Hubbry Logo
MyositisMyositisMain
Open search
Myositis
Community hub
Myositis
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Myositis
Myositis
Myositis
View on Wikipedia
from Wikipedia
Myositis
A muscle biopsy from someone who is diagnosed with[clarification needed][further explanation needed] myositis.
SpecialtyRheumatology
ComplicationsAmplified musculoskeletal pain syndrome[1]
CausesAutoimmunity, idiopathic, adverse drug reaction

Myositis is a rarely-encountered medical condition characterized by inflammation affecting the muscles.[2] The manifestations of this condition may include skin issues, muscle weakness, and the potential involvement of other organs.[3] Additionally, systemic symptoms like weight loss, fatigue, and low-grade fever can manifest in individuals with myositis.

Causes

[edit]

Myositis can arise from various causes, including injury, certain medications, infections, inherited muscle disorders, or autoimmune conditions. In some instances, the origins of myositis remain idiopathic, without a discernible cause.

Diagnosis

[edit]

There are various tools that can be used to help diagnose myositis. The most common methods are physical examination, electromyography (EMG), magnetic resonance imaging (MRI), muscle biopsy, and blood tests. The first course of action a doctor will likely take is perform a physical exam.[2] The doctor assesses for muscle weakness or rashes.

Another possible test is electromyography. This test involves the insertion of small needles into the patient's muscles.[4] This allows a physician to look at the muscles' responses to various electrical nerve stimuli and evaluate which muscles potentially have myositis.[4] Magnetic resonance imaging can be useful in diagnosis,[9] allowing painless, non-invasive visualisation of any muscle wastage.[4]

Muscle biopsies, however, are the most reliable tests for diagnosing myositis.[4]

There are also a variety of blood tests available that help in the diagnosis of myositis. The doctor may look for an elevation of creatine kinase in the blood, which is indicative of muscle inflammation.[4] Certain autoantibodies (antibodies that target muscle cells) can also be found in the blood, which can indicate that myositis is caused by an autoimmune disease.[3] Some specific examples of autoantibodies are Anti-Jo-1, Anti-HMGCR, Anti-TIF1, etc.[3]

Treatment

[edit]

Treatment for myositis depends on the underlying cause.[4] For myositis, which is caused by a viral infection, no treatment is typically needed.[4] For myositis caused by a bacterial infection, antibiotics can be used.[4] For myositis caused by a medication, it is important to stop using that medication.[4]

There are a variety of treatment options available if myositis is caused by an autoimmune disease. Glucocorticoids are often the first choice for treatment.[10] This drug works to weaken the immune system so that it is not able to attack the muscles. It is a type of steroid and can cause a wide array of side effects, such as mood changes, increased hunger, trouble sleeping, etc. Another treatment option is a steroid-sparing immunosuppressive agent.[10] This also works to weaken the immune system but does not cause the side effects that steroids do. Another treatment option is a class of drugs called biologics.[10] Also, intravenous immunoglobulins (IVIg) have been shown to be effective in the treatment of myositis caused by an autoimmune disease.[11]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Myositis

View on Grokipedia
from Grokipedia
Myositis is a group of rare, chronic inflammatory diseases affecting the skeletal muscles, characterized by immune-mediated damage that leads to , pain, and fatigue. These conditions, collectively known as idiopathic inflammatory myopathies, primarily involve the proximal muscles (those closest to the , such as shoulders and hips), impairing everyday activities like climbing stairs, rising from a chair, or lifting objects. The most common types include , which causes symmetric without skin involvement; , distinguished by accompanied by distinctive skin rashes (such as on the face, eyelids, knuckles, or chest); , a progressive form often affecting older adults with asymmetric weakness and ; and immune-mediated necrotizing myopathy, featuring severe muscle damage with minimal . Juvenile variants, like , can occur in children. The underlying causes of myositis are multifactorial and not fully understood, but most cases are autoimmune, where the mistakenly targets muscle fibers and associated tissues, leading to and degeneration. Secondary forms may result from infections (e.g., viral triggers like or ), certain medications (such as statins or inhibitors), malignancies (with sometimes paraneoplastic), or other rheumatologic conditions like . Symptoms often develop gradually over weeks to months and can include , low-grade fever, joint pain, weight loss, and in some cases, involvement of other organs such as the lungs (), heart, or esophagus (). may present with photosensitive rashes resembling Gottron's papules or heliotrope rash. typically requires a combination of clinical evaluation, elevated muscle enzyme levels (e.g., ), , MRI imaging, and often a muscle to confirm and rule out mimics like . Treatment focuses on suppressing the and managing symptoms, with high-dose corticosteroids (e.g., ) as first-line therapy to reduce inflammation, often combined with immunosuppressive agents like , , or rituximab for steroid-sparing effects. is essential to maintain muscle function and prevent , while intravenous immunoglobulin may be used for refractory cases, particularly in . varies by type and timeliness of intervention; and often respond well to treatment, potentially achieving remission, whereas is notoriously resistant and progressive, leading to significant disability over time. Early diagnosis and multidisciplinary care involving rheumatologists, neurologists, and pulmonologists are crucial for optimizing outcomes and addressing complications like or increased malignancy risk.

