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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> © 2011 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>66</prism:volume><prism:number>6</prism:number><prism:publicationDate>June 2012</prism:publicationDate><prism:copyright> © 2011 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/PIIS0190962211008140/abstract?rss=yes"/><rdf:li 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rdf:resource="http://www.eblue.org/article/PIIS0190962210004007/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS019096221000695X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962211005305/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962210021122/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962211007961/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962212003714/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962212003726/abstract?rss=yes"/><rdf:li rdf:resource="http://www.eblue.org/article/PIIS0190962212003738/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.eblue.org/article/PIIS0190962211008140/abstract?rss=yes"><title>Human papillomavirus–related genital disease in the immunocompromised host: Part I</title><link>http://www.eblue.org/article/PIIS0190962211008140/abstract?rss=yes</link><description>Human papillomavirus (HPV) is responsible for common condyloma acuminata and a number of premalignant and malignant anogenital lesions. These conditions are of particular concern in immunocompromised individuals who have higher risk of malignant transformation and are more difficult to treat. This is part I of a two-part review that will highlight the cutaneous features of condyloma acuminata and vaginal, vulvar, penile, and anal intraepithelial neoplasias, with an emphasis on presentation of these HPV-mediated diseases in the immunocompromised host. Counseling patients about these conditions requires a thorough understanding of the epidemiology, natural history of HPV, transmission and infectivity, risk of malignancy, and the role of the host immune response in clearing HPV lesions. Part II will provide an updated review of available treatments, with a focus on recent advances and the challenges faced in successfully treating HPV lesions in immunocompromised patients.</description><dc:title>Human papillomavirus–related genital disease in the immunocompromised host: Part I</dc:title><dc:creator>Rachel H. Gormley, Carrie L. Kovarik</dc:creator><dc:identifier>10.1016/j.jaad.2010.12.050</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>867.e1</prism:startingPage><prism:endingPage>867.e14</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212001053/abstract?rss=yes"><title>CME examination</title><link>http://www.eblue.org/article/PIIS0190962212001053/abstract?rss=yes</link><description></description><dc:title>CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2012.01.020</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>881</prism:startingPage><prism:endingPage>881</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212001065/abstract?rss=yes"><title>Answers to CME examination</title><link>http://www.eblue.org/article/PIIS0190962212001065/abstract?rss=yes</link><description></description><dc:title>Answers to CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2012.01.021</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>882</prism:startingPage><prism:endingPage>882</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212004276/abstract?rss=yes"><title>American Board of Dermatology Examination Dates</title><link>http://www.eblue.org/article/PIIS0190962212004276/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(12)00427-6</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>882</prism:startingPage><prism:endingPage>882</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008139/abstract?rss=yes"><title>Human papillomavirus–related genital disease in the immunocompromised host: Part II</title><link>http://www.eblue.org/article/PIIS0190962211008139/abstract?rss=yes</link><description>Human papillomavirus is responsible for common condyloma acuminata and a number of premalignant and malignant anogenital lesions. The immunocompromised population is at particular risk because of a higher incidence of malignant transformation. Lesions in this population may prove refractory to standard treatment. This is part II of a two-part review that will discuss the treatment of condyloma acuminata and vaginal, vulvar, penile, and anal intraepithelial neoplasias. This article will provide an updated review of available treatments, with a focus on recent advances and the challenges faced in successfully treating human papillomavirus lesions in the immunocompromised host.</description><dc:title>Human papillomavirus–related genital disease in the immunocompromised host: Part II</dc:title><dc:creator>Rachel H. Gormley, Carrie L. Kovarik</dc:creator><dc:identifier>10.1016/j.jaad.2010.12.049</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>883.e1</prism:startingPage><prism:endingPage>883.e17</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212001089/abstract?rss=yes"><title>Answers to CME examination</title><link>http://www.eblue.org/article/PIIS0190962212001089/abstract?rss=yes</link><description></description><dc:title>Answers to CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2012.01.023</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>899</prism:startingPage><prism:endingPage>899</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212001077/abstract?rss=yes"><title>CME examination</title><link>http://www.eblue.org/article/PIIS0190962212001077/abstract?rss=yes</link><description></description><dc:title>CME examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jaad.2012.01.022</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Continuing Medical Education</prism:section><prism:startingPage>900</prism:startingPage><prism:endingPage>900</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211006943/abstract?rss=yes"><title>Molecular profiling and gene expression analysis in cutaneous sarcoidosis: The role of interleukin-12, interleukin-23, and the T-helper 17 pathway</title><link>http://www.eblue.org/article/PIIS0190962211006943/abstract?rss=yes</link><description>Background: Cutaneous sarcoidosis (CS) skin provides relatively noninvasive access to granulomatous sarcoidosis tissue.Objective: We sought to explore the role of the T-helper (Th)1 and Th17 pathways in sarcoidosis.Methods: We used molecular profiling and gene expression analysis to analyze the Th1 and Th17 pathways and other immune-mediated pathways in CS. Molecular profiles were obtained from sarcoidosis skin lesions (lesional skin [LS]), unaffected skin from patients with CS (non-LS), and the skin of healthy control subjects. Whole blood was collected to compare the molecular profile of sarcoidosis skin lesions and whole blood.Results: Twenty participants were enrolled: 15 with active CS and 5 healthy volunteers. Microarray analyses comparing non-LS and healthy volunteer skin with LS showed several thousand genes differentially expressed (≥2-fold change false discovery rate, P &lt; .01). Targeted selections of genes associated with Th1 and Th17 phenotypes showed a strong Th1 profile of sarcoidosis and expression of interleukin (IL)-23 and IL-23R with limited expression of other Th17 pathway genes. IL-21 and signal transducer and activator of transcription 3 (STAT3) were also dysregulated in skin and whole blood, providing additional evidence for involvement of the IL-12 pathway and potential activation of the Th17 pathway.Limitations: Measurements were made at a single point in time and may not identify mechanisms that may be identified in patients followed up longitudinally.Conclusion: These findings provide novel insight into the dysregulated pathways that may be involved in the pathogenesis of sarcoidosis.</description><dc:title>Molecular profiling and gene expression analysis in cutaneous sarcoidosis: The role of interleukin-12, interleukin-23, and the T-helper 17 pathway</dc:title><dc:creator>Marc A. Judson, Richard M. Marchell, MaryAnn Mascelli, Alexa Piantone, Elliot S. Barnathan, Kevin J. Petty, Dion Chen, Hongtao Fan, Heidi Grund, Keying Ma, Frédéric Baribaud, Carrie Brodmerkel</dc:creator><dc:identifier>10.1016/j.jaad.2011.06.017</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-09-19</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-09-19</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>901</prism:startingPage><prism:endingPage>910.e2</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211005482/abstract?rss=yes"><title>HLA antigen expression in melanocytic lesions: Is acquisition of HLA antigen expression a biomarker of atypical (dysplastic) melanocytes?</title><link>http://www.eblue.org/article/PIIS0190962211005482/abstract?rss=yes</link><description>Background: Although criteria are established for the histologic diagnosis of atypical nevi (AN), consensus about the criteria in the diagnosis of and in the definition of AN is limited. Moreover, intraobserver and interobserver differences in the application of these criteria for the diagnosis of AN have been observed.Objective: We sought to determine the usefulness of HLA antigen expression as a biomarker of AN.Methods: The immunoperoxidase reaction was used to mark common nevi and AN with HLA class I heavy chain–, β2microglobulin (β2m)-, and HLA class II β chain–specific monoclonal antibodies.Results: HLA class I heavy chain, β2m, and HLA class II β chain were expressed in 5 (8.6%) of the 58 common nevi and in 46 (∼72%) of the 64 atypical melanocytic lesions. Among common lesions, only halo nevi expressed HLA class I heavy chain, β2m, and HLA class II β chain. The level of HLA class I heavy chain β2m and of HLA class II β chain expression correlated with the degree of cytologic atypia and architectural disorder.Limitations: The number of lesions tested and the subjective nature of the analysis of immunohistochemical staining of tissue sections are both limitations.Conclusions: The data presented suggest that HLA antigen expression is an objective biomarker that correlates well with the degree of cytologic atypia in AN and may: (1) be useful to distinguish common nevi from AN, and (2) represent a more objective measure to determine which AN should be excised.</description><dc:title>HLA antigen expression in melanocytic lesions: Is acquisition of HLA antigen expression a biomarker of atypical (dysplastic) melanocytes?