Medicine:Dermatomyositis

From HandWiki

Dermatomyositis (DM) is a group of sytemic autoimmune inflammatory diseases primarily affecting the skin and skeletal muscles.[1][2] Its symptoms are generally a skin rash and worsening muscle weakness over time. These may occur suddenly or develop over months. Other symptoms may include weight loss, fever, lung inflammation, or light sensitivity. Complications may include calcium deposits in muscles or skin. Distinct myositis-specific autoantibodies (MSA) define clinically and pathologically distinct DM subtypes, each associated with characteristic disease manifestations, prognosis, and treatment response.[1][3]

Eighty percent of adults[4] and sixty percent of children with juvenile dermatomyositis have a MSA.[5] These autoantibodies, produced by locally infiltrating plasma cells, can enter various cell types and disrupt the function of their target autoantigens, inducing cellular damage and inflammation that directly drive disease pathogenesis.[6][7][8][9] Dermatomyositis may develop as a paraneoplastic syndrome associated with several malignancies, in which tumors harbor genetic alterations, including somatic mutations, in genes encoding the specific autoantigens targeted by the patient's corresponding autoantibodies.[10][11][12][13] It is known to be associated with several viruses, especially coxsackievirus, but no definitive causal link has been found.[14] Diagnosis is typically based on some combination of symptoms, blood tests, electromyography, and muscle biopsies.[1]

Current treatment of dermatomyositis relies on immunosuppressive agents such as corticosteroids, methotrexate, mycophenolate mofetil, azathioprine, tacrolimus, and cyclosporine, with intravenous immunoglobulin (IVIG) widely used for refractory or severe disease.[15][16] Rituximab remains an important therapeutic option despite mixed clinical trial results.[17] Emerging targeted therapies, including Janus kinase (JAK) inhibitors[18][19][20][21][22] and agents targeting the type I interferon pathway, such as dazukibart,[23] have demonstrated promising efficacy. Novel approaches such as CD19 chimeric antigen receptor (CAR) T-cell therapy,[24] plasma cell–directed therapies,[25][26] and neonatal Fc receptor (FcRn) inhibitors, such as efgartigimod, are also showing encouraging results,[27] offering the potential for sustained treatment-free disease control in the case of CD19 CAR-T cell therapy. Overall, with timely diagnosis and appropriate treatment, the prognosis of DM is generally favorable.

About one in 100,000 people receive a new diagnosis of dermatomyositis each year.[28] The condition usually occurs in those in their 40s and 50s with women being affected more often than men.[28] People of any age, however, may be affected.[28] The condition was first described in the 1800s.[29]

Signs and symptoms

The main symptoms include several kinds of skin rash along with muscle weakness in both upper arms or thighs.[1]

Skin

One form the rashes take is called "heliotrope" (a purplish color) or lilac, but may also be red. It can occur around the eyes along with swelling, but also occurs on the upper chest or back what is called the "shawl" (around the neck) or "V-sign" above the breasts and may also occur on the face, upper arms, thighs, or hands.[30] Another form the rash takes is called Gottron's sign, which is red or violet, sometimes scaly, slightly raised papules that erupt on any of the finger joints (the metacarpophalangeal joints or the interphalangeal joints).[30][31] Gottron's papules may also be found over other bony prominences including the elbows, knees, or feet. All these rashes are made worse by exposure to sunlight, and are often very itchy, painful, and may bleed.[31]

If a person exhibits only skin findings characteristic of DM, without weakness or abnormal muscle enzymes, may be classified as having amyopathic or clinically amyopathic dermatomyositis (ADM), formerly known as "dermatomyositis sine myositis".[32]

Muscles

People with DM experience progressively worsening muscle weakness in the proximal muscles (for example, the shoulders and thighs).[33] Tasks that use these muscles: standing from sitting, lifting, and climbing stairs, can become increasingly difficult for people with dermatomyositis.[33]

Respiratory

The primary cause of respiratory failure in dermatomyositis is interstitial lung disease, resulting from damage to the lung interstitium.[1] This is particularly prominent in patients with anti–MDA5 autoantibodies, who are at high risk of developing rapidly progressive interstitial lung disease.[14] In some people, the condition affects the diaphragm muscle, the lungs directly (through inflammation), or both. This causes difficulty breathing, and dermatomyositis is considered to be a restrictive lung disease in patients with these symptoms. Respiratory symptoms occur in about 40% of people with dermatomyositis, and in these people, the symptoms may slowly progress, contributing to increased morbidity and mortality.

Cardiac

In dermatomyositis, patients can develop myocarditis and cardiac conduction system abnormalities which may be detected if the patient undergoes special testing. However, these abnormalities typically have no symptoms or clinical consequences.[14]

More rarely, these abnormalities can cause greater issues and lead to arrhythmias, heart failure, or damage to heart valves.[14] For those dermatomyositis patients who do have cardiac symptoms caused by the disease, their clinical course may be much worse than usual.[34]

Other

Around 30% of people have swollen, painful joints, but this is generally mild.[35]

Later in the course of the disease, patients often experience difficulty swallowing, called dysphagia, which makes it hard to move food from the mouth to the stomach. The muscles of the esophagus may become weak, leading to reduced or irregular movements that prevent proper swallowing. Additionally, individuals might suffer from gastroesophageal reflux disease (GERD), where stomach acid flows back into the esophagus, causing heartburn and irritation.[14]

