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Dermatomyositis Autoantibodies: Clinical Markers of Patients Past, Present, and Future

Dermatomyositis Autoantibodies: Clinical Markers of Patients Past, Present, and Future It has been almost 50 years since autoantibodies (Abs) were identified in the blood of patients with myositis.1 Since then, the targets of several myositis-specific antibodies (MSAs) have been identified as ubiquitous proteins involved in critical cellular processes, such as protein translation, DNA repair, transcription, and viral recognition.2 Several pieces of evidence suggest that these Abs are not merely epiphenomena but are markers of an immune response that is central to disease propagation: the most compelling of these is the finding that patients typically have only 1 MSA type (eg, Mi-2 vs Jo-1), and those with a particular MSA often share similar clinical features regarding organ system involvement, prognosis, and response to therapy.3,4 The antigens are often preferentially overexpressed in diseased tissue; for example, Mi-2 and Jo-1 are overexpressed in the muscle tissue of patients with dermatomyositis (DM) compared with those with polymyositis (PM) or healthy muscle.5 Local environment is also critical; for example, many autoantigens, such as Ro-52 and melanoma differentiation–associated gene 5 (MDA-5), are induced by type I or II interferon, and activity of interferon is significantly increased in myositis tissues.6 In addition to expression level, many proteins are likely rendered immunogenic by processes, such as cleavage (which can occur in the context of granzyme B–mediated CD8+ killing), and posttranslational modification.7 Thus, the paradigm emerges that self-proteins are rendered antigenic in a tissue-specific manner that depends on the differentiation state or the microenvironment of the target cell. Thus, antigens have the potential to provide insight regarding the exact cell(s) that is undergoing attack and producing the disease we recognize clinically as DM. This paradigm explains why MSAs in DM are associated with patient prognosis and phenotype and are, thus, important tools for the physician caring for patients with DM. For example, it has long been known that patients with anti–tRNA synthetase antibodies tend to have a high risk of interstitial lung disease (ILD), arthritis, Raynaud phenomenon, and mechanic hands4; Mi-2 antibodies tend to be associated with low mortality, treatable disease, and classic cutaneous signs, such as the shawl sign and cuticular overgrowth.4 Until a few years ago, these 2 classes of Abs were the only MSAs in patients with DM, representing less than 20% of patients. Thus, the notion of a serologic test to diagnose DM with high sensitivity was still not realized. In the past several years, we have seen the discovery of several novel MSAs in DM,2 including antibodies to p155/140 and MDA-5 (CADM-140), whose frequency and associated phenotypes are further detailed by Hamaguchi et al8 in this issue of the Archives. This study is significant in that it is the largest study to date to compare the prevalence of and clinical characteristics associated with all the aforementioned MSAs in a large DM cohort. The antibodies to p155/140 and MDA-5 (CADM-140) were found in 18% of the patient cohort, meaning that more than 40% of their patients with DM were able to be characterized by a single dominant MSA. One caveat to this discovery is that the authors enriched their cohort with a separate group of 13 MSA-positive patients from another institution, which represents almost 10% of their MSA-positive cohort; thus, some of their prevalence data for MSAs is confounded by selection bias. In addition, this information may or may not be applicable to DM seen in other ethnic populations or geographic regions. For example, the frequency of Mi-2 Abs is known to be increased in areas of high UV exposure.9 In general, Hamaguchi et al8 confirm previous clinical data that are associated with Mi-2 and antisynthetase antibodies. The importance of the study lies in the further characterization of anti–155/140 and anti-MDA serotypes. The anti–155/140 Ab has previously been suggested to identify adult patients with DM at higher risk for cancer.10,11 The study by Hamaguchi et al8 confirms this, with 68% of patients with anti–155/140 Abs having an underlying malignancy and 41% of these patients dying of their malignancy. For the entire group of patients with DM, 10.4% had underlying