Overview

Definition

Myositis encompasses a heterogeneous group of disorders characterized by chronic inflammation of the skeletal muscles, resulting in progressive muscle weakness and pain, with potential systemic involvement affecting organs such as the lungs, heart, and skin. These conditions are primarily autoimmune in nature, though infectious, toxic, or paraneoplastic etiologies can also contribute, distinguishing myositis as an inflammatory myopathy rather than a purely degenerative process. Major subtypes include dermatomyositis, polymyositis, and inclusion body myositis, each sharing the core feature of muscle inflammation but varying in clinical presentation and organ involvement. The term myositis was first introduced in the 19th century, with Leberecht Wagner providing one of the earliest detailed descriptions in 1863, coining "" to denote affecting multiple muscles. This marked the initial recognition of these rare conditions as distinct from other muscle disorders, paving the way for subsequent classifications in the mid-20th century that refined subtypes based on histopathological and clinical criteria. Myositis is differentiated from broader myopathies, which refer to any disease impairing muscle structure or function without a predominant inflammatory component, such as metabolic or toxic myopathies. In contrast to —an acute syndrome involving rapid skeletal muscle necrosis and release of into the bloodstream, often triggered by trauma, exertion, or drugs—myositis typically follows a subacute or chronic course driven by immune-mediated damage rather than immediate cell lysis. The idiopathic inflammatory myopathies, the most common form of myositis, have an estimated incidence of 0.2–2 cases per 100,000 person-years and a of 2–25 per 100,000 individuals, with higher rates in women (female-to-male ratio approximately 2:1) and peak onset in adults over 40 years. These figures underscore the rarity of the condition, though geographic and methodological variations in studies influence reported estimates.

Epidemiology

Myositis, encompassing idiopathic inflammatory myopathies (IIM) such as , , and , is a rare group of disorders with global incidence rates estimated at 2-11 cases per million person-years. These rates vary by subtype and region, with DM incidence ranging from 1 to 15 per million and overall IIM incidence reported as high as 11 per million in population-based studies from . Recent estimates as of 2022 indicate up to 32.2 per 100,000 in some populations. Higher incidence is observed in , including , where point for IBM is notably elevated—up to seven times higher than earlier European estimates—and relative of DM increases with . Demographically, myositis exhibits a 2:1 female-to-male ratio across most subtypes, though IBM shows a reversal with males affected approximately twice as often as females. The peak age of onset is typically 40-60 years for DM and PM, while IBM predominantly affects individuals over 50 years, making it the most common in older adults. Prevalence estimates reflect this age skew, with IIM rates reaching 13.93 per 100,000 overall and up to 18.20 per 100,000 among those aged 50 and older for IBM. Key risk factors include genetic predispositions, such as the HLA 8.1 ancestral haplotype, which is the strongest associated genetic factor for major IIM phenotypes, and HLA-DR3 alleles particularly linked to DM. Environmental triggers encompass ultraviolet radiation exposure, , certain pollutants, medications like statins, and . Myositis also shows significant overlap with other autoimmune diseases, with 20-30% of systemic sclerosis patients developing myositis . Geographic variations extend beyond Northern Europe, with underdiagnosis prevalent in developing regions due to limited diagnostic infrastructure and awareness, potentially skewing global prevalence data lower in and . In the United States, prevalence differs by region, with higher rates in the Northeast possibly reflecting denser population interactions and access to care.

Clinical Presentation

Signs and Symptoms

The hallmark symptom of myositis is typically symmetric proximal in most forms, such as and , though asymmetric in ; it develops gradually over weeks to months and affects muscles closest to the trunk, such as those in the shoulders, hips, and thighs. In , weakness is often asymmetric and may involve distal muscles, such as finger flexors. Patients often experience difficulty rising from a seated position, climbing stairs, combing their hair, or lifting objects overhead due to weakness in the deltoids, hip flexors, and . This weakness can lead to frequent tripping or falling, particularly in the lower extremities. Muscle pain, or , occurs in approximately 60-90% of cases, often described as aching or soreness that worsens with activity, alongside profound and unintentional . Systemic symptoms may include low-grade fever and, in , affecting about 30% of patients due to involvement of pharyngeal and esophageal muscles. Respiratory can manifest as or dyspnea on exertion. In , a subset of myositis, characteristic skin manifestations accompany muscle symptoms, distinguishing it from other forms. The heliotrope rash appears as a violaceous or dusky red discoloration on the upper eyelids, often with periorbital , giving a purplish hue (as depicted in clinical images from references). Gottron's papules present as erythematous, scaly plaques over the knuckles and extensor surfaces of the fingers, elbows, and knees, resembling psoriatic changes but with a violaceous tint. The sign is a poikilodermatous rash—featuring redness, scaling, and pigmentation changes—distributed across the upper back, shoulders, and posterior neck, resembling a shawl draped over the body (illustrated in atlases). These cutaneous features are unique to and absent in pure , which lacks any rash.

Complications

Myositis can lead to several serious complications that impact multiple organ systems and overall quality of life. One of the most common is interstitial lung disease (ILD), which affects approximately 20-40% of patients with idiopathic inflammatory myopathies, with a higher prevalence in those with antisynthetase syndrome where ILD occurs in up to 90% of cases. ILD often presents with progressive dyspnea and dry cough, potentially leading to pulmonary fibrosis and respiratory failure if untreated. Cardiac involvement is another significant complication, occurring in 10-30% of myositis patients and manifesting as , conduction abnormalities, or . These issues can result in arrhythmias, , or sudden cardiac death, particularly in and subtypes. Adult is associated with an increased risk of 15-25%, with cancers such as ovarian, lung, and gastrointestinal tumors being most frequent. This paraneoplastic association necessitates enhanced protocols, including age-appropriate tests plus computed of the chest, , and for high-risk patients, as recommended by international guidelines. Functional impairments arise from chronic muscle inflammation and damage, leading to disability through , joint contractures, and complications from such as . In long-term follow-up of juvenile myositis, up to 63% of patients may develop joint contractures and 49% experience , contributing to reduced mobility and independence. Rare but notable complications include , particularly in where it affects up to 40% of cases and can cause painful subcutaneous deposits, skin ulceration, and further joint immobility.

