Dermatomyositis 

  • Author: Jeffrey P Callen, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Oct 12, 2011
 

Background

Dermatomyositis is an idiopathic inflammatory myopathy (IIM) with characteristic cutaneous findings. It is a systemic disorder that most frequently affects the skin and muscles, but may also affect the joints, the esophagus, the lungs, and, less commonly, the heart.[1, 2] Calcinosis is a complication of dermatomyositis that is observed most often in children and adolescents. An association between dermatomyositis and cancer has long been recognized.[3, 4, 5, 6, 7, 8]

In 1975, Bohan and Peter first suggested a set of 5 criteria to aid in the diagnosis and classification of dermatomyositis and polymyositis.[9, 10] Four of the 5 criteria are related to the muscle disease, as follows: progressive proximal symmetrical weakness, elevated levels of muscle enzymes, an abnormal finding on electromyography, and an abnormal finding on muscle biopsy. The fifth criterion was compatible with cutaneous disease.

Bohan and Peter suggested 5 subsets of myositis, as follows[10] :

  • Dermatomyositis
  • Polymyositis
  • Myositis with malignancy
  • Childhood dermatomyositis/polymyositis
  • Myositis overlapping with another collagen-vascular disorder

In a subsequent publication, Bohan et al noted that cutaneous disease may precede the development of the myopathy.[9] 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 have controlled myopathy but 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 have muscle involvement, and their condition may be better classified as hypomyopathic dermatomyositis. Patients with ADM or hypomyopathic DM may also reflect an underlying malignancy, and some develop severe pulmonary disease, particularly persons in Asian countries.

Patients exist in whom myositis resolves after therapy but whose 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 is the major and often only manifestation of the disease. Germani and colleagues have suggested the term postmyopathic dermatomyositis for these patients.[11]

Rare cutaneous manifestations include vesiculobullous erosive lesions and an exfoliative erythroderma. Biopsy samples from patients reveal an interface dermatitis similar to that seen in biopsy samples of heliotrope rash, Gottron papules, poikiloderma, or scalp lesions. These cutaneous manifestations may be more common in patients with an associated malignancy than in those without a malignancy.

Therapy for the muscle component of dermatomyositis involves the use of corticosteroids, with or without an immunosuppressive agent. The skin disease is treated with sun avoidance, sunscreens, topical corticosteroids, antimalarial agents, methotrexate, mycophenolate mofetil, or intravenous (IV) immunoglobulin. Rituximab may be useful in the treatment of muscle disease of dermatomyositis and has had mixed results in treatment of skin disease.[12, 13]

Physical therapy and rehabilitative measures are necessary in selected patients. Sun protective measures are necessary for patients with skin disease. Patients may visit The Myositis Association Web site for more information.

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.

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Pathophysiology

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.[14]

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.

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.[15]

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Etiology

The cause of dermatomyositis is unknown; however, the following factors have been implicated.

A genetic component may predispose to dermatomyositis. Dermatomyositis rarely occurs in multiple family members. However, a link to certain human leukocyte antigen (HLA) types (eg, DR3, DR5, DR7. may exist. Polymorphisms of tumor necrosis factor may be involved; specifically, the presence of the -308A allele is linked to photosensitivity in adults and calcinosis in children.[15, 16, 17]

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, including viruses (eg, coxsackievirus, parvovirus, echovirus, human T-cell lymphotropic virus type 1 [HTLV-1], HIV) and Toxoplasma and Borrelia species, have been suggested as possible triggers of dermatomyositis.

Several cases of drug-induced dermatomyositis have been reported. Dermatomyositislike skin changes have been reported with hydroxyurea in patients with chronic myelogenous leukemia or essential thrombocytosis.[18, 19] Other agents that may trigger the disease include penicillamine, statin drugs, quinidine, and phenylbutazone.

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 detailed HLA differences among women in whom inflammatory myopathy develops after they received silicone implants.[20]

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Epidemiology

The estimated incidence of dermatomyositis is 9.63 cases per million population. The estimated incidence of AMD is 2.08 cases per million.[21]

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.