malignancy. However, patients with the anti–155/140 Ab tended to have classical DM, which may suggest that those with clinically amyopathic DM (CADM) are less prone to underlying malignancy, a finding seen in several other cohorts.12,13 One population-based study14 in the United States of 29 patients did not find this difference in the rate of malignancy in DM relative to CADM, in which 30% of patients (6 of 20) with classical DM and 17% with CADM (1 of 6) had a malignancy. Larger studies are needed to confirm that there is a lower rate of malignancy in patients with CADM. Patients with MDA Abs have been described as typically having mild or absent muscle disease, which was confirmed in this study.15 This group has also been shown to have a high risk of ILD, sometimes rapidly progressive and fatal, which was seen in this cohort.15 Patients with the anti-MDA Ab have a 93% incidence of ILD (compared with an overall ILD incidence of 39.6%), which is frequently rapidly progressive. The anti-MDA was also associated with high serum KL-6 levels. This Ab was associated with increased CADM relative to classical DM, and 37% of patients died of ILD. Of interest, there were many more females in the anti-MDA Ab group relative to the other DM-specific Abs. Studies of patients with CADM in the United States have also suggested a female predominance.16 In addition, the investigators found that patients with anti-MDA also have a higher risk of cutaneous ulceration and arthritis, which is in agreement with data in US patients with DM.17 The correlation between Ab and the clinical findings gives the hope that many of these patients may be recognized by their clinical phenotype. In terms of prognosis, the study by Hamaguchi et al8 suggests that Japanese patients with CADM and ILD are less likely to develop malignancy. Despite this, survival of patients with either anti–155/140 or MDA Abs was quite low. It is stated that the frequency of ILD in patients with CADM in the United States is low, but 1 retrospective US study in which 78% of patients underwent pulmonary function tests found that the frequency of ILD in CADM and DM was comparable. Approximately 50% of the patients with both CADM and DM in this referral population had evidence of lung abnormalities, a number not so dissimilar to that in the Japanese group presented in this issue.13 Few other studies have systematically examined the incidence of lung disease in the United States in CADM or DM, and the percentage of rapidly progressive ILD (RP-ILD) is not known. The study by Hamaguchi et al8 and others18,19 suggest that there may be ethnic differences in the incidence of RP-ILD in the Asian population relative to the US population which would need to be confirmed with more systematic studies in the United States. It is apparent from the article by Hamaguchi et al8 that improving treatment of RP-ILD is an urgent issue for the Japanese (and likely other races). Several studies20,21 suggest that mycophenolate mofetil treatment can reverse ILD in patients with DM, but prospective studies are needed, and it is not clear that this approach would be effective in RP-ILD. One study22 concludes that ILD associated with DM, defined by criteria requiring the presence of myositis, is in most cases mild and chronic, and has a nonprogressive course during immunosuppressive treatment. Routine pulmonary function test screening of patients with CADM is needed; because these patients do not necessarily receive immunosuppressive agents for their muscle disease, studies to determine the natural history and role of interventions for subclinical lung disease are needed. A few commercial laboratories now perform testing on these and other novel MSAs for DM (eg, RDL Reference Laboratory [http://www.rdlinc.com/index.html]). Two other Ab targets, SAE1/2 and NXP-2, are also described as DM specific, but whose phenotype is not yet clearly defined in adult patients with DM.2 Even with testing, we are still left with approximately 50% to 60% of our patients with DM who cannot yet be assigned a known serologic specificity. We must continue to carefully phenotype patients so that the maximum amount of clinical information can be associated with these serologic profiles. Prognostic information and optimal treatment strategies may well depend on knowledge of the serologic status of the patient. The study by Hamaguchi et al8 also demonstrates the power in numbers and the need for multicenter collaborations to study