  • Examples of dermatomyositis
  • Gottron's papules on finger joints
    Gottron's papules on finger joints
  • Gottron's papules on the elbows of a person with juvenile DM
    Gottron's papules on the elbows of a person with juvenile DM
  • Gottron's papules
    Gottron's papules
  • Gottron's bumps on a person with juvenile DM
    Gottron's bumps on a person with juvenile DM
  • Gottron's papules in a severe case of juvenile dermatomyositis
    Gottron's papules in a severe case of juvenile dermatomyositis
  • Heliotrope with swelling around the eyes
    Heliotrope with swelling around the eyes
  • Heliotrope
    Heliotrope
  • Facial rash
    Facial rash
  • Severe rash on the hands, extending up the forearm
    Severe rash on the hands, extending up the forearm
  • Forearm rash
    Forearm rash

Etiopathogenesis

See also: List of human leukocyte antigen alleles associated with cutaneous conditions

Recent studies suggest that the pathogenesis of DM is driven by the pathogenic internalization of autoantibodies.[7][6][8] Although these antibodies target intracellular proteins, evidence indicates that they can enter different cell types and disrupt the function of their target autoantigens causing inflammation and damage.[6][8] For example, anti-Mi-2 autoantibodies bind PHD-containing proteins,[36][37] including component of the NuRD complex, inducing derepression of multiple genes,[6] and in anti-MDA5 dermatomyositis, autoantibodies activate MDA5 directly inducing the activation of type I interferon pathways.[6]

The type I interferon pathway is especially prominent in DM and has become a major therapeutic target.[38][39] Clinical responses to JAK inhibitors,[40][41][42][43][44] anti-IFNβ therapy,[45] and agents targeting the interferon receptor support the importance of this pathway in disease activity. Conversely, a negative trial of complement inhibition in immune-mediated necrotizing myopathy[46] has challenged earlier models in which complement-mediated muscle injury was considered central to that subtype.[47][48][49]

The characteristic pathological feature is perifascicular muscle involvement, often accompanied by vasculopathy. Plasma cells are found in close proximity to affected areas with high type I interferon expression and have been observed to externalize immunoglobulin heavy- and light-chain RNA into surrounding muscle cells, suggesting that this may be a potential mechanism for immunoglobulin entry into affected cell types shared across different forms of DM.[8]

DM is paraneoplastic in up to 40% of cases, most commonly in association with underlying malignancy in patients with anti–TIF1γ autoantibodies.[14] A majority of patients with paraneoplastic dermatomyositis harbor somatic mutations or other genetic alterations in tumor genes encoding the target autoantigens of their corresponding autoantibodies, suggesting that, in this context, autoantibody production arises secondary to an anti-tumor immune response that fails to achieve effective tumor control.[10][11][12][13]The most commonly associated cancers are ovarian cancer, breast cancer, and lung cancer overall,[50] but the most frequent associations can vary depending on patient race or ethnicity.[14]

Inherited genetic factors confer a predisposition to developing these diseases, and HLA subtypes HLA-DR3, HLA-DR52, and HLA-DR6 seem to create a disposition to DM.[35]

Diagnosis and classification

Calcinosis from dermatomyositis
X-Ray of the knee in a person with dermatomyositis with calcinosis.
Micrograph of dermatomyositis, muscle biopsy, H&E stain

There are several diagnostic and classification criteria have been proposed for dermatomyositis.[51][52][53][54] Contemporary approaches generally combine clinical features with myositis-specific and myositis-associated autoantibody testing, supported by complementary laboratory, imaging, histopathologic, and electrophysiologic investigations. Some criteria are designed to establish a broad syndromic diagnosis of DM, whereas others provide greater granularity by identifying distinct autoantibody-defined clinical subsets. Despite these differences, the principal diagnostic features include:

  1. Detection of myositis-specific autoantibodies (MSAs), including anti-Mi-2, anti-NXP2, anti-TIF1-γ, anti-MDA5, and anti-SAE. These autoantibodies are considered pathogenic[6][8][7] and are typically mutually exclusive, with most patients harboring only a single MSA.
  2. Muscle weakness in both thighs or both upper arms.
  3. Using a blood test, finding higher levels of enzymes found in skeletal muscle, including creatine kinase, aldolase, and glutamate oxaloacetate, pyruvate transaminases or lactate dehydrogenase.
  4. Using electromyography (testing of electric signalling in muscles), finding all three of: erratic, repetitive, high-frequency signals; short, low-energy signals between skeletal muscles and motor neurons that have multiple phases; and sharp activity when a needle is inserted into the muscle.
  5. Examining a muscle biopsy under a microscope demonstrating perifascicular atrophy, increased expression of type I interferon–inducible markers (predominantly in the perifascicular regions), mononuclear white blood cells between the muscle cells, and finding abnormal muscle cell degeneration and regeneration, dying muscle cells, and muscle cells being consumed by other cells (phagocytosis).[38][55]
  6. Rashes typical of dermatomyositis, which include heliotrope rash, Gottron's sign, and Gottron's papules.

The fifth criterion is what differentiates dermatomyositis from other forms of inflammatory myopathy. Patients with antisynthetase autoantibodies, such as anti-Jo-1, may also present with dermatomyositis-like skin manifestations. Although these patients were historically classified as having DM, they are now generally considered to have the distinct clinical entity antisynthetase syndrome, even in the presence of characteristic cutaneous features.[1]

Magnetic resonance imaging may be useful for guiding muscle biopsy and for distinguishing active inflammation from irreversible muscle damage as contributors to muscle weakness. In addition to muscle inflammation, MRI frequently demonstrates fascial inflammation (fasciitis) in patients with DM.[56][57] X-ray may be used to investigate joint involvement and calcifications.[58]

A case of DM may be classified as clinically amyopathic dermatomyositis (CADM) when cutaneous manifestations predominate and there is little or no clinical evidence of muscle involvement.[59] Anti-MDA5 autoantibodies are strongly associated with CADM and are frequently accompanied by rapidly progressive interstitial lung disease.[60] Patients with anti-TIF1-γ autoantibodies also commonly present with clinically amyopathic disease, although less frequently than those with anti-MDA5 autoantibodies.

