Idiopathic inflammatory myopathies

Summary

Idiopathic inflammatory myopathies (IIM) are a group of rare systemic diseases characterized by progressive weakness due to chronic skeletal muscle inflammation. They are classified based on clinicopathological findings into dermatomyositis (DM), overlap myositis (OM), immune-mediated necrotizing myopathy (IMNM), inclusion-body myositis (IBM), and polymyositis (PM). If onset occurs before the age of 18 years, it is called juvenile IIM, or JIIM. IIM typically manifests with proximal, symmetric weakness in appendicular muscles, which leads to difficulty reaching overhead, climbing the stairs, and/or standing up. The severity of muscle involvement can vary significantly between forms of IIM. In advanced disease, weakness may also affect oropharyngeal muscles (causing dysphagia and aspiration) and respiratory muscles (causing restrictive lung disease or even respiratory failure.) Patients may also have cutaneous features (including Gottron papules, heliotrope rash, and the shawl sign) and an increased risk of various malignancies (in DM, PM, and IMNM), and interstitial lung disease in some forms of DM, IMNM, and OM.

The diagnosis of suspected IIM is supported by laboratory tests, which show elevated muscle enzymes (e.g., creatine kinase, aldolase) as well as characteristic electromyogram (EMG) and biopsy findings. Management consists of supportive treatment (such as physical and occupational therapy) alongside immunosuppression with glucocorticoids and drugs such as methotrexate and azathioprine (except for IBM, for which treatment is supportive only).

Definitions

Dermatomyositis (DM): : an inflammatory myopathy characterized by progressive symmetrical proximal muscle weakness and distinctive skin findings
Overlap myositis (OM): any inflammatory myopathy that occurs in association with features of another autoimmune connective tissue disease. A classic form of OM is antisynthetase syndrome.
Immune-mediated necrotizing myopathy (IMNM): an inflammatory myopathy affecting the proximal skeletal muscles that is particularly severe and associated with a markedly elevated CK level
Inclusion body myositis (IBM): : an inflammatory myopathy affecting both the proximal and distal skeletal muscles
Polymyositis (PM): : an inflammatory myopathy affecting the proximal skeletal muscles, with evidence of elevated CK and myositis on EMG and biopsy in the absence of any of the characteristic findings of the other IIM (a rare diagnosis of exclusion)
Juvenile idiopathic inflammatory myopathy (JIIM): any inflammatory myopathy manifesting in an individual < 18 years old [1]

References:[2][3]

Epidemiology

Incidence
- PM and DM: 2/100,000 per year
- In the US, PM disproportionately affects the black population.
Sex
- PM and DM: ♀ > ♂ (2:1)
- IBM: ♂ > ♀ (2:1)
Peak
incidence
- PM: 30–60 years
- DM
  
  5–15 years (juvenile dermatomyositis)
  
  40–60 years (adult dermatomyositis)
- IBM: > 50 years

Epidemiological data refers to the US, unless otherwise specified.

Etiology

The origin is unknown, but most forms of IM seem to involve an autoimmune reaction that leads to muscle inflammation, particularly in genetically susceptible individuals. Viral infections, malignancies, and connective tissue disorders may play a role.
Polymyositis (PM): cell-mediated cytotoxicity: against unidentified skeletal muscle antigens, chiefly affecting the endomysium
Dermatomyositis (DM): idiopathic or paraneoplastic antibody-mediated: vasculopathy, associated with malignancies (non-Hodgkin lymphoma; lung, stomach, colorectal, or ovarian cancer )

References:[4][5]

Clinical features

Clinical manifestations of IIM vary widely both between and within the subtypes. Symptoms can be grouped into three categories: muscle weakness, cutaneous features, and systemic manifestations. [2][6]

Muscle weakness

Limb
weakness
- Symmetrical proximal muscle weakness and atrophy
- Commonly affects pelvic and shoulder girdle muscles, leading to difficulties combing hair, standing up from a sitting position, and climbing stairs
- Can also affect neck muscles (flexors more than extensors)
- May be accompanied by myalgia [7]
- In inclusion body myositis, the weakness may be:
  
  Asymmetrical
  
  Additionally affecting distal muscle groups, making it hard to grip objects
Axial
muscle weakness
- Oropharyngeal muscle weakness leading to dysphagia [8][9]
- Respiratory muscle weakness leading to restrictive lung disease

Cutaneous features [8]

Cutaneous features are characteristic of dermatomyositis but may be found in other subtypes.

