise in other areas of dermatology. To investigate this, we surveyed those responsible for resident education: dermatology residency program directors and department chairmen.</description><dc:title>The perceived influence of cosmetic dermatology on dermatology resident education</dc:title><dc:creator>Rachel Schleichert, Sarah Grim Hostetler, Matt Zirwas</dc:creator><dc:identifier>10.1016/j.jaad.2009.07.054</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>352</prism:startingPage><prism:endingPage>353</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209005416/abstract?rss=yes"><title>Partial unilateral lentiginosis associated with nevus of Ota</title><link>http://www.eblue.org/article/PIIS0190962209005416/abstract?rss=yes</link><description>To the Editor: A 25-year-old otherwise healthy female was referred to our department for the evaluation of pigmented facial lesions. Localized hyperpigmentation over the right eye had been present since birth. In the last 4 years, she noticed development of ipsilateral multiple brown lentigines extending onto the right forehead, temple, and eyelids, as well as a progressive blue-gray pigmentation on the right eyelid and tip of the nose.</description><dc:title>Partial unilateral lentiginosis associated with nevus of Ota</dc:title><dc:creator>Beatriz González-Sixto, Carlos De la Torre, Celia Posada, Carlos Sevillano</dc:creator><dc:identifier>10.1016/j.jaad.2009.04.049</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>353</prism:startingPage><prism:endingPage>355</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220900615X/abstract?rss=yes"><title>Apparent safe use of single dose rituximab for recalcitrant atopic dermatitis in the first trimester of a twin pregnancy</title><link>http://www.eblue.org/article/PIIS019096220900615X/abstract?rss=yes</link><description>To the Editor: Rituximab, a chimeric monoclonal anti-CD20 antibody originally developed for the therapy of B-cell malignancies, has recently been suggested as an option for severe atopic dermatitis (AD), particularly in patients with elevated levels of total immunoglobulin E (IgE) and/or specific IgE to environmental allergens.</description><dc:title>Apparent safe use of single dose rituximab for recalcitrant atopic dermatitis in the first trimester of a twin pregnancy</dc:title><dc:creator>Pedro Ponte, Maria João Paiva Lopes</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.015</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>355</prism:startingPage><prism:endingPage>356</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006689/abstract?rss=yes"><title>Development of pemphigus vulgaris in a patient with psoriasis treated with cyclosporine</title><link>http://www.eblue.org/article/PIIS0190962209006689/abstract?rss=yes</link><description>To the Editor: In July 2008, a 60-year-old man who had had psoriasis since 28 years of age presented to our department with erosive lesions on the oral and genital mucosa and erosive bullous lesions on the skin, predominantly on the back and chest. The lesions had arisen at a time when his psoriasis had regressed almost completely, with few residual erythematous, finely scaling lesions on scalp and elbows. The patient had been on continuous cyclosporine therapy (initial dosage, 250 mg/day) for his psoriasis for the previous 9 months. When he came to us, the cyclosporine dose had been decreased to 140 mg/day and he was using no topical treatment. The patient also had congenital deaf-mutism and diabetes mellitus, for which he had been taking glimepiride for several years.</description><dc:title>Development of pemphigus vulgaris in a patient with psoriasis treated with cyclosporine</dc:title><dc:creator>Giacomo Caldarola, Angelo Carbone, Clara De Simone, Riccardo Pellicano</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.032</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>356</prism:startingPage><prism:endingPage>357</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006690/abstract?rss=yes"><title>Metal-induced granule deposition with pseudoochronosis</title><link>http://www.eblue.org/article/PIIS0190962209006690/abstract?rss=yes</link><description>To the Editor: A healthy 49-year-old woman presented to our department with an irregularly bordered and pigmented black-gray plaque of 30 years' duration in the right popliteal fossa. At 15 years of age, she was struck by a firecracker in this location. She denied any previous treatment and did not note any change in size, shape, or color. She did not recall using silver sulfadiazine on the burn injury, and denied taking silver solutions for health reasons.