Juvenile dermatomyositis (JDM) has traditionally been regarded as a distinct entity from adult-onset DM. However, there is no convincing evidence that the two differ fundamentally in their pathophysiology, and they are now generally considered age-specific presentations of the same group of conditions.

Treatment

Multiple effective therapies are available for the treatment of DM.[1] Standard treatment typically consists of a combination of glucocorticoids and steroid-sparing immunosuppressive agents, including methotrexate, mycophenolate mofetil, azathioprine, tacrolimus, and cyclosporine. Intravenous immunoglobulin (IVIG) has demonstrated efficacy in DM.[61][62] Although rituximab did not meet its primary endpoint in randomized clinical trials, it remains an important treatment option in clinical practice, particularly for refractory disease, often in combination with IVIG.[63]

More recently, Janus kinase (JAK) inhibitors, including tofacitinib,[64] ruxolitinib,[65][66] baricitinib,[67] and brepocitinib,[68] have shown efficacy in dermatomyositis. Additional strategies targeting the type I interferon pathway have also demonstrated benefit, including blockade of interferon-β with dazukibart.[69]

Deep B-cell depletion with CD19 chimeric antigen receptor (CAR) T-cell therapy has shown preliminary evidence of inducing sustained, and potentially treatment-free, remission in DM.[70][71][72] Similarly, plasma cell–targeted therapies, including CAR T-cell approaches and monoclonal antibodies,[73] as well as inhibitors of the neonatal Fc receptor (FcRn), such as efgartigimod,[74] have emerged as promising therapeutic strategies for DM.

Antimalarial medications, such as hydroxychloroquine,[75] have historically been used to manage the cutaneous manifestations of DM. However, given the potential for hypersensitivity reactions in DM,[76] their use is generally limited to patients who have previously responded well and tolerated these therapies, rather than being routinely employed in DM.

Overall, with timely diagnosis and appropriate treatment, the prognosis of DM is generally favorable.

Prognosis

The cutaneous manifestations of dermatomyositis may or may not improve with therapy in parallel with the improvement of the myositis. In some people, the weakness and rash resolve together. In others, the two are not linked, with one or the other being more challenging to control. Often, cutaneous disease persists after adequate control of the muscle disease.[77][78]

The risk of death from the condition is much higher if the heart or lungs are affected.[79][80]

Before the advent of modern therapies, the prognosis was poor. However, with timely diagnosis and appropriate management, the prognosis has improved substantially, and outcomes are now generally favorable.[81]

Epidemiology

Incidence of DM peaks at ages 40–50, but the disease can affect people of all ages.[82][28] It tends to affect more women than men.[28] The prevalence of DM ranges from one to 22 per 100,000 people.[83][84][85]

