ࡱ>  bjbj 4ee/   xxxxx8DS """" R R R R R R R$UX/Rx/Rxx""R % % %x"x" R % R % %ND-P"c!#O&QR0SP&pY$LpYL-P-PpYxP %/R/R %SpY >: LUPUS Activation of T-Follicular Helper Cells and B Cells in Ultraviolet Light-Induced Murine Model of Systemic Lupus Erythematosus Misha Zarbafian1, Mehran Ghoreishi2 and Jan Dutz2, 1Medicine, University of British Columbia Vancouver Fraser Medical Program, Vancouver, BC, Canada, 2University of British Columbia Department of Dermatology and Skin Science, Vancouver, BC, Canada Background/Purpose: Non-obese diabetic (NOD) mice repeatedly exposed to ultraviolet (UV) light and Toll-like receptor-7 (TLR7) agonist cream (imiquimod) develop lupus-like disease, modeling a possible cutaneous trigger for systemic lupus erythematosus (SLE) in genetically predisposed individuals. Previous research has supported that T-follicular helper (TFH) cells support B cell maturation in germinal centers, leading to auto-antibody production in the context of SLE. Increased frequency of circulating TFH cells in the peripheral blood of human SLE patients has been associated with more severe disease, characterized by more lupus-associated auto-antibodies and end-organ manifestations. High-mobility group protein B1 (HMGB1) is a pro-inflammatory cytokine which facilitates auto-antibody production in SLE, both locally and systemically. HMGB1 release from the cell nucleus in skin occurs early in sun-induced lesions, and has been found to correlate with the progression of SLE disease. We sought to characterize TFH cells and B cells in skin-draining lymph nodes of NOD mice treated with UV and topical imiquimod cream (TLR7 agonist). Methods: NOD and Balb/C mice received weekly UVB radiation (5000 J/m2) and 25 g of topical imiquimod cream. Skin-draining lymph nodes were analyzed by flow cytometry after four treatments to determine the activation status and number of TFH cells and B cells. Serum was collected to measure inflammatory cytokines such as TNFa, IL-6, and IFNg. Extra-nuclear expression of HMGB1 was evaluated in skin samples from both strains after four treatments. Results: There was expansion of both TFH and B cells, as well as increased expression of the B cell activation marker CD40 in skin-draining lymph nodes of NOD mice following combined UV and imiquimod therapy, in contrast to Balb/C mice. Extra-nuclear expression of HMGB1 was greater in NOD mice, whereas expression in Balb/C mice was largely limited to the nucleus. Conclusion: Skin-draining lymph node TFH cell expansion is an early event after UV and TLR7 agonist therapy and is correlated with auto-antibody production. HMGB1 redistribution in the skin also correlates with auto-antibody production. Quantification of circulating TFH cells and local HMGB1 expression may serve as markers for predicting SLE onset in genetically predisposed individuals. Immunohistochemical characterization of acute and chronic discoid lupus erythematosus skin lesions Jack C. OBrien, BS1, Gregory A. Hosler, MD1,2, Benjamin F. Chong, MD, MSCS1 1University of Southwestern Medical Center, Department of Dermatology, Dallas, TX 2ProPath, Dallas, TX Background: Cells of both the innate and adaptive immune system have been implicated in the pathogenesis of discoid lupus erythematosus (DLE). The inflammatory cell infiltrate in DLE has been described as containing CD4+ and CD8+ T cells, B cells, macrophages, and plasmacytoid dendritic cells. Histologically, DLE skin lesions can be thought of as having two phases, acute and chronic, which can be distinguished based on the absence or presence of dermal sclerosis. Characterizing the changes in the composition of the inflammatory cell infiltrate of acute and chronic DLE lesions would elucidate the disease course of DLE. Objective: To characterize the inflammatory infiltrate in acute and chronic DLE skin lesions using immunohistochemistry. Methods: We identified 25 skin biopsies from untreated DLE skin lesions from DLE patients seen at UT Southwestern Medical Center and Parkland Memorial Hospital between 2006 and 2015. Patients were classified as having acute (N=7) or chronic (N=18) DLE based on the presence or absence of deep dermal fibrosis, respectively. Immunostains for T cells (CD3, CD4, CD8), B cells (CD20), plasmacytoid dendritic cells (CD123), macrophages (CD163), neutrophils (MPO), and plasma cells (CD138) were performed. Two independent observers graded the overall intensity of the infiltrate in three areas, interfollicular interface, perifollicular, and perivascular, on a 0 to 3 scale (0 = none, 1 = mild, 2 = moderate, 3 = marked). Each immunostain was graded on a 0 to 3 scale based on percentage of positive-staining cells (0 = <1%, 1 = <10%, 2 = 10-50%, 3 = >50%). Median staining intensities for each group were calculated and compared using nonparametric tests. Results: Chronic DLE skin had increased CD20 staining in perifollicular (p=0.002) and perivascular regions (p=0.009) compared to acute DLE skin. CD8+ cells trended towards being more frequent in the interfollicular interface (p=0.07) and perifollicular regions (p=0.05) in acute DLE skin. The CD4:CD8 T cell ratio was higher in perifollicular (p=0.005) and in perivascular (p=0.02) regions in chronic DLE. Conclusions: The inflammatory infiltrate in DLE patients changes as the histology progresses to dermal fibrosis, as evidenced by fewer CD8+ lymphocytes and increased CD20+ B cells in different regions of chronic DLE skin. These changes could reflect an initial inflammatory process driven by a cytotoxic T cell response that is later mediated by a B cell response in DLE. Belimumab for the treatment of recalcitrant cutaneous lupus A pilot project Priyanka Vashisht MD, Manpreet Sethi MD, Melanie Rohr MD, Debbie Lim MD, Michelene Hearth-Holmes MD Background/Purpose: Belimumab (Benlysta) is a monoclonal antibody that prevents the survival of B lymphocytes by blocking the binding of soluble human B lymphocyte stimulator (BLyS) to its B cell receptors. Approved by the U.S. Food & Drug Administration in 2011 for the treatment of adult patients with active, autoantibody-positive systemic lupus erythematosus (SLE) who are receiving standard therapy, belimumab reduces B-cell mediated immunity and autoimmune responses. The utility of benlysta for management of resistant SLE skin manifestations has not been reported. We present our experience of using this novel molecule for the successful management of cutaneous lupus at our center. Methods: We studied 4 patients with severe SLE skin manifestations. All patients met 1997 ACR SLE criteria and were ANA positive. Two patients had low complements and 1 patient had positive double-stranded (dS) DNA antibodies. All patients had failed multiple medications, including anti-malarial therapy and high-dose glucocorticoids, to control their skin disease. SLE disease activity indexes (SLEDAI) and patients global assessment (PGA) were recorded before and after benlysta treatment. Benlysta was added to concomitant standard therapy, as a loading dose of 10 mg/kg intravenously (IV) every 2 weeks for 3 doses followed by maintenance of 10 mg/kg every 4 weeks. All patients were pre-medicated with 40 mg prednisone. Patients were followed closely for clinical improvement every 4 weeks. Baseline patient characteristics and clinical images are outlined in the Table and Figure 1. Results: All the 4 patients demonstrated marked clinical improvement after benlysta treatment (Figure 2). The average time to clinical improvement after treatment initiation was 8-12 weeks. There were no changes in complement levels or dsDNA antibodies with treatment. All patients had a decrease in prednisone dose and improvement in both SLEDAI and PGA scores with therapy (Table). Conclusion: In this case series, the addition of benlysta to standard therapy improved the signs and symptoms of refractory cutaneous lupus in our patients. This is one of the first reports highlighting the potential utility of this medication for treatment of severe skin involvement in SLE. Additional studies need to be performed to assess use of benlysta in skin lupus. DERMATOMYOSITIS The Cutaneous Dermatomyositis Disease Area and Severity Index as a primary efficacy endpoint in a Phase 2 clinical trial of IMO-8400 in patients with dermatomyositis David Fiorentino1, Mark Hurtt2, Julie Brevard2, Victoria Werth3 1 Department of Dermatology, Stanford University School of Medicine, Redwood City, California, 2 Idera Pharmaceuticals, Inc., Cambridge, Massachusetts, 3 Division of Dermatology, Philadelphia Veteran's Affairs Medical Center, Philadelphia, Pennsylvania Introduction: The Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI) was developed to evaluate skin manifestations of dermatomyositis (DM), which can be the most active and severe components of DM in patients. Multiple studies have demonstrated the validity and reliability of the CDASI in patients with DM. In addition, it has been established that a difference of about 5 points on the CDASI activity score is clinically meaningful. IMO-8400 is an investigational oligonucleotide-based antagonist of Toll-like receptors (TLRs) 7, 8 and 9 that previously demonstrated activity on the Psoriasis Area and Severity Index in patients with moderate to severe plaque psoriasis. To evaluate the CDASI as a potential primary efficacy endpoint in a Phase 2 clinical trial of IMO-8400 in patients with DM, analyses were conducted on available longitudinal CDASI outcome data. Methods: Retrospective analyses were conducted on de-identified CDASI assessments for 115 unique DM patients with a total of 345 clinic visits. Patients with multiple assessments approximately 12 or 24 weeks apart were grouped by the first visit CDASI activity score (<15, 15-19, 20-24 and e"25), and the change in CDASI activity score between the visits was assessed. In addition, a simulation-based analysis was conducted to estimate the number of subjects needed for a trial using the CDASI as an outcome measure. Results: Over 24 weeks, a 5 point or greater decrease in CDASI activity score was observed at 31.8% of patient visits, with the change in CDASI activity score ranging from -23 to +27 points across all patients. Patients with a high first visit CDASI activity scores demonstrated larger decreases over 24 weeks compared to patients with low first visit CDASI activity scores. Because some patients experienced clinically meaningful changes of 4 to 5 points on the CDASI following treatment with standard of care therapies, a 7 point treatment effect was targeted for the IMO-8400 trial. Sample size calculations resulted in 10 patients per treatment group, assuming a standard deviation of 8.5 points over 24 weeks using a Repeated Measures Mixed Model analysis of change from baseline on monthly CDASI assessments (>80% power on a 1-sided test; alpha=0.05). Conclusion: Analyses of longitudinal CDASI outcome data demonstrated the feasibility of the CDASI as a primary efficacy endpoint for use in the Phase 2 clinical trial of IMO-8400 in patients with DM. The Janus kinase inhibitor tofacitinib is an alternative treatment option for refractory cutaneous dermatomyositis Drew Kurtzman, MD; Natalie Wright, MD; Janice Lin, MD; Alisa Femia, MD; Henry Townsend, MD; Mital Patel, MD; Ruth Ann Vleugels, MD, MPH Department of Dermatology, Brigham and Womens Hospital, Boston, MA Background: Dermatomyositis is an idiopathic inflammatory myopathy with characteristic cutaneous findings. As a rare disorder, few validated therapies exist for disease management, and when traditional agents fail, effective alternatives have been scarcely reported. Recently, ruxolitinib, a selective inhibitor of the Janus kinases JAK1 and JAK2, was demonstrated to be effective for inducing remission of refractory dermatomyositis in a single case report. A related Janus kinase inhibitor, tofacitinib, is commercially labeled for use in select inflammatory conditions, however, its use in patients with dermatomyositis has not yet been reported. Objective: We sought to assess the efficacy of the Janus kinase inhibitor tofacitinib for treating refractory cutaneous dermatomyositis. Methods: We identified patients with cutaneous dermatomyositis refractory to traditional agents. The clinical response to tofacitinib was evaluated. The primary endpoint was improvement of skin disease as measured by the validated Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI). Secondary endpoints included necessity for concurrent therapies, improvement of muscle disease when applicable, tolerability, and incidence of adverse events. Results: Three patients with refractory cutaneous dermatomyositis were evaluated including one with amyopathic dermatomyositis. All patients were female. The mean prescribed dose of tofacitinib was 6.67 mg (range 5-10 mg, n=3) administered orally twice daily for a mean period of 8.6 months (range 5-14 months). The mean age at treatment initiation was 40 years (range 30-50 