Symmetric
erythematous rash on the: ; [10]

Extensor surfaces of the hand joints; , elbows, and knees (Gottron sign); scaly papules; may form (Gottron papules)

Upper eyelids (heliotrope rash); often associated with periorbital edema

Mid-face [11]

Upper back, posterior neck, and shoulders; (shawl sign)

Upper chest and anterior neck (V sign)

Hips and lateral thighs (Holster sign)
Poikiloderma may be seen in chronic disease. [12][13]
Mechanic's hands: thickened and cracked skin on the sides of the fingers and palms (horizontal fissures may appear darkened or dirty, hence the name)
Periungual telangiectasias
Calcinosis cutis (in children)

Gottron papules in dermatomyositis Heliotrope rash V sign of dermatomyositis Calcinosis cutis Cutaneous manifestations of dermatomyositis

Systemic manifestations

Interstitial lung disease
Cardiac involvement (primarily in
dermatomyositis and
polymyositis), including:
[14]
- Myocarditis
- AV block
- Heart failure
Constitutional symptoms
Increased risk of malignancy (DM, PM, IMNM)
Raynaud phenomenon
Arthritis
Gastrointestinal symptoms (e.g., abdominal pain, hematemesis, melena)

Characteristic presentations of idiopathic inflammatory myopathies (IIM) [2][6][15][16]
	Muscle weakness	Cutaneous features	Systemic features
Dermatomyositis (DM)	Progresses over weeks to months Mild to moderately severe weakness	Typically present	Common Typically: Increased risk of malignancy Interstitial lung disease (may be severe)
Polymyositis (PM)		Absent
Antisynthetase syndrome	May be present depending on the subtype	Common: mechanic's hands	Common Typically: Interstitial lung disease Constitutional symptoms Raynaud phenomenon Arthritis (usually nonerosive polyarthritis) may be seen. [17]
Immune-mediated necrotizing myopathy (IMNM)	Severe Progression over weeks to months	Rare	Rare
Inclusion body myositis (IBM)	Progresses over years Symmetrical or asymmetrical Distal muscles also affected	Absent	Rare
Juvenile IIM (JIIM)	Variable in severity; may be absent	Present in juvenile DM Calcinosis cutis common	Common: gastrointestinal and constitutional symptoms, arthritis Other extramuscular features: rare

Think HAIR, CHAIRS, and STAIRS for the problems in activities of daily living caused by inflammatory myopathy: Muscle weakness causes difficulty raising the arms, getting up from a seated position, and climbing stairs.

Polymyositis and dermatomyositis fact sheet

**Gottron papules in dermatomyositis**
Scaly, erythematous papules and periungual erythema are visible on the dorsal aspect of the interphalangeal and metacarpophalangeal joints.
Both localization and appearance are typical of Gottron papules, which are pathognomonic of dermatomyositis.

Source: “Gottron papules .dermatomyocitis” by Mohammad2018, Wikimedia commons, licensed under CC BY-SA 4.0.

**Heliotrope rash**
A confluent macular, erythematous rash is visible on both upper eyelids with concurrent periorbital edema.
This is a characteristic finding in dermatomyositis.

Source: “Figure 3, in: Lupus Erythematosus, Dermatomyositis and Systemic Sclerosis: Assessment and Differentials from A Dermatologic Point of View” by S. B. Fadhel, A. C. Diniz Silva, Enliven Archive, licensed under CC BY 3.0.

**V sign of dermatomyositis**
This photograph of the anterior chest and neck shows a large, irregular shaped area of erythema with petechiae on the right breast.
The shown features are termed “V sign” and is a characteristic cutaneous finding of dermatomyositis.

Source: “Figure 6, in: Paraneoplastic Dermatoses: A Brief General Review and an Extensive Analysis of Paraneoplastic Pemphigus and Paraneoplastic Dermatomyositis” by Didona D, Fania L, Didona B, Eming R, Hertl M, Di Zenzo G, International Journal of Molecular Sciences Online Journal; eScholarship, licensed under CC BY 4.0. Modifications: image has been cropped.