People who were affected with dermatomyositis

  • Opera singer Maria Callas (1923–1977) allegedly had dermatomyositis from 1975 until her death.[86]
  • Actor Laurence Olivier (1907–1989) had dermatomyositis from 1974 until his death.[87]
  • American football running back Ricky Bell (1955–1984), the runner-up for the Heisman Trophy in 1976, and the number-one pick in the NFL draft in 1977, died at the age of 29 from heart failure caused by this disease.[88]
  • Rob Buckman (1948–2011) a doctor, comedian, and author, and the president of the Humanist Association of Canada.[89]
  • Samantha, Indian actress diagnosed in 2022.
  • Suhani Bhatnagar (2005–2024), Indian actress.[90]
  • Tim Rooney (1947–2006), American actor and son of Mickey Rooney.[91]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Selva-O'Callaghan, Albert; Pinal-Fernandez, Iago; Trallero-Araguás, Ernesto; Milisenda, José César; Grau-Junyent, Josep Maria; Mammen, Andrew L. (September 2018). "Classification and management of adult inflammatory myopathies". The Lancet. Neurology 17 (9): 816–828. doi:10.1016/S1474-4422(18)30254-0. ISSN 1474-4465. PMID 30129477. 
  2. ↑ Allenbach, Yves; Benveniste, Olivier (2026-05-14). "Inflammatory Myopathies" (in en). New England Journal of Medicine 394 (19): 1925–1938. doi:10.1056/NEJMra2415426. ISSN 0028-4793. PMID 42127392. http://www.nejm.org/doi/10.1056/NEJMra2415426. 
  3. ↑ Casal-Dominguez, Maria; Pinal-Fernandez, Iago; Pak, Katherine; Huang, Wilson; Selva-O'Callaghan, Albert; Albayda, Jemima; Casciola-Rosen, Livia; Paik, Julie J. et al. (March 2022). "Performance of the 2017 European Alliance of Associations for Rheumatology/American College of Rheumatology Classification Criteria for Idiopathic Inflammatory Myopathies in Patients With Myositis-Specific Autoantibodies". Arthritis & Rheumatology 74 (3): 508–517. doi:10.1002/art.41964. ISSN 2326-5205. PMID 34480833. 
  4. ↑ "Adult and juvenile dermatomyositis: are the distinct clinical features explained by our current understanding of serological subgroups and pathogenic mechanisms?". Arthritis Research & Therapy 15 (2): 211. April 2013. doi:10.1186/ar4198. PMID 23566358. "Myositis-specific autoantibodies (MSAs) can now be identified in 80% of adults.". 
  5. ↑ "Juvenile idiopathic inflammatory myositis: an update on pathophysiology and clinical care". Nature Reviews. Rheumatology 19 (6): 343–362. June 2023. doi:10.1038/s41584-023-00967-9. PMID 37188756. "Approximately 60% of patients with JDM are positive for a myositis-specific antibody (MSA).". 
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 Pinal-Fernandez, Iago; Muñoz-Braceras, Sandra; Casal-Dominguez, Maria; Pak, Katherine; Torres-Ruiz, Jiram; Musai, Jon; Dell'Orso, Stefania; Naz, Faiza et al. (2024-10-21). "Pathological autoantibody internalisation in myositis". Annals of the Rheumatic Diseases 83 (11): 1549–1560. doi:10.1136/ard-2024-225773. ISSN 1468-2060. PMID 38902010. 
  7. ↑ 7.0 7.1 7.2 Pinal-Fernandez, Iago; Milisenda, Jose Cesar; Pak, Katherine; Muñoz-Braceras, Sandra; Casal-Dominguez, Maria; Torres-Ruiz, Jiram; Dell'Orso, Stefania; Naz, Faiza et al. (August 2023). "Transcriptional derepression of CHD4/NuRD-regulated genes in the muscle of patients with dermatomyositis and anti-Mi2 autoantibodies". Annals of the Rheumatic Diseases 82 (8): 1091–1097. doi:10.1136/ard-2023-223873. ISSN 1468-2060. PMID 37130727. 
  8. ↑ 8.0 8.1 8.2 8.3 8.4 Pinal-Fernandez, Iago; Pak, Katherine; Casal-Dominguez, Maria; Muñoz-Braceras, Sandra; Wigerblad, Gustaf; Dell'Orso, Stefania; Naz, Faiza; Islam, Shamima et al. (July 2026). "Spatial transcriptomics reveals mechanism of autoimmunity driven by internalised autoantibodies". Annals of the Rheumatic Diseases. doi:10.1016/j.ard.2026.06.028. ISSN 0003-4967. PMID 42493309. https://linkinghub.elsevier.com/retrieve/pii/S0003496726004139. 
  9. ↑ Giannini, Margherita; Quiring, Giulia; Oulad-Abdelghani, Mustapha; Lannes, Béatrice; Allenbach, Yves; Benveniste, Olivier; Boyer, Olivier; Pakleza, Aleksandra Nadaj et al. (October 2025). "In immune-mediated necrotising myopathy, anti-HMGCR antibodies inhibit HMGCR activity, leading to the sarcoplasmic accumulation of lipid droplets and myofibres necrosis". Annals of the Rheumatic Diseases 84 (10): 1752–1755. doi:10.1016/j.ard.2025.04.027. ISSN 1468-2060. PMID 40410054. 
  10. ↑ 10.0 10.1 "A Study on Dermatomyositis and the Relation to Malignancy". Current Health Sciences Journal 47 (3): 377–382. July 2021. doi:10.12865/CHSJ.47.03.07. PMID 35003769. 