a rare disease such as DM. Given the heterogeneity of DM, ideal studies would link experts in rheumatology, pulmonology, neurology, and dermatology because they see different subsets of the CADM and classic DM populations. For example, patients with CADM tend to be seen in dermatology clinics because of the predominance of skin symptoms.16 The North American Rheumatologic Dermatology Society (http://www.rheumaderm-society.org/) has collaborated on such cutaneous DM studies, providing an infrastructure that should be further developed to expand knowledge of DM subtypes (including CADM) in the United States. The North American Rheumatologic Dermatology Society has undertaken several studies specifically related to the dermatologic aspects of DM, and funding to support prospective studies would advance knowledge of how to evaluate and treat such patients.23,24 Correspondence: Dr Werth, Department of Dermatology, Perelman Center for Advanced Medicine, 3400 Civic Center Blvd, Ste 1-330A, Philadelphia, PA 19104 (werth@mail.med.upenn.edu). Financial Disclosure: None reported. Funding/Support: This study was supported in part by grant K24-AR 02207 from the National Institutes of Health (Dr Werth). Role of the Sponsor: The National Institutes of Health had no role in the design and conduct of the study; in the collection, analysis, and interpretation of data; or in the preparation, review, or approval of the manuscript. References 1. Caspary EAGubbay SSStern GM Circulating antibodies in polymyositis and other muscle-wasting disorders. Lancet 1964;2 (7366) 94114203937Google Scholar 2. Gunawardena HBetteridge ZE McHugh NJ Myositis-specific autoantibodies: their clinical and pathogenic significance in disease expression. Rheumatology (Oxford) 2009;48 (6) 607- 61219439503Google Scholar 3. Joffe MMLove LALeff RL et al. Drug therapy of the idiopathic inflammatory myopathies: predictors of response to prednisone, azathioprine, and methotrexate and a comparison of their efficacy. Am J Med 1993;94 (4) 379- 3878386437Google Scholar 4. Love LALeff RLFraser DD et al. A new approach to the classification of idiopathic inflammatory myopathy: myositis-specific autoantibodies define useful homogeneous patient groups. Medicine (Baltimore) 1991;70 (6) 360- 3741659647Google Scholar 5. Casciola-Rosen LNagaraju KPlotz P et al. Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy. J Exp Med 2005;201 (4) 591- 60115728237Google Scholar 6. Greenberg SA Dermatomyositis and type 1 interferons. Curr Rheumatol Rep 2010;12 (3) 198- 20320425524Google Scholar 7. Rosen ACasciola-Rosen L Autoantigens in systemic autoimmunity: critical partner in pathogenesis. J Intern Med 2009;265 (6) 625- 63119493056Google Scholar 8. Hamaguchi YKuwana MHoshino K et al. Clinical correlations with dermatomyositis-specific autoantibodies in adult Japanese patients with dermatomyositis: a multicenter, cross-sectional study. Arch Dermatol 2011;147 (4) 391- 398Google Scholar 9. Love LAWeinberg CR McConnaughey DR et al. Ultraviolet radiation intensity predicts the relative distribution of dermatomyositis and anti-Mi-2 autoantibodies in women. Arthritis Rheum 2009;60 (8) 2499- 250419644877Google Scholar 10. Targoff INMamyrova GTrieu EP et al. Childhood Myositis Heterogeneity Study Group; International Myositis Collaborative Study Group, A novel autoantibody to a 155-kd protein is associated with dermatomyositis. Arthritis Rheum 2006;54 (11) 3682- 368917075819Google Scholar 11. Kaji KFujimoto MHasegawa M et al. Identification of a novel autoantibody reactive with 155 and 140 kDa nuclear proteins in patients with dermatomyositis: an association with malignancy. Rheumatology (Oxford) 2007;46 (1) 25- 2816728436Google Scholar 12. Azuma KYamada HOhkubo M et al. Incidence and predictive factors for malignancies in 136 Japanese patients with dermatomyositis, polymyositis and clinically amyopathic dermatomyositis [published online ahead of print October 5, 2010]. Mod Rheumatol 2010;2092245310.1007/s10165-010-0362-yGoogle Scholar 13. Morganroth PAKreider MEOkawa JTaylor LWerth VP Interstitial lung disease in classic and skin-predominant dermatomyositis: a retrospective study with screening recommendations. Arch Dermatol 2010;146 (7) 729- 73820644033Google Scholar 14. Bendewald MJWetter DALi XDavis MD Incidence of dermatomyositis and clinically amyopathic dermatomyositis: a population-based study in Olmsted County, Minnesota. Arch Dermatol 2010;146 (1) 26- 3020083689Google Scholar 15. Sato SHirakata