Classification

Autoimmune Myositides

Autoimmune myositides, also known as idiopathic inflammatory myopathies (IIMs), represent a group of rare systemic autoimmune disorders characterized by chronic muscle inflammation leading to progressive weakness, primarily affecting skeletal muscles but often involving other organs such as the skin, lungs, and joints. These conditions are distinguished from other forms of myositis by their idiopathic nature and immune-mediated , with traditionally relying on clinical, serological, and histopathological features. The major subtypes include , , , immune-mediated necrotizing myopathy, overlap syndromes, and juvenile myositis, each with unique diagnostic criteria and phenotypic expressions. While early systems like the Bohan and Peter criteria from 1975 have been foundational, more recent frameworks such as the 2017 European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) criteria incorporate myositis-specific autoantibodies and improve specificity. Dermatomyositis (DM) is defined by the combination of proximal symmetric muscle weakness and distinctive cutaneous manifestations, such as the heliotrope rash (violaceous periorbital edema) and Gottron's papules (erythematous scaly plaques over the knuckles). Muscle involvement typically presents with fatigue and weakness in the shoulders, hips, and neck, often confirmed by elevated serum muscle enzymes, electromyography (EMG) abnormalities, and muscle biopsy showing perivascular inflammation. A key subtype is amyopathic dermatomyositis (also called clinically amyopathic DM), where characteristic skin lesions persist for at least six months without clinical evidence of muscle weakness or only minimal subclinical muscle involvement on testing. This variant accounts for approximately 20% of DM cases and is associated with specific autoantibodies like anti-MDA5, highlighting the spectrum from skin-predominant to full myopathic disease. Polymyositis (PM) is characterized by pure muscle inflammation without cutaneous involvement, featuring insidious onset of symmetric proximal that impairs activities like rising from a or combing , typically in adults over 40 years. Diagnostic features include elevated levels, myopathic changes on EMG, and muscle revealing endomysial inflammation with + T-cell invasion of non-necrotic fibers. PM frequently overlaps with other connective tissue diseases (CTDs), such as systemic lupus erythematosus or Sjögren's syndrome, in up to 30% of cases, where myositis-specific autoantibodies like anti-Ku may be present, complicating classification and requiring evaluation for extramuscular manifestations. Immune-mediated necrotizing (IMNM) is characterized by severe muscle fiber with minimal lymphocytic infiltration on , leading to profound proximal and markedly elevated levels, often exceeding 10 times the upper limit of normal. It typically affects adults and is associated with autoantibodies such as anti-signal recognition particle (SRP) or anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the latter linked to exposure. Unlike other IIMs, IMNM shows little to no or regeneration on , and it responds partially to but may require aggressive therapy including intravenous immunoglobulin. Inclusion body myositis (IBM) is the most common acquired in individuals over age 50, distinguished by its slowly progressive course affecting both proximal and distal muscles, particularly the finger flexors, wrist flexors, and , leading to early functional impairment like difficulty gripping or walking. Unlike other autoimmune myositides, IBM shows mixed degenerative and inflammatory pathology on muscle , including rimmed vacuoles, congophilic inclusions, and filamentous inclusions resembling those in neurodegenerative diseases. It is notably resistant to immunosuppressive therapies, with progression continuing despite treatment, emphasizing the need for early to differentiate it from treatable forms like PM. Overlap syndromes occur when myositis coexists with features of other CTDs, such as (systemic sclerosis) or , fulfilling diagnostic criteria for at least two autoimmune conditions and often involving multisystem involvement like Raynaud's phenomenon or . A prominent subset is the antisynthetase syndrome, defined by the presence of antisynthetase autoantibodies (most commonly anti-Jo-1 against histidyl-tRNA synthetase, found in 20-30% of PM/DM cases), accompanied by myositis, non-erosive arthritis, mechanic's hands (hyperkeratotic skin on palms), fever, and rapidly progressive . These syndromes are distinguished by their serological profiles and require integrated assessment to avoid misclassification as isolated myositis. Juvenile myositis primarily refers to (JDM), with onset before age 18 years (peak at 5-10 years), presenting with similar features to adult DM but a higher propensity for (subcutaneous calcium deposits in up to 30% of cases), , and gastrointestinal involvement. Juvenile is rarer and lacks skin findings. Classification often adapts the Bohan and Peter criteria, which for definite JDM require the characteristic plus three of four additional criteria: progressive proximal symmetric weakness, elevated muscle enzymes, abnormal EMG, and compatible muscle . These criteria provide a structured approach but have limitations in pediatric populations, where autoantibodies like anti-NXP2 correlate with increased risk. The Bohan and Peter criteria, established in 1975, remain a reference for classifying autoimmune myositides despite their outdated status. For , definite diagnosis requires all four criteria (symmetric proximal weakness, elevated enzymes, abnormal EMG, positive biopsy), probable requires three, and possible requires two. adds the fifth criterion of characteristic skin rash, with definite requiring the rash plus three others. These have been largely superseded by EULAR/ACR criteria for greater accuracy in incorporating modern diagnostics like autoantibodies.