</description><dc:title>Metal-induced granule deposition with pseudoochronosis</dc:title><dc:creator>Ikue Shimizu, Sara Worthing Dill, Jason McBean, Leslie Robinson-Bostom</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.031</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Case Letters</prism:section><prism:startingPage>357</prism:startingPage><prism:endingPage>359</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209014777/abstract?rss=yes"><title>Clinical and basic immunodermatology</title><link>http://www.eblue.org/article/PIIS0190962209014777/abstract?rss=yes</link><description>This volume is a welcome addition to the somewhat sparsely populated list of current texts in immunodermatology. The importance of the immune system in the mechanisms underlying or contributing to the pathogenesis of many skin diseases has long been recognized, and any perusal of current journals reveals a seemingly exponential growth in the body of information in the field. The editors and the numerous expert contributors have valiantly addressed the task of presenting key new findings in the context of previous knowledge and clinical disease. The first of the four sections of this book comprises 11 chapters that include overviews of the major components of systemic and cutaneous immunology. It is clear at the outset that the authors assume that the reader possesses at least a foundational knowledge and understanding of the field. This section opens with a thorough discussion of the production and function of the cytokines and chemokines that mediate the numerous functions of the immune system, which are increasingly being examined for their potential therapeutic benefit in many diseases. The section continues with reviews of several key aspects of innate and specific immunity, with particularly informative chapters on the function of T lymphocytes and their numerous subsets, and photoimmunology. A topic notable for its absence is genetics—particularly a discussion of genetic association and predisposition toward disease. Some specific information is found in the clinical sections of the book; for example, the chapters on psoriasis and atopic dermatitis include short explanations of genetic analyses and the detection of candidate disease susceptibility genes and gene polymorphisms.</description><dc:title>Clinical and basic immunodermatology</dc:title><dc:creator>Gillian M. Galbraith</dc:creator><dc:identifier>10.1016/j.jaad.2009.09.052</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Book Review</prism:section><prism:startingPage>360</prism:startingPage><prism:endingPage>360</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209010573/abstract?rss=yes"><title>Scarring alopecia followed by a progressive eruption</title><link>http://www.eblue.org/article/PIIS0190962209010573/abstract?rss=yes</link><description>A 58-year-old white man presented with a 10-year history of a progressive eruption that began on his scalp, resulting in widespread alopecic patches, and gradually spread to involve his trunk and extremities. He was otherwise healthy.  shows representative lesions on the scalp and flank. Histologic findings from biopsies obtained from lesions on the trunk are shown in .</description><dc:title>Scarring alopecia followed by a progressive eruption</dc:title><dc:creator>Matthew J. Meier, Diya F. Mutasim</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.025</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Images in Dermatology</prism:section><prism:startingPage>e19</prism:startingPage><prism:endingPage>e20</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209010603/abstract?rss=yes"><title>Strange occurrence of lip indentation</title><link>http://www.eblue.org/article/PIIS0190962209010603/abstract?rss=yes</link><description>A 24-year-old white man presented for a vascular malformation of the right forearm that had been present since birth. He had bilateral symmetrical lip indentations (). The lip indentations were asymptomatic other than the rare drainage of clear fluid. A careful examination of his mucous membranes, head, and neck was otherwise normal. The rest of his cutaneous examination revealed the vascular anomaly of his forearm and was otherwise normal.