years, n=3). Prior failed therapies included topical and systemic corticosteroids, hydroxychloroquine, methotrexate, azathioprine, mycophenolate mofetil, dapsone, thalidomide, lenalidomide, isotretinoin, intravenous and subcutaneous immunoglobulin (IVIG and SCIG), and rituximab. Tofacitinib as a monotherapy produced skin improvement in all three patients. Mean CDASI scores before and after treatment were 28.3 (range 23-32, n=3) and 17.6 (range 10-27, n=3), respectively. Muscle disease in the two patients with classic dermatomyositis remained in remission while on therapy; one patient noted subjective improvement of strength. Tofacitinib was uniformly tolerated without side effects. No laboratory abnormalities were encountered throughout the duration of treatment. Limitations: Small sample size, heterogeneous past treatment regimens. Conclusions: Tofacitinib is a well-tolerated, easily administered oral medication capable of improving recalcitrant cutaneous dermatomyositis in select patients. Additional large-scale and comparative studies are warranted to further support its use in this setting. Evaluation of the Reliability and Validity of the Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI) and the Cutaneous Assessment Tool-Binary Method (CAT-BM) Among Pediatric Dermatologists, Rheumatologists, and Neurologists in Juvenile Dermatomyositis Janice Tiao, BA,*1, 2 Neelam Khan, MS,*1, 2 Rui Feng, PhD,3 Emily M. Berger, MD,4 John Brandsema, MD,5 Carrie C. Coughlin, MD,6 Elizabeth A. Kichula, MD, PhD,5 Melissa A. Lerman, MD, PhD,7 Svetlana Lvovich, DO,8 Patrick J. McMahon, MD,10 Lisa G. Rider, MD,11 Adam I. Rubin, MD,1,10 Lisabeth V. Scalzi, MD,12 Douglas M. Smith, MD,5 Alysha J. Taxter, MD, MSCE,9 James R. Treat, MD,10 Sabrina W. Yum, MD,5 Joyce Okawa, MBE, RN,1 Victoria P. Werth, MD1, 2 *co-first authors 1Department of Dermatology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 2Philadelphia VA Medical Center, Philadelphia, PA 3Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, PA 4Hackensack University Medical Center, Hackensack, NJ 5Division of Neurology, Childrens Hospital of Philadelphia, Philadelphia, PA 6Division of Dermatology, Washington University School of Medicine, St. Louis, MO 7 HYPERLINK "http://www.chop.edu/centers-programs/center-childhood-arthritis-and-rheumatic-diseases" Division of Rheumatology, Childrens Hospital of Philadelphia, Philadelphia, PA 8St. Christophers Hospital for Children, Philadelphia, PA 9Wake Forest Baptist Brenner Childrens Hospital, Winston-Salem, NC 10Division of Dermatology, Childrens Hospital of Philadelphia, Philadelphia, PA 11National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD 12Penn State Hershey Rheumatology, Penn State Milton S. Hershey Medical Center, Hershey, PA Background/Purpose: The Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI) has been shown to be a reliable and valid outcome measure to assess cutaneous disease in the adult dermatomyositis (DM) population. Better instruments are needed to assess cutaneous disease in the juvenile DM (JDM) population. The purpose of this study is to compare two outcome measures, the CDASI and the Cutaneous Assessment Tool-Binary Method (CAT-BM), for use by pediatric dermatologists, rheumatologists, and neurologists in JDM patients. Methods: Five pediatric dermatologists, 5 pediatric rheumatologists, and 5 pediatric neurologists evaluated 14 JDM patients using the CDASI, CAT-BM, and Physician Global Assessment (PGA) scales. Patients were scored independently by each physician. Inter-rater reliability, intra-rater reliability, and construct validity were compared. Results: Inter-rater reliability for CDASI activity and damage scores was good to moderate for dermatologists and rheumatologists, but poor for neurologists. The inter-rater reliability for CAT-BM activity and damage scores was moderate for dermatologists and rheumatologists, but poor for neurologists (Table 1). Notably, the inter-rater reliability for neurologists for CDASI activity and damage improved to moderate (0.66 and 0.61, respectively) when an outlier neurologist and patient were removed. Intra-rater reliability for CDASI activity and damage scores was excellent for dermatologists, moderate for neurologists, and moderate to excellent for rheumatologists. Intra-rater