</dc:title><dc:creator>Michael Campoli, James E. Fitzpatrick, Whitney High, Soldano Ferrone</dc:creator><dc:identifier>10.1016/j.jaad.2011.04.025</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-03-26</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-03-26</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>911</prism:startingPage><prism:endingPage>916.e8</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211006955/abstract?rss=yes"><title>Integrating clinical/dermatoscopic findings and fluorescence in situ hybridization in diagnosing melanocytic neoplasms with less than definitive histopathologic features</title><link>http://www.eblue.org/article/PIIS0190962211006955/abstract?rss=yes</link><description>Background: Early diagnosis of melanoma remains of paramount importance, because it has been widely demonstrated that survival is strongly related to Breslow thickness. Several studies have shown that dermatoscopy improves accuracy in the diagnosis of melanoma. Although histopathology is considered the gold standard to differentiate melanoma from nevi, there are some cases of melanoma in which the histopathologic features are less than definitive. It has also been demonstrated that fluorescence in situ hybridization can be used to differentiate melanomas from nevi based on chromosomal copy number aberrations.Objective: In this study we present a case series to demonstrate the value of combining fluorescence in situ hybridization and dermatoscopy/clinical history to enhance diagnostic capability for selected cases of early melanoma.Methods: Cases were identified that had dermatoscopic findings or clinical history highly suggestive of melanoma and fluorescence in situ hybridization evaluation positive for melanoma, but histopathologic features that were less than definitive. Two dermatopathologists performed independent histologic analysis of specimens and two dermatologists experienced in dermatoscopy reviewed dermatoscopic and clinical data.Results: Nine cases meeting inclusion criteria were identified. In 6 cases the histologic differential diagnosis was dysplastic nevus versus early melanoma whereas in 3 cases the differential diagnosis included Spitz nevus versus early melanoma.Limitations: Limitations of this study include restrictive inclusion criteria and study design restricted to a case series.Conclusion: This exploratory study demonstrates that in a subset of early melanoma cases, combining multiple diagnostic modalities such as dermatoscopy and molecular techniques with histology enhances detection of early melanoma.</description><dc:title>Integrating clinical/dermatoscopic findings and fluorescence in situ hybridization in diagnosing melanocytic neoplasms with less than definitive histopathologic features</dc:title><dc:creator>Beatrice Nardone, Mary Martini, Klaus Busam, Ashfaq Marghoob, Dennis P. West, Pedram Gerami</dc:creator><dc:identifier>10.1016/j.jaad.2011.05.051</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-10-03</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-10-03</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>917</prism:startingPage><prism:endingPage>922</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211006980/abstract?rss=yes"><title>Dermatoscopic vascular patterns in cutaneous Merkel cell carcinoma</title><link>http://www.eblue.org/article/PIIS0190962211006980/abstract?rss=yes</link><description>Background: Merkel cell carcinoma (MCC) is one of the most aggressive primary cutaneous malignancies. The clinical diagnosis of MCC is often delayed. Although the rarity of this skin cancer partially explains the low clinical suspicion by physicians, the absence of characteristic clinical features contributes to the delay in diagnosis. Dermatoscopy has proven a useful diagnostic tool in other cutaneous malignancies; however, the dermatoscopic features of cutaneous MCC are unknown.Objective: We performed dermatoscopy on 10 primary cutaneous MCC to describe the dermatoscopic features and correlate these findings with the histopathologic parameters.Methods: Consecutive patients with cutaneous MCC were identified and their tumors were evaluated under dermatoscopy. An 8-point MCC histopathology profile was recorded for each primary tumor in an attempt to correlate individual parameters with dermatoscopic features.Results: All 10 tumors showed an irregular vascular pattern under dermatoscopy and demonstrated milky-red areas/globules and numerous linear irregular vessels. No correlation was noted between dermatoscopic and histopathologic features.Limitations: The patients were from a single institution and tumors evaluated by a single dermatoscopic reviewer. Because of the rarity of this tumor, a small number of tumors were evaluated (10).Conclusion: MCC exhibits a variety of dermatoscopic vascular patterns, most commonly milky-red areas/globules, polymorphous vessels, and linear-irregular vessels. Although we found no specific dermatoscopic pattern for MCC in our series, the polymorphous vascular pattern was atypical and suggestive of a malignant process. Further studies should be done to investigate the potential correlation between dermatoscopic features and histopathologic parameters.</description><dc:title>Dermatoscopic vascular patterns in cutaneous Merkel cell carcinoma</dc:title><dc:creator>Mandy S. Harting, Mathew W. Ludgate, Douglas R. Fullen, Timothy M. Johnson, Christopher K. Bichakjian</dc:creator><dc:identifier>10.1016/j.jaad.2011.06.020</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-10-07</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-10-07</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>923</prism:startingPage><prism:endingPage>927</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008012/abstract?rss=yes"><title>In search of prognostic indicators for lymphomatoid papulosis: A retrospective study of 123 patients</title><link>http://www.eblue.org/article/PIIS0190962211008012/abstract?rss=yes</link><description>Background: Lymphomatoid papulosis (LyP) is a benign recurrent papulonodular skin eruption with histologically malignant features that sometimes (10%-20%) progresses to lymphoma.Objective: We retrospectively evaluated the clinical course of patients with LyP and identify prognostic factors possibly indicating a malignant course.Methods: Clinical, histopathologic, and immunologic features and molecular genetics were examined and correlated with clinical course and outcomes. Immunophenotyping and chemokine profiling were performed in select skin biopsy samples. A follow-up questionnaire was sent to patients. Clinical course and association with neoplastic disorders were correlated with LyP subtypes, molecular genetics, and immunophenotyping studies.Results: Of 123 patients with LyP (1991-2008) followed up a mean of 4 years (range, 2 months to 14 years), 17 (14%) had an associated hematologic malignancy, 8 of which were mycosis fungoides. Histopathologic analyses demonstrated classic LyP type A (n = 69), B (n = 13), or C (n = 6), and a slight predominance of T-cell CD8 marker expression for type A. More than one type of lesion was present in 9 patients with a higher incidence of hematologic malignancies. T-cell receptor gene rearrangement positivity was about two times higher, with LyP associated with hematologic malignancy (82% vs 44%; odds ratio 5.7; P = .02). Chemokine studies in a subset of 25 patients showed chemokine receptor (CCR) CCR4+ and thymus and activation-related chemokine (TARC+) in all LyP types and CCR3+ and chemokine-related receptor (CXCR) CXCR3+ in types B and C.Limitations: Retrospective study design is a limitation.Conclusions: Positive T-cell receptor gene rearrangement or diagnosis of mixed-type LyP may be a prognostic indicator of disease more prone to progress to lymphoma.</description><dc:title>In search of prognostic indicators for lymphomatoid papulosis: A retrospective study of 123 patients</dc:title><dc:creator>Aieska de Souza, Rokea A. el-Azhary, Michael J. Camilleri, David A. Wada, David L. Appert, Lawrence E. Gibson</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.012</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>928</prism:startingPage><prism:endingPage>937</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212004288/abstract?rss=yes"><title>Change of Address</title><link>http://www.eblue.org/article/PIIS0190962212004288/abstract?rss=yes</link><description></description><dc:title>Change of Address</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(12)00428-8</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>937</prism:startingPage><prism:endingPage>937</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211006906/abstract?rss=yes"><title>Children’s sun exposure and sun protection: Prevalence in Australia and related parental factors</title><link>http://www.eblue.org/article/PIIS0190962211006906/abstract?rss=yes</link><description>Background: Reducing childhood exposure to ultraviolet radiation is important to minimize lifetime skin cancer risk.Objectives: We sought to describe the prevalence of children’s sun-related behaviors and associated parental and other factors.Methods: In weekly cross-sectional telephone interviews during summer, 1140 parents/guardians of children aged 0 to 11 years were recruited. Parents provided proxy reports for one of their children. Key questions related to weekend sun protection and sunburn, parent’s sun-related attitudes, and demographic characteristics. Potential predictors of children’s sun protection and sunburn were analyzed adjusting for covariates including weather conditions on the previous weekend.Results: On summer weekends, 73% of children spent longer than 15 minutes outdoors in peak ultraviolet radiation periods. Of these, 64% were protected by a hat and 58% by sun-protection factor 15 or higher sunscreen, 32% stayed under shade, and 18% wore three-quarter or long-sleeved tops. Overall, 8% of children had sunburn. Parental attitudes were typically supportive of children’s sun protection. Parental use of hats (odds ratio [OR] 3.1; 95% confidence interval [CI] 1.6-6.2), shade (OR 9.6; 95% CI 4.4-20.8), sunscreen (OR 12.6; 95% CI 5.2-30.4), longer leg cover (OR 10.3; 95% CI 4.4-24.0), and two or more protective behaviors (OR 5.7; 95% CI 2.8-11.9) increased the odds of their children practicing these behaviors, as did some parental attitudes.Limitations: We relied on cross-sectional parent reports.Conclusion: Although children’s sun protection was favorable, there was room for improvement. Health promotion to improve sun-protection practices in adults may benefit children’s sun-safe behaviors.</description><dc:title>Children’s sun exposure and sun protection: Prevalence in Australia and related parental factors</dc:title><dc:creator>Suzanne Dobbinson, Melanie Wakefield, David Hill, Afaf Girgis, Joanne F. Aitken, Kerri Beckmann, Anthony I. Reeder, Natalie Herd, Matthew J. Spittal, Andrew Fairthorne, Kelly-Ann Bowles</dc:creator><dc:identifier>10.1016/j.jaad.2011.06.015</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-09-05</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-09-05</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>938</prism:startingPage><prism:endingPage>947</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211006876/abstract?rss=yes"><title>Patient-centered online management of psoriasis: A randomized controlled equivalency trial</title><link>http://www.eblue.org/article/PIIS0190962211006876/abstract?rss=yes</link><description>Background: Previous research suggests that technology-enabled health care delivery may improve access to dermatologic specialty care. Outcomes research using validated outcomes measures is necessary for evaluation of novel health care delivery models.Objective: We sought to compare the clinical equivalence of a novel patient-centered online health care delivery model with standard in-office care for follow-up treatment of patients with psoriasis.Methods: A total of 64 participants with psoriasis were randomized to receive follow-up care either in-office or online over a 24-week period. Patients randomized to the online group underwent standardized training on capturing high-quality digital images of their psoriatic skin and transmitting these images and clinical history to a dermatologist securely. The dermatologist then performed asynchronous, online evaluation and provided recommendations directly to patients. We used clinically validated disease severity and quality-of-life measures to assess effectiveness between the models.Results: Both online and in-office groups showed improvement in psoriasis disease severity as measured by mean improvement in Psoriasis Area and Severity Index (online group: mean = –3.4, in-office: mean = –3.4). Patient-centered online care resulted in similar improvement in psoriasis severity compared with in-person follow-up care (mean difference in Psoriasis Area and Severity Index change 0.1, 95% confidence interval –2.2 to 2.3, a priori equivalence margin of 2.5). Investigator Global Assessment and Dermatology Life Quality Index scores also improved during the study period; no significant differences existed between the two groups.Limitations: The follow-up period was limited to 24 weeks.Conclusion: A patient-centered online model may be an effective alternative to in-office care for follow-up management of psoriasis.