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Dermatomyositis is an idiopathic inflammatory myopathy with characteristic cutaneous findings that occur in children and adults (see the image below). This systemic disorder most frequently affects the skin and muscles but may also affect the joints; the esophagus; the lungs; and, less commonly, the heart. [1,2]Dystrophic calcinosis may complicate dermatomyositis and is most often observed in children and adolescents.
These lesions on dorsal hands demonstrate photodistribution of dermatomyositis. Note sparing of interdigital web spaces.Persons with dermatomyositis often present with skin disease as one of the initial manifestations, and it may be the sole manifestation at onset in perhaps as many as 40% of individuals with this condition. Cutaneous involvement may manifest as follows:
Muscle disease may occur concurrently, may precede the skin disease, or may follow the skin disease by weeks to years. Muscle involvement manifests as the following:
Systemic manifestations that may occur include the following:
SeePresentation for more detail.
Examination for cutaneous dermatomyositis may reveal the following findings:
Examination for muscle disease in dermatomyositis may demonstrate the following:
Testing
Laboratory and other studies that may be helpful include the following:
Imaging studies
The following imaging studies may be used in the evaluation of dermatomyositis:
Procedures
The following procedures may be helpful in the evaluation of dermatomyositis:
SeeWorkup for more detail.
Therapy for the muscle component of dermatomyositis involves the use of corticosteroids, typically with an immunosuppressive agent. Therapy for the skin disease includes the following, among other options:
Pharmacotherapy
Medications used in the management of dermatomyositis include the following:
Rituximab may be useful in the treatment of muscle disease in dermatomyositis, and has had mixed results in treatment of skin disease. [11,12,13]In addition to the medications listed above, diltiazem, colchicine, alendronate, and warfarin are among the medications that have shown potential benefit in treating calcinosis. Surgical excision of focal, tender calcinotic lesions is also considered a therapeutic option.
Nonpharmacotherapy
General therapeutic measures may include the following:
Surgery
Surgical care is usually unnecessary in the management of dermatomyositis. However, some patients may benefit from surgical removal of localized areas of calcinosis, particularly those that are painful.
SeeTreatment andMedication for more detail.
The prognosis of dermatomyositis depends on the severity of the myopathy, the presence of malignancy, and/or the presence of esophageal and/or cardiopulmonary involvement. Residual weakness is common, even in patients who fully recover.
For discussion of dermatomyositis in pediatric patients, seeJuvenile Dermatomyositis. For patient education information, seeDermatomyositis andThe Myositis Association Web site.
In 1975, Bohan and Peter first suggested a set of five criteria to aid in the diagnosis and classification of dermatomyositis. [14,15]Four of the five criteria are related to the muscle disease, as follows:
The fifth criterion is compatible cutaneous disease.
In addition to dermatomyositis, Bohan and Peter suggested the following four subsets of myositis [15]:
In a subsequent publication, Bohan et al noted that cutaneous disease may precede the development of the myopathy in patients with dermatomyositis. [14]In addition, the existence of another subset of patients with dermatomyositis that affects only the skin (ie, amyopathic dermatomyositis [ADM], or dermatomyositis sine myositis) has been recognized. Finally, another subset of patients with dermatomyositis are those with controlled myopathy who continue to have severe and sometimes debilitating skin disease (ie, postmyopathic dermatomyositis).
ADM is diagnosed in patients with typical cutaneous disease who show no evidence of muscle weakness and in whom serum muscle enzyme levels are repeatedly normal over a 2-year period in the absence of the use of disease-modifying therapies such as corticosteroids, immunosuppressive agents, or both for 2 months or longer.
When studied, some ADM patients may have abnormal findings on ultrasonography, electromyography, magnetic resonance imaging (MRI), magnetic resonance spectroscopy, or muscle biopsy. These patients are better classified as having hypomyopathic dermatomyositis. ADM or hypomyopathic dermatomyositis may also be related to an underlying malignancy.