</description><dc:title>Strange occurrence of lip indentation</dc:title><dc:creator>Anik Amin, Tor Shwayder</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.028</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Images in Dermatology</prism:section><prism:startingPage>e21</prism:startingPage><prism:endingPage>e21</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210003129/abstract?rss=yes"><title>The canary seems fine: The effects of the economy on job-seeking experiences of recent dermatology training program graduates</title><link>http://www.eblue.org/article/PIIS0190962210003129/abstract?rss=yes</link><description>On November 28, 2008, the Business Cycle Dating Committee of the National Bureau of Economic Research (NBER) announced that a peak in the US economic activity had occurred in December 2007, ending an expansion that began in 2001 and marking an abrupt beginning of the current recession. Commonly defined by the financial press as two consecutive quarters of decline in real gross domestic product, the NBER defines a recession as a significant decrease in activity spread across the economy and determined by a number of measures including job losses, declines in personal income, in addition to declines in real gross domestic product.</description><dc:title>The canary seems fine: The effects of the economy on job-seeking experiences of recent dermatology training program graduates</dc:title><dc:creator>Carol Erin Cheng, Alexa Boer Kimball</dc:creator><dc:identifier>10.1016/j.jaad.2010.02.043</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-06-24</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-06-24</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e23</prism:startingPage><prism:endingPage>e28</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210004901/abstract?rss=yes"><title>Physician performance measures in dermatology</title><link>http://www.eblue.org/article/PIIS0190962210004901/abstract?rss=yes</link><description>Performance measures serve as a method of assessing and reporting on the quality of care that physicians are delivering to their patients. Although measures have been developed and integrated into other fields of medicine, a comprehensive set of measures specific to the specialty of dermatology is lacking. It is likely that quality measures will become an increasingly significant component of health care, thus it is important for dermatologists to actively participate in their development. There are multiple topics relevant to the various components of dermatology practice (medical, surgical, and cosmetic dermatology and dermatopathology) upon which measures can be based.</description><dc:title>Physician performance measures in dermatology</dc:title><dc:creator>Rebekah L. Wilson, Steven R. Feldman</dc:creator><dc:identifier>10.1016/j.jaad.2010.04.018</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e29</prism:startingPage><prism:endingPage>e35</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210001143/abstract?rss=yes"><title>Management of subcutaneous implantation of mercury after broken thermometer</title><link>http://www.eblue.org/article/PIIS0190962210001143/abstract?rss=yes</link><description>To the Editor: In their interesting case report, Vano-Galvan et al describe a 29-year-old woman who presented with painful skin lesion on her right knee associated with subcutaneous implantation of elemental metallic mercury (Hg0) derived from 30 broken thermometers. We would like to raise some points about this case.</description><dc:title>Management of subcutaneous implantation of mercury after broken thermometer</dc:title><dc:creator>Paolo D. Pigatto, Gianpaolo Guzzi</dc:creator><dc:identifier>10.1016/j.jaad.2009.12.060</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e37</prism:startingPage><prism:endingPage>e37</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210000058/abstract?rss=yes"><title>Indications of therapy in subcutaneous implantation of mercury</title><link>http://www.eblue.org/article/PIIS0190962210000058/abstract?rss=yes</link><description>To the Editor: I appreciate the comments of Guzzi et al regarding our article. As they stated, the measurement of blood mercury level is the most precise tool for the diagnosis of mercury poisoning. When available, it should be the main criterion for starting chelation therapy. Unfortunately, the test is not available in all hospitals. When it is not available, it may be better to begin chelation therapy based on systemic signs and symptoms rather than delaying therapy until a blood mercury level can be obtained. Symptoms of acute intoxication of elemental mercury include shortness of breath, chest pain, dyspnea, paroxysmal cough, chills, nausea and vomiting, diffuse joint swelling, and rash.