**Calcinosis cutis**
Photograph of the palmar aspect of the fingertips of a patient
A multinodular white lesion with superficial ulceration is visible at the fingertip of the index finger.
A yellowish-white plaque can be seen over the pulp of the middle finger.
These features are characteristic of calcinosis cutis, a subcutaneous calcium deposit seen in various connective tissue diseases (CREST, dermatomyositis, and SLE), hypercalcemic conditions (e.g., hyperparathyroidism, paraneoplastic syndromes), and secondary to trauma.

Source: Courtesy of Dr. Gary M. White, MD

**Cutaneous manifestations of dermatomyositis**
A series of photographs of a 4-year-old with dermatomyositis
A: Edema with hyperpigmentation can be seen above the upper eyelids (heliotrope rash).
B: An ecthyma‐like ulcer can be seen on the left shoulder as well as nonscarring alopecia on the scalp.
C: A hyperpigmented rash can be seen on the neck.
D: Calcified papules and nodules appear around the knee, some of which are expelling calcified material (calcinosis cutis).
E: Small flat‐topped papules are located over the extensor aspects of the proximal and distal interphalangeal joints (possible early manifestation of Gottron papules).
These findings are typical of dermatomyositis.

Source: “Figure 1, in: Juvenile dermatomyositis in a 4‐year‐old Kenyan girl” by Marlous L. Grijsen, Deborah Mchaile, Inge Geut et al, Wiley Online Library, licensed under CC BY 4.0.

**Polymyositis and dermatomyositis fact sheet**
© AMBOSS

Diagnosis

General principles [2][18]

There are different sets of diagnostic criteria for IIM; (e.g., the 2017 EULAR/ACR criteria) but none are universally accepted. [19]
Diagnosis is made based on the presence of characteristic clinical features and diagnostic studies.
[6]

Suspect IIM in patients with classic clinical features and elevated levels of muscle enzymes.

Confirm the diagnosis with muscle biopsy.

Patients with DM, PM, and IMNM: Arrange cancer screening at the time of diagnosis.
The Peter and Bohan criteria are still widely referenced but have significant limitations. The criteria are as follows:
[20][21]

DM: characteristic skin findings and ≥ 3 additional features

Symmetric proximal muscle weakness

Elevated muscle enzymes

Electromyogram (EMG) suggestive of inflammatory myopathy

Evidence of myositis on muscle biopsy

PM: all four of the above features in the absence of skin involvement

Laboratory studies [3][22]

Routine

CBC: may show leukocytosis [23]
ESR and CRP: normal or mildly elevated
↑ Muscle enzymes
[24]
- ↑ CK
  
  Typically elevated 2–100 times the normal value [9]
  
  May be normal in IBM and in 20–30% of DM cases
  
  Levels do not correlate with symptom severity.
- Liver chemistries: ↑ AST, ↑ ALT [6]
- ↑ LDH
- ↑ Aldolase
- ↑ Myoglobin
Exclusion of differential diagnoses
- Serum electrolytes (BMP and magnesium): to rule out electrolyte disturbances causing muscle weakness
- TSH: to rule out myopathy secondary to hypothyroidism

Antibodies

The choice of antibody tests depends on the type of inflammatory myopathy under investigation and whether other connective tissue disorders are suspected. Consult rheumatology prior to ordering.

Antinuclear antibodies (ANAs)

ANA: sensitive for autoimmune processes; but still negative in > ⅓ of IIM cases

Depending on symptoms, consider specific ANAs to rule out myopathy due to other connective tissue disorders.
Myositis-specific antibodies (MSAs): The choice of test depends on the suspected underlying condition. [2]

Condition-specific antibody testing in IIM
Dermatomyositis	First-line test: anti-Mi-2 antibodies (helicase): present in 7–30% of patients with DM [16] Consider also requesting anti-NXP-2, anti-TIF-1, anti-SAE, and anti-MDA-5 antibodies.
Antisynthetase syndrome	First-line test: antisynthetase antibodies, e.g., anti-Jo-1 antibodies (histidyl-tRNA synthetase) Typically associated with interstitial lung disease Present in up to 20% of IIM patients [3][22] Consider also requesting anti-PL-7, anti-PL-12 antibodies.
Immune-mediated necrotizing myopathy (severe form)	First-line test: anti-signal recognition particle antibodies (anti-SRP) Present in 5–10% of IIM patients May also be seen in DM [25] Consider also requesting anti-HMGCR antibodies.