The term clinically amyopathic dermatomyositis (CADM) is often used to encompass patients with both amyopathic and hypomyopathic dermatomyositis. [16]CADM is estimated to account for about 20% of patients with dermatomyositis, [17]and one large review suggests that CADM is associated with malignancy and lung disease as frequently as classic dermatomyositis. [18]In addition, some patients with CADM develop severe pulmonary disease, particularly persons from Asian countries. [19]
Patients exist in whom myositis resolves after therapy but skin disease remains an active and important feature of the disorder. These patients are not classified as having ADM, even though by this point the skin lesions are the major and often only manifestation of the disease. Germani and colleagues have suggested the term postmyopathic dermatomyositis for these patients. [20]
Dermatomyositis is considered to be the result of a humoral attack against the muscle capillaries and small arterioles (endothelium of the endomysial blood vessels). Since 1966, there has been evidence supporting an ongoing microangiopathy. [21]
Like other idiopathic inflammatory myopathies, dermatomyositis is characterized by the presence of autoantibodies that are conventionally divided into myositis-specific autoantibodies (MSAs) and myositis-associated autoantibodies (MAAs). Individual patients rarely generate more than one MSA simultaneously. MSAs found in dermatomyositis include anti–Mi-2, anti-MDA5, anti–TIF1γ, anti-NXP2, and anti-SAE. [22]
The disease starts when putative antibodies or other factors activate C3, forming C3b and C4b fragments that lead to formation of C3bNEO and membrane attack complex (MAC), which are deposited in the endomysial vasculature. Complement C5b-9 MAC is deposited and is needed in preparing the cell for destruction in antibody-mediated disease. B cells and CD4 (helper) cells are also present in abundance in the inflammatory reaction associated with the blood vessels.
As the disease progresses, the capillaries are destroyed, and the muscles undergo microinfarction. Perifascicular atrophy occurs in the beginning; however, as the disease advances, necrotic and degenerative fibers are present throughout the muscle.
The pathogenesis of the cutaneous component of dermatomyositis is poorly understood, but is thought to be similar to that of muscle involvement.
Studies on the pathogenesis of the muscle component have been controversial. Some suggest that the myopathy in dermatomyositis is pathogenetically different from that in polymyositis. The former is probably caused by complement-mediated (terminal attack complex) vascular inflammation, the latter by the direct cytotoxic effect of CD8+ lymphocytes on muscle. However, other cytokine studies suggest that some of the inflammatory processes may be similar. One report has linked tumor necrosis factor (TNF) abnormalities with dermatomyositis. [23]
The cause of dermatomyositis is unknown. However, genetic, immunologic, infectious, and environmental factors have been implicated.
A genetic component may predispose to dermatomyositis. Dermatomyositis rarely occurs in multiple family members, but a link to certain human leukocyte antigen (HLA) types (eg, DR3, DR5, DR7) may exist.
Polymorphisms of tumor necrosis factor (TNF) may be involved; specifically, the presence of the -308A allele is linked to photosensitivity in adults and calcinosis in children. [23,24,25]A meta-analysis demonstrated that the TNF-α-308A/G polymorphism might contribute to dermatomyositis susceptibility, especially in a European population. [26]
Immunologic abnormalities are common in patients with dermatomyositis. Patients frequently have circulating autoantibodies. Abnormal T-cell activity may be involved in the pathogenesis of both the skin disease and the muscle disease. In addition, family members may manifest other diseases associated with autoimmunity.
Antinuclear antibodies (ANAs) and antibodies to cytoplasmic antigens (ie, antitransfer RNA synthetases) may be present. Although their presence may help to define subtypes of dermatomyositis and polymyositis, their role in pathogenesis is uncertain.