reliability for CAT-BM activity and damage scores was excellent for dermatologists and neurologists and moderate to excellent for rheumatologists (Table 2). Strong positive associations were found between the change in PGA activity and damage scores and the respective CDASI activity and damage scores (0.224 with p<0.0001 and 0.343 with p<0.0001), as well as between the change in PGA activity and damage scores and the respective CAT-BM activity and damage scores (0.484 with p<0.0001 and 0.256 with p=0.0019). Conclusion: Our data confirm the reliability and validity of the CDASI activity and damage scores and the CAT-BM activity scores when used by pediatric dermatologists and rheumatologists. Significant variation in the pediatric neurologists scores suggests that outliers affect results considerably. Table 1. Inter-observer correlation coefficient Within pediatric dermatologists (n=5)Within pediatric neurologists (n=5)Within pediatric rheumatologists (n=5)CDASI Activity0.52 (0.44-0.61)0.47 (0.39-0.56)0.81 (0.76-0.85) Damage0.59 (0.51-0.67)0.46 (0.37-0.54)0.59 (0.51-0.66)CAT-BM Activity0.58 (0.50-0.66)0.42 (0.33-0.51)0.67 (0.60-0.74) Damage0.49 (0.41-0.58)0.29 (0.20-0.38)0.48 (0.39-0.57)PGA Activity0.64 (0.50-0.78)0.38 (0.29-0.47)0.47 (0.39-0.56) Damage0.71 (0.65-0.83)0.73 (0.67-0.79)0.31 (0.22-0.40) Table 2. Intra-rater reliability ICC (95% C.I.) Within pediatric dermatologists (n=5)Within pediatric neurologists (n=5)Within pediatric rheumatologists (n=5)CDASI Activity0.90 (0.78-1.00)0.65 (0.29-1.00)0.91 (0.79-1.00) Damage0.97 (0.94-1.00)0.78 (0.53-1.00)0.64 (0.27-1.00)CAT-BM Activity0.86 (0.70-1.00)0.91 (0.80-1.00)0.88 (0.74-1.00) Damage0.93 (0.85-1.00)0.89 (0.76-1.00)0.73 (0.44-1.00)PGA Activity0.95 (0.90-1.00)0.83 (0.64-1.00)0.50 (0.03-0.96) Damage0.84 (0.66-1.00)0.96 (0.91-1.00)0.55 (0.12-0.98)*ICC scores between 0.50 and 0.70 are considered moderate and minimally acceptable, 0.70 to 0.81 good, and >0.81 excellent. Scores <0.5 are considered poor. Activity of Type I and Type II Interferons in Dermatomyositis Skin is Correlated with Characteristic Pathologic Features Hayley Leatham1, Kerri Rieger2, Lorinda Chung3, Shufeng Li1, Brandon Higgs4, Yihong Yao4, Kavita Sarin1, David Fiorentino1 Departments of Dermatology1 and Dermatopathology2, Stanford University Division of Immunology and Rheumatology3, Stanford University Translational Sciences, MedImmune4, Gaithersburg, MD Background/Purpose: Interferon (IFN) signaling is upregulated in dermatomyositis (DM) skin, but the relationship to classic histopathologic features is unknown. Methods: Thirty-nine skin biopsies from patients with dermatomyositis underwent gene expression analysis using Affymetrix arrays, as well as histologic analysis by a blinded dermatopathologist. Biopsies were scored for severity of several cardinal histopathologic features, including basal vacuolar change (BV), dermal mucin deposition, and perivascular inflammation. Type I and type II IFN scores were generated based on the average relative expression of selected genes previously demonstrated to be specifically upregulated by IFN-alpha and IFN-gamma, respectively. Expression levels of IFN transcripts were measured by quantitative PCR. Univariate analysis was performed to evaluate the association between IFN scores and IFN transcripts with key histopathologic features, with subsequent multivariate models constructed to include potentially confounding variables such as biopsy site, medication use, age, and length of disease. Results: Skin biopsies were heterogeneous with regard to both histopathologic features as well as type I and II IFN scores. The type I IFN gene set was comprised of three genes (OAS1, OAS2, IFIT1) and the type II IFN gene set consisted of six genes (GBP1, GBP2, HLA-DMB, HLA-DRA, IL18BP, WARS); these scores were significantly correlated (r=0.6636, p<0.0001). Type I IFN scores correlated strongly with IFN beta expression (r=0.70956, p<0.0001) but not other type I (alpha, kappa, omega) transcript levels; type I IFN scores also correlated with IFN gamma transcripts (r=0.4539, p=0.008). Type II IFN scores correlated strongly with IFN gamma (r=0.839, p<0.0001), as well as IFN beta (r=0.481, p=0.0046). In univariate analysis, keratinocyte injury (reflected by BV score) was found to be associated with both type I and