Other procedures [2][22]

Muscle biopsy: Gold standard for diagnosis of IIM ; [22]

Perform on a muscle that is clinically affected but not wasted (MRI can be used to help select a site). [26]

Typical findings [6]

Muscle fiber damage

Necrosis, degeneration, and regeneration

IBM: rimmed vacuoles within muscle fibers

Inflammatory cellular infiltrates (except in IMNM)

DM: antibody-mediated inflammatory infiltrates that predominantly involve CD4+ T cells, plasmacytoid dendritic cells, and B lymphocytes in the perimysium (the connective tissue surrounding the fascicle); can lead to perifascicular atrophy

IBM and PM: cell-mediated inflammatory infiltrates that predominantly involve cytotoxic CD8+ T cells in the endomysium (the connective tissue surrounding each muscle fiber)

Immunohistochemistry in PM and IBM: overexpression of MHC-I on the sarcolemma
Electromyography:
irritable myopathic pattern in all forms of IIM

Characteristic of myopathy

Can help distinguish between myopathic and neuropathic processes

Include myopathic motor unit action potentials (polyphasic and of short duration and low amplitude), an increase in spontaneous activity (e.g., fibrillations, positive sharp waves), and early recruitment

Dermatomyositis Inclusion body myositis Structure of skeletal muscle

Evaluation for extramuscular features [3][22]

Evaluation for lung disease: baseline chest x-ray and pulmonary function tests
Malignancy
workup in patients with DM, PM, and
IMNM [22][27][28]

Standard age-appropriate cancer screenings, including: [3]

Breast, pelvic, and prostate exams

Mammography

Colonoscopy

Additional evaluation should be performed after consultation with rheumatology.

All patients diagnosed with DM, PM, and IMNM should be tested for malignancies.

**Dermatomyositis**
MRI thigh (T2-weighted with fat suppression, STIR sequence; axial plane)
A hyperintense signal, indicating inflammation (green overlay), is present in the quadriceps femoris group anteriorly and semitendinosus muscle posteriorly.

Source: © IMPP

**Inclusion body myositis**
Photomicrograph of a biopsy sample of striated muscle tissue
Vacuoles (dotted white outlines) are present within the muscle fibers. The fibers vary in size, from smaller atrophic (green overlay) to larger hypertrophic (yellow overlay).
There is an abundance of inflammatory cells between the fibers.
These are typical histological findings in inclusion body myositis.

Source: “Figure 10, in: Idiopathic Inflammatory Myopathies: Clinical Approach and Management” by Asma Malik, Ghazala Hayat, Junaid S. Kalia, Miguel A. Guzman, Frontiers in Neurology, licensed under CC BY 4.0. Modifications: image cropped and labels removed. The supplementary image with overlays of relevant areas was adapted from the image mentioned above (© AMBOSS).