  11. ↑ 11.0 11.1 Pinal-Fernandez, Iago; Ferrer-Fabregas, Berta; Trallero-Araguas, Ernesto; Balada, Eva; Martínez, Maria Angeles; Milisenda, Jose César; Aparicio-Español, Gloria; Labrador-Horrillo, Moises et al. (2018-02-01). "Tumour TIF1 mutations and loss of heterozygosity related to cancer-associated myositis". Rheumatology 57 (2): 388–396. doi:10.1093/rheumatology/kex413. ISSN 1462-0332. PMID 29149307. 
  12. ↑ 12.0 12.1 Cordel, Nadège; Derambure, Céline; Coutant, Sophie; Mariette, Xavier; Jullien, Denis; Debarbieux, Sébastien; Chosidow, Olivier; Meyer, Alain et al. (2021-12-01). "TRIM33 gene somatic mutations identified by next generation sequencing in neoplasms of patients with anti-TIF1γ positive cancer-associated dermatomyositis". Rheumatology 60 (12): 5863–5867. doi:10.1093/rheumatology/keab260. ISSN 1462-0332. PMID 33764396. 
  13. ↑ 13.0 13.1 Moreno-Cárdenas, Ana Belén; Ros, Javier; Gil-Vila, Albert; Datta, Debayan; Fasani, Roberta; Serna, Garazi; Jimenez, Jose; Trallero-Araguás, Ernesto et al. (March 2026). "Frequent genetic alterations in myositis autoantigen genes in cancer-associated dermatomyositis" (in en). Annals of the Rheumatic Diseases 85 (3): 519–533. doi:10.1016/j.ard.2025.10.018. PMID 41290487. 
  14. ↑ 14.0 14.1 14.2 14.3 14.4 14.5 14.6 "Dermatomyositis: a comprehensive review of clinical manifestations, serological features, and therapeutic approaches". Italian Journal of Dermatology and Venereology 158 (2): 84–98. April 2023. doi:10.23736/S2784-8671.23.07458-3. PMID 37153943. 
  15. ↑ Dalakas, Marinos C.; Illa, Isabel; Dambrosia, James M.; Soueidan, Shawke A.; Stein, Daniel P.; Otero, Carlos; Dinsmore, Steven T.; McCrosky, Susan (1993-12-30). "A Controlled Trial of High-Dose Intravenous Immune Globulin Infusions as Treatment for Dermatomyositis" (in en). New England Journal of Medicine 329 (27): 1993–2000. doi:10.1056/NEJM199312303292704. ISSN 0028-4793. PMID 8247075. http://www.nejm.org/doi/abs/10.1056/NEJM199312303292704. 
  16. ↑ Aggarwal, Rohit; Charles-Schoeman, Christina; Schessl, Joachim; Bata-Csörgő, Zsuzsanna; Dimachkie, Mazen M.; Griger, Zoltan; Moiseev, Sergey; Oddis, Chester et al. (2022-10-06). "Trial of Intravenous Immune Globulin in Dermatomyositis" (in en). New England Journal of Medicine 387 (14): 1264–1278. doi:10.1056/NEJMoa2117912. ISSN 0028-4793. PMID 36198179. http://www.nejm.org/doi/10.1056/NEJMoa2117912. 
  17. ↑ Oddis, Chester V.; Reed, Ann M.; Aggarwal, Rohit; Rider, Lisa G.; Ascherman, Dana P.; Levesque, Marc C.; Barohn, Richard J.; Feldman, Brian M. et al. (February 2013). "Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: A randomized, placebo-phase trial" (in en). Arthritis & Rheumatism 65 (2): 314–324. doi:10.1002/art.37754. ISSN 0004-3591. PMID 23124935. 
  18. ↑ Paik, Julie J.; Casciola-Rosen, Livia; Shin, Joseph Yusup; Albayda, Jemima; Tiniakou, Eleni; Leung, Doris G; Gutierrez-Alamillo, Laura; Perin, Jamie et al. (May 2021). "Study of Tofacitinib in Refractory Dermatomyositis: An Open-Label Pilot Study of Ten Patients" (in en). Arthritis & Rheumatology 73 (5): 858–865. doi:10.1002/art.41602. ISSN 2326-5191. PMID 33258553. 
  19. ↑ Ladislau, Leandro; Suárez-Calvet, Xavier; Toquet, Ségolène; Landon-Cardinal, Océane; Amelin, Damien; Depp, Marine; Rodero, Mathieu P; Hathazi, Denisa et al. (2018-06-01). "JAK inhibitor improves type I interferon induced damage: proof of concept in dermatomyositis" (in en). Brain 141 (6): 1609–1621. doi:10.1093/brain/awy105. ISSN 0006-8950. PMID 29741608. https://academic.oup.com/brain/article/141/6/1609/4993951. 
  20. ↑ Hornung, Thorsten; Janzen, Viktor; Heidgen, Franz-Josef; Wolf, Dominik; Bieber, Thomas; Wenzel, Joerg (2014-12-25). "Remission of Recalcitrant Dermatomyositis Treated with Ruxolitinib" (in en). New England Journal of Medicine 371 (26): 2537–2538. doi:10.1056/NEJMc1412997. ISSN 0028-4793. PMID 25539124. http://www.nejm.org/doi/10.1056/NEJMc1412997. 
  21. ↑ Kim, Hanna; Dill, Samantha; O'Brien, Michelle; Vian, Laura; Li, Xiaobai; Manukyan, Manuk; Jain, Minal; Adeojo, Lilian W et al. (March 2021). "Janus kinase (JAK) inhibition with baricitinib in refractory juvenile dermatomyositis" (in en). Annals of the Rheumatic Diseases 80 (3): 406–408. doi:10.1136/annrheumdis-2020-218690. PMID 32843325. 
  22. ↑ Vleugels, Ruth Ann; Paik, Julie J.; Bauer Ventura, Iazsmin; Mangold, Aaron R.; Gandiga, Prateek C.; Haemel, Anna; Chinoy, Hector; Hussain, Yessar M. et al. (2026-05-14). "A Phase 3 Trial of Brepocitinib in Dermatomyositis" (in en). New England Journal of Medicine 394 (19): 1883–1893. doi:10.1056/NEJMoa2503531. ISSN 0028-4793. PMID 41910335. http://www.nejm.org/doi/10.1056/NEJMoa2503531. 