Infectious agents have been suggested as possible triggers of dermatomyositis. These include the following:
New cases of dermatomyositis have been reported following COVID-19 infection or vaccination. [27,28]
Cases of drug-induced dermatomyositis have been reported. Dermatomyositis-like skin changes have been reported with hydroxyurea in patients withchronic myelogenous leukemia oressential thrombocytosis. [29,30]Other agents that may trigger the disease include the following:
Dermatomyositis may be initiated or exacerbated by silicone breast implants or collagen injections, but the evidence for this is anecdotal and has not been verified in case-control studies. One report identified a distinct immunogenetic profile in women who developed inflammatory myopathy after receiving silicone implants. [33]
The estimated incidence of dermatomyositis is 9.63 cases per million population. The estimated incidence of AMD is 2.08 cases per million. [17]
Dermatomyositis can occur in people of any age. Two peak ages of onset exist: in adults, the peak age of onset is approximately 50 years, whereas in children, the peak age is approximately 5-10 years. Dermatomyositis and polymyositis are twice as common in women as in men. Neither condition shows any racial predilection.
Dermatomyositis may spontaneously remit in as many as 20% of affected patients. About 5% of patients have a fulminant progressive course with eventual death. However, patients who survive the disease may experience residual weakness and disability. Children with severe dermatomyositis may develop contractures. Therefore, many patients require long-term therapy.
Risk factors for a poorer prognosis in patients with dermatomyositis include the following:
Dermatomyositis may cause death because of muscle weakness or cardiopulmonary involvement. [34]Patients with an associated cancer may die of the malignancy.
The association between malignancy and dermatomyositis has long been recognized. An estimated 25% of patients with dermatomyositis have or will develop an associated malignancy, and the risk appears to remain elevated for 3-5 years. [35,36,37]Strong data from Scandinavia, Australia, North America, and Asia continue to confirm this association with malignancy, and existing data supports that risk of malignancy is similar in patients with little or no evidence of muscle involvement (clinically amyopathic dermatomyositis [CADM]) and in those with classic dermatomyositis. [18,20,36,37,38,39,40,41]
The presence of specific circulating autoantibodies has been linked with risk of malignancy in patients with dermatomyositis. The strongest reported correlation is with circulating anti–transcriptional intermediary factor 1 (TIF1), anti-nuclear matrix protein 2 (NXP2), and anti–SUMO-1 activating enzyme (SAE) autoantibodies. [42]
Ovarian cancer is clearly over-represented in patients with dermatomyositis; however, any malignancy may occur. Reported maligancies include lung, colon, prostate, breast, pancreatic, cervical, and hematologic malignancies. [43]Predilection for certain types of malignancy may be more common in specific populations. For example, nasopharyngeal carcinoma appears to be over-represented in certain Asian populations. [44,45,46]
In an approximately 10-year retrospective study from southern China, 60 of 246 dermatomyositis patients developed malignancies. The risk of malignancy was highest in the first year after diagnosis of dermatomyositis, and nasopharyngeal carcinoma and ovarian carcinoma were the most common malignancies. Male gender, dysphagia and elevated erythrocyte sedimentation rate were risk factors for malignancy, whereas the presence of interstitial lung disease appeared to reduce the risk of malignancy. [47]Older age appears to be the strongest predictor of malignancy in patients with dermatomyositis.
Calcinosis may also complicate dermatomyositis. It is rare in adults but is more common in children and has been linked to delay in diagnosis and to less-aggressive therapy. [48]Contractures can occur if the patient is immobile.
Population-based studies from British Columbia concluded that patients with dermatomyositis (or polymyositis) are at increased risk for venous thromboembolism (deep venous thrombosis or pulmonary embolism) and myocardial infarction, especially in the first year after diagnosis. [49,50]However, dermatomyositis was not associated with an increased risk of ischemic stroke. [50]
A study from Taiwan reported that the risk of osteoporosis in persons with dermatomyositis (or polymyositis) was 2.99 times higher than in those without these disorders. This risk was independent of treatment with corticosteroids and immunosuppressant drugs. [51]
In a study of patients with dermatomyositis with cutaneous involvement, 28 of 74 achieved clinical remission of the skin disease during a 3-year follow-up period. Clinical remission of skin disease was more likely to occur in older patients (odds ratio [OR], 1.07; 95% CI, 1.02-1.12; P = 0.01), those with a dermatomyositis-associated malignancy (OR, 14.46; 95% CI, 2.18-96.07; P =0 .01), and those treated with mycophenolate mofetil (OR, 6.00; 95% CI, 1.66-21.78; P = 0.01). Patients with antimelanoma differentiation–associated protein 5 antibodies had a significantly lower probability of achieving clinical remission. [52]
African Americans and patients in lower socioeconomic groups are more likely to experience a delay in diagnosis. The prognosis in children with dermatomyositis is worse in those in whom diagnosis is delayed.
