Journal of Investigative Dermatology Symposium Proceedings

Publisher: Society for Investigative Dermatology; European Society for Dermatological Research, Nature Publishing Group

Journal description

Current impact factor: 3.73

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2011 Impact Factor 3.733
2010 Impact Factor 1.19
2009 Impact Factor 1.435
2008 Impact Factor 1.576
2007 Impact Factor 1.576
2006 Impact Factor 2.191
2005 Impact Factor 2.392
2004 Impact Factor 0.308
2003 Impact Factor 0.867
2002 Impact Factor 0.613
2001 Impact Factor 0.962

Impact factor over time

Impact factor

Additional details

5-year impact 2.48
Cited half-life 7.80
Immediacy index 0.88
Eigenfactor 0.00
Article influence 0.73
Other titles Journal of investigative dermatology., The journal of investigative dermatology. Symposium proceedings, JID symposium proceedings, Symposium proceedings
ISSN 1529-1774
OCLC 43647738
Material type Conference publication, Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Author's pre-print on arXiv or bioRXiv
    • Author's post-print on author's personal website, institutional repository, PubMed Central or funding body's archive
    • Published source must be acknowledged
    • Must link to publisher version with DOI
    • Publisher's version/PDF cannot be used
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Although the association between alopecia areata (AA), psoriasis, and other autoimmune diseases has been well reported in the literature, an association with metabolic syndrome has not been reported. We present two young women with the combination of severe psoriasis, androgen excess, metabolic syndrome, thyroiditis, and AA. Both women ultimately progressed to treatment-resistant alopecia universalis. This constellation of autoimmunity and metabolic syndrome presents a therapeutic challenge while highlighting the need for full laboratory assessment of AA patients. Careful selection of biological treatment regimens may offer therapeutic benefit for both their psoriasis and AA while giving us experience with the newer biologics in AA.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S56-7. DOI:10.1038/jidsymp.2013.22
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    ABSTRACT: Although alopecia areata (AA) is not life threatening, it may lead to severe psychological disturbances, reducing the quality of life in all ages. Thus, a new animal model is needed for shedding more light onto the pathogenesis of this cell-mediated, organ-specific autoimmune disease to identify more effective therapeutic strategies. Recently, we succeeded in developing a new humanized mouse model of AA, which includes transplantation of healthy human scalp skin obtained from normal volunteers on to severe-combined immunodeficient mice. This is followed by intradermal injection of either autologous or allogeneic peripheral blood mononuclear cells, which had been cultured with high dose of IL-2 and enriched for natural killer group 2D-positive (NKG2D+) and CD56+ cells. This protocol leads to rapid and predictable development of focal hair loss, with all the characteristic clinical, histological, and immunohistochemical features of AA. This humanized mouse AA model underscores the functional importance of NKG2D+ and CD56+ cells in AA pathogenesis and promises to be instrumental for identifying novel AA treatment strategies.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S37-8. DOI:10.1038/jidsymp.2013.11
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    ABSTRACT: Alopecia areata, alopecia totalis, and alopecia universalis likely represent a constellation of related diseases with similar, yet distinct heritability markers. There is currently no known curative therapy that works universally for all patients. Pharmacogenomic research enables the pharmaceutical industry to understand variability of patient responses to drugs during clinical drug development and during post-marketing surveillance. Understanding the genetic basis for patient response/non-response can enable the development of individualized therapies for those patients with an inherited basis for altered response to drug therapy. There are multiple examples of drugs that now contain a recommendation for genetic testing before dosing in their drug labels, directing clinicians to obtain genetic information for each individual patient in order to help direct drug therapy.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S39-40. DOI:10.1038/jidsymp.2013.12
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    ABSTRACT: Alopecia areata is the only condition that can cause complete hair loss in 3 months without symptoms or signs.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S65-6. DOI:10.1038/jidsymp.2013.27
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    ABSTRACT: Alopecia areata (AA) is a nonscarring and recurrent disease characterized by hair loss that may significantly affect patient health-related quality of life (HRQoL). Given the lack of reliable and accurate reporting of HRQoL status in patients with AA, we analyzed data from 532 AA patients from the National Alopecia Areata Registry whose registry record included HRQoL assessments using three validated instruments: Skindex-16, brief version of the Fear of Negative Evaluation Scale, and Dermatology Life Quality Index. The mean HRQoL scores were compared with previously reported HRQoL levels from healthy controls and patients with other skin diseases. Two-step cluster analysis of Skindex-16 scales divided patients into two groups: 481 (57%) with good HRQoL and 361 (43%) with poor HRQoL. Multivariate logistic regression modeling revealed a set of risk factors for poor HRQoL: age <50 years (odds ratio (OR) 3.99, 95% confidence interval (CI) 1.66-9.58), female gender (OR 2.74, 95% CI 1.73-4.34), hair loss 25-99% (OR 2.47, 95% CI 1.12-5.45), family stress (OR 1.8, 95% CI 1.13-2.86), and job change (OR 2.01, 95% CI 1.02-3.94). The current analysis provides an overview of the HRQoL status of AA patients and may guide patient care in the future.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S49-50. DOI:10.1038/jidsymp.2013.18