</description><dc:title>Indications of therapy in subcutaneous implantation of mercury</dc:title><dc:creator>Sergio Vano-Galvan</dc:creator><dc:identifier>10.1016/j.jaad.2009.12.049</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e37</prism:startingPage><prism:endingPage>e37</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209013668/abstract?rss=yes"><title>Subgroup analyses of etanercept in pediatric patients with psoriasis</title><link>http://www.eblue.org/article/PIIS0190962209013668/abstract?rss=yes</link><description>To the Editor: The efficacy and safety of etanercept therapy in a large, 48-week, phase III clinical trial in a pediatric population with moderate to severe plaque psoriasis has been reported. Subgroup analyses are generally performed to address the possibility of different outcomes, treatment effects, or pathophysiology between treatment groups. The current analysis examines patients from the pediatric trial to determine the possible effects of variations in baseline characteristics based on the subgroups of age, gender, body surface area, Psoriasis Area and Severity Index (PASI), Physician's Global Assessment, disease duration, and previous systemic therapy or phototherapy.</description><dc:title>Subgroup analyses of etanercept in pediatric patients with psoriasis</dc:title><dc:creator>Amy S. Paller, Lawrence F. Eichenfield, Richard G. Langley, Craig L. Leonardi, Elaine C. Siegfried, Kara Creamer, Gregory Kricorian</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.001</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e38</prism:startingPage><prism:endingPage>e41</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209014431/abstract?rss=yes"><title>Acute patchy exanthematous pustulosis caused by sulfamethoxazole-trimethoprim</title><link>http://www.eblue.org/article/PIIS0190962209014431/abstract?rss=yes</link><description>To the Editor: We describe a patient with an acute eruption of asymptomatic, erythematous, edematous, oval plaques studded with pinpoint, nonfollicular pustules on her torso and proximal extremities caused by sulfamethoxazole-trimethoprim (SMZ-TMP). This 40-year-old female had a history of chronic myelogenous leukemia unresponsive to etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, rituximab, and fludarabine (EPOCH-RF) therapy. She subsequently received a matched, related-donor peripheral blood stem cell transplant and donor lymphocyte infusion (DLI of TH2 cells). She presented on posttransplant day 15 (post-DLI day 1) with acute onset of the aforementioned eruption (). There were no vesicles, bullae, or mucosal lesions and experienced no fever, chills, lymphadenopathy, angioedema, or gastrointestinal symptoms. Her medications included valacyclovir, fluconazole, cyclosporine, insulin, heparin, and SMZ-TMP. Valacyclovir and fluconazole were started 6 weeks before the eruption. Cyclosporine, insulin, and heparin were started 15 days before the eruption. SMP-TMZ was instituted 3 days before the eruption; however, the patient had previously received SMP-TMZ, 6 weeks earlier, during induction chemotherapy. The patient had no known drug allergies or personal or family history of psoriasis. Laboratory examinations revealed a chronic pancytopenia without neutrophilia or eosinophilia. Serum metabolic panel, liver function tests, and calcium levels were unremarkable. Gram stain and bacterial culture of a pustule were negative for organisms. A punch biopsy specimen revealed subcorneal neutrophilic pustules, mild spongiosis, and a superficial dermal, perivascular lymphocytic inflammatory infiltrate with rare eosinophils ().</description><dc:title>Acute patchy exanthematous pustulosis caused by sulfamethoxazole-trimethoprim</dc:title><dc:creator>Ivy Lee, Maria Turner, Chyi-Chia Richard Lee</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.008</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e41</prism:startingPage><prism:endingPage>e43</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209002552/abstract?rss=yes"><title>Autoimmune hepatitis in two psoriasis patients treated with inflixmab</title><link>http://www.eblue.org/article/PIIS0190962209002552/abstract?rss=yes</link><description>To the Editor: A 37-year-old man was referred to our hospital with a 12-year history of severe plaque-type psoriasis without psoriatic arthritis. He did not drink alcohol. His only medication was omeprazole for a hiatal hernia. Six weeks after the third infusion of infliximab (5 mg/kg at weeks 0, 2, and 6), the patient complained of asthenia, abdominal pain, and arthritis of the wrist. No other drugs or alcohol were taken. Blood tests () showed a strong elevation in transaminase levels, without evidence of cholestatis, but with positive tests for antinuclear antibodies (ANA), double stranded DNA antibodies, and smooth muscle antibodies. Viral serologies were negative. Computed tomography of the liver was normal. No liver biopsy was performed. Spontaneously, the liver function tests (LFTs) became normal within 2 months, with a disappearance of the clinical symptoms. The hepatologist diagnosed autoimmune hepatitis (AIH). Infliximab was responsible for AIH for three reasons: (1) there was no other explanation for the AIH; (2) the delay of 10 weeks between the last infusion and the hepatitic damage; and (3) the spontaneous and complete recovery after stopping infliximab.