Overall, data suggest that the mortality rate in persons with dermatomyositis is higher than that in the general population. Population-based data from Sweden demonstrate that mortality in idiopathic inflammatory myopathies is increased within 1 year of diagnosis and plateaus around 10 years after diagnosis, with the increase in mortality largely attributed to malignancy, as well as to diseases of the respiratory and vascular systems. [53]
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Autoantibody | Clinical Associations |
Anti–Mi-2 | Typical dermatomyositis rashes |
Anti–MDA5 | Particular skin signs Clinically amyopathic dermatomyositis Rapidly progressive interstitial lung disease |
Anti–TIF1γ | Skin disease with photoexposed pattern Clinically amyopathic dermatomyositis in younger patients Increased risk of malignancy and muscle weakness in older patients |
Anti-NXP2 | Subcutaneous calcinosis and edema Severe muscle disease Increased risk of malignancy |
Anti-SAE | High frequency of dysphagia Skin involvement prior to muscle disease |
Alisa N Femia, MD Assistant Professor, Ronald O Perelman Department of Dermatology, New York University Medical Center
Alisa N Femia, MD is a member of the following medical societies:Alpha Omega Alpha,American Academy of Dermatology,Society for Investigative Dermatology,Medical Dermatology Society,Rheumatologic Dermatology Society
Disclosure: Nothing to disclose.
Ruth Ann Vleugels, MD, MPH Assistant Professor of Dermatology, Harvard Medical School; Associate Physician, Department of Dermatology, Brigham and Women's Hospital; Associate Physician, Department of Immunology and Allergy, Children's Hospital Boston
Ruth Ann Vleugels, MD, MPH is a member of the following medical societies:Alpha Omega Alpha,American Academy of Dermatology,American College of Rheumatology,American Medical Association,Society for Investigative Dermatology,Medical Dermatology Society,Dermatology Foundation
Disclosure: Nothing to disclose.
Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine
Jeffrey P Callen, MD is a member of the following medical societies:Alpha Omega Alpha,American Academy of Dermatology,American College of Physicians,American College of Rheumatology
Disclosure: Received income in an amount equal to or greater than $250 from: Biogen US (Adjudicator for study entry cutaneous lupus erythematosus); Priovant (Adjudicator for entry into a dermatomyositis study); IQVIA (Serono - adjudicator for a study of cutaneous LE) <br/>Received honoraria from UpToDate for author/editor; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for these trust accounts for: Stocks held in various trust accounts: Allergen; Amgen; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble;; Celgene; Gilead; CVS; Walgreens; Bristol-Myers Squibb.
Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies:Alpha Omega Alpha,American College of Physicians,American College of Rheumatology,American Medical Association,Phi Beta Kappa
Disclosure: Nothing to disclose.
Lawrence H Brent, MD Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center
Lawrence H Brent, MD is a member of the following medical societies:American Association for the Advancement of Science,American Association of Immunologists,American College of Physicians, andAmerican College of Rheumatology
Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching
William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
William D James, MD is a member of the following medical societies:American Academy of Dermatology andSociety for Investigative Dermatology
Disclosure: Nothing to disclose.
Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Center for the Advancement of Women's Health and Division of Rheumatology, Director, Rheumatology Training Program, University of Kentucky College of Medicine
Kristine M Lohr, MD, MS is a member of the following medical societies:American College of Physicians andAmerican College of Rheumatology
Disclosure: Nothing to disclose.
Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio
Jeffrey Meffert, MD is a member of the following medical societies:American Academy of Dermatology,American Medical Association,Association of Military Dermatologists, andTexas Dermatological Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies:American Academy of Dermatology,Association of Military Dermatologists,Texas Dermatological Society, andTexas Medical Association
Disclosure: Nothing to disclose.