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    ABSTRACT: Within the area of alopecia areata research, there is an obvious need for well-designed clinical trials of therapeutic agents. The National Alopecia Areata Foundation (NAAF) has created an initiative for the development of a unified protocol with guidelines for clinical studies. The NAAF universal protocol represents a joint effort of clinicians and investigators with experience in treating alopecia areata. This protocol will serve as a tremendous resource to facilitate future clinical studies.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S48. DOI:10.1038/jidsymp.2013.17
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    ABSTRACT: The differential diagnosis of a strongly positive and painless hair pull test includes alopecia areata and loose anagen syndrome. A hair mount examined with low power light microscopy easily clarifies the diagnosis.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S63-4. DOI:10.1038/jidsymp.2013.26
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    ABSTRACT: Alopecia areata is a complex genetic, immune-mediated disease that targets anagen hair follicles. The disease affects children and adults and is characterized by round or oval patches of hair loss, loss of all scalp hair (alopecia totalis), body hair (alopecia universalis), or ophiasis pattern hair loss. Patients may also present with patchy loss in multiple hair-bearing areas. Commonly associated diseases include asthma, allergic rhinitis, atopic dermatitis, thyroid disease, and automimmune diseases, such as thyroiditis and vitiligo. Nail abnormalities may precede, follow, or occur concurrently with hair loss activity. Alopecia areata has no known age, race, or ethnic preponderance and in contrast to other autoimmune diseases such as thyroiditis or lupus, the hair follicle does not usually sustain permanent injury and maintains its potential to regrow hair. It is estimated that alopecia areata affects between six and seven million individuals in the United States. Genes, the immune and nervous systems have all been implicated in the pathogenesis of alopecia areata. Although many treatments are available, there is still no cure. Bolstered by new scientific and translational opportunities from recently published genome-wide association studies, an ambitious treatment development program has recently been initiated by the National Alopecia Areata Foundation.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S13-5. DOI:10.1038/jidsymp.2013.4
  • Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S10-2. DOI:10.1038/jidsymp.2013.3
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    ABSTRACT: Founded in 1981, the National Alopecia Areata Foundation (NAAF) is dedicated to research to find a cure or acceptable treatment for alopecia areata (AA), to develop support for people affected by the disease, and to educate the public about it. NAAF has developed into an international organization advancing patient interests in a number of ways. Beginning in 2008, NAAF organized a series of research summits that focused AA research investments into genetic, molecular, and immunological investigations as well as laying the groundwork for clinical trials and support for regulatory evaluation of prospectively available treatments. This multifaceted initiative is called the Alopecia Areata Treatment Development Program (TDP). It is representative of initiatives among voluntary patient advocacy organizations to partner with academic, clinical, government, and biotechnology interests to accelerate the development and approval of treatments for understudied diseases. The article describes key steps in the development of TDP, its progress, and future direction.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S46-7. DOI:10.1038/jidsymp.2013.16
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    ABSTRACT: The onset of alopecia areata creates a roller coaster of emotions. Like the disease, a patient's emotions are unpredictable. The lack of control over one's body is both frightening and intimidating. Alopecia areata not only impacts an individual but it also has a halo effect, impacting family and friends, thereby increasing the number of people affected by the disease.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S41. DOI:10.1038/jidsymp.2013.13
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    ABSTRACT: A major impetus to initiating the Human Genome Project was the belief that information encoded in the human genome would "accelerate progress in understanding disease pathogenesis and in developing new approaches to diagnosis, treatment, and prevention in many areas of medicine". Alopecia areata (AA) is a notable example of how understanding the genetic basis of a disease can have an impact on the care of patients in a relatively short time. Our first genome-wide association study in AA identified an initial set of common variants that increase risk of AA, some of which are shared with other autoimmune diseases. Thus, there has already been rapid progress in the translation of this information into new therapeutic strategies for patients, as drugs are already on the market for some of these disorders that can now be tested in AA. Informed by the progress achieved with genetic studies for mechanistically aligned autoimmune diseases, we are poised to carry this work forward and interrogate the underlying disease mechanisms in AA. Importantly, future genetic studies aimed at identifying additional susceptibility genes will further establish the foundation for the application of precision medicine in the care of AA patients.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S16-22. DOI:10.1038/jidsymp.2013.5
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    ABSTRACT: The author has been treating extensive cases of alopecia areata with 1-chloro-2, 4-dinitrobenzene (DNCB) for 35 years with considerable success. This presentation outlines the protocol that has been used.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S45. DOI:10.1038/jidsymp.2013.15