MKuwana M et al. Autoantibodies to a 140-kd polypeptide, CADM-140, in Japanese patients with clinically amyopathic dermatomyositis. Arthritis Rheum 2005;52 (5) 1571- 157615880816Google Scholar 16. Klein RQTeal VTaylor LTroxel ABWerth VP Number, characteristics, and classification of patients with dermatomyositis seen by dermatology and rheumatology departments at a large tertiary medical center. J Am Acad Dermatol 2007;57 (6) 937- 94317923170Google Scholar 17. Fiorentino DChung LZwerner JRoen ACasciola-Rosen L The mucocutaneous and systemic phenotype in dermatomyositis patients with antibodies to MDA5 (CADM-140): a retrospective study. J Am Acad Dermatol In pressGoogle Scholar 18. Ye SChen XXLu XY et al. Adult clinically amyopathic dermatomyositis with rapid progressive interstitial lung disease: a retrospective cohort study. Clin Rheumatol 2007;26 (10) 1647- 165417308858Google Scholar 19. Mukae HIshimoto HSakamoto N et al. Clinical differences between interstitial lung disease associated with clinically amyopathic dermatomyositis and classic dermatomyositis. Chest 2009;136 (5) 1341- 134719581351Google Scholar 20. Morganroth PAKreider MEWerth VP Mycophenolate mofetil for interstitial lung disease in dermatomyositis. Arthritis Care Res (Hoboken) 2010;62 (10) 1496- 150120506189Google Scholar 21. Saketkoo LAEspinoza LR Experience of mycophenolate mofetil in 10 patients with autoimmune-related interstitial lung disease demonstrates promising effects. Am J Med Sci 2009;337 (5) 329- 33519295413Google Scholar 22. Fathi MVikgren JBoijsen M et al. Interstitial lung disease in polymyositis and dermatomyositis: longitudinal evaluation by pulmonary function and radiology. Arthritis Rheum 2008;59 (5) 677- 68518438901Google Scholar 23. Klein RQBangert CACostner M et al. Comparison of the reliability and validity of outcome instruments for cutaneous dermatomyositis. Br J Dermatol 2008;159 (4) 887- 89418616782Google Scholar 24. Goreshi RChock MFoering K et al. Quality of life in dermatomyositis. J Am Acad Dermatol In pressGoogle Scholar http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Dermatology American Medical Association

Dermatomyositis Autoantibodies: Clinical Markers of Patients Past, Present, and Future

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American Medical Association
Copyright
Copyright © 2011 American Medical Association. All Rights Reserved.
ISSN
0003-987X
eISSN
1538-3652
DOI
10.1001/archdermatol.2011.41
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Abstract

It has been almost 50 years since autoantibodies (Abs) were identified in the blood of patients with myositis.1 Since then, the targets of several myositis-specific antibodies (MSAs) have been identified as ubiquitous proteins involved in critical cellular processes, such as protein translation, DNA repair, transcription, and viral recognition.2 Several pieces of evidence suggest that these Abs are not merely epiphenomena but are markers of an immune response that is central to disease propagation: the most compelling of these is the finding that patients typically have only 1 MSA type (eg, Mi-2 vs Jo-1), and those with a particular MSA often share similar clinical features regarding organ system involvement, prognosis, and response to therapy.3,4 The antigens are often preferentially overexpressed in diseased tissue; for example, Mi-2 and Jo-1 are overexpressed in the muscle tissue of patients with dermatomyositis (DM) compared with those with polymyositis (PM) or healthy muscle.5 Local environment is also critical; for example, many autoantigens, such as Ro-52 and melanoma differentiation–associated gene 5 (MDA-5), are induced by type I or II interferon, and activity of interferon is significantly increased in myositis tissues.6 In addition to expression level, many proteins are likely rendered immunogenic by processes, such as cleavage (which can occur in the context of granzyme B–mediated CD8+ killing), and posttranslational modification.7 Thus, the paradigm emerges that self-proteins are rendered antigenic in a tissue-specific manner that depends on the differentiation state or the microenvironment of the target cell. Thus, antigens have the potential to provide insight regarding the exact cell(s) that is undergoing attack and producing the disease we recognize clinically as DM. This paradigm explains why MSAs in DM are associated with patient prognosis and phenotype and are, thus, important tools for the physician caring for patients