</description><dc:title>Autoimmune hepatitis in two psoriasis patients treated with inflixmab</dc:title><dc:creator>Catherine Goujon, Karima Dahel, Frédéric Bérard, Isabelle Guillot, Nathalie Gunera-Saad, Jean-François Nicolas</dc:creator><dc:identifier>10.1016/j.jaad.2009.02.029</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e43</prism:startingPage><prism:endingPage>e44</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096220900601X/abstract?rss=yes"><title>Acute localized exanthematous pustulosis induced by docetaxel</title><link>http://www.eblue.org/article/PIIS019096220900601X/abstract?rss=yes</link><description>To the Editor: A 44-year-old woman who was receiving chemotherapy after surgery for breast cancer complained of symmetric pustular skin lesions on an erythematous background on both cheeks (). The lesions developed abruptly 2 days after the first infusion of docetaxel which began after four cycles of chemotherapy composed of adriamycin and cyclophophamide. The last infusion of adriamycin and cyclophophamide was 3 weeks earlier, and no medications were administered between the chemotherapies. Itching, localized warmth, and mild myalgias were noted, but there was no fever. Bacterial culture from the exudate revealed no growth of either Gram-positive or -negative microorganisms. A Tzanck smear was also negative.</description><dc:title>Acute localized exanthematous pustulosis induced by docetaxel</dc:title><dc:creator>Sung Woo Kim, Un Ha Lee, Sang Jai Jang, Hyun Su Park, Yoo Seok Kang</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.007</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e44</prism:startingPage><prism:endingPage>e46</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006665/abstract?rss=yes"><title>Erythema palmare hereditarium (Lane's red palms): A forgotten entity?</title><link>http://www.eblue.org/article/PIIS0190962209006665/abstract?rss=yes</link><description>To the Editor: In March 2009, a 52-year-old woman was referred to our department for bilateral red palms. Her medical history was notable for chronic sciatica and bilateral carpal tunnel syndrome. Erythema was permanent and unrelated to cold, heat, or exercise; the erythema was bright with scattered purplish telangiectasia and spider naevi and was asymptomatic without pain, scaling, hyperhidrosis, or hyperkeratosis. The erythema was restricted to the thenar and hypothenar eminences, palmar monticule, and phalanges (). The feet were mildly affected. The physical examination was otherwise unremarkable. Laboratory tests, including liver enzymes and autoimmune antibodies, were normal. The patient clearly recalled that the erythema had been present since her childhood. She stated that her mother had similar lesions, but we did not examine her mother. A diagnosis of erythema palmare hereditarium was made.</description><dc:title>Erythema palmare hereditarium (Lane's red palms): A forgotten entity?</dc:title><dc:creator>Nicolas Kluger, Bernard Guillot</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.033</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e46</prism:startingPage><prism:endingPage>e46</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209006768/abstract?rss=yes"><title>Lipodystrophy in association with adult-onset dermatomyositis sine myositis: A rare manifestation</title><link>http://www.eblue.org/article/PIIS0190962209006768/abstract?rss=yes</link><description>To the Editor: Lipodystrophy is a rare disease that is characterized by the loss of subcutaneous adipose tissue. The exact pathogenesis remains unclear; however, it has been associated with autoimmunity, particularly juvenile dermatomyositis (JDM). We report a case of partial lipodystrophy in an adult patient with dermatomyositis (DM) sine myositis who did not develop metabolic abnormalities.</description><dc:title>Lipodystrophy in association with adult-onset dermatomyositis sine myositis: A rare manifestation</dc:title><dc:creator>Elizabeth N. Le, Rachel Abuav</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.001</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e46</prism:startingPage><prism:endingPage>e48</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007270/abstract?rss=yes"><title>Cutaneous metastases of cervical adenosquamous carcinoma</title><link>http://www.eblue.org/article/PIIS0190962209007270/abstract?rss=yes</link><description>To the Editor: A 32-year-old woman with a history of cervical cancer presented with skin lesions involving her lower abdomen, hips, and groin in January 2007. The patient had undergone total abdominal hysterectomy in 2004 for recurrent cervical intraepithelial neoplasia (CIN III) and microinvasive adenosquamous