</description><dc:title>Patient-centered online management of psoriasis: A randomized controlled equivalency trial</dc:title><dc:creator>Cindy J. Chambers, Kory K. Parsi, Clayton Schupp, April W. Armstrong</dc:creator><dc:identifier>10.1016/j.jaad.2011.05.047</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-09-05</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-09-05</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>948</prism:startingPage><prism:endingPage>953</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211007997/abstract?rss=yes"><title>Childhood- and later-onset vitiligo have diverse epidemiologic and clinical characteristics</title><link>http://www.eblue.org/article/PIIS0190962211007997/abstract?rss=yes</link><description>Background: Vitiligo onset during childhood is common. There are limited data regarding childhood-onset vitiligo.Objective: We sought to provide an epidemiologic and clinical comparison between childhood- and later-onset vitiligo.Methods: Two groups of patients were included in this cross-sectional study. Consecutive patients examined at the Vitiligo Clinic of Andreas Sygros Hospital for Skin and Venereal Diseases, Athens, Greece, from January 2005 to December 2009 with a disease onset before the age of 12 years were included in the childhood-onset group. The later-onset group included randomly selected patients who were examined at the same period and had a disease onset after the age of 12 years. After clinical examination, a standardized questionnaire was completed for each patient.Results: In all, 126 patients were included in the childhood-onset and 107 patients in the later-onset group. Childhood-onset vitiligo: (1) involved different sites at initial presentation, (2) included more cases of segmental type, and (3) was characterized by a higher prevalence of allergic diseases and a lower prevalence of thyroid diseases. Longer duration of disease and a positive family history of thyroid disease were associated with the presence of thyroid disease only in the childhood-onset group. In the later-onset group, only female sex was associated with the presence of thyroid disease.Limitations: The study was conducted in a hospital specializing in skin diseases and a selection bias toward more severe vitiligo cases is possible.Conclusions: Childhood-onset vitiligo had distinct epidemiologic and clinical characteristics, compared with later-onset disease.</description><dc:title>Childhood- and later-onset vitiligo have diverse epidemiologic and clinical characteristics</dc:title><dc:creator>Electra Nicolaidou, Christina Antoniou, Alexandra Miniati, Eirini Lagogianni, Athina Matekovits, Alex Stratigos, Andreas Katsambas</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.010</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>954</prism:startingPage><prism:endingPage>958</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008024/abstract?rss=yes"><title>Fibroblastic rheumatism: A report of 4 cases with potential therapeutic implications</title><link>http://www.eblue.org/article/PIIS0190962211008024/abstract?rss=yes</link><description>Background: Fibroblastic rheumatism is a rare dermatoarthropathy characterized by the sudden onset of cutaneous nodules, flexion contractures, and polyarthritis. Histopathology in the correct clinical context confirms the diagnosis. Treatment is based on observational data from single case reports.Objective: We describe 4 cases, review histologic findings, and discuss therapeutic responses.Methods: Cases coded as fibroblastic rheumatism were retrieved from institutional and consultation files. Medical charts and biopsy specimens were reviewed. Elastic stains and immunostains for smooth muscle actin, S100, CD34, desmin, and epithelial membrane antigen were performed on selected cases.Results: Four cases were identified. Patients displayed cutaneous nodules and arthralgias. Flexion contractures/decreased motion were present in two patients; one patient had associated Raynaud phenomenon and erosive joint disease. Biopsy specimens demonstrated a fibroblastic proliferation associated with a collagenous stroma. Growth patterns varied from cellular fascicles to paucicellular randomly arranged spindle cells. Elastic fibers were absent in all cases tested (3/3). Immunohistochemical stains demonstrated immunoreactivity for smooth muscle actin in one of 3 cases in a myofibroblastic pattern. Other stains were negative. One patient had complete resolution of disease with methotrexate. One patient partially responded to interferon-alfa and ribavirin and was subsequently treated with methotrexate with additional improvement. One patient had limited response to all therapies attempted. One patient was lost to follow-up.Limitations: Small sample size (n = 4) is a limitation.Conclusion: Our data expand the clinical, histologic, and therapeutic response data on fibroblastic rheumatism. Correlation with clinical history is critical to avoid misdiagnosis as other fibrosing lesions. Methotrexate and interferon-alfa are potential therapies.</description><dc:title>Fibroblastic rheumatism: A report of 4 cases with potential therapeutic implications</dc:title><dc:creator>Sara A. Jurado, G.K. Glen Alvin, M. Angelica Selim, Clare A. Pipkin, Douglas Kress, Maria Jasmin J. Jamora, Steven D. Billings</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.013</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>959</prism:startingPage><prism:endingPage>965</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008097/abstract?rss=yes"><title>Expression of innate defense antimicrobial peptides in hidradenitis suppurativa</title><link>http://www.eblue.org/article/PIIS0190962211008097/abstract?rss=yes</link><description>Background: Hidradenitis suppurativa (HS) is a chronic inflammatory disorder of apocrine gland-bearing skin. It is associated with alterations in innate immunity and frequent bacterial infections.Objective: We investigated the expression of innate defense antimicrobial peptides in patients with HS and different grades of severity.Methods: Skin biopsy specimens and sweat were collected from 36 patients with HS and 57 healthy control subjects for analysis of epithelial antimicrobial peptides by real-time reverse transcription–polymerase chain reaction, immunohistochemistry, enzyme-linked immunosorbent assay, and surface-enhanced laser desorption ionization time-of-flight mass spectrometry.Results: We provide evidence that human β-defensin-3 expression is induced in lesional HS skin on transcriptional and protein levels, yet, this up-regulation was not detectable in patients with severe HS (Hurley grade III). In contrast, messenger RNA expression of ribonuclease 7 was significantly diminished in lesional HS skin specimens irrespective of HS severity. Overall levels of dermcidin/dermcidin-derived peptides in sweat and messenger RNA expression of psoriasin in skin biopsy specimens did not differ between patients with HS and healthy control subjects.Limitation: The relatively small number of samples, in particular in the group of patients with HS and Hurley grade III, is a limitation.Conclusion: Deficient constitutive production of ribonuclease 7 and, in severe HS, reduced human β-defensin-3 induction may contribute to impaired immunity within the hair follicle and thereby boost HS inflammation and severity.</description><dc:title>Expression of innate defense antimicrobial peptides in hidradenitis suppurativa</dc:title><dc:creator>Silke C. Hofmann, Viola Saborowski, Sylke Lange, Winfried V. Kern, Leena Bruckner-Tuderman, Siegbert Rieg</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.020</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>966</prism:startingPage><prism:endingPage>974</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008231/abstract?rss=yes"><title>Cutaneous and mucosal mucormycosis mimicking pancreatic panniculitis and gouty panniculitis</title><link>http://www.eblue.org/article/PIIS0190962211008231/abstract?rss=yes</link><description>Background: Histopathologic study of lesions of cutaneous mucormycosis usually shows suppurative granulomas involving the deep dermis and subcutaneous fat. Large, broad and non-septate fungal hyphae are easily identified within the necrotic areas.Objective: The main goal of our study is to describe the histopathologic features of 13 cases of cutaneo-mucous mucormycosis, which mimicked the findings of pancreatic and/or gouty panniculitis and discuss the histopathologic differential diagnosis among these 3 disorders.Methods: Histopathologic examination of sections stained with hematoxylin-eosin, periodic acid–Schiff (PAS), Gomori methenamine, and Grocott stains. All sections were examined under polarized light. One case was immunohistochemically studied with anti-BCG antibody.Results: Histopathologically, the most striking feature consisted of the presence of groups of necrotic adipocytes lacking nuclei and large cytoplasm with pale basophilic hue due to calcium salts deposition. In other areas, groups of necrotic adipocytes filled with radially oriented needle-shaped and slightly eosinophilic crystals were seen. These intracellular crystals were refractile under polarized light examination. Numerous thick-walled non-septate fungal hyphae scattered throughout the necrotic areas were also seen in all cases.Limitations: The study was limited to 13 cases.Conclusions: Histopathologic study of 13 cases of subcutaneous mucormycosis demonstrated features closely resembling those of pancreatic panniculitis and/or gouty panniculitis. Ghost adipocytes should be not considered as diagnostic of pancreatic panniculitis and necrotic adipocytes containing needle-shaped refractile crystals should be not interpreted as specific of gouty panniculitis.