Infectious and Toxic Myositides

Infectious and toxic myositides encompass a diverse group of inflammatory muscle conditions triggered by microbial pathogens or exogenous agents, distinct from the chronic, immune-mediated idiopathic forms. These entities often present with acute muscle , , or formation, and their identification is crucial for targeted antimicrobial or supportive therapies that can lead to resolution. Unlike autoimmune myositides, which tend to be insidious and symmetric, infectious and toxic variants frequently involve identifiable causative agents and respond to etiology-specific interventions. Viral infections represent a common cause of acute myositis, particularly in otherwise healthy individuals. viruses A and B frequently induce , characterized by sudden calf pain and difficulty walking, often following a respiratory illness, with elevated levels and potential in severe cases. Human immunodeficiency virus () can cause a with proximal weakness and elevated enzymes, manifesting early in infection or later due to direct viral effects or opportunistic complications. Coxsackieviruses, especially types A9 and B5, lead to focal myositis with muscle necrosis, sometimes mimicking but resolving with supportive care. Bacterial infections typically result in , a suppurative process often due to hematogenous spread of , leading to intramuscular , particularly in tropical regions or immunocompromised hosts. This condition presents with localized pain, swelling, and fever, progressing through stages of invasive infection to abscess formation if untreated, with risk factors including trauma, , or . Parasitic agents cause myositis through larval invasion or tissue cysts, often in endemic areas or with undercooked meat consumption. Trichinellosis, from Trichinella species, induces systemic symptoms including fever, myalgia, periorbital edema, and marked eosinophilia due to migrating larvae encysting in skeletal muscle, typically 2-8 weeks post-exposure. Toxoplasmosis, caused by Toxoplasma gondii, manifests as polymyositis or disseminated muscle involvement primarily in immunocompromised patients, such as those with AIDS, featuring weakness, elevated enzymes, and potential myocarditis. Drug-induced myositides arise as adverse reactions to medications, often involving immune or direct toxic effects on muscle fibers. Statins, such as simvastatin, can trigger immune-mediated necrotizing , characterized by severe proximal weakness, high levels, and persistent symptoms even after discontinuation, due to autoantibodies against . Immune checkpoint inhibitors like , used in , provoke myositis in up to 20% of cases, often overlapping with or , presenting as subacute weakness shortly after initiation. Toxic exposures contribute to myositis through metabolic disruption and muscle breakdown. Chronic leads to acute alcoholic myopathy, manifesting as with dark urine, severe pain, and , exacerbated by and immobility. Carbon monoxide poisoning induces via hypoxia and direct myotoxicity, particularly in enclosed-space exposures, resulting in elevated and potential . Clinically, infectious and toxic myositides often feature acute onset with focal or asymmetric involvement, fever, and , contrasting with the symmetric, insidious progression of autoimmune counterparts. Diagnosis relies on history, for abscesses, , or , and treatment focuses on addressing the underlying cause—antibiotics and drainage for bacterial , antiparasitics like for trichinellosis, discontinuation and for drug-induced cases, or supportive hydration for toxic —leading to resolution in most instances without chronic sequelae.

Other Forms

Paraneoplastic myositis represents a subset of inflammatory myopathies triggered by an underlying , most commonly observed in adults over 50 years of age, where the muscle serves as a remote effect of the tumor rather than direct invasion. This condition frequently manifests with proximal , elevated muscle enzymes, and skin findings akin to , with a notably higher cancer association in (up to 25-30% of cases) compared to . Common associated include ovarian, lung, and gastrointestinal cancers, and the myositis often precedes or coincides with tumor detection; treatment of the underlying typically leads to resolution of muscular symptoms, though persistent can occur post-tumor therapy. requires thorough malignancy screening, including and tumor markers, as paraneoplastic myositis may not respond well to standard immunosuppressive therapies alone. Metabolic myositides encompass muscle disorders mimicking due to endocrine or iatrogenic disruptions, distinct from primary autoimmune processes. Hypothyroid myopathy, affecting 30-80% of patients with , presents with proximal weakness, muscle cramps, and elevated levels, often resolving with hormone replacement therapy. Pathologically, it features type II fiber without significant , though rare cases overlap with autoimmune myositis, complicating differentiation. Steroid-induced myopathy, a common iatrogenic complication of chronic use (doses >10 mg/day equivalent), preferentially affects type II muscle fibers, leading to insidious proximal weakness and without rash or . This condition arises from glucocorticoid-mediated and mitochondrial dysfunction, and management involves dose minimization or switching to alternative agents, with recovery possible upon discontinuation. Orbital myositis involves isolated inflammation of the extraocular muscles, presenting with acute-onset pain on eye movement, proptosis, diplopia, and eyelid swelling, often affecting a single muscle group and mimicking infectious or neoplastic processes. While many cases are idiopathic and respond rapidly to corticosteroids, a significant proportion—up to 20-30% in some series—is linked to IgG4-related disease, characterized by IgG4-positive plasma cell infiltration, fibrosis, and elevated serum IgG4 levels. In IgG4-related orbital myositis, bilateral involvement and association with lacrimal gland or salivary enlargement are common, with biopsy confirming storiform fibrosis and obliterative phlebitis; rituximab or systemic steroids provide effective control, distinguishing it from typical idiopathic forms. Focal myositis is a rare, benign inflammatory pseudotumor confined to a single , most frequently involving the lower extremities such as the calf or , and typically presenting as a rapidly enlarging, painful mass without systemic symptoms. Histologically, it shows localized lymphocytic and histiocytic infiltration with muscle fiber , but lacks the widespread of ; the condition is self-limiting in over 90% of cases, resolving spontaneously within months, though recurrence occurs in 10-20%. Diagnosis relies on MRI demonstrating muscle and to exclude , with conservative management preferred over unless compressive symptoms arise. Eosinophilic myositis is an uncommon variant marked by eosinophil-predominant infiltration of , often accompanied by peripheral (>1,500 /mm³), and subdivided into focal, diffuse (polymyositis-like), or perimyositis forms based on extent. It may occur idiopathically or as part of hypereosinophilic syndrome (HES), a multisystem disorder with sustained causing organ damage, where muscle involvement presents with myalgias, weakness, and edema, potentially leading to in severe cases. In HES-associated eosinophilic myositis, mediate tissue injury via and release, with treatment targeting eosinophil reduction using corticosteroids, hydroxyurea, or for refractory disease. Prognosis varies, with focal forms often self-resolving, while HES-linked cases require vigilant monitoring for cardiac or pulmonary complications.