cervical carcinoma. Pathologic margins were negative and the patient was well until June 2006, when she developed significant constitutional symptoms. Imaging and tumor markers were consistent with metastatic cervical cancer with extensive lymph node involvement. A biopsy specimen of the vaginal vault showed poorly differentiated adenosquamous carcinoma, and fine needle aspiration of the pelvic lymph nodes confirmed metastatic spread. She was treated palliatively with cisplatinum and radiation therapy. One month later, the patient presented with her skin lesions. On physical examination, multiple erythematous nodules and plaques were seen on the patient's lower abdomen and inner thighs outside the field of previous irradiation ().</description><dc:title>Cutaneous metastases of cervical adenosquamous carcinoma</dc:title><dc:creator>Raina Fumerton, Tarek Afifi, Magdalena Martinka, Gillian de Gannes</dc:creator><dc:identifier>10.1016/j.jaad.2009.05.050</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e48</prism:startingPage><prism:endingPage>e49</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007877/abstract?rss=yes"><title>Eyelid metastasis as an initial presentation of a gastric adenocarcinoma</title><link>http://www.eblue.org/article/PIIS0190962209007877/abstract?rss=yes</link><description>To the Editor: We report a 75-year-old white man who presented with a 4-month history of painless swelling of the left superior and inferior eyelid. His medical history included type 2 diabetes mellitus and hypertension. The physical examination showed an indurated erythematous plaque involving the left upper and lower eyelid that was hard to the touch (). A biopsy specimen of the skin lesion revealed diffuse infiltration with tumor cells arranged in small islands, cords, and ribbons between the collagen bundles throughout the dermis. The infiltrating tumor cells were mostly histiocytoid with an abundant, vacuolated, eosinophilic cytoplasm. Signet ring cells with a large intracytoplasmic vacuole compressing the nucleus to the periphery of the cell were less frequent. The nuclei were round and slightly pleomorphic with inconspicuous nucleoli with a few mitotic figures (). Cytoplasmic vacuoles stained positively with periodic acid–Schiff stain. With immunohistochemistry, the tumor cells expressed pancytokeratin and epithelial membrane antigen but not carcinoembryonic antigen.</description><dc:title>Eyelid metastasis as an initial presentation of a gastric adenocarcinoma</dc:title><dc:creator>Cristina Rodríguez-García, Sorahaya González-Hernández, Nuria Pérez-Robayna, Antonio Martín-Herrera, Rosalba Sánchez, Francisco Guimerá</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.055</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e49</prism:startingPage><prism:endingPage>e50</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209007889/abstract?rss=yes"><title>Folliculotropic mycosis fungoides masquerading as alopecia areata</title><link>http://www.eblue.org/article/PIIS0190962209007889/abstract?rss=yes</link><description>To the Editor: Early in 2004, a 27-year-old male presented to our department with a 2-year history of progressive patchy alopecia of the left side of the pubis and upper thigh without signs of inflammation (, A).</description><dc:title>Folliculotropic mycosis fungoides masquerading as alopecia areata</dc:title><dc:creator>Matilde Iorizzo, Laila El Shabrawi Caelen, Colombina Vincenzi, Cosimo Misciali, Antonella Tosti</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.056</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e50</prism:startingPage><prism:endingPage>e52</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209008391/abstract?rss=yes"><title>Primary cutaneous Hodgkin lymphoma</title><link>http://www.eblue.org/article/PIIS0190962209008391/abstract?rss=yes</link><description>To the Editor: A 70-year-old man presented in December 2001 with a 6-month history of erythematous papules and nodules on the right back (). He denied previous skin disease or a history of malignancy or autoimmune disorders.</description><dc:title>Primary cutaneous Hodgkin lymphoma</dc:title><dc:creator>Guglielmo Pranteda, Mattia Falchetto Osti, Maria Cristina Cox, Claudio Cacchi, Marta Carlesimo, Miriam Grimaldi, Laura Fidanza, Armando Bartolazzi</dc:creator><dc:identifier>10.1016/j.jaad.2009.06.076</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e52</prism:startingPage><prism:endingPage>e53</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209014820/abstract?rss=yes"><title>Subcutaneous morphea with dystrophic calcification with response to ceftriaxone treatment</title><link>http://www.eblue.org/article/PIIS0190962209014820/abstract?rss=yes</link><description>To the Editor: In March 2005, an otherwise healthy 16-year-old Austrian male presented to our department with a 2-year history of multiple asymptomatic, subcutaneous, firm nodules on both arms ranging in size from 3 to 6 mm with sequestration of whitish chalky material. In addition, the patient showed symmetric gynecomastia and a discrete lividoid, reticular discoloration with skin atrophy on the left chest ().