</description><dc:title>Cutaneous and mucosal mucormycosis mimicking pancreatic panniculitis and gouty panniculitis</dc:title><dc:creator>Luis Requena, Panitta Sitthinamsuwan, Carlos Santonja, María Teresa Fernández-Figueras, José Luis Rodríguez-Peralto, Zsolt Argenyi, Antonio Torrelo, Lorenzo Cerroni, Heinz Kutzner</dc:creator><dc:identifier>10.1016/j.jaad.2011.06.024</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-09-29</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-09-29</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Dermatopathology</prism:section><prism:startingPage>975</prism:startingPage><prism:endingPage>984</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211023619/abstract?rss=yes"><title>The unsolicited ominous diagnosis: Legal, moral, and ethical considerations</title><link>http://www.eblue.org/article/PIIS0190962211023619/abstract?rss=yes</link><description>   A respected physician affiliated with an academic medical center is shopping at a local gift shop with his spouse. The physician is being helped by the owner of the shop, a fair-skinned woman that he estimates to be in her mid-forties. During this interaction, the physician cannot help but notice an asymmetric lesion with variable pigmentation on the woman’s left upper arm. Although this physician is not a dermatologist, he is a general surgeon with experience in excising malignant melanomas and performing sentinel lymph node biopsies. His experience and clinical acumen leads him to be clinically suspicious that this lesion might be a melanoma.</description><dc:title>The unsolicited ominous diagnosis: Legal, moral, and ethical considerations</dc:title><dc:creator>Jane M. Grant-Kels, Julia K. Anderson, Barry D. Kels</dc:creator><dc:identifier>10.1016/j.jaad.2011.12.026</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Dermatoethics Consultation</prism:section><prism:startingPage>985</prism:startingPage><prism:endingPage>987</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211010644/abstract?rss=yes"><title>A critical reappraisal of the current data on drug-induced linear immunoglobulin A bullous dermatosis: A real and separate nosological entity?</title><link>http://www.eblue.org/article/PIIS0190962211010644/abstract?rss=yes</link><description>Background: Linear IgA disease (LAD) has been associated with a variety of drugs over the past 30 years.Objective: To review current literature on all available cases of drug-induced LAD, in order to ascertain whether a close relationship is justified, so that it constitutes a real and separate nosological entity.Methods: The PubMed database was searched for all articles written in English related to drug-induced LAD published between January 1980 and December 2010.Results: The literature review shows that at least 84 articles were published, describing a total of 103 patients. Of these articles, only 46, from 13 countries, were included in this analysis, with a total of 52 patients: 24 (46.2%) were believed to be induced by vancomycin and 28 (53.8%) by drugs other than vancomycin. Challenge-dechallenge-rechallenge testing protocol was performed on only 6 (11.5%) of 52 patients, of which only 5 showed a positive result, while the Naranjo algorithm was performed on only 2 of them (0.3%).Limitations: The evidence of this review analysis is based only on case reports. No study on large samples of drug-induced LAD is currently available.Conclusions: The literature analysis reveals no strong scientific evidence to support the notion that some drugs have induced LAD; therefore in many reviewed cases, we must question whether drug-induced LAD is really the underlying entity. Further and thorough investigations using one of the available algorithms for adverse drug reaction are warranted.</description><dc:title>A critical reappraisal of the current data on drug-induced linear immunoglobulin A bullous dermatosis: A real and separate nosological entity?</dc:title><dc:creator>Giulio Fortuna, Julio Cesar Salas-Alanis, Eugenio Guidetti, M. Peter Marinkovich</dc:creator><dc:identifier>10.1016/j.jaad.2011.09.018</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-12-12</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-12-12</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Reviews</prism:section><prism:startingPage>988</prism:startingPage><prism:endingPage>994</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211010772/abstract?rss=yes"><title>Toxic epidermal necrolysis: Review of pathogenesis and management</title><link>http://www.eblue.org/article/PIIS0190962211010772/abstract?rss=yes</link><description>Toxic epidermal necrolysis (TEN) is a severe cutaneous drug reaction with a mortality rate of approximately 30%. The hallmark of TEN is widespread epidermal sloughing due to keratinocyte apoptosis. Multiple genetic associations between TEN and specific ethnic populations have been determined. The pathophysiology of TEN has yet to be fully elucidated; however, current pathogenic models implicate Fas ligand, granulysin, and reactive oxygen species. The value of current therapies, such as intravenous immunoglobulin and corticosteroids, remains under evaluation.</description><dc:title>Toxic epidermal necrolysis: Review of pathogenesis and management</dc:title><dc:creator>Andrew Downey, Chris Jackson, Nadia Harun, Alan Cooper</dc:creator><dc:identifier>10.1016/j.jaad.2011.09.029</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-12-12</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-12-12</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Reviews</prism:section><prism:startingPage>995</prism:startingPage><prism:endingPage>1003</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212002526/abstract?rss=yes"><title>Calcinosis cutis: An additional therapy to consider</title><link>http://www.eblue.org/article/PIIS0190962212002526/abstract?rss=yes</link><description>To the Editor: Reiter et al provide a comprehensive review of treatment options for calcinosis cutis (CC). However, they do not discuss the role of hematopoietic stem cell transplantation (HSCT), a treatment modality that has shown some promise in this condition and may have an increasing role as a potential treatment option as the evidence for this modality continues to evolve.</description><dc:title>Calcinosis cutis: An additional therapy to consider</dc:title><dc:creator>Nicole F. Velez, Jeffrey P. Callen, Ruth Ann Vleugels</dc:creator><dc:identifier>10.1016/j.jaad.2011.11.967</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>1004</prism:startingPage><prism:endingPage>1005</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212002599/abstract?rss=yes"><title>Reply</title><link>http://www.eblue.org/article/PIIS0190962212002599/abstract?rss=yes</link><description>To the Editor: We thank Dr Velez and coauthors for their comments on our article, “Calcinosis cutis, part II: Treatment options.” Autologous stem cell transplantation (ASCT) exerts a positive effect on soft-tissue calcification. We agree with the author's suggestion that ASCT might be a reasonable choice for the treatment of extensive lifestyle-limiting and painful dystrophic calcinosis cutis that does not respond to traditional therapy. In ASCT, conditioning with high-dose cyclophosphamide, antithymocyte globulin, and/or total-body irradiation nullifies the majority of autoreactive effector cells involved in the adaptive and innate immune response, including B and T lymphocytes, monocytes, natural killer cells, and dendritic cells. Thus, the immunosuppressive effect of ASCT may be regarded as the key factor in autoimmune diseases. A favorable response of the underlying disease to ASCT will logically lead to the resolution of all accompanying symptoms, including skin calcification. Nevertheless, one should keep in mind the fact that the transplant-related mortality is approximately 7%, whereas transplant-related toxicity registered 2 years after ASCT was as high as 33%. Therefore, a careful risk-benefit evaluation must be performed for each patient. What we miss in the letter of Dr Velez and colleagues is the fact that not only dystrophic calcinosis cutis in connective tissue disease, but also calciphylaxis (in most cases a result of end-stage renal disease) may benefit from ASCT. In this context Mandelbrot et al described the resolution of extensive calciphylactic lesions in a young woman with systemic lupus erythematosus, undergoing hemodialysis for the treatment of lupus nephritis. It is not clear whether the calciphylaxis arose from systemic lupus erythematosus or was secondary to hemodialysis. However, the impressive fact was that the previously painful calciphylactic lesions had healed fully after ASCT treatment and the patient required no further medication for pain relief. In conclusion, ASCT may be regarded as a maximal variant of immunosuppressive therapy in autoimmune diseases and even reverses calcinosis cutis. We suggest ASCT as a therapy option for patients with severe therapy-refractory dystrophic calcinosis caused by autoimmune disease and in patients with extensive calciphylaxis.</description><dc:title>Reply</dc:title><dc:creator>Nadine Reiter, Elisabeth Aberer</dc:creator><dc:identifier>10.1016/j.jaad.2012.02.028</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>1005</prism:startingPage><prism:endingPage>1005</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212002575/abstract?rss=yes"><title>Evidence for fractional laser treatment in the improvement of cutaneous scars</title><link>http://www.eblue.org/article/PIIS0190962212002575/abstract?rss=yes</link><description>To the Editor: We read with great interest the article by Tziotzios and colleagues describing strategies to reduce cutaneous scarring, published in January 2012. This valuable review article very briefly touches on fractional laser therapy for scars, and comments that “there is a limited evidence base to support use of fractional laser therapy.”</description><dc:title>Evidence for fractional laser treatment in the improvement of cutaneous scars</dc:title><dc:creator>Kavitha K. Reddy, Jeremy A. Brauer, Roy G. Geronemus</dc:creator><dc:identifier>10.1016/j.jaad.2012.01.047</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>1005</prism:startingPage><prism:endingPage>1006</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212002563/abstract?rss=yes"><title>Reply</title><link>http://www.eblue.org/article/PIIS0190962212002563/abstract?rss=yes</link><description>To the Editor: We thank Dr Reddy et al for their comments and for suggesting a wider review of current evidence for the use of fractional lasers in the treatment of scars. The focus of our CME series was on the molecular pathobiology of hypertrophic and keloid scarring and on strategies to avoid or treat such scarring after dermatologic procedures, as conveyed by the titles of each part. We had therefore not evaluated treatments for atrophic scars nor those after burns or acne.</description><dc:title>Reply</dc:title><dc:creator>Christos Tziotzios, Christos Profyris, Jane Sterling</dc:creator><dc:identifier>10.1016/j.jaad.2012.02.026</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Notes &amp; Comments</prism:section><prism:startingPage>1006</prism:startingPage><prism:endingPage>1007</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211011340/abstract?rss=yes"><title>Stability of sunscreens and sunblocks following exposure to extreme temperatures</title><link>http://www.eblue.org/article/PIIS0190962211011340/abstract?rss=yes</link><description>To the Editor: Sunscreens and sunblocks are significant means of protection from the cutaneous damages imparted by ultraviolet radiation (UVR). Chemical sunscreens, as opposed to physical sunblocks, typically consist of a combination of lipophilic organic compounds in order to absorb the broad UVR spectrum. These sunscreen oils are incorporated into the lipophilic phase of oil-in-water or water-in-oil emulsions to achieve an efficacious and esthetically acceptable product. Sunscreens are frequently exposed to temperature extremes. For example, depending on the ambient temperature, the interior temperature of an automobile can range from –3°C to 89°C. These extreme temperature exposures may have a profound effect on the chemical stability of sunscreens and induce irreversible emulsion instability via alteration of droplet-droplet interactions and phase transitions. These physical and chemical changes could reduce the ability of sunscreens to protect the skin by filtering and/or absorbing UVR.