  23. ↑ Fiorentino, David; Mangold, Aaron R; Werth, Victoria P; Christopher-Stine, Lisa; Femia, Alisa; Chu, Myron; Musiek, Amy C M; Sluzevich, Jason C et al. (January 2025). "Efficacy, safety, and target engagement of dazukibart, an IFNβ specific monoclonal antibody, in adults with dermatomyositis: a multicentre, double-blind, randomised, placebo-controlled, phase 2 trial" (in en). The Lancet 405 (10473): 137–146. doi:10.1016/S0140-6736(24)02071-3. PMID 39798982. https://linkinghub.elsevier.com/retrieve/pii/S0140673624020713. 
  24. ↑ Müller, Fabian; Taubmann, Jule; Bucci, Laura; Wilhelm, Artur; Bergmann, Christina; Völkl, Simon; Aigner, Michael; Rothe, Tobias et al. (2024-02-22). "CD19 CAR T-Cell Therapy in Autoimmune Disease — A Case Series with Follow-up" (in en). New England Journal of Medicine 390 (8): 687–700. doi:10.1056/NEJMoa2308917. ISSN 0028-4793. PMID 38381673. http://www.nejm.org/doi/10.1056/NEJMoa2308917. 
  25. ↑ Müller, Fabian; Wirsching, Andreas; Hagen, Melanie; Völkl, Simon; Tur, Carlo; Raimondo, Maria Gabriella; Taubmann, Jule; Bucci, Laura et al. (June 2025). "BCMA CAR T cells in a patient with relapsing idiopathic inflammatory myositis after initial and repeat therapy with CD19 CAR T cells" (in en). Nature Medicine 31 (6): 1793–1797. doi:10.1038/s41591-025-03718-3. ISSN 1078-8956. PMID 40245922. 
  26. ↑ Hagen, Melanie; Bucci, Laura; Böltz, Sebastian; Nöthling, Danae-Mona; Rothe, Tobias; Anoshkin, Kirill; Raimondo, Maria G.; Tur, Carlo et al. (2024-09-05). "BCMA-Targeted T-Cell–Engager Therapy for Autoimmune Disease" (in en). New England Journal of Medicine 391 (9): 867–869. doi:10.1056/NEJMc2408786. ISSN 0028-4793. PMID 39231353. http://www.nejm.org/doi/10.1056/NEJMc2408786. 
  27. ↑ Chinoy, H.; Rodriguez-Garcia, S.; Neto, A.; Papadopoulou, D.; Van Baelen, B.; Duncombe, P.; De Ceuninck, L.; van der Woning, B. et al. (June 2025). "Op0002 Efficacy and Safety of Efgartigimod Ph20 Sc in Adult Participants with Active Idiopathic Inflammatory Myopathy: Phase 2 Results from the Alkivia Study" (in en). Annals of the Rheumatic Diseases 84: 2–3. doi:10.1016/j.ard.2025.05.025. 
  28. ↑ 28.0 28.1 28.2 28.3 28.4 "Dermatomyositis". 2015. https://rarediseases.org/rare-diseases/dermatomyositis/. 
  29. ↑ "History of Dermatomyositis". Dermatomyositis. 2009. pp. 5–8. doi:10.1007/978-3-540-79313-7_2. ISBN 978-3-540-79312-0. 
  30. ↑ 30.0 30.1 "Cutaneous manifestations of dermatomyositis and their management". Current Rheumatology Reports 12 (3): 192–197. June 2010. doi:10.1007/s11926-010-0100-7. PMID 20425525. 
  31. ↑ 31.0 31.1 "The skin in autoimmune diseases-Unmet needs". Autoimmunity Reviews 15 (10): 948–954. October 2016. doi:10.1016/j.autrev.2016.07.013. PMID 27481041. 
  32. ↑ "Treatment of clinically amyopathic dermatomyositis in adults: a systematic review". The British Journal of Dermatology 179 (6): 1248–1255. December 2018. doi:10.1111/bjd.14726. PMID 27167896. 
  33. ↑ 33.0 33.1 "Inflammatory muscle diseases". The New England Journal of Medicine 372 (18): 1734–1747. April 2015. doi:10.1056/NEJMra1402225. PMID 25923553. 
  34. ↑ "Cardiac involvement in polymyositis and dermatomyositis: diagnostic approaches". Reumatologia 61 (3): 202–212. 2023-07-02. doi:10.5114/reum/168362. PMID 37522146. 
  35. ↑ 35.0 35.1 "Polymyositis and Dermatomyositis – Musculoskeletal and Connective Tissue Disorders". Merck Manuals Professional Edition. June 2013. http://www.merckmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/autoimmune-rheumatic-disorders/polymyositis-and-dermatomyositis. 
  36. ↑ Musai, Jon; Jayaraman, Sahana; Pak, Katherine; Pinal-Fernandez, Iago; Muñoz-Braceras, Sandra; Casal-Dominguez, Maria; Cho, Eric; Fitisemanu, Fa'alataitaua M. et al. (2026-02-01). "Myositis-specific autoantibodies recognising Mi2 also target the AIRE protein at a shared PHD zinc finger". Annals of the Rheumatic Diseases 85 (2): 351–359. doi:10.1016/j.ard.2025.08.023. ISSN 1468-2060. PMID 40957771. 
  37. ↑ Pinal-Fernandez, Iago; Musai, Jon; Casal-Dominguez, Maria; Pak, Katherine; Kaplan, Mariana; Warner, Blake M.; Rider, Lisa G.; Aggarwal, Rohit et al. (2025-12-01). "Anti-Mi2 autoantibodies target PHD fingers of SP140L and TIF1γ, while anti-TIF1γ autoantibodies primarily bind TIF1γ outside the PHD region". Rheumatology (Oxford, England) 64 (12): 6371–6377. doi:10.1093/rheumatology/keaf426. ISSN 1462-0332. PMID 40795062. 
  38. ↑ 38.0 38.1 Greenberg, Steven A.; Pinkus, Jack L.; Pinkus, Geraldine S.; Burleson, Travis; Sanoudou, Despina; Tawil, Rabi; Barohn, Richard J.; Saperstein, David S. et al. (2005-05-01). "Interferon-alpha/beta-mediated innate immune mechanisms in dermatomyositis". Annals of Neurology 57 (5): 664–678. doi:10.1002/ana.20464. ISSN 0364-5134. PMID 15852401. 