</description><dc:title>Subcutaneous morphea with dystrophic calcification with response to ceftriaxone treatment</dc:title><dc:creator>Nadine Reiter, Laila El-Shabrawi, Bernd Leinweber, Elisabeth Aberer</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.016</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e53</prism:startingPage><prism:endingPage>e55</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209014935/abstract?rss=yes"><title>Cutaneous epithelioid angiosarcoma occurring at a peristomal site</title><link>http://www.eblue.org/article/PIIS0190962209014935/abstract?rss=yes</link><description>To the Editor: Peristomal skin disease is common. Close to 75% of abdominal stoma patients will incur a skin condition affecting their stoma site within 10 years from the time of surgery. The most frequently reported skin disorders around stoma sites are irritant reactions, preexisting skin diseases, infections, and nonspecific dermatitis.</description><dc:title>Cutaneous epithelioid angiosarcoma occurring at a peristomal site</dc:title><dc:creator>Chris Kon Fessa, Raghwa Sharma, Pablo Fernández-Peñas</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.026</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e55</prism:startingPage><prism:endingPage>e56</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209021136/abstract?rss=yes"><title>Facial hypertrichosis and trichomegaly developing in patients treated with the epidermal growth factor receptor inhibitor erlotinib</title><link>http://www.eblue.org/article/PIIS0190962209021136/abstract?rss=yes</link><description>To the Editor: Agents that target the epidermal growth factor receptor (EGFR) are being used as a therapy against a variety of malignancies, including lung cancer. The use of EGFR inhibitors is associated with a constellation of hair disorders, such as brittle, curly hair, diffuse nonscarring alopecia, and abnormal lengthening of the hair, eyebrows, eyelashes. We report three patients who developed facial hypertrichosis and eyelash trichomegaly while receiving erlotinib. The age, sex, underlying disease, previous therapies, and coexisting manifestations of the patients are shown in .</description><dc:title>Facial hypertrichosis and trichomegaly developing in patients treated with the epidermal growth factor receptor inhibitor erlotinib</dc:title><dc:creator>Theognosia Vergou, Alexander J. Stratigos, Eleni M. Karapanagiotou, Athina E. Matekovits, Kalliopi D. Dilana, Sotirios Tsimboukis, Christina Antoniou, Vassiliki Chasapi, Kostas N. Syrigos</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.589</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e56</prism:startingPage><prism:endingPage>e58</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209023068/abstract?rss=yes"><title>Epidermal growth factor receptor inhibition with erlotinib for palmoplantar keratoderma</title><link>http://www.eblue.org/article/PIIS0190962209023068/abstract?rss=yes</link><description>To the Editor: Olmsted syndrome is a rare autosomal dominant disorder of unknown cause characterized by symmetric mutilating hyperkeratotic plaques of palmoplantar and periorificial areas, with significant pain and disability. Treatment with oral retinoids and surgery is usually ineffective and is associated with significant toxicities. We describe the use of the epidermal growth factor receptor (EGFR) inhibitor erlotinib in a patient with Olmsted syndrome.</description><dc:title>Epidermal growth factor receptor inhibition with erlotinib for palmoplantar keratoderma</dc:title><dc:creator>Brandi M. Kenner-Bell, Amy S. Paller, Mario E. Lacouture</dc:creator><dc:identifier>10.1016/j.jaad.2009.10.052</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e58</prism:startingPage><prism:endingPage>e59</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210002136/abstract?rss=yes"><title>Cutaneous marginal zone B-cell lymphoma in a patient previously diagnosed with cutaneous Waldenström macroglobulinemia</title><link>http://www.eblue.org/article/PIIS0190962210002136/abstract?rss=yes</link><description>To the Editor: We report a case of cutaneous marginal zone B-cell lymphoma. This patient has been twice reported in the literature as having an atypical cutaneous presentation of Waldenström macroglobulinemia (WM). In 1991, at 46 years of age, our patient