</description><dc:title>Stability of sunscreens and sunblocks following exposure to extreme temperatures</dc:title><dc:creator>Gordon W. Jung, Patricia T. Ting, Thomas G. Salopek</dc:creator><dc:identifier>10.1016/j.jaad.2011.10.010</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>1007</prism:startingPage><prism:endingPage>1009</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211011881/abstract?rss=yes"><title>The infra-auricular fissure: A bedside marker of disease severity in patients with atopic dermatitis</title><link>http://www.eblue.org/article/PIIS0190962211011881/abstract?rss=yes</link><description>To the Editor: Monitoring the severity of atopic dermatitis (AD) is crucial to disease management. Tools exist to assess disease severity for experimental studies; these tools are not practical in a high-volume clinical setting. Thus, a simple bedside marker of AD severity would be a useful addition to the armamentarium of AD management.</description><dc:title>The infra-auricular fissure: A bedside marker of disease severity in patients with atopic dermatitis</dc:title><dc:creator>Shawn G. Kwatra, Hong Liang Tey, Saba M. Ali, Tushar Dabade, Yiong-Huak Chan, Gil Yosipovitch</dc:creator><dc:identifier>10.1016/j.jaad.2011.10.031</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>1009</prism:startingPage><prism:endingPage>1010</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211022407/abstract?rss=yes"><title>Refusal of shingles vaccine: Implications for public health</title><link>http://www.eblue.org/article/PIIS0190962211022407/abstract?rss=yes</link><description>To the Editor: While the varicella-zoster virus (VZV; chickenpox) vaccine (Varivax) is widely utilized and has produced a dramatic decline in VZV-related morbidity and mortality, the herpes zoster virus (HZV) (shingles) vaccine (Zostavax) is used in only 2% to 7% of the target population over 50 years of age in the United States. Research has shown that the HZV vaccine is effective. A randomized, double-blind, placebo-controlled trial involving 38,546 patients 60 years of age or older demonstrated a reduction of 51.3% (P &lt; .001) in the incidence of HZ. Furthermore, those who did develop HZ after receiving the vaccine benefited from a 66.5% (P &lt; .001) decrease in the incidence of postherpetic neuralgia (PHN). Cost-effectiveness is more difficult to prove. Our society generally finds it acceptable to pay at least $100,000 per quality-adjusted life year (QALY). Utilizing the HZ vaccine, extending life by one QALY costs $44,000 for a 70-year-old woman and $191,000 for an 80-year-old man. The cost per QALY for a patient 80 years old falls by approximately 40% when PHN is considered. Finally, if the HZ vaccine were administered to 1,000,000 eligible recipients, it would prevent over 75,000 cases of HZ and over 20,000 cases of PHN, resulting in savings of $82 million to $103 million.</description><dc:title>Refusal of shingles vaccine: Implications for public health</dc:title><dc:creator>Angela L. Funovits, Kyle L. Wagamon, Eliot N. Mostow, Robert T. Brodell</dc:creator><dc:identifier>10.1016/j.jaad.2011.11.931</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>1011</prism:startingPage><prism:endingPage>1012</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211022444/abstract?rss=yes"><title>Association between pediatric psoriasis and the metabolic syndrome</title><link>http://www.eblue.org/article/PIIS0190962211022444/abstract?rss=yes</link><description>To the Editor: Psoriasis is an inflammatory skin disease that affects approximately 2% of the general population, and roughly 1% of children. Numerous large population-based studies have demonstrated the systemic effects of psoriatic disease in adults showing an increased risk of coronary artery disease, myocardial infarction, and stroke. Although the increased risk of cardiovascular disease in adults with psoriasis has been well documented, there are more limited data available on cardiovascular risk factors in children with psoriasis.</description><dc:title>Association between pediatric psoriasis and the metabolic syndrome</dc:title><dc:creator>Shiu-chung Au, Ari M. Goldminz, Daniel S. Loo, Nicole Dumont, Danielle Levine, Eva Volf, Melissa Michelon, Andrew Wang, Noori Kim, Shimrat Yaniv, Paul F. Lizzul, Todd Kerensky, Jorge M. Lopez-Benitez, Marc Natter, Laurie Miller, Christina F. Pelajo, Trevor Davis, Alice B. Gottlieb</dc:creator><dc:identifier>10.1016/j.jaad.2011.11.935</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>1012</prism:startingPage><prism:endingPage>1013</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211022511/abstract?rss=yes"><title>Lipodermatosclerosis: Improvement noted with hydroxychloroquine and pentoxifylline</title><link>http://www.eblue.org/article/PIIS0190962211022511/abstract?rss=yes</link><description>To the Editor: Lipodermatosclerosis (LDS) is believed to be associated with chronic venous insufficiency. Abnormal fibrinolysis, the excessive proteolytic activity by matrix metalloproteinase, and the up-regulation of inflammatory response by interleukin-8 are thought to be the causes for this condition. Treatment of LDS is difficult and therapeutic trials have shown variations in the response rate. Pentoxifylline has been shown to decrease platelet aggregation, fibrinogen levels, and production of cytokines, and to inhibit leukocyte/endothelial cell binding. Antimalarials may decrease the production of proinflammatory cytokines and affect matrix metalloprotein production. Jorizzo et al treated 6 patients with LDS using many systemic agents including hydroxychloroquine in one patient and pentoxifylline in two other patients, but no clinical benefit was observed. There was, however, no information about dosage and duration of the treatment for either agent. Because there is no universally accepted therapy for LDS, we have tried using a combination of hydroxychloroquine and pentoxifylline, based on the pharmacologic mechanisms described previously.</description><dc:title>Lipodermatosclerosis: Improvement noted with hydroxychloroquine and pentoxifylline</dc:title><dc:creator>Charoen Choonhakarn, Suteeraporn Chaowattanapanit</dc:creator><dc:identifier>10.1016/j.jaad.2011.11.942</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Research Letters</prism:section><prism:startingPage>1013</prism:startingPage><prism:endingPage>1014</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210007474/abstract?rss=yes"><title>Dermatophytoma: Description of 7 cases</title><link>http://www.eblue.org/article/PIIS0190962210007474/abstract?rss=yes</link><description>To the Editor: Dermatophytoma is a little-known microscopic manifestation of fungal nail infection only recently mentioned in the literature. It is characterized by abundant fungal filaments, large spores, or both, compacted and forming a fungal ball. Definitive diagnosis is made microscopically by observation of this fungal conglomerate via direct potassium hydroxide or chlorazol black E examination of nail samples from patients with suspected onychomycosis (). Clinically, it has been described as a linear band of white or yellowish color. Unfortunately, published clinical descriptions are scarce.</description><dc:title>Dermatophytoma: Description of 7 cases</dc:title><dc:creator>Erick Martinez-Herrera, Gabriela Moreno-Coutiño, Ramon F. Fernández-Martínez, Justin Finch, Roberto Arenas</dc:creator><dc:identifier>10.1016/j.jaad.2010.06.034</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Case Letter</prism:section><prism:startingPage>1014</prism:startingPage><prism:endingPage>1016</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212004240/abstract?rss=yes"><title>Cover Sheet for Index</title><link>http://www.eblue.org/article/PIIS0190962212004240/abstract?rss=yes</link><description></description><dc:title>Cover Sheet for Index</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(12)00424-0</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Index to Volume 66</prism:section><prism:startingPage>1017</prism:startingPage><prism:endingPage>1018</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212004252/abstract?rss=yes"><title>Author index∗</title><link>http://www.eblue.org/article/PIIS0190962212004252/abstract?rss=yes</link><description>Aarons E (see Benton et al). 2012;66:e123-4 (Case letter)   Abdel Halim DM (see El-Darouti et al). 2012;66:511-3 (Research letter)</description><dc:title>Author index∗</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(12)00425-2</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Index to Volume 66</prism:section><prism:startingPage>1019</prism:startingPage><prism:endingPage>1033</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212004264/abstract?rss=yes"><title>Subject index</title><link>http://www.eblue.org/article/PIIS0190962212004264/abstract?rss=yes</link><description>Acne   Prospective randomized controlled clinical and histopathological study of acne vulgaris treated with dual mode of quasi-long pulse and Q-switched 1064-nm Nd:YAG laser assisted with a topically applied carbon suspension (Jung et al). 2012;66:626-33 (Derm. surgery)</description><dc:title>Subject index</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(12)00426-4</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Index to Volume 66</prism:section><prism:startingPage>1034</prism:startingPage><prism:endingPage>1057</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096221200374X/abstract?rss=yes"><title>Dermatology Calendar</title><link>http://www.eblue.org/article/PIIS019096221200374X/abstract?rss=yes</link><description></description><dc:title>Dermatology Calendar</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(12)00374-X</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Index to Volume 66</prism:section><prism:startingPage>1058</prism:startingPage><prism:endingPage>1058</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211004816/abstract?rss=yes"><title>Linear erythematous papules from previous scratching</title><link>http://www.eblue.org/article/PIIS0190962211004816/abstract?rss=yes</link><description>A 63-year-old man presented with erythematous papules in a linear distribution (). Each linear lesion persisted beyond 24 hours. He complained of severe itching but otherwise felt well. A complete blood cell count revealed no pathologic findings. The patient denied taking any oral medications. On direct questioning, he affirms the consumption of Chinese food about 24 hours before the severely itching skin changes first appeared.