**Structure of skeletal muscle**
© AMBOSS

Differential diagnoses

Differential diagnosis of myopathy [29]
		Features	ESR	CK	Muscle biopsy findings
Inflammatory myopathies	Dermatomyositis	Peak incidence: 5–10 years and ∼ 50 years ♀ > ♂ Proximal and symmetrical muscle weakness (esp. pelvic and shoulder girdle) Weakness progresses within weeks to months. Skin involvement: heliotrope rash, Gottron papules Associated with malignancies	↑	↑↑	Autoantibody-mediated Perimysial and perivascular inflammation Muscle atrophy
	Polymyositis	Peak incidence: > 20 years ♀ > ♂ Proximal and symmetrical muscle weakness (especially of the pelvic girdle and shoulder girdle) Weakness progresses within weeks to months. No skin involvement	↑	↑↑	Intrafascicular infiltration of CD8+ T cells Endomysial inflammation Muscle atrophy (late finding in chronic disease)
	Inclusion body myositis	Peak incidence: > 50 years ♂ > ♀ Proximal and distal, asymmetrical muscle involvement Weakness progresses slowly over years. No skin involvement	↑	Normal or mildly ↑	Endomysial inflammation Intramuscular vacuoles resembling inclusion bodies of aggregated proteins Muscle atrophy
Polymyalgia rheumatica		Affects mainly older women Fatigue and malaise Often rapid-onset: symmetric pain in the shoulder, pelvic girdle, and neck (proximal muscles) Morning stiffness (> 45 min) Associated with giant cell arteritis	↑↑	Normal	Temporal artery biopsy if giant cell arteritis is suspected
Fibromyalgia		Peak incidence: 20–50 years Tender points over multiple areas of the body with no signs of inflammation Chronic fatigue, sleep disturbances Morning stiffness	Normal		Not helpful in establishing diagnosis
Hypothyroid myopathy		Muscle stiffness Proximal muscle weakness affecting both sides of the body Myoedema: localized painless muscle contraction induced by light muscle percussion or pressure that is visible as a palpable muscle swelling Exercise intolerance Symptoms of hypothyroidism	Normal	↑–↑↑	Not helpful in establishing diagnosis
Drug-induced myopathies	Corticosteroid-induced myopathy	History of glucocorticoid intake Insidious-onset proximal muscle weakness of upper and lower limbs Adverse effects of glucocorticoid therapy	Normal	↑ in approx. 50% of cases	Not helpful in establishing diagnosis
	Statin-induced myopathy [30]	History of statin intake Muscle pain and weakness Fatigue	Normal	↑	Not helpful in establishing diagnosis
	Zidovudine-induced myopathy [31]	History of zidovudine intake Fatigue Muscle pain and weakness that improves after discontinuing drug therapy	Normal	↑	Varying degrees of mitochondrial disorganization Presence of ragged red fibers
	Alcohol-induced myopathy [32]	Acute alcohol-induced myopathy Recent history of consuming large quantities of alcohol in a short period of time Proximal muscle pain and weakness Possibly rhabdomyolysis, acute kidney injury	No information available	↑	Not helpful in establishing diagnosis
	Alcohol-induced myopathy [32]	Chronic alcohol-induced myopathy History of long-standing alcohol use Proximal muscle weakness	No information available	Normal, ↑, or mildly ↑	Not helpful in establishing diagnosis
	Cocaine-induced myopathy [33]	History of cocaine use Muscle pain Proximal muscle weakness, predominantly of the lower extremities Other symptoms: delirium, chest pain, fever, hypotension Possibly massive rhabdomyolysis	Normal	↑–↑↑↑	Not helpful in establishing diagnosis

Further differential diagnoses
- SLE
- Acute myopathy
- ALS
- Myasthenia gravis
- Muscular dystrophy

The differential diagnoses listed here are not exhaustive.

Treatment

Approach [2][3][22]

Refer to a rheumatologist experienced in the management of IIM.
All patients: Start supportive therapies (physical, occupational, and/or speech therapy, as appropriate) as soon as possible.
Patients with any form of IIM except IBM: Start pharmacological therapy.
Advise patients with cutaneous manifestations to use photoprotective measures.
Educate patients on the possible increased risk of malignancy and the importance of attending screenings.

Pharmacologic therapy

Initial treatment [2][16]

First-line: glucocorticoids

Prednisone [2][16]

In severe disease or with multisystem involvement, consider an initial short course of pulsed IV methylprednisolone.
AND (usually) a
steroid-sparing
immunosuppressive agent, e.g.: ; [16]

Methotrexate

Azathioprine

Subsequent treatment [2][6]

Depending on the clinical presentation, additional medications may need to be added to the initial treatment regimen.

Severe or refractory disease
- Intravenous immunoglobulins [34]
- AND/OR rituximab
Dysphagia: intravenous immunoglobulins
Rapidly progressive ILD: Consider plasmapheresis.

Complications

Respiratory failure
Myocarditis
Esophageal disease
Dystrophic calcinosis (common in juvenile dermatomyositis): Calcium deposits may be subcutaneous, intracutaneous, or intramuscular.

We list the most important complications. The selection is not exhaustive.

External Resources

References

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