Pathophysiology

Immune-Mediated Mechanisms

Idiopathic inflammatory myopathies, commonly known as myositides, are primarily driven by dysregulated autoimmune responses targeting tissue, involving both cellular and humoral components of the . In (PM) and inclusion body myositis (IBM), the pathogenesis centers on T-cell mediated , where CD8+ T cells infiltrate and invade non-necrotic muscle fibers expressing major histocompatibility complex (MHC) class I antigens, leading to direct cytotoxic damage through perforin and granzyme release. These CD8+ T cells, often lacking expression (CD28null), exhibit heightened and contribute to chronic inflammation in endomysial regions. In contrast, (DM) involves predominant , characterized by complement activation and microvascular injury. Autoantibodies bind to endothelial cells in muscle capillaries, activating the membrane attack complex (C5b-9) and causing , perivascular , and ischemia-induced muscle fiber without direct invasion. This process is mediated by CD4+ T cells and B cells, with immunoglobulin deposition along the and vascular walls exacerbating tissue damage. Myositis-specific autoantibodies (MSAs) play a central role in humoral pathogenesis and disease subtyping. Anti-Jo-1 antibodies, targeting histidyl-tRNA synthetase, are present in approximately 20-30% of PM and DM cases and are associated with antisynthetase syndrome, where they promote immune complex formation and predict through enhanced T-cell activation and cytokine release. In DM, anti-Mi-2 antibodies against nuclear target muscle-specific antigens, correlating with complement-mediated capillary destruction and a favorable response to . Anti-TIF1-γ antibodies, directed at transcriptional intermediary factor 1-gamma, drive B-cell responses and are linked to humoral attack on regenerating myofibers in adult DM. Additionally, anti-HMGCR antibodies in statin-associated immune-mediated necrotizing recognize 3-hydroxy-3-methylglutaryl-coenzyme A reductase, inducing antibody-dependent complement activation and macrophage-mediated necrosis independent of prior exposure in some cases. Cytokines amplify these immune processes by recruiting inflammatory cells and promoting muscle damage. Type I interferons (IFN-α and IFN-β), produced by plasmacytoid dendritic cells, upregulate on muscle fibers and sustain chronic inflammation, particularly in DM, while IFN-γ from + T cells enhances and in PM and . Tumor necrosis factor-α (TNF-α), secreted by macrophages and T cells, inhibits myoblast differentiation, induces MHC expression, and directly contributes to fiber via activation. These cytokines form a feedback loop, with IFN-α driving TNF-α production and vice versa, perpetuating endomysial infiltrates. Genetic predisposition influences susceptibility through (HLA) associations. The HLA 8.1 ancestral (HLA-A01, B08:01, DRB103:01, DQA105:01, DQB102:01) confers the strongest risk for antisynthetase and anti-Jo-1 positive myositis, enhancing autoantigen by antigen-presenting cells. HLA-DRB103:01 alleles are linked to juvenile DM and overall myositis risk, while HLA-DRB107 and DQB102 alleles associate with anti-TIF1-γ positive DM, promoting aberrant T- and B-cell responses. These HLA variants likely facilitate molecular mimicry, potentially triggered by environmental factors such as infections. The culmination of these mechanisms results in endomysial , where mononuclear infiltrates surround and invade muscle fibers, causing , by macrophages, and attempted regeneration with basophilic fibers. In PM and IBM, CD8+ T-cell invasion directly perforates , releasing intracellular contents that recruit further immune cells, while in DM, ischemic from leads to perifascicular . This immune assault disrupts myofiber integrity, with upregulated on all fibers amplifying ongoing damage and fibrosis.

Infectious and Metabolic Pathways

Infectious myositis arises from direct pathogen invasion or toxin-mediated damage to tissue. RNA viruses, such as enteroviruses including B3, can replicate within muscle cells, leading to cytopathic effects and focal . This replication occurs in the of myocytes, where viral proteins disrupt cellular integrity, causing myocyte and release of intracellular contents. Bacterial infections contribute through toxin production, as seen in clostridial myonecrosis or caused by . The alpha-toxin, a lecithinase, hydrolyzes phospholipids, leading to pore formation, imbalance, and rapid myocyte death. This results in extensive , gas production from , and systemic due to additional exotoxins like theta-toxin, which impairs vascular integrity. Metabolic derangements induce myositis by disrupting muscle , often culminating in . imbalances, particularly , impair the sodium-potassium pump, causing membrane depolarization, uncontrolled calcium influx, and sustained that exhausts energy stores, leading to and toxic release into the bloodstream. Ischemia from vascular compromise similarly triggers ATP depletion and , exacerbating myocyte damage and . Drug-induced metabolic pathways, such as those involving statins, target inhibition, which depletes intermediates like essential for mitochondrial electron transport. This leads to impaired respiratory chain function, particularly complex III inhibition, increased , and activation of apoptotic cascades in muscle fibers via cytochrome c release and caspase activation. Resolution of infectious and metabolic myositis typically involves clearance or correction of the underlying , allowing host repair mechanisms to predominate. In infectious cases, antimicrobials eradicate or inhibit , while innate immunity—through and cytokine-mediated —facilitates debris removal and tissue regeneration, often resolving symptoms within weeks without persistent damage. Metabolic disruptions resolve upon normalization or drug discontinuation, with supportive hydration preventing complications like renal failure from .