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    ABSTRACT: Alopecia areata (AA) is a cell-mediated autoimmune disease that targets actively growing hair follicles in mammals, including humans and mice. Development of the C3H/HeJ spontaneous mouse model AA nearly 20 years ago provided a much needed tool to test the hypotheses and ultimately serve as a preclinical model for drug testing. Discoveries in both human AA patients and the mouse model supported each other and lead to discoveries on the incredibly complex genetic basis of this disease. The discovery that A/J, MRL/MpJ, SJL/J, and SWR/J strains also develop AA now allows genome-wide association mapping studies to expand the list of genes underlying this disease. Potential new targets for unraveling the pathogenesis of AA include the role of retinoic acid metabolism in the severity of disease and hair shaft proteins that may be either the inciting antigen or ultimate target of the immune reaction leading to breakage of the shaft causing clinical alopecia. Comparing these model systems with human and mouse clinical disease, for both discovery and validation of the discoveries, continues to resolve the complex questions surrounding AA.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S23-4. DOI:10.1038/jidsymp.2013.6
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    ABSTRACT: Alopecia areata (AA) is an autoimmune condition characterized by T cell-mediated attack of the hair follicle. The inciting antigenic stimulus is unknown. A dense perbulbar lymphocytic infiltrate and reproducible immunologic abnormalities are hallmark features of the condition. The cellular infiltrate primarily consists of activated T lymphocytes and antigen-presenting Langerhans cells. The xenon chloride excimer laser emits its total energy at the wavelength of 308 nm and therefore is regarded as a "super-narrowband" UVB light source. Excimer laser treatment is highly effective in psoriasis, another T cell-mediated disorder that shares many immunologic features with AA. The excimer laser is superior in inducing T cell apoptosis in vitro compared with narrowband UVB, with paralleled improved clinical efficacy. The excimer laser has been used successfully in patients with AA. In this context, evaluation of the potential benefit of 308-nm excimer laser therapy in the treatment of AA is clinically warranted. Herein, the use of a common treatment protocol with a specifically designed module to study the outcome of excimer laser treatment on moderate-to-severe scalp AA in adults is described.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S77-9. DOI:10.1038/jidsymp.2013.31
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    ABSTRACT: Alopecia areata is an autoimmune skin disease resulting in the loss of hair on the scalp and elsewhere on the body. The disease most often occurs in childhood and affects males and females of all ages. The National Alopecia Areata Foundation conducts research summits every 2 years to review progress and create new directions in its funded and promoted research. The Foundation brings together scientists from all disciplines to get a broad and varied perspective. These summits are part of the Foundation's main strategic initiative, the Alopecia Areata Treatment Development Program to accelerate progress toward a viable alopecia areata treatment.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S1-4. DOI:10.1038/jidsymp.2013.1
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    ABSTRACT: Alopecia areata (AA) may represent a CD8+T cell-mediated, organ-specific autoimmune disease in which as yet elusive autoantigens are recognized, once they become exposed by ectopic major histocompatibility complex class I expression by anagen hair follicles (HFs) that have lost their relative immune privilege (IP). On this basis, AA research is chiefly challenged with identifying the autoreactive CD8+T cells and their cognate autoantigens as well as key inducers of HF-IP collapse and "HF-IP guardians" that prevent and/or can restore IP collapse. However, natural killer group 2D-positive (NKG2D+) cells (incl. NK, NKT, and CD8+T cells) and NKG2D-activating ligands from the MICA (MHC I-related chain A) family may also have a key role in AA pathogenesis, as a massive infiltrate of IFN-γ-secreting NKG2D+ cells alone suffices to induce the AA phenotype. Therefore, we speculate that AA may represent a stereotypic, but distinct HF response pattern to inflammatory insults associated with HF-IP collapse.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S25-7. DOI:10.1038/jidsymp.2013.7
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    ABSTRACT: The existing literature on alopecia areata (AA) clearly demonstrates patients' concerns related to physical symptoms, emotional well-being, mental health, social functioning, and other dimensions of daily functioning. Although questionnaires such as the Skindex-16 and the Dermatology Life Quality Index have been used, these questionnaires were validated for skin conditions other than AA as a chronic condition. The goals of this study are to develop a measure of quality of life, symptoms, and their impact for patients with AA called the Alopecia Areata Symptom Impact Scale (AASIS) and to provide psychometric evidence for its use. We used data from 1,400 patients from the National Alopecia Areata Registry together with clinical experts' reviews and quantitative approaches. The preliminary version of the AASIS with 13 items was administered to about 210 patients with AA. Results indicated that the AASIS measures three underlying constructs related to AA. These dimensions were impact of AA, hair loss, and physical skin symptoms. The internal consistency reliabilities of these subscales are 0.93, 0.86, and 0.81, respectively. Cognitive debriefing results showed that patients find the AASIS items easy to understand, clear, and concise. Preliminary evidence suggests that the AASIS is a reliable and valid measure of the symptoms and their impact in patients with AA.
    Journal of Investigative Dermatology Symposium Proceedings 12/2013; 16(1):S51-2. DOI:10.1038/jidsymp.2013.19