</description><dc:title>Linear erythematous papules from previous scratching</dc:title><dc:creator>Corinna Hamsch, Martin Hartmann</dc:creator><dc:identifier>10.1016/j.jaad.2011.04.013</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Images in Dermatology</prism:section><prism:startingPage>e189</prism:startingPage><prism:endingPage>e190</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211009558/abstract?rss=yes"><title>A scaling rash preferentially involving a recent tattoo</title><link>http://www.eblue.org/article/PIIS0190962211009558/abstract?rss=yes</link><description>An 18-year-old woman developed an asymptomatic rash 2 weeks after having a tattoo applied that preferentially affected both the red and black areas of the tattoo. There was no history of a sore throat or other infections. The physical examination revealed white scaling overlying the areas where tattoo ink was injected ( and ). Salmon-colored, scaled, guttate lesions 5 mm to 2 cm in diameter appeared at the same time, scattered over numerous areas on her legs, arms, trunk, and scalp. The rash cleared in 1 month with triamcinolone 0.1% cream twice daily, and graded exposure to natural sun producing a tan.</description><dc:title>A scaling rash preferentially involving a recent tattoo</dc:title><dc:creator>Vindhya Veerula, Jenifer R. Lloyd, Robert T. Brodell</dc:creator><dc:identifier>10.1016/j.jaad.2011.08.024</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Images in Dermatology</prism:section><prism:startingPage>e191</prism:startingPage><prism:endingPage>e192</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211001423/abstract?rss=yes"><title>An appraisal of oral retinoids in the treatment of pachyonychia congenita</title><link>http://www.eblue.org/article/PIIS0190962211001423/abstract?rss=yes</link><description>Background: Pachyonychia congenita (PC), a rare autosomal-dominant keratin disorder caused by mutations in keratin genes KRT6A/B, KRT16, or KRT17, is characterized by painful plantar keratoderma and hypertrophic nail dystrophy. Available studies assessing oral retinoid treatment for PC are limited to a few case reports.Objective: We sought to assess overall effectiveness, adverse effects, and patient perspective in patients with PC receiving oral retinoids.Methods: In a questionnaire-based retrospective cross-sectional survey of 30 patient with PC assessing oral retinoids (10-50 mg/d for 1-240 months), we determined the clinical score, satisfaction score, visual analog pain scale, and adverse effects.Results: In 50% of patients there was thinning of hyperkeratoses (average improvement 1.6 on a scale from –3 to +3) (95% confidence interval 1.2-1.9, P &lt; .001). In all, 14% observed amelioration of their pachyonychia; 79% did not experience any nail change. The self-reported overall satisfaction score with oral retinoid treatment was 2 or greater in 50% of the patients (mean 4.5 on a scale of 1-10). Although 33% reported decreased and 27% increased plantar pain with treatment, 40% did not notice any pain change. All patients experienced adverse effects, and 83% reported to have discontinued medication. Risk/benefit analysis favored lower retinoid doses (≤25 mg/d) over a longer time period (&gt;5 months), compared with higher doses (&gt;25 mg/d) for a shorter time (≤5 months).Limitations: The retrospective, cross-sectional study design is prone to a recall bias.Conclusion: Oral retinoids are effective in some patients with PC. However, many patients discontinued medication because adverse effects outweighed the benefits. Careful dose titration is warranted in patients informed about potential adverse effects.</description><dc:title>An appraisal of oral retinoids in the treatment of pachyonychia congenita</dc:title><dc:creator>Robert Gruber, Michael Edlinger, Roger L. Kaspar, C. David Hansen, Sancy Leachman, Leonard M. Milstone, Frances J.D. Smith, Alexis Sidoroff, Peter O. Fritsch, Matthias Schmuth</dc:creator><dc:identifier>10.1016/j.jaad.2011.02.003</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-05-23</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-05-23</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e193</prism:startingPage><prism:endingPage>e199</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211002404/abstract?rss=yes"><title>Neuropeptide Y expression in cutaneous melanoma</title><link>http://www.eblue.org/article/PIIS0190962211002404/abstract?rss=yes</link><description>Background: Neuropeptide Y (NPY) is widely found in the nervous system and has a role in numerous physiologic processes. In addition, NPY receptors are expressed in neuroendocrine tumors, breast cancer, prostate cancer, kidney cancer, and some types of sarcomas. Different neuropeptides, particularly α-melanocyte-stimulating hormone (MSH), seem to play a role in the pathogenesis of melanoma.Objective: We sought to analyze the expression of NPY in cutaneous melanoma, its association with clinical and histologic features, and its correlation with α-MSH.Methods: This was an observational study of the immunohistochemical expression of NPY and α-MSH in tissue samples of cutaneous melanomas, different types of melanocytic nevi, and melanoma metastases diagnosed from 2004 to 2008 in San Jorge Hospital, Huesca, Spain.Results: A total of 184 lesions were studied: 49 primary cutaneous melanomas, 12 melanoma metastases (9 cutaneous and 3 lymphatic), and 123 melanocytic nevi. Immunostaining revealed that levels of NPY and α-MSH were significantly higher in melanomas than in melanocytic nevi (P &lt; .001). Melanoma metastases were negative for both neuropeptides. Nodular melanomas showed the highest median percentage of NPY positive cells (75% [20-95]) followed by superficial spreading melanoma (25% [2-92]), whereas lentigo maligna were negative (0% [0-0]). Significant, direct associations between NPY expression and vertical growth (P = .0141) and presence of metastasis (P = .0196) were observed. NPY and α-MSH were positively correlated in cutaneous melanoma (0.49, P &lt; .001).Limitations: The sample size of melanomas was not very large.Conclusion: Our study demonstrates that NPY is significantly expressed in melanomas, especially the nodular type, being associated with invasiveness independently of proliferative markers such as thickness, ulceration, and mitotic index.</description><dc:title>Neuropeptide Y expression in cutaneous melanoma</dc:title><dc:creator>Yolanda Gilaberte, M. Jose Roca, M. Dolores Garcia-Prats, Carmen Coscojuela, M. Dolores Arbues, Jesús J. Vera-Alvarez</dc:creator><dc:identifier>10.1016/j.jaad.2011.02.015</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-05-27</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-05-27</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e201</prism:startingPage><prism:endingPage>e208</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211003033/abstract?rss=yes"><title>A randomized, investigator-blinded, controlled pilot study to evaluate the safety and efficacy of a poly-N-acetyl glucosamine–derived membrane material in patients with venous leg ulcers</title><link>http://www.eblue.org/article/PIIS0190962211003033/abstract?rss=yes</link><description>Background: Standard care for venous leg ulcers (VLUs) has remained unchanged over several decades despite high rates of initial treatment failure and ulcer recurrence.Objective: We sought to evaluate the efficacy, safety, and tolerability of an advanced, poly-N-acetyl glucosamine (pGlcNAc), nanofiber-derived, wound-healing technology among patients with VLUs (Talymed, Marine Polymer Technologies Inc, Danvers, MA).Methods: In this randomized, investigator-blinded, parallel-group, controlled study, eligible patients were randomized to treatment with standard care plus pGlcNAc (applied only once, every other week, or every 3 weeks) or to standard care alone. The primary end point was the proportion of patients with complete wound healing at week 20 in the intent-to-treat population (all randomized subjects), with last observation carried forward.Results: Among 82 randomized patients, 71 completed the study with 7 lost to follow-up and 4 discontinued because of systemic infection. There were no significant group differences with regard to baseline demographic, illness, and VLU characteristics. At 20 weeks, the proportion of patients with completely healed VLUs was 45.0% (n = 9 of 20), 86.4% (n = 19 of 22), and 65.0% (n = 13 of 20) for groups receiving standard care plus pGlcNAc only once, every other week, and every 3 weeks, respectively, versus 45.0% (n = 9 of 20) for those receiving standard care alone (P &lt; .01 for pGlcNAc every other week vs standard care). The novel pGlcNAc advanced wound-healing technology was well tolerated and safe.Limitations: Limitations were small sample size and patients unblinded to treatment allocation.Conclusion: These pilot study results suggest that the pGlcNAc advanced wound-healing technology is well tolerated and effective.</description><dc:title>A randomized, investigator-blinded, controlled pilot study to evaluate the safety and efficacy of a poly-N-acetyl glucosamine–derived membrane material in patients with venous leg ulcers</dc:title><dc:creator>Teresa J. Kelechi, Martina Mueller, Cheryl S. Hankin, Amy Bronstone, John Samies, Phyllis A. Bonham</dc:creator><dc:identifier>10.1016/j.jaad.2011.01.031</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-05-27</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-05-27</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e209</prism:startingPage><prism:endingPage>e215</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210008194/abstract?rss=yes"><title>Chronic mucocutaneous herpes simplex virus and varicella zoster virus infections</title><link>http://www.eblue.org/article/PIIS0190962210008194/abstract?rss=yes</link><description>Chronic herpes simplex virus (CHSV) and chronic varicella zoster virus (CVZV) are defined as atypical mucocutaneous wart-like and/or ulcerative HSV or VZV infections, persisting for at least 1 month. Both are commonly associated with HIV infection and may occasionally present with other types of immunosuppression. CHSV and CVZV occur despite the immune restoration effect of highly active antiretroviral therapy for HIV. The clinical polymorphism of CHSV and CVZV makes recognition difficult. Histology, immunohistology, PCR and viral culture all help to confirm the diagnosis. Treatment is frequently complicated by resistance to thymidine kinase (TK)–dependent antivirals, including acyclovir, valacyclovir and famciclovir. Viral culture remains an essential tool for antiviral drug susceptibility testing. Therapeutic alternatives include non-TK-dependent antivirals, such as foscarnet or cidofovir, which directly target viral DNA polymerase. With few exceptions, CHSV and CVZV infections do not constitute significant risk factors for disseminated cutaneous or systemic infection. This review compares the similarities of and differences between CHSV and CVZV infections.