Diagnosis

History and Physical Examination

The history in suspected myositis focuses on eliciting symptoms suggestive of inflammatory muscle disease, particularly a subacute onset of progressive muscle weakness over weeks to months, often affecting activities such as climbing stairs, rising from a chair, or combing hair. Patients may describe associated fatigue, myalgias, or arthralgias, and a detailed inquiry into family history of autoimmune disorders, such as rheumatoid arthritis or systemic lupus erythematosus, is essential to identify potential genetic predispositions. Exposure to potential triggering agents, including medications like statins or immune checkpoint inhibitors, should be explored, as these can precipitate drug-induced myositis. In cases of dermatomyositis, patients often report characteristic skin manifestations, such as a violaceous rash on the eyelids (heliotrope rash) or erythematous papules over the knuckles (Gottron's papules), which may precede or accompany muscle symptoms. The physical examination begins with a systematic assessment of muscle strength, typically using the , which grades power from 0 (no contraction) to 5 (normal strength against full resistance). In myositis, weakness is characteristically symmetrical and predominantly proximal, involving the shoulder and hip girdles more than distal muscles, with neck flexor weakness also common; for instance, patients may struggle to lift their head from a . examination is crucial, particularly for heliotrope rash, Gottron's papules, or shawl sign ( over the shoulders and upper back), which support a of . Pharyngeal involvement may manifest as dysphonia or nasal regurgitation, indicating risk of aspiration. Certain findings raise red flags for specific subtypes, such as asymmetric or distal-predominant weakness, which suggests () rather than classic , or early involvement leading to falls. These clinical features help differentiate myositis from neuropathy, where sensory symptoms and deficits are typically present without the sensory sparing seen in pure myopathies, or from endocrine myopathies like those in , which often lack inflammatory signs such as rash or rapid progression. While the Bohan and Peter criteria (1975) provided a foundational framework for suspecting myositis, requiring symmetrical proximal as a core clinical element plus supportive evidence from other modalities for as definite, probable, or possible disease, current of idiopathic inflammatory myopathies relies on the 2017 European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) criteria. These assign a probability score based on core variables such as , skin manifestations, autoantibodies, and biopsy findings to classify the condition. This initial clinical evaluation guides subsequent laboratory and imaging studies to confirm the .

Laboratory and Imaging Studies

Laboratory evaluation plays a crucial role in supporting the diagnosis of myositis by identifying markers of muscle damage and immune dysregulation. Serum muscle enzymes are typically elevated in active disease, with creatine kinase (CK) levels often rising 5 to 50 times the upper limit of normal, reflecting skeletal muscle breakdown. Aldolase and lactate dehydrogenase (LDH) levels are also commonly increased, while aspartate aminotransferase (AST) and alanine aminotransferase (ALT) may be elevated, sometimes mimicking hepatic involvement. These enzyme abnormalities are nonspecific but help assess disease activity and response to treatment. Autoantibody testing is essential for classifying idiopathic inflammatory myopathies, with myositis-specific autoantibodies (MSAs) such as anti-Jo-1 and myositis-associated antibodies (MAAs) detected via methods like or line blot assays. MSAs are present in 60-80% of idiopathic myositis cases, aiding in subtype identification and prognostic assessment. For instance, anti-Jo-1 is associated with antisynthetase syndrome, featuring and alongside myositis. Inflammatory markers like (ESR) and (CRP) are frequently normal or only mildly elevated in myositis, distinguishing it from other rheumatologic conditions where these are more consistently raised. Elevated ESR or CRP occurs in about 50% of cases and may correlate with extramuscular involvement, but their absence does not exclude active disease. Imaging modalities provide noninvasive visualization of muscle inflammation and guide biopsy site selection. (MRI) is highly sensitive for detecting muscle , appearing as T2-weighted hyperintensity, particularly in proximal muscles during early or active phases. Electromyography (EMG) reveals characteristic abnormalities, including spontaneous fibrillations, positive sharp waves, and polyphasic potentials with early recruitment, supporting an inflammatory myopathic pattern. can identify fascial and perifascial in early disease, offering a bedside tool for assessing muscle involvement, though it is less specific than MRI.

Muscle Biopsy and Definitive Tests

Muscle biopsy serves as the gold standard for confirming the of myositis and distinguishing its subtypes, providing histopathological evidence of muscle and damage. The procedure typically involves either an open surgical , which removes a larger sample under , or a needle using a specialized gun to extract smaller cores, often from the , deltoid, or muscles to target affected areas while minimizing cosmetic impact. It is advisable to avoid strenuous exercise or trauma to the target muscle in the days to weeks immediately preceding the to minimize potential artifactual changes that could mimic . Histopathological examination reveals distinct patterns across myositis subtypes. In dermatomyositis, perifascicular atrophy—characterized by smaller, atrophic fibers at the periphery of muscle fascicles—is a hallmark finding, often accompanied by perivascular and dropout. shows endomysial with CD8+ T-cell infiltrates invading non-necrotic muscle fibers, leading to fiber and regeneration. In , biopsies demonstrate rimmed vacuoles within muscle fibers, congophilic inclusions, and mixed inflammatory infiltrates, alongside degenerative changes like mitochondrial abnormalities. Immunohistochemistry enhances diagnostic specificity by identifying immune cell markers and molecular alterations. Widespread upregulation of class I (MHC-I) on the of muscle fibers is a consistent feature in idiopathic inflammatory myopathies, indicating immune targeting of muscle tissue. In , complement deposition, particularly membrane attack complex (MAC/C5b-9), is observed in intramuscular blood vessels, supporting a humorally mediated vasculopathy. + T cells predominate in perivascular and perimysial areas in , while + T cells are prominent in endomysial regions in and . Electron microscopy provides ultrastructural insights, particularly in , where tubuloreticular inclusions—cylindrical structures within the cisternae of in endothelial cells—are frequently observed and linked to interferon-alpha exposure in the microvascular pathology. Beyond , definitive tests address associated complications to establish . Pulmonary function tests, including forced vital capacity and diffusion capacity for carbon monoxide, confirm in up to 30-50% of myositis cases, guiding subtype classification. In high-risk patients, such as those with or anti-TIF1γ antibodies, screening with computed tomography (CT) or (PET)-CT is essential to detect paraneoplastic associations, as cancer precedes or coincides with myositis in approximately 15-25% of such cases. Laboratory abnormalities like elevated levels offer supportive evidence but require for confirmation.