with DM. For example, it has long been known that patients with anti–tRNA synthetase antibodies tend to have a high risk of interstitial lung disease (ILD), arthritis, Raynaud phenomenon, and mechanic hands4; Mi-2 antibodies tend to be associated with low mortality, treatable disease, and classic cutaneous signs, such as the shawl sign and cuticular overgrowth.4 Until a few years ago, these 2 classes of Abs were the only MSAs in patients with DM, representing less than 20% of patients. Thus, the notion of a serologic test to diagnose DM with high sensitivity was still not realized. In the past several years, we have seen the discovery of several novel MSAs in DM,2 including antibodies to p155/140 and MDA-5 (CADM-140), whose frequency and associated phenotypes are further detailed by Hamaguchi et al8 in this issue of the Archives. This study is significant in that it is the largest study to date to compare the prevalence of and clinical characteristics associated with all the aforementioned MSAs in a large DM cohort. The antibodies to p155/140 and MDA-5 (CADM-140) were found in 18% of the patient cohort, meaning that more than 40% of their patients with DM were able to be characterized by a single dominant MSA. One caveat to this discovery is that the authors enriched their cohort with a separate group of 13 MSA-positive patients from another institution, which represents almost 10% of their MSA-positive cohort; thus, some of their prevalence data for MSAs is confounded by selection bias. In addition, this information may or may not be applicable to DM seen in other ethnic populations or geographic regions. For example, the frequency of Mi-2 Abs is known to be increased in areas of high UV exposure.9 In general, Hamaguchi et al8 confirm previous clinical data that are associated with Mi-2 and antisynthetase antibodies. The importance of the study lies in the further characterization of anti–155/140 and anti-MDA serotypes. The anti–155/140 Ab has previously been suggested to identify adult patients with DM at higher risk for cancer.10,11 The study by Hamaguchi et al8 confirms this, with 68% of patients with anti–155/140 Abs having an underlying malignancy and 41% of these patients dying of their malignancy. For the entire group of patients with DM, 10.4% had underlying malignancy. However, patients with the anti–155/140 Ab tended to have classical DM, which may suggest that those with clinically amyopathic DM (CADM) are less prone to underlying malignancy, a finding seen in several other cohorts.12,13 One population-based study14 in the United States of 29 patients did not find this difference in the rate of malignancy in DM relative to CADM, in which 30% of patients (6 of 20) with classical DM and 17% with CADM (1 of 6) had a malignancy. Larger studies are needed to confirm that there is a lower rate of malignancy in patients with CADM. Patients with MDA Abs have been described as typically having mild or absent muscle disease, which was confirmed in this study.15 This group has also been shown to have a high risk of ILD, sometimes rapidly progressive and fatal, which was seen in this cohort.15 Patients with the anti-MDA Ab have a 93% incidence of ILD (compared with an overall ILD incidence of 39.6%), which is frequently rapidly progressive. The anti-MDA was also associated with high serum KL-6 levels. This Ab was associated with increased CADM relative to classical DM, and 37% of patients died of ILD. Of interest, there were many more females in the anti-MDA Ab group relative to the other DM-specific Abs. Studies of patients with CADM in the United States have also suggested a female predominance.16 In addition, the investigators found that patients with anti-MDA also have a higher risk of cutaneous ulceration and arthritis, which is in agreement with data in US patients with DM.17 The correlation between Ab and the clinical findings gives the hope that many of these patients may be recognized by their clinical phenotype. In terms of prognosis, the study by Hamaguchi et al8 suggests that Japanese patients with CADM and ILD are less likely to develop malignancy. Despite this, survival of patients with either anti–155/140 or MDA Abs was quite low. It is stated that the frequency of ILD in patients with CADM in the United States is low, but 1 retrospective US study in which 78% of patients underwent pulmonary function tests found that the frequency of ILD in CADM and DM was comparable. Approximately 50% of the patients