type II IFN scores (p=0.0046 and p=0.004, respectively); these associations remained significant in multivariate analysis. Similar analysis of additional histopathologic features showed an association between mucin deposition and higher type I IFN scores (OR 1.13, p=0.0001) but not type II IFN scores (OR 1.32, p=0.071); additionally, lymphocytic dermal inflammation was associated with type II IFN scores (OR 1.36, p=0.0413) but not type I IFN scores (OR 1.03, p=0.3275). Other analyzed histologic features, including epidermal atrophy, basement membrane thickening, and vessel damage were not statistically associated with either IFN score. Conclusion: Our results highlight that IFN signaling in DM skin likely represents a combination of at least type I and II activity. Furthermore, our data suggest that both type I and II IFN signaling may be associated with shared as well as distinct pathologic processes in DM skin, although there is a clearly a high correlation and degree of overlap in gene expression between our two scores. Keratinocyte injury, the sine qua non finding in DM skin, is associated with both type I and II IFN activity. Finally, our results imply that IFN beta is the relevant IFN driving type I IFN signaling in DM skin and point to both IFN beta and IFN gamma as potential targets of pharmacologic inhibition in cutaneous DM.  MORPHEA Changes of disease activity and damage over time in morphea patients Jack C. OBrien, BS1 and Heidi T. Jacobe MD, MSCS1 1University of Southwestern Medical Center, Department of Dermatology, Dallas, TX Background: Morphea, also known as localized scleroderma, is characterized by inflammation followed by sclerosis, producing devastating functional and cosmetic impairment in those affected. Very little is known about the natural history of morphea. It was previously thought to burn out within 5 years. Newer studies, including our own, imply some patients have a remitting relapsing course. However, no studies have prospectively examined morphea disease activity over time. Understanding the course of morphea is important, not only in determining how to counsel and evaluate patients, but also for appropriately planning outcome and interventional studies. Objective: To define the disease course of morphea with respect to activity and damage based on validated clinical outcome measures in a prospective, longitudinal cohort of patients. Methods: This is prospective cohort study including 118 study patients from the Morphea in Adults and Children (MAC) cohort. Patients were included if they had at least three study visits with localized scleroderma activity index (LoSAI) scores recorded. Patients were divided into two groups based on disease activity at baseline visit, with those with LoSAI scores <10 being considered to have mild disease and those e" 10 were classified as having moderate to severe disease activity. Mean disease activity over time was measured by plotting time on the x-axis and LoSAI on the y-axis for each patient. Area under the curve per year (AUC/yr), reflecting disease activity over time, was determined for each patient using the trapezoidal rule. Linear regression analysis was used to determine the slope of each line, reflecting the overall disease course for each patient. Similar analyses were conducted using the Modified Rodnan Skin Score (MRSS), localized scleroderma damage index (LoSDI), and physicians global assessment of activity (PGA-A), and damage (PGA-D). Longitudinal regression analyses are currently underway to model the relationship between baseline demographic and clinical features and activity and damage over time. We compared mean AUC/yr and mean slopes in patients with mild disease activity and in those with moderate to severe disease activity with the Mann-Whitney U Test using GraphPad Prism 6.0. Results: 118 patients with a total of 535 study visits were included in this study. 71 patients had four visits, 49 had five visits, and 36 had six or more study visits. 39% were children and 61% adults at baseline visit. The majority of patients were Caucasian (75%) and female (79%). 