  39. ↑ Pinal-Fernandez, Iago; Casal-Dominguez, Maria; Derfoul, Assia; Pak, Katherine; Plotz, Paul; Miller, Frederick W.; Milisenda, Jose C.; Grau-Junyent, Josep M. et al. (2019-09-17). "Identification of distinctive interferon gene signatures in different types of myositis". Neurology 93 (12): e1193–e1204. doi:10.1212/WNL.0000000000008128. ISSN 1526-632X. PMID 31434690. 
  40. ↑ Hornung, Thorsten; Janzen, Viktor; Heidgen, Franz-Josef; Wolf, Dominik; Bieber, Thomas; Wenzel, Joerg (2014-12-25). "Remission of Recalcitrant Dermatomyositis Treated with Ruxolitinib". New England Journal of Medicine 371 (26): 2537–2538. doi:10.1056/nejmc1412997. ISSN 0028-4793. PMID 25539124. 
  41. ↑ Ladislau, Leandro; Suárez-Calvet, Xavier; Toquet, Ségolène; Landon-Cardinal, Océane; Amelin, Damien; Depp, Marine; Rodero, Mathieu P; Hathazi, Denisa et al. (2018-05-08). "JAK inhibitor improves type I interferon induced damage: proof of concept in dermatomyositis". Brain 141 (6): 1609–1621. doi:10.1093/brain/awy105. ISSN 0006-8950. PMID 29741608. 
  42. ↑ Paik, Julie J.; Casciola-Rosen, Livia; Shin, Joseph Yusup; Albayda, Jemima; Tiniakou, Eleni; Leung, Doris G.; Gutierrez-Alamillo, Laura; Perin, Jamie et al. (2021-03-24). "Study of Tofacitinib in Refractory Dermatomyositis: An Open-Label Pilot Study of Ten Patients". Arthritis & Rheumatology 73 (5): 858–865. doi:10.1002/art.41602. ISSN 2326-5191. PMID 33258553. 
  43. ↑ Kim, Hanna; Dill, Samantha; O'Brien, Michelle; Vian, Laura; Li, Xiaobai; Manukyan, Manuk; Jain, Minal; Adeojo, Lilian W. et al. (2021-03-01). "Janus kinase (JAK) inhibition with baricitinib in refractory juvenile dermatomyositis". Annals of the Rheumatic Diseases 80 (3): 406–408. doi:10.1136/annrheumdis-2020-218690. ISSN 1468-2060. PMID 32843325. 
  44. ↑ Vleugels, Ruth Ann; Paik, Julie J.; Bauer Ventura, Iazsmin; Mangold, Aaron R.; Gandiga, Prateek C.; Haemel, Anna; Chinoy, Hector; Hussain, Yessar M. et al. (2026-05-14). "A Phase 3 Trial of Brepocitinib in Dermatomyositis" (in en). New England Journal of Medicine 394 (19): 1883–1893. doi:10.1056/NEJMoa2503531. ISSN 0028-4793. PMID 41910335. http://www.nejm.org/doi/10.1056/NEJMoa2503531. 
  45. ↑ Fiorentino, David; Mangold, Aaron R; Werth, Victoria P; Christopher-Stine, Lisa; Femia, Alisa; Chu, Myron; Musiek, Amy C M; Sluzevich, Jason C et al. (2025-01-01). "Efficacy, safety, and target engagement of dazukibart, an IFNβ specific monoclonal antibody, in adults with dermatomyositis: a multicentre, double-blind, randomised, placebo-controlled, phase 2 trial". The Lancet 405 (10473): 137–146. doi:10.1016/s0140-6736(24)02071-3. ISSN 0140-6736. PMID 39798982. 
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  47. ↑ Bergua, Cécile; Chiavelli, Hélène; Allenbach, Yves; Arouche-Delaperche, Louiza; Arnoult, Christophe; Bourdenet, Gwladys; Jean, Laetitia; Zoubairi, Rachid et al. (2019-01-01). "In vivo pathogenicity of IgG from patients with anti-SRP or anti-HMGCR autoantibodies in immune-mediated necrotising myopathy". Annals of the Rheumatic Diseases 78 (1): 131–139. doi:10.1136/annrheumdis-2018-213518. ISSN 0003-4967. PMID 30309969. 
  48. ↑ Allenbach, Yves; Arouche-Delaperche, Louiza; Preusse, Corinna; Radbruch, Helena; Butler-Browne, Gillian; Champtiaux, Nicolas; Mariampillai, Kuberaka; Rigolet, Aude et al. (2018-02-06). "Necrosis in anti-SRP + and anti-HMGCR + myopathies". Neurology 90 (6): e507–e517. doi:10.1212/wnl.0000000000004923. ISSN 0028-3878. PMID 29330311. 
  49. ↑ Julien, Sarah; Vadysirisack, Douangsone; Sayegh, Camil; Ragunathan, Sharan; Tang, Yalan; Briand, Emma; Carrette, Marion; Jean, Laetitia et al. (2022-08-20). "Prevention of Anti-HMGCR Immune-Mediated Necrotising Myopathy by C5 Complement Inhibition in a Humanised Mouse Model". Biomedicines 10 (8): 2036. doi:10.3390/biomedicines10082036. ISSN 2227-9059. PMID 36009583. 
  50. ↑ "Cancer risk in dermatomyositis: a systematic review of the literature". Giornale Italiano di Dermatologia e Venereologia 149 (5): 525–537. October 2014. PMID 24975953. http://www.minervamedica.it/index2.t?show=R23Y2014N05A0525. 
  51. ↑ Lundberg, Ingrid E; Tjärnlund, Anna; Bottai, Matteo; Werth, Victoria P; Pilkington, Clarissa; Visser, Marianne de; Alfredsson, Lars; Amato, Anthony A et al. (December 2017). "2017 European League Against Rheumatism/American College of Rheumatology classification criteria for adult and juvenile idiopathic inflammatory myopathies and their major subgroups" (in en). Annals of the Rheumatic Diseases 76 (12): 1955–1964. doi:10.1136/annrheumdis-2017-211468. PMID 29079590. 