</description><dc:title>Chronic mucocutaneous herpes simplex virus and varicella zoster virus infections</dc:title><dc:creator>Odile Wauters, Eglantine Lebas, Arjen F. Nikkels</dc:creator><dc:identifier>10.1016/j.jaad.2010.07.011</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2010-11-09</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2010-11-09</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e217</prism:startingPage><prism:endingPage>e227</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210022474/abstract?rss=yes"><title>A review of DRESS-associated myocarditis</title><link>http://www.eblue.org/article/PIIS0190962210022474/abstract?rss=yes</link><description>DRESS (drug rash with eosinophilia and systemic symptoms), also known as drug-induced hypersensitivity syndrome, is a severe, systemic drug reaction most commonly associated with aromatic anticonvulsants and sulfonamides. Patients typically present with fever, facial edema, cervical lymphadenopathy and a morbilliform eruption, which may progress to erythroderma. Hematologic abnormalities are a hallmark of the condition, including eosinophilia and atypical lymphocytosis. Visceral organ involvement typically manifests as hepatic dysfunction but may include lymphadenopathy, nephritis, interstitial pneumonitis, and myocarditis. Five to ten percent of patients with DRESS die from systemic complications, making timely recognition and treatment essential to prevent life-threatening manifestations. Myocarditis is a fatal and under-recognized manifestation of DRESS, which may occur long after the initial diagnosis. We review the literature of previously reported cases of DRESS and myocardial involvement, highlighting the presenting symptoms associated with cardiac involvement, treatments used, and the outcome for each patient. In addition, we offer an algorithm for early diagnosis, treatment, and subsequent monitoring of these patients.</description><dc:title>A review of DRESS-associated myocarditis</dc:title><dc:creator>Greg P. Bourgeois, Jennifer A. Cafardi, Vlada Groysman, Lauren C. Hughey</dc:creator><dc:identifier>10.1016/j.jaad.2010.11.057</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2011-06-09</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2011-06-09</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e229</prism:startingPage><prism:endingPage>e236</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211003896/abstract?rss=yes"><title>Chemical leukoderma after the application of a transdermal methylphenidate patch</title><link>http://www.eblue.org/article/PIIS0190962211003896/abstract?rss=yes</link><description>To the Editor: Chemical leukoderma is a chemically induced acquired hypopigmented dermatosis. We report a case of chemical leukoderma induced by a transdermal methylphenidate medicated patch for the treatment of attention deficit hyperactive disorder (ADHD).</description><dc:title>Chemical leukoderma after the application of a transdermal methylphenidate patch</dc:title><dc:creator>Pedram Ghasri, Shilpa Gattu, Naz Saedi, Anand K. Ganesan</dc:creator><dc:identifier>10.1016/j.jaad.2011.03.030</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e237</prism:startingPage><prism:endingPage>e238</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096221100805X/abstract?rss=yes"><title>Blastic plasmacytoid dendritic cell neoplasm in a child</title><link>http://www.eblue.org/article/PIIS019096221100805X/abstract?rss=yes</link><description>To the Editor: Blastic plasmacytoid dendritic cell neoplasm (BPDCN) has been described as a distinct clinicopathologic entity in the last World Health Organization classification of tumors of hematopoietic and lymphoid tissue. It is a very rare neoplasm, even more infrequent in children than in adults, with an aggressive clinical course and a poor outcome (mean survival: 12-14 months). Herein we report a case of BPDCN in a 15-year-old boy and discuss treatment options.</description><dc:title>Blastic plasmacytoid dendritic cell neoplasm in a child</dc:title><dc:creator>Carla Ferrándiz-Pulido, Ingrid López-Lerma, Constantino Sábado, Berta Ferrer, Sandra Pisa, Vicente García-Patos</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.016</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e238</prism:startingPage><prism:endingPage>e240</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008061/abstract?rss=yes"><title>Mycosis fungoides–associated follicular mucinosis after bone-marrow transplantation</title><link>http://www.eblue.org/article/PIIS0190962211008061/abstract?rss=yes</link><description>To the Editor: A 32-year-old woman with acute myelogenous leukemia presented with a 2-month history of subtle papules on her cheeks and forehead 100 days after allogenic bone-marrow transplantation (). She was on cyclosporine for graft-versus-host disease prophylaxis. A punch biopsy specimen from her cheek revealed a dermal folliculocentric infiltrate with exocytosis of atypical lymphocytes into the follicular epithelium and mucin deposition (, A). The infiltrate was positive for CD3 and CD4 and negative for CD7, CD8, and myeloperoxidase (, B). Histologic features of graft-versus-host disease were not present. T-cell receptor gene rearrangements were detected by polymerase chain reaction analysis.</description><dc:title>Mycosis fungoides–associated follicular mucinosis after bone-marrow transplantation</dc:title><dc:creator>Faith A. Stewart, Aleodor Andea, Lauren C. Hughey</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.017</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e240</prism:startingPage><prism:endingPage>e241</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008115/abstract?rss=yes"><title>Onychopapilloma presenting as longitudinal melanonychia</title><link>http://www.eblue.org/article/PIIS0190962211008115/abstract?rss=yes</link><description>To the Editor: Onychopapilloma is a benign neoplasm of the distal matrix and the nail bed.   It typically presents with longitudinal erythronychia with hemorrhagic lines. One case of onychopapilloma causing longitudinal leukonychia has also been published.</description><dc:title>Onychopapilloma presenting as longitudinal melanonychia</dc:title><dc:creator>Mariya Miteva, Piero A. Fanti, Paolo Romanelli, Martin Zaiac, Antonella Tosti</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.022</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e242</prism:startingPage><prism:endingPage>e243</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008267/abstract?rss=yes"><title>Pemphigus foliaceus clearance status postmyomectomy for an enlarged infarcted subserous uterine fibroid</title><link>http://www.eblue.org/article/PIIS0190962211008267/abstract?rss=yes</link><description>To the Editor: Pemphigus foliaceus is a well-defined clinical disease that has been linked to thymic neoplasmsm; however, most cases are idiopathic in origin. The purpose of this letter is to describe a novel observation of an association between pemphigus foliaceus and uterine fibroids.</description><dc:title>Pemphigus foliaceus clearance status postmyomectomy for an enlarged infarcted subserous uterine fibroid</dc:title><dc:creator>Samantha H. Fisher, Ann A. Church, Christina L. Mitchell, Carlos H. Nousari</dc:creator><dc:identifier>10.1016/j.jaad.2011.06.027</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e243</prism:startingPage><prism:endingPage>e245</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008395/abstract?rss=yes"><title>Nodular scleroderma presenting as multiple spontaneous keloidal scars</title><link>http://www.eblue.org/article/PIIS0190962211008395/abstract?rss=yes</link><description>To the Editor: A 13-year-old African American girl presented with a history of several keloidal scars arising in areas of previously normal-appearing skin involving the face, neck, trunk, and lower and upper extremities. History of trauma, piercings, or acne was negative. The lesions arose spontaneously 23 months earlier, and were initially pruritic but currently asymptomatic. She was evaluated a few months before presentation by a rheumatologist who suspected a connective tissue disease based on a laboratory workup, started hydroxychloroquine sulfate, but did not diagnose scleroderma. Her medical history was significant for Raynaud phenomenon, positive antinuclear antibody titer of 1:1280 in a nucleolar pattern, negative antitopoisomerase I antibodies (anti-scleroderma 70 antibody), and a diagnosis of vitiligo versus postinflammatory hypopigmentation. There was no esophageal dysmotility, sclerodactyly, or pulmonary or cardiac dysfunction, but she reported history of digital tip erosions. Before presentation, the cutaneous lesions were treated with topical and intralesional corticosteroids, which resulted in flattening of the lesions on her chin, neck, upper aspect of her chest, proximal aspect of right arm, and lower aspect of left leg ().</description><dc:title>Nodular scleroderma presenting as multiple spontaneous keloidal scars</dc:title><dc:creator>Candrice R. Heath, Jennifer N. David, Susan C. Taylor</dc:creator><dc:identifier>10.1016/j.jaad.2011.06.031</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e245</prism:startingPage><prism:endingPage>e246</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008413/abstract?rss=yes"><title>Multiple cutaneous metastatic chordomas from the sacrum</title><link>http://www.eblue.org/article/PIIS0190962211008413/abstract?rss=yes</link><description>To the Editor: A 78-year-old woman with a history of sacral chordoma presented 2 years after wide local resection with multiple rubbery, flesh-colored, nodular lesions of the scalp measuring 0.9 × 0.7 × 0.5 cm, 0.6 × 0.5 × 0.5 cm, and 0.5 × 0.4 × 0.4 cm, and one 0.8 × 0.7 × 0.6 cm rubbery gray nodule on the left forearm (). A bone scan performed because of low back pain indicated sacral recurrence and bony metastases in the L2 and T7 vertebrae, right scapula, and left 10th rib.</description><dc:title>Multiple cutaneous metastatic chordomas from the sacrum</dc:title><dc:creator>Ryan M. Svoboda, Donald Mackay, Michael Jude Welsch, Bryan E. Anderson</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.037</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e246</prism:startingPage><prism:endingPage>e247</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008437/abstract?rss=yes"><title>Mycobacterium celatum skin infection with sporotrichoid spread in an HIV-negative immunocompromised man</title><link>http://www.eblue.org/article/PIIS0190962211008437/abstract?rss=yes</link><description>To the Editor: A 68-year-old man presented with a 2-month history of progressing plaques on his right arm after he had punctured the tip of his fourth finger with a fishhook. A first plaque had appeared on his forearm 1 month after the injury and two others appeared successively in a sporotrichoid pattern over the following weeks. He was known to have myelodysplastic syndrome, diabetes mellitus, and temporal arteritis, treated with prednisone 45 mg daily and azathioprine 50 mg twice daily for the last 8 months.</description><dc:title>Mycobacterium celatum skin infection with sporotrichoid spread in an HIV-negative immunocompromised man</dc:title><dc:creator>Jean-Michel Leduc, Simon F. Dufresne, Christian Lavallée, Simon Nigen, Annie-Claude Labbé, Louise Poirier</dc:creator><dc:identifier>10.1016/j.jaad.2011.06.034</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e247</prism:startingPage><prism:endingPage>e249</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008474/abstract?rss=yes"><title>Successful treatment of lamotrigine-associated drug hypersensitivity syndrome with intravenous IgG</title><link>http://www.eblue.org/article/PIIS0190962211008474/abstract?rss=yes</link><description>To the Editor: Anticonvulsant hypersensitivity syndrome is an adverse and potentially fatal condition associated with the use of certain anticonvulsants. It is characterized by the presence of fever, generalized cutaneous eruption, lymphadenopathy, and internal organ involvement. We present the case of a 30-year-old woman with history of tonic-clonic seizures who developed a generalized, erythematous, morbilliform skin eruption along with oral and ocular ulcerations 4 months into treatment with lamotrigine. Skin examination was remarkable for confluent and discrete bright red, flat-topped papules on her trunk, extremities, face, neck, palms, and soles over a background of vascular hyperemia. Mucosal surfaces presented multiple ill-defined superficial erosions and ulcerations over her lips extending onto the oral commissures. Histopathologic examination demonstrated lichenoid interface dermatitis and mixed dermal infiltrate with eosinophils and direct immunofluorescence confirmed lichenoid dermatosis suggestive of a drug reaction. Laboratory evaluation showed leukocytosis with eosinophilia, elevated creatinine, serum urea nitrogen, and liver transaminases. Viral serologies for hepatitis B and C, HIV, CMV, and EBV were negative. Antihuman herpesvirus 6 IgG was elevated at titer of 1:5120, antihuman herpesvirus 6 IgM titer was less than 1:20, and serum human herpesvirus 6 polymerase chain reaction was negative.