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Prognosis

Most patients with dermatomyositis survive, in which case they may develop residual weakness and disability. Children with severe dermatomyositis may develop contractures. The disease may spontaneously remit in as many as 20% of affected patients. About 5% of patients have a fulminant progressive course with eventual death. Therefore, many patients require long-term therapy. Patients with dermatomyositis who have malignancy, cardiac involvement, or pulmonary involvement or who are elderly (ie, > 60 years) have a poorer prognosis.

Dermatomyositis may cause death because of muscle weakness or cardiopulmonary involvement. Patients with an associated malignancy may die of the malignancy.

Calcinosis may complicate dermatomyositis. It is very rare in adults but is more common in children and has been linked to delay in diagnosis and to less-aggressive therapy. Contractures can occur if the patient is immobile.

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Proceed to Clinical Presentation
 
 
Contributor Information and Disclosures
Author

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, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Consulting fee Consulting; Celgene Honoraria Safety Monitoring Committee; GSK - Glaxo Smith Kline Consulting fee Consulting; TenXBioPharma Consulting fee Safety Monitoring Committee

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; 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, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

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, and American 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

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 and American College of Rheumatology

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

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Heliotrope flower, for which characteristic manifestation of dermatomyositis is named.
Heliotrope rash in a woman with dermatomyositis.
Gottron papules and nailfold telangiectasia are present in this patient with dermatomyositis.
These lesions on dorsal hands demonstrate photodistribution of dermatomyositis. Note sparing of interdigital web spaces.
Diffuse alopecia with scaly scalp dermatosis is common in patients with dermatomyositis.
Dermatomyositis is often associated with a poikiloderma in a photodistribution.
Histopathology of dermatomyositis is interface dermatitis.
Calcinosis caused by dermatomyositis in childhood can be observed in patient who had active dermatomyositis 15 years before time of this photograph.
Histopathology of dermatomyositis showing inflammatory myopathic changes with a predominantly perivascular chronic inflammatory infiltrate.
Calcifying panniculitis in patient with dermatomyositis.
Ulceration over dorsal and lateral fingers in patient with dermatomyositis.
Hematoxylin and eosin paraffin section shows polymyositis. Longitudinal section shows dense, chronic, endomysial inflammatory infiltrate. Image courtesy of Roberta J Seidman, MD.
Hematoxylin and eosin frozen section shows polymyositis. Endomysial chronic inflammation is present among intact myofibers that are remarkable only for increased variability of fiber size. Image courtesy of Roberta J Seidman, MD.
Hematoxylin and eosin paraffin section shows polymyositis. Patient had dense endomysial inflammation that contains abundance of plasma cells, which can be observed in patients with chronic polymyositis. Two necrotic myofibers, characterized by dense eosinophilic staining, are observed. Focal fatty infiltration of muscle is present in lower left quadrant of photomicrograph. Image courtesy of Roberta J Seidman, MD.
Hematoxylin and eosin paraffin section shows polymyositis. Photomicrograph illustrates attack on nonnecrotic myofiber by autoaggressive T lymphocytes. On left, central myofiber is intact. On right, it is obliterated by segmental inflammatory attack. If immunohistochemistry were performed, expected findings would include admixture of CD8 T lymphocytes and macrophages in inflammatory process. Image courtesy of Roberta J Seidman, MD.
Hematoxylin and eosin paraffin shows dermatomyositis. In dermatomyositis, inflammation is characteristically perivascular and perimysial. Vessel oriented approximately vertically in center has mild perivascular chronic inflammatory infiltrate. Endothelium is plump; wall is not necrotic. A few lymphocytes in wall of vessel are probably in transit from lumen to external aspect of vessel. Some observers may interpret this finding as vasculitis, but it is certainly neither necrotizing vasculitis nor arteritis. Image courtesy of Roberta J. Seidman, MD.
Hematoxylin and eosin frozen section shows perifascicular atrophy in dermatomyositis. Fascicles in this sample show atrophy, predominantly at periphery, along connective-tissue border. Ischemia is considered to cause perifascicular atrophy. This finding is characteristic of dermatomyositis, mostly associated with juvenile form but also observed in adult form. Image courtesy of Roberta J Seidman, MD.
Immunofluorescence for membrane attack complex of complement (MAC) in dermatomyositis. Bright ring of yellow-green fluorescence at center represents MAC in wall of microvessel. Finding was not present after treatment with steroids. Image courtesy of Roberta J Seidman, MD.
 
 
 
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