  52. ↑ Allenbach, Yves; Mammen, Andrew L.; Benveniste, Olivier; Stenzel, Werner; Allenbach, Yves; Amato, Anthony; Aussey, Audrey; Benveniste, Olivier et al. (January 2018). "224th ENMC International Workshop" (in en). Neuromuscular Disorders 28 (1): 87–99. doi:10.1016/j.nmd.2017.09.016. PMID 29221629. https://linkinghub.elsevier.com/retrieve/pii/S0960896617312075. 
  53. ↑ Mammen, Andrew L.; Allenbach, Yves; Stenzel, Werner; Benveniste, Olivier; Allenbach, Yves; Benveniste, Olivier; Bleecker, Jan De; Boyer, Olivier et al. (January 2020). "239th ENMC International Workshop: Classification of dermatomyositis, Amsterdam, the Netherlands, 14–16 December 2018" (in en). Neuromuscular Disorders 30 (1): 70–92. doi:10.1016/j.nmd.2019.10.005. PMID 31791867. https://linkinghub.elsevier.com/retrieve/pii/S0960896619311617. 
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  56. ↑ "Autoimmune Myopathies: Where Do We Stand?". Frontiers in Immunology 7: 234. 14 June 2016. doi:10.3389/fimmu.2016.00234. PMID 27379096. 
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  58. ↑ "Dermatomyositis-Part 2: Diagnosis, Association With Malignancy, and Treatment". Skinmed 14 (5): 354–358. 1 October 2016. PMID 27871347. 
  59. ↑ Euwer, Rebecca L.; Sontheimer, Richard D. (1993). "Amyopathic Dermatomyositis: A Review" (in en). Journal of Investigative Dermatology 100 (1): S124–S127. doi:10.1038/jid.1993.35. https://linkinghub.elsevier.com/retrieve/pii/S0022202X15509731. 
  60. ↑ Sato, Shinji; Hirakata, Michito; Kuwana, Masataka; Suwa, Akira; Inada, Shinichi; Mimori, Tsuneyo; Nishikawa, Takeji; Oddis, Chester V. et al. (2005). "Autoantibodies to a 140-kd polypeptide, CADM-140, in Japanese patients with clinically amyopathic dermatomyositis" (in en). Arthritis & Rheumatism 52 (5): 1571–1576. doi:10.1002/art.21023. ISSN 1529-0131. PMID 15880816. https://onlinelibrary.wiley.com/doi/abs/10.1002/art.21023. 
  61. ↑ Dalakas, Marinos C.; Illa, Isabel; Dambrosia, James M.; Soueidan, Shawke A.; Stein, Daniel P.; Otero, Carlos; Dinsmore, Steven T.; McCrosky, Susan (1993-12-30). "A Controlled Trial of High-Dose Intravenous Immune Globulin Infusions as Treatment for Dermatomyositis". New England Journal of Medicine 329 (27): 1993–2000. doi:10.1056/NEJM199312303292704. ISSN 0028-4793. PMID 8247075. https://www.nejm.org/doi/full/10.1056/NEJM199312303292704. 
  62. ↑ Aggarwal, Rohit; Charles-Schoeman, Christina; Schessl, Joachim; Bata-Csörgő, Zsuzsanna; Dimachkie, Mazen M.; Griger, Zoltan; Moiseev, Sergey; Oddis, Chester et al. (2022-10-05). "Trial of Intravenous Immune Globulin in Dermatomyositis". New England Journal of Medicine 387 (14): 1264–1278. doi:10.1056/NEJMoa2117912. ISSN 0028-4793. PMID 36198179. https://www.nejm.org/doi/full/10.1056/NEJMoa2117912. 
  63. ↑ Oddis, Chester V.; Reed, Ann M.; Aggarwal, Rohit; Rider, Lisa G.; Ascherman, Dana P.; Levesque, Marc C.; Barohn, Richard J.; Feldman, Brian M. et al. (February 2013). "Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: A randomized, placebo-phase trial" (in en). Arthritis & Rheumatism 65 (2): 314–324. doi:10.1002/art.37754. ISSN 0004-3591. PMID 23124935. 
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  65. ↑ Hornung, Thorsten; Janzen, Viktor; Heidgen, Franz-Josef; Wolf, Dominik; Bieber, Thomas; Wenzel, Joerg (2014-12-25). "Remission of Recalcitrant Dermatomyositis Treated with Ruxolitinib". New England Journal of Medicine 371 (26): 2537–2538. doi:10.1056/NEJMc1412997. ISSN 0028-4793. PMID 25539124. https://www.nejm.org/doi/full/10.1056/NEJMc1412997. 
  66. ↑ Ladislau, Leandro; Suárez-Calvet, Xavier; Toquet, Ségolène; Landon-Cardinal, Océane; Amelin, Damien; Depp, Marine; Rodero, Mathieu P; Hathazi, Denisa et al. (2018-06-01). "JAK inhibitor improves type I interferon induced damage: proof of concept in dermatomyositis". Brain 141 (6): 1609–1621. doi:10.1093/brain/awy105. ISSN 0006-8950. PMID 29741608. 
  67. ↑ Kim, Hanna; Dill, Samantha; O'Brien, Michelle; Vian, Laura; Li, Xiaobai; Manukyan, Manuk; Jain, Minal; Adeojo, Lilian W. et al. (2021-03-01). "Janus kinase (JAK) inhibition with baricitinib in refractory juvenile dermatomyositis" (in English). Annals of the Rheumatic Diseases 80 (3): 406–408. doi:10.1136/annrheumdis-2020-218690. ISSN 0003-4967. PMID 32843325. PMC 7904969. https://ard.eular.org/article/S0003-4967(24)00538-7/abstract. 
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 This article incorporates public domain material from the United States Department of Health and Human Services document "NINDS Dermatomyositis Information Page".

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