Management

Pharmacologic Treatments

The primary pharmacologic treatment for myositis involves corticosteroids as first-line therapy to rapidly suppress and improve muscle strength. High-dose , administered orally at 1 mg/kg/day (up to 80 mg daily), is the standard initial regimen for most forms of idiopathic inflammatory myopathies, including (DM), (PM), and immune-mediated necrotizing (IMNM). This dose is typically maintained for 4-6 weeks before gradual tapering over several months, guided by clinical response, muscle enzyme levels, and imaging to minimize relapse. Intravenous pulses (e.g., 1 g/day for 3 days) may be used in severe cases with or respiratory involvement to achieve faster onset. Steroid-sparing immunosuppressants are introduced early, often within 1-3 months, to reduce dependence and long-term toxicity. (15-25 mg/week orally or subcutaneously) or (2-3 mg/kg/day) are commonly used as second-line agents, particularly for PM and DM, with evidence from randomized trials showing improved remission rates when combined with glucocorticoids. For refractory cases, especially in DM with skin or lung involvement, intravenous immunoglobulin (IVIG) at 2 g/kg body weight divided over 2-5 days monthly is recommended, following its FDA approval in 2021 based on phase 3 trials demonstrating significant muscle strength gains. inhibitors like (0.075 mg/kg/day, targeting trough levels of 5-10 ng/mL) are used in , with evidence of efficacy in pediatric populations. Biologic therapies target specific immune pathways in resistant myositis. Rituximab, a B-cell depleting monoclonal antibody (1 g intravenously on days 1 and 15, repeated every 6 months), shows benefit in anti-synthetase syndrome with anti-Jo-1 antibodies, with observational studies reporting response rates up to 70% in refractory PM and DM. Anti-TNF agents like infliximab have limited efficacy and are generally avoided due to risk of exacerbating myositis, as evidenced by case reports of disease flares. For inclusion body myositis (IBM), as of 2025, systematic reviews indicate no effective pharmacologic treatments, as it remains resistant to standard immunosuppressive therapies. Emerging options include Janus kinase (JAK) inhibitors, such as ruxolitinib, under investigation in clinical trials for IBM (e.g., phase 2 trial NCT06536166). Adverse effects are a major consideration in long-term pharmacologic management. Corticosteroids commonly cause (with bisphosphonates recommended for prophylaxis in patients on >7.5 mg/day for >3 months), weight gain, , and , necessitating calcium/ supplementation and bone density monitoring. Immunosuppressants increase risk (e.g., with , requiring prophylaxis in high-risk cases) and hepatotoxicity ( monitoring via TPMT ), while IVIG may lead to headache, , or renal impairment in 5-10% of infusions. Biologics like rituximab carry risks of infusion reactions and late-onset , with overall rates elevated by 20-30% in treated cohorts. Treatment regimens are individualized, with multidisciplinary monitoring to balance efficacy and safety.

Non-Pharmacologic Interventions

Non-pharmacologic interventions play a crucial role in managing myositis by addressing , preventing complications, and improving , often complementing immunosuppressive therapies to optimize outcomes. These strategies focus on rehabilitation, lifestyle adjustments, and supportive measures tailored to the individual's disease subtype and severity. is a cornerstone of care, emphasizing graded exercise programs that begin with low-intensity activities to combat and gradually progress to build strength and endurance. Such programs, typically involving aerobic exercises three times per week alternated with anaerobic sessions, have been shown to safely reduce and enhance muscle performance in adults with myositis without exacerbating inflammation. offers a low-impact alternative, allowing patients to perform strength-building exercises in , which supports weakened limbs, minimizes joint stress, and facilitates balance and . Occupational therapy complements physical efforts by promoting independence in daily activities through the use of adaptive devices, such as reachers or modified utensils, to accommodate proximal . Splinting, particularly for hands or wrists, helps prevent contractures by maintaining alignment and supporting function during periods of active . Nutritional support aids muscle repair and counters treatment-related side effects, with recommendations for a incorporating lean sources like and nuts to support tissue recovery. supplementation, at least 800 international units daily, is advised to mitigate loss associated with long-term use, often combined with calcium intake for optimal absorption. For patients with (ILD), a common complication, respiratory includes pulmonary rehabilitation programs that improve endurance and breathing efficiency through supervised exercises. Supplemental oxygen may be provided as needed to alleviate dyspnea and enhance participation in daily activities. Patient education empowers individuals to manage risks specific to their condition, such as strict sun protection for , involving broad-spectrum (SPF 30 or higher), protective clothing, and avoidance of midday exposure to prevent flares. protocols are emphasized, recommending inactivated against and pneumococcus while avoiding live to reduce risk, particularly in those with compromised immunity.