61% of patients had mild disease activity at baseline and 39% of patients had moderate-severe disease activity. Mean disease activity and damage measurements for patients at baseline visit were LoSAI 13.2 20.1, LoSDI 16.8 17.3, PGA-A 31.4 29.6, PGA-D 34.0 23.7, and MRSS 6.6 5.7. Mean AUC/yr for LoSAI scores in patients with moderate-severe activity was higher than those with mild activity (27.7 vs. 4.1; p<0.0001). Patients with moderate-severe disease activity also had higher disease damage scores as measured by LoSDI and MRSS (p=0.001 and p=0.005, respectively). The mean slope for patients with mild disease activity was -0.76 while the mean slope for patients with moderate-severe disease activity was -9.20 (p<0.0001). Conclusions: Disease activity improves in the majority of morphea patients over time. As expected, morphea patients with higher disease activity at baseline progress to having higher damage scores than those with mild disease activity as activity resolves with damage. An unexpected finding was that damage scores in patients, after initially worsening as activity subsided, improved in many patients. We hypothesize that this may occur more frequently in the subgroup with dermal involvement, as compared to those with deep involvement. Acknowledgements: We are grateful to Jeannette Olazagasti and Victoria P. Werth, MD, for sharing their data analysis plan for this project. Epidemiology and treatment of post-irradiation morphea: a retrospective analysis from three large tertiary care centers *Renee Fruchter BA1, *Drew Kurtzman MD2, Daniel R. Mazori BA1, Natalie A. Wright MD2, Mital Patel MD2, Ruth Ann Vleugels MD MPH2, Alisa N. Femia MD1 1. The Ronald O. Perelman Department of Dermatology, New York University Langone Medical Center 2. Brigham and Women s Hospital Department of Dermatology, Harvard Medical School *represent co-first authors represent co-last authors Background: Post-irradiation morphea (PIM) is a rare and potentially disabling cutaneous complication of radiotherapy, affecting approximately 2 in every 1000 patients treated with radiation. Only 67 cases are reported in the literature to date, and treatment data is reported in only half of cases. Objective: The objective of this retrospective cohort study was to characterize the nature and treatment of patients with PIM. Methods: Using medical record databases at New York University (2005-2015) and Partners Healthcare (Brigham and Womens and Massachusetts General Hospitals; 2000-2015), we reviewed all charts with ICD-9 code 701.0 to identify all patients with PIM at three large tertiary care centers. Results: Twenty-four patients with PIM were identified. All were female. Twenty-three of the 24 were treated with radiotherapy for breast cancer, while one patient had a history of an acinic cell carcinoma of the parotid gland treated with radiation. The mean age of onset was 57.9 years. Where data was available, 24% (n=5) developed PIM within 1 year of first radiation exposure, 52% (n=11) within 1-5 years, and 24% (n=5) after 5 years. All had PIM within the irradiated site, and 46% (n=11) had PIM extending beyond the irradiation field to sites including the contralateral breast, abdomen, back, groin, extremities, and face. Fifty-four percent (n=13) were asymptomatic, 29% (n=7) complained of pruritus, 17% (n=4) endorsed pain, and 8% (n=2) reported a sensation of tightening. One patient had a documented history of radiation dermatitis, and only one had a prior history of a connective tissue disease. All but one patient were referred to a dermatologist. Where treatment data was available (n=22), 91% (n=20) were treated with topical agents including corticosteroids, vitamin D analogues, tacrolimus, dapsone, and azelaic acid; of these, 40% (n=8) had improvement with topical therapy alone. Thirty-six percent (n=8) of patients received systemic agents (methotrexate, prednisone, etanercept, doxycycline, colchicine, calcitriol, and pentoxifylline) and/or phototherapy. Although only utilized in four patients, methotrexate led to disease stabilization or improvement in all of those treated with this medication. Post-irradiation morphea was treatment-refractory in 36% (n=8) of patients, requiring trials of three or more therapies. Conclusion: In conclusion, this study represents the largest PIM cohort to date as well as the largest study to describe treatment outcomes. This study highlights the varied nature of PIM in terms of associated symptoms, latency period from treatment with radiotherapy, and