with both CADM and DM in this referral population had evidence of lung abnormalities, a number not so dissimilar to that in the Japanese group presented in this issue.13 Few other studies have systematically examined the incidence of lung disease in the United States in CADM or DM, and the percentage of rapidly progressive ILD (RP-ILD) is not known. The study by Hamaguchi et al8 and others18,19 suggest that there may be ethnic differences in the incidence of RP-ILD in the Asian population relative to the US population which would need to be confirmed with more systematic studies in the United States. It is apparent from the article by Hamaguchi et al8 that improving treatment of RP-ILD is an urgent issue for the Japanese (and likely other races). Several studies20,21 suggest that mycophenolate mofetil treatment can reverse ILD in patients with DM, but prospective studies are needed, and it is not clear that this approach would be effective in RP-ILD. One study22 concludes that ILD associated with DM, defined by criteria requiring the presence of myositis, is in most cases mild and chronic, and has a nonprogressive course during immunosuppressive treatment. Routine pulmonary function test screening of patients with CADM is needed; because these patients do not necessarily receive immunosuppressive agents for their muscle disease, studies to determine the natural history and role of interventions for subclinical lung disease are needed. A few commercial laboratories now perform testing on these and other novel MSAs for DM (eg, RDL Reference Laboratory [http://www.rdlinc.com/index.html]). Two other Ab targets, SAE1/2 and NXP-2, are also described as DM specific, but whose phenotype is not yet clearly defined in adult patients with DM.2 Even with testing, we are still left with approximately 50% to 60% of our patients with DM who cannot yet be assigned a known serologic specificity. We must continue to carefully phenotype patients so that the maximum amount of clinical information can be associated with these serologic profiles. Prognostic information and optimal treatment strategies may well depend on knowledge of the serologic status of the patient. The study by Hamaguchi et al8 also demonstrates the power in numbers and the need for multicenter collaborations to study a rare disease such as DM. Given the heterogeneity of DM, ideal studies would link experts in rheumatology, pulmonology, neurology, and dermatology because they see different subsets of the CADM and classic DM populations. For example, patients with CADM tend to be seen in dermatology clinics because of the predominance of skin symptoms.16 The North American Rheumatologic Dermatology Society (http://www.rheumaderm-society.org/) has collaborated on such cutaneous DM studies, providing an infrastructure that should be further developed to expand knowledge of DM subtypes (including CADM) in the United States. The North American Rheumatologic Dermatology Society has undertaken several studies specifically related to the dermatologic aspects of DM, and funding to support prospective studies would advance knowledge of how to evaluate and treat such patients.23,24 Correspondence: Dr Werth, Department of Dermatology, Perelman Center for Advanced Medicine, 3400 Civic Center Blvd, Ste 1-330A, Philadelphia, PA 19104 (werth@mail.med.upenn.edu). Financial Disclosure: None reported. Funding/Support: This study was supported in part by grant K24-AR 02207 from the National Institutes of Health (Dr Werth). Role of the Sponsor: The National Institutes of Health had no role in the design and conduct of the study; in the collection, analysis, and interpretation of data; or in the preparation, review, or approval of the manuscript. References 1. Caspary EAGubbay SSStern GM Circulating antibodies in polymyositis and other muscle-wasting disorders. Lancet 1964;2 (7366) 94114203937Google Scholar 2. Gunawardena HBetteridge ZE McHugh NJ Myositis-specific autoantibodies: their clinical and pathogenic significance in disease expression. Rheumatology (Oxford) 2009;48 (6) 607- 61219439503Google Scholar 3. Joffe MMLove LALeff RL et al. Drug therapy of the idiopathic inflammatory myopathies: predictors of response to prednisone, azathioprine, and methotrexate and a comparison of their efficacy. Am J Med 1993;94 (4) 379- 3878386437Google Scholar 4. Love LALeff RLFraser DD et al. A new approach to the classification of idiopathic inflammatory myopathy: myositis-specific autoantibodies define useful homogeneous patient groups. Medicine (Baltimore) 1991;70 (6) 360- 3741659647Google Scholar 5. Casciola-Rosen LNagaraju KPlotz P et al. Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy. J Exp Med 2005;201 (4) 591- 60115728237Google Scholar 6. Greenberg SA Dermatomyositis and type 1 interferons. Curr Rheumatol Rep 2010;12 (3) 198- 20320425524Google Scholar 7. Rosen ACasciola-Rosen L Autoantigens in systemic autoimmunity: critical partner in pathogenesis. J Intern Med 2009;265 (6) 625- 63119493056Google Scholar 8. Hamaguchi YKuwana MHoshino K et al. Clinical correlations with dermatomyositis-specific autoantibodies in adult Japanese patients with dermatomyositis: a multicenter, cross-sectional study. Arch Dermatol 2011;147 (4) 391- 398Google Scholar 9. Love LAWeinberg CR McConnaughey DR et al. Ultraviolet radiation intensity predicts the relative distribution of dermatomyositis and anti-Mi-2 autoantibodies in women. Arthritis Rheum 2009;60 (8) 2499- 250419644877Google Scholar 10. Targoff INMamyrova GTrieu EP et al. Childhood Myositis Heterogeneity Study Group; International Myositis Collaborative Study Group, A novel autoantibody to a 155-kd protein is associated with dermatomyositis. Arthritis Rheum 2006;54 (11) 3682- 368917075819Google Scholar 11. Kaji KFujimoto MHasegawa M et al. Identification of a novel autoantibody reactive with 155 and 140 kDa nuclear proteins in patients with dermatomyositis: an association with malignancy. Rheumatology (Oxford) 2007;46 (1) 25- 2816728436Google Scholar 12. Azuma KYamada HOhkubo M et al. Incidence and predictive factors for malignancies in 136 Japanese patients with dermatomyositis, polymyositis and clinically amyopathic dermatomyositis [published online ahead of print October 5, 2010]. Mod Rheumatol 2010;2092245310.1007/s10165-010-0362-yGoogle Scholar 13. Morganroth PAKreider MEOkawa JTaylor LWerth VP Interstitial lung disease in classic and skin-predominant dermatomyositis: a retrospective study with screening recommendations. Arch Dermatol 2010;146 (7) 729- 73820644033Google Scholar 14. Bendewald MJWetter DALi XDavis MD Incidence of dermatomyositis and clinically amyopathic dermatomyositis: a population-based study in Olmsted County, Minnesota. Arch Dermatol 2010;146 (1) 26- 3020083689Google Scholar 15. Sato SHirakata MKuwana M et al. Autoantibodies to a 140-kd polypeptide, CADM-140, in Japanese patients with clinically amyopathic dermatomyositis. Arthritis Rheum 2005;52 (5) 1571- 157615880816Google Scholar 16. Klein RQTeal VTaylor LTroxel ABWerth VP Number, characteristics, and classification of patients with dermatomyositis seen by dermatology and rheumatology departments at a large tertiary medical center. J Am Acad Dermatol 2007;57 (6) 937- 94317923170Google Scholar 17. Fiorentino DChung LZwerner JRoen ACasciola-Rosen L The mucocutaneous and systemic phenotype in dermatomyositis patients with antibodies to MDA5 (CADM-140): a retrospective study. J Am Acad Dermatol In pressGoogle Scholar 18. Ye SChen XXLu XY et al. Adult clinically amyopathic dermatomyositis with rapid progressive interstitial lung disease: a retrospective cohort study. Clin Rheumatol 2007;26 (10) 1647- 165417308858Google Scholar 19. Mukae HIshimoto HSakamoto N et al. Clinical differences between interstitial lung disease associated with clinically amyopathic dermatomyositis and classic dermatomyositis. Chest 2009;136 (5) 1341- 134719581351Google Scholar 20. Morganroth PAKreider MEWerth VP Mycophenolate mofetil for interstitial lung disease in dermatomyositis. Arthritis Care Res (Hoboken) 2010;62 (10) 1496- 150120506189Google Scholar 21. Saketkoo LAEspinoza LR Experience of mycophenolate mofetil in 10 patients with autoimmune-related interstitial lung disease demonstrates promising effects. Am J Med Sci 2009;337 (5) 329- 33519295413Google Scholar 22. Fathi MVikgren JBoijsen M et al. Interstitial lung disease in polymyositis and dermatomyositis: longitudinal evaluation by pulmonary function and radiology. Arthritis Rheum 2008;59 (5) 677- 68518438901Google Scholar 23. Klein RQBangert CACostner M et al. Comparison of the reliability and validity of outcome instruments for cutaneous dermatomyositis. Br J Dermatol 2008;159 (4) 887- 89418616782Google Scholar 24. Goreshi RChock MFoering K et al. Quality of life in dermatomyositis. J Am Acad Dermatol In pressGoogle Scholar

Journal

Archives of DermatologyAmerican Medical Association

Published: Apr 1, 2011

Keywords: dermatomyositis,autoantibodies

References