was diagnosed with WM based on findings of monoclonal immunoglobulin M (IgM) paraproteinemia, plasmacytoid lymphocytic bone marrow infiltrate, and the presence of urine kappa light chains. Three years after his initial presentation, he developed violaceous plaques of the scalp and chest. Immunohistochemical analysis revealed CD20- and CD79a-positive B cells with no light chain restriction. These findings were reported by Libow et al as a cutaneous manifestation of the patient's previously diagnosed WM. In 2002, the patient developed severe anemia, hepatosplenomegaly, and retroperitoneal adenopathy and was successfully treated with rituximab. The patient presented in 2005 with erythematous patches and plaques on the scalp. A biopsy specimen revealed dense dermal infiltrates of large to medium-sized lymphoid cells with plasmacytoid features. Immunohistochemical analysis demonstrated CD20- and CD79a-positive B cells with aberrant expression of BCL-2 and no light chain restriction. These findings were again reported as cutaneous manifestations of WM. In 2006, a bone marrow biopsy specimen revealed sheets of intermediate size CD20-positive lymphocytes comprising approximately 90% of the marrow and serum concentrations of IgM reaching 5074 mg/dL (range, 50-300 mg/dL). During this time, the patient developed extensive lymphadenopathy and responded well to bortezamib and dexamethasone.</description><dc:title>Cutaneous marginal zone B-cell lymphoma in a patient previously diagnosed with cutaneous Waldenström macroglobulinemia</dc:title><dc:creator>Marsha Mitchum, Melissa Scorza, Brian Thomas, Kenneth Galeckas</dc:creator><dc:identifier>10.1016/j.jaad.2010.02.013</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e59</prism:startingPage><prism:endingPage>e61</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209002710/abstract?rss=yes"><title>Iotaderma #199</title><link>http://www.eblue.org/article/PIIS0190962209002710/abstract?rss=yes</link><description></description><dc:title>Iotaderma #199</dc:title><dc:creator>Robert I. Rudolph</dc:creator><dc:identifier>10.1016/j.jaad.2009.03.002</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e63</prism:startingPage><prism:endingPage>e63</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209001388/abstract?rss=yes"><title>July iotaderma (#198)</title><link>http://www.eblue.org/article/PIIS0190962209001388/abstract?rss=yes</link><description></description><dc:title>July iotaderma (#198)</dc:title><dc:creator>Robert I. Rudolph</dc:creator><dc:identifier>10.1016/j.jaad.2009.02.003</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e63</prism:startingPage><prism:endingPage>e63</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210007140/abstract?rss=yes"><title>Editorial Board</title><link>http://www.eblue.org/article/PIIS0190962210007140/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00714-0</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</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/PIIS0190962210007085/abstract?rss=yes"><title>Contents</title><link>http://www.eblue.org/article/PIIS0190962210007085/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00708-5</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</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/PIIS0190962210007097/abstract?rss=yes"><title>Information for Readers</title><link>http://www.eblue.org/article/PIIS0190962210007097/abstract?rss=yes</link><description></description><dc:title>Information for Readers</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00709-7</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A27</prism:startingPage><prism:endingPage>A28</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210007103/abstract?rss=yes"><title>Instructions for Category 1 CME Credit</title><link>http://www.eblue.org/article/PIIS0190962210007103/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)00710-3</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A34</prism:startingPage><prism:endingPage>A34</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210007115/abstract?rss=yes"><title>Dermatology Calendar</title><link>http://www.eblue.org/article/PIIS0190962210007115/abstract?rss=yes</link><description></description><dc:title>Dermatology Calendar</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(10)00711-5</dc:identifier><dc:source>Journal of the American Academy of Dermatology 63, 2 (2010)</dc:source><dc:date>2010-08-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-08-01</prism:publicationDate><prism:volume>63</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0190-9622(10)X0007-X</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A41</prism:startingPage><prism:endingPage>A41</prism:endingPage></item></rdf:RDF>