sites of disease involvement. In addition, this study underscores the potentially refractory nature of PIM, as well as the need to better define a treatment algorithm for this condition. Additional investigations are warranted to further characterize this disorder. MISCELLANEOUS Myelodysplastic Syndrome Presenting as Generalized Granulomatous Dermatitis Oral Presentation: David A. Wetter, M.D. Abstract was previously published in the following article:   { |  Z y ; tvp&2#ȽȽȽȽȽ|n|||aYhoh~5hoh~PJnH tH hohf 2H*PJnH tH hohf 2PJnH tH hohf 25PJ\nH tH hoh)OJQJhohf 25OJQJ\hoh~OJQJhohf 2OJQJhohf 2H*OJQJhohf 2OJQJ\hohf 2CJOJQJaJhoh~>*CJOJQJaJ"| p&^?w; "n&'g)h)gd~$dd[$\$a$gd+F$a$gd~$a$gdf 2#$&;>\]^_?Iw; N """m&n&x&''f)g)h)j)z)!*1*2*>*?*N*O*_*`*a*b*c*******H+^+糥 hu6h~hoh~H*h~hoh~5>*CJaJhoh~PJnH tH hoh~5>*^Jhoh~^Jhoh~5^Jhoh~H* hoh~hoh~5hoh~5H*9h)i)j)z){)!*a*^+.1<5666y67E79X:!<@@AABDD$a$gd~gd~$dd[$\$a$gd+F^+k+..1122<5G566y6E7Q799X:`:!<)<@@@@ABCC$C(C7C8CMCNCbCcC{C|CCCCCCCCCCCDD.D0DFDGDcDdDxDzDDDDDDDDDDD@EAErEsEEE F FXFYFFF hoh2ohoh~H*hoh2o5hoh~hmK hoh~hoh~5PD@ErEE FXFFbGGG2HHH K[L Q6RfRgRRRR$<&`#$/Ifgdol "gd~dgd~gd~FFGG)G*GbGcGGGGG2H4HHHHIIKKKZLcLeLQQQQ5R6RfRRRRR"S#S`SaSkSlSSSSSSS1T2ToTpTTUU픋hoh~PJhoh~5OJQJ^JaJhoh~B*\phhoh2o5hoh~5hoh~H*(jhoh~0J>*B*U\phhoh~0JB*\ph hoh~jhoh~U6RRRRR?%%%$<&`#$/Ifgdol kd$$Ifl&\a,"   t 6`<0644 lap(ytoRRRRS%kd$$Ifl \a,"   t 6`<0644 lap(yto$<&`#$/Ifgdol SS"S#S-S%kd$$Ifl \a,"   t 6`<0644 lap(yto$<&`#$/Ifgdol -S>SOS`SaS%kd$$Ifl \a,"   t 6`<0644 lap(yto$<&`#$/Ifgdol aShSiSjSkS$<&`#$/Ifgdol kSlSxSSS?%%%$<&`#$/Ifgdol kdT$$Ifl \a,"   t 6`<0644 lap(ytoSSSSS%kd)$$Ifl \a,"   t 6`<0644 lap(yto$<&`#$/Ifgdol SSSSS%kd$$Ifl \a,"   t 6`<0644 lap(yto$<&`#$/Ifgdol SSSSS%kd$$Ifl \a,"   t 6`<0644 lap(yto$<&`#$/Ifgdol SST T1T$<&`#$/Ifgdol 1T2TX?XZX[XpXqXXXXXXYYYYYYI]P]Q]S]]^cccceee$jhoh~UmHnHtH uhoh~PJ^Jhoh2o5hoh~H* hoh2ohoh~5 hoh~hoh~PJB;ULU]U^UhU%kd $$Ifl \f8,"X 2 2 t 6`<0644 lap(yto$<&`#$/Ifgdol hUyUUUU%kd $$Ifl \f8,"X 2 2 t 6`<0644 lap(yto$<&`#$/Ifgdol UUUUU$<&`#$/Ifgdol UUUUU?%%%$<&`#$/Ifgdol kd $$Ifl \f8,"X 2 2 t 6`<0644 lap(ytoUUUUV%kdw $$Ifl \f8,"X 2 2 t 6`<0644 lap(yto$<&`#$/Ifgdol VV$V%V)V%kdL $$Ifl \f8,"X 2 2 t 6`<0644 lap(yto$<&`#$/Ifgdol )V*V+V,V-V%kd!$$Ifl \f8,"X 2 2 t 6`<0644 lap(yto$<&`#$/Ifgdol -V9VJV[VlV$<&`#$/Ifgdol lVmVwVVV?%%%$<&`#$/Ifgdol kd$$Ifl \f8,"X 2 2 t 6`<0644 lap(ytoVVVIW% gd~kd$$Ifl \f8,"X 2 2 t 6`<0644 lap(yto$<&`#$/Ifgdol IWJWKWLWW@XXXXYI]ceeeeeeeeeee+f^ffLigd2ogd2o$a$gd~gd~eeee>f?f@fCfDf\f]f^f_fffLiVij jqqu'u7wHwwww~xxxxxxxxxxx(y*yJyLyPyRyyyyyyûûì}}}}}}}}}}hoh~CJH*OJQJaJhoh~5CJOJQJaJhoh2oCJOJQJaJhoh~CJOJQJaJhoh~H* hoh~hoh~5H*hoh~5hoh2o5hoh~5>*CJaJhoh2o5>*CJaJ1Lijqu7wwww~xxyyrz{N{{{|r}~"#12~ !d *$gd2o$a$gd~ $a$gd~gd~yyypzrz{{{L{N{P{{{{{|||q}r}|}~~~!"#0ѭ~q]&hoh2o0J!5>*CJaJmH sH hoh~0J!mH sH  hoh~0J!CJaJmH sH  hoh2o0J!CJaJmH sH hoh~0J!CJaJ#hoh2o0J!5CJaJmH sH #hoh~0J!CJH*OJQJaJ hoh~0J!CJOJQJaJhoh~0J!OJQJhoh~CJH*OJQJaJ012~U^tuo|н׳ШЛhojhoUhoh~PJnH tH hoh~mH sH hoh2o5aJhoh~56U hoh2o hoh~hoh~5hoh~0J!mH sH &hoh~0J!5>*CJaJmH sH ~Utuogd4$dd[$\$a$gd+Fgd~$a$gd~ !d*$gd~dgd~ !d *$gd~ !d *$gd2oSamuel J. Balin, *David A. Wetter, Paul J. Kurtin, Louis Letendre, Mark R. Pittelkow Arch Derm 2011;147(3):331-335. Background: Granulomatous dermatitis rarely has been reported as a manifestation of leukemia or myelodysplastic syndromes. We describe a case of widespread granulomatous dermatitis that preceded the diagnosis of myelodysplastic syndrome by 2 years. Observations: A 71-year-old man had development of a generalized, mildly pruritic eruption that slowly progressed over a 2-year period. Punch biopsy specimens demonstrated interstitial dermal granulomatous inflammation. Complete blood count with differential showed marked monocytosis, and subsequent biopsy of the bone marrow confirmed myelodysplastic syndrome. The patient started treatment with lenalidomide and his skin condition improved after 6 weeks of treatment; however, the myelodysplastic syndrome progressed to acute leukemia, and he died shortly thereafter. Conclusions: A paucity of literature exists documenting the occurrence of granulomatous dermatitis as a manifestation of an underlying hematologic disorder. This case illustrates a striking example of widespread granulomatous dermatitis heralding the onset of myelodysplastic syndrome. 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