</description><dc:title>Successful treatment of lamotrigine-associated drug hypersensitivity syndrome with intravenous IgG</dc:title><dc:creator>Nneka I. Comfere, Julio C. Sartori-Valinotti, Alison J. Bruce, Lisa A. Drage</dc:creator><dc:identifier>10.1016/j.jaad.2011.06.038</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e249</prism:startingPage><prism:endingPage>e250</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211008516/abstract?rss=yes"><title>Galli-Galli disease is an acantholytic variant of Dowling-Degos disease: Additional genetic evidence in a German family</title><link>http://www.eblue.org/article/PIIS0190962211008516/abstract?rss=yes</link><description>To the Editor: Dowling-Degos disease (DDD) is a rare autosomal dominant genodermatosis with variable penetrance. It is characterized by reticular hyperpigmentation and pruritic follicular hyperkeratotic papules in the axillae, groin, and other body folds. Comedo-like lesions on the back or neck, pitted perioral scars, and hypopigmented macules are also described. Histopathologically, DDD shows acanthotic elongation of rete ridges in conjunction with basal hyperpigmentation. Galli-Galli disease (GGD) is an eponym introduced in 1982 to describe a skin disease in two affected brothers with reticulated hyperpigmentation and erythematous lichenoid papules resembling DDD, but with the histopathologic finding of prominent acantholysis. We report a family with this acantholytic variant of DDD.</description><dc:title>Galli-Galli disease is an acantholytic variant of Dowling-Degos disease: Additional genetic evidence in a German family</dc:title><dc:creator>Astrid Schmieder, Sandra M. Pasternack, Dieter Krahl, Regina C. Betz, Martin Leverkus</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.038</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e250</prism:startingPage><prism:endingPage>e251</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096221100911X/abstract?rss=yes"><title>A case of rapid improvement of severe psoriasis during molecular-targeted therapy using an epidermal growth factor receptor tyrosine kinase inhibitor for metastatic lung adenocarcinoma</title><link>http://www.eblue.org/article/PIIS019096221100911X/abstract?rss=yes</link><description>To the Editor: We describe a patient with severe psoriasis whose skin lesions regressed after the oral administration of erlotinib, an epidermal growth factor receptor (EGFR)-specific tyrosine kinase inhibitor (TKI), for the treatment of metastatic lung adenocarcinoma.</description><dc:title>A case of rapid improvement of severe psoriasis during molecular-targeted therapy using an epidermal growth factor receptor tyrosine kinase inhibitor for metastatic lung adenocarcinoma</dc:title><dc:creator>Noritaka Oyama, Fumio Kaneko, Ari Togashi, Toshiyuki Yamamoto</dc:creator><dc:identifier>10.1016/j.jaad.2011.08.009</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e251</prism:startingPage><prism:endingPage>e253</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209012250/abstract?rss=yes"><title>Aesthetic rejuvenation: A regional approach</title><link>http://www.eblue.org/article/PIIS0190962209012250/abstract?rss=yes</link><description>Aesthetic Rejuvenation: A Regional Approach edited by Ranell Hirsch, Neil Sadick, and Joel L. Cohen is a lightweight, but comprehensive, easy-to-use textbook. The book's focus is on specific regions of the body, giving practitioners a way to effectively determine the most appropriate procedure, similar to what we do in practice when evaluating cosmetic patients. The text starts with the initial approach of the cosmetic patient and covers procedures, outcomes, results, and side effects of each, on the basis of the region of concern. The chapter on facial rejuvenation covers multiple modalities from nonablative techniques, fractional resurfacing, Botox, fillers, chemical peels, photodynamic therapy, threads, minilifts, and tightening devices.</description><dc:title>Aesthetic rejuvenation: A regional approach</dc:title><dc:creator>Theresa Conologue</dc:creator><dc:identifier>10.1016/j.jaad.2009.08.059</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e255</prism:startingPage><prism:endingPage>e255</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962209021197/abstract?rss=yes"><title>The cutaneous lymphoid proliferations: A comprehensive textbook of lymphocytic infiltrates of the skin</title><link>http://www.eblue.org/article/PIIS0190962209021197/abstract?rss=yes</link><description>Magro et al have succeeded in filling a vacuum in our libraries. This is the first truly comprehensive book on the subject of lymphoid-rich infiltrates of the skin covering the entire spectrum of cutaneous pathology from benign dermatoses to malignant lymphomas, including a section on cutaneous lymphoid dyscrasias, a theme Magro has pioneered and written about extensively.</description><dc:title>The cutaneous lymphoid proliferations: A comprehensive textbook of lymphocytic infiltrates of the skin</dc:title><dc:creator>Joan Guitart</dc:creator><dc:identifier>10.1016/j.jaad.2009.11.595</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e255</prism:startingPage><prism:endingPage>e256</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210004007/abstract?rss=yes"><title>History of German language dermatology</title><link>http://www.eblue.org/article/PIIS0190962210004007/abstract?rss=yes</link><description>In the late decades of the 18th century, the ravages of syphilis and other contagions aroused widespread public alarm. Syphilis and other venereal diseases were rampant. Scabies was endemic. Many disorders of the skin were thought to be signs of the dreaded leprosy. Clinics for skin disorders were established, and the specialty of dermatology and syphilology was born.</description><dc:title>History of German language dermatology</dc:title><dc:creator>Robert W. Goltz</dc:creator><dc:identifier>10.1016/j.jaad.2010.04.008</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e256</prism:startingPage><prism:endingPage>e257</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS019096221000695X/abstract?rss=yes"><title>Consultant pathology: Tumorigenic melanocytic proliferations</title><link>http://www.eblue.org/article/PIIS019096221000695X/abstract?rss=yes</link><description>Tumorigenic melanocytic proliferations, by David Elder, is part of the Consultant Pathology series published by Demos Medical Publishing. Given that most medical titles are now published by Elsevier or Wolters Kluwer, this book might escape notice during a casual stroll down publisher's row at the annual meeting. It is worth seeking out. The book is a gem, and we have made it part of the core curriculum for our dermatopathogy fellowship.</description><dc:title>Consultant pathology: Tumorigenic melanocytic proliferations</dc:title><dc:creator>Dirk M. Elston</dc:creator><dc:identifier>10.1016/j.jaad.2010.06.015</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e257</prism:startingPage><prism:endingPage>e258</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211005305/abstract?rss=yes"><title>Psoriasis</title><link>http://www.eblue.org/article/PIIS0190962211005305/abstract?rss=yes</link><description>Another book dedicated to psoriasis is always welcomed, especially if it is current and meticulously updated by a renowned authority and his colleague. Psoriasis is such a book, and it is succinct, consisting of only 124 pages before the appendix, references, and index. The authors attempt to cover all aspects of the disease and, in some chapters, are successful, for example, summarizing the most important susceptibility genes and the latest pathways of immunopathogenesis including antigen-presenting cells, the roles of Th1 and Th17 cells and interleukins 12, 23, 22, and 17 with clear and concise cartoons.</description><dc:title>Psoriasis</dc:title><dc:creator>Charles Camisa</dc:creator><dc:identifier>10.1016/j.jaad.2011.05.005</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e258</prism:startingPage><prism:endingPage>e258</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962210021122/abstract?rss=yes"><title>Iotaderma #221</title><link>http://www.eblue.org/article/PIIS0190962210021122/abstract?rss=yes</link><description></description><dc:title>Iotaderma #221</dc:title><dc:creator>Robert I. Rudolph</dc:creator><dc:identifier>10.1016/j.jaad.2010.11.012</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e259</prism:startingPage><prism:endingPage>e259</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962211007961/abstract?rss=yes"><title>May iotaderma (#220)</title><link>http://www.eblue.org/article/PIIS0190962211007961/abstract?rss=yes</link><description></description><dc:title>May iotaderma (#220)</dc:title><dc:creator>Robert I. Rudolph</dc:creator><dc:identifier>10.1016/j.jaad.2011.07.007</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>JAAD Online</prism:section><prism:startingPage>e259</prism:startingPage><prism:endingPage>e259</prism:endingPage></item><item rdf:about="http://www.eblue.org/article/PIIS0190962212003714/abstract?rss=yes"><title>Editorial Board</title><link>http://www.eblue.org/article/PIIS0190962212003714/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(12)00371-4</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-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/PIIS0190962212003726/abstract?rss=yes"><title>Table of Contents</title><link>http://www.eblue.org/article/PIIS0190962212003726/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(12)00372-6</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-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/PIIS0190962212003738/abstract?rss=yes"><title>Information for Readers</title><link>http://www.eblue.org/article/PIIS0190962212003738/abstract?rss=yes</link><description></description><dc:title>Information for Readers</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0190-9622(12)00373-8</dc:identifier><dc:source>Journal of the American Academy of Dermatology 66, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Journal of the American Academy of Dermatology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>66</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0190-9622(11)X0021-X</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A31</prism:startingPage><prism:endingPage>A32</prism:endingPage></item></rdf:RDF>