Monitoring and Follow-Up

Monitoring and follow-up in myositis involve regular evaluation of disease activity, treatment efficacy, and potential complications to guide therapeutic adjustments and prevent long-term damage. Standardized tools from the International Myositis Assessment and Clinical Studies Group (IMACS) are recommended for assessing overall disease activity, including the Myositis Disease Activity Assessment Tool (MYOACT), which uses visual analog scales (VAS) to score involvement across organ systems such as muscle, skin, joints, and lungs based on clinical and laboratory findings. The MYOACT helps quantify reversible inflammatory manifestations and is typically completed by physicians during clinic visits to track changes over time. Routine laboratory monitoring includes serial measurements of (CK) levels every 1-3 months during active treatment to detect flares or response to therapy, as elevations often correlate with muscle inflammation. For patients at elevated risk of malignancy, particularly those with or certain autoantibodies, annual enhanced is advised for the first 3 years following diagnosis, incorporating age- and sex-appropriate tests plus targeted imaging like CT of the chest, , and as per IMACS guidelines. Treatment adjustments are based on these assessments; for example, immunosuppressive doses may be escalated during flares indicated by rising CK or worsening MYOACT scores, while transition to maintenance therapy—such as lower-dose corticosteroids combined with steroid-sparing agents—occurs after 6-12 months of sustained remission to minimize side effects. A multidisciplinary approach enhances follow-up, involving rheumatologists for core management, pulmonologists for interstitial lung disease monitoring via pulmonary function tests, and oncologists for ongoing cancer surveillance in high-risk cases. Patient-reported outcomes are integrated into monitoring using tools like the Health Assessment Questionnaire (HAQ), which evaluates functional status and disability on a 0-3 scale, providing insights into daily impacts and correlating with clinical measures in myositis trials. Regular HAQ assessments, often at 3- to 12-month intervals, help capture subjective improvements or deteriorations not evident in objective tests.

Prognosis

Short-Term Outcomes

In idiopathic inflammatory myopathies (IIMs), initial treatment with high-dose corticosteroids typically results in clinical improvement in many patients with (PM) or (DM) within the first three months, as measured by reductions in muscle weakness and elevated levels. Refractory cases, where symptoms persist despite standard therapy, occur in approximately 20-30% of patients and often necessitate escalation to immunosuppressive agents like or . Type-specific short-term outcomes vary significantly. generally shows faster remission compared to (), with many DM patients achieving partial or complete response to initial steroids within months due to its inflammatory nature. In contrast, is largely refractory to , with minimal to no meaningful response in most patients during the first year. () exhibits favorable early recovery, with 70% of children achieving full or near-full remission on within the initial treatment phase, often within one to two years. Early and prompt initiation of are key factors influencing short-term outcomes, as delays beyond six months from symptom onset correlate with lower response rates and higher risk of persistent . In anti-synthetase , a subset of IIM, there is an elevated short-term risk of (ILD), affecting up to 75% of patients at presentation and contributing to acute respiratory complications. Subtypes like anti-MDA5-positive DM have poorer short-term outcomes, with elevated mortality risk from rapidly progressive ILD. Early complications from treatment, such as steroid-induced or opportunistic infections due to , contribute to approximately 5% mortality in the first year in , particularly in severe cases with or ILD. Overall one-year survival in IIM exceeds 90%, though it is lower in overlap syndromes involving systemic sclerosis or other connective tissue diseases, where rates can drop to around 80-85% due to multi-organ involvement.

Long-Term Considerations

Myositis often follows a chronic course, with approximately 40% of patients with idiopathic inflammatory myopathies (IIMs) able to discontinue glucocorticoids at long-term follow-up (median ~5 years). In contrast, (IBM) exhibits a relentlessly progressive trajectory, typically leading to significant mobility loss; most patients require assistive devices within 5 to 10 years of onset, and become wheelchair-dependent after 10 years. This chronicity underscores the need for sustained management strategies to mitigate disease progression and complications. Disability rates in myositis vary by subtype but are notable, with 30-40% of patients experiencing moderate to severe functional impairment affecting daily activities, particularly in untreated or cases where persists despite intervention. Higher occurs in due to its poor response to standard therapies, resulting in progressive and increased fall risk over time. Quality of life in myositis patients remains compromised long-term, with persistent and reported as major contributors to reduced physical function and mental health burdens. These symptoms often lead to ongoing challenges in productivity and emotional well-being, necessitating psychological support to address relapses, depression, and coping mechanisms. Patient surveys highlight that and exert a profound impact, comparable to in limiting independence. Emerging research focuses on advancing personalized approaches, including trials of CAR-T cell therapies targeting autoimmune pathways in refractory myositis as of 2024, alongside investigations into biomarkers like myositis-specific autoantibodies for tailoring treatments. Studies on safety confirm general tolerability in myositis patients, with low rates of flares and recommendations for to prevent severe . Key gaps persist, particularly in where limited effective therapies highlight the need for targeted interventions, and international registries like EuroMyositis are essential for aggregating data to drive collaborative research and improve outcomes.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK584479/
  2. https://medlineplus.gov/myositis.html
  3. https://my.clevelandclinic.org/health/diseases/24170-myositis
  4. https://www.hss.edu/health-library/conditions-and-treatments/list/myositis
  5. https://www.mayoclinic.org/departments-centers/inflammatory-myositis-clinic/overview/ovc-20477805
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC7538050/
  7. https://www.mayoclinic.org/diseases-conditions/dermatomyositis/symptoms-causes/syc-20353188
  8. https://www.mayoclinic.org/diseases-conditions/polymyositis/diagnosis-treatment/drc-20353212
  9. https://www.ncbi.nlm.nih.gov/medgen/44564
  10. https://pmc.ncbi.nlm.nih.gov/articles/PMC6297649/
  11. https://www.ninds.nih.gov/health-information/disorders/inclusion-body-myositis
  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC10495079/
  13. https://www.nejm.org/doi/abs/10.1056/NEJM197502132920706
  14. https://www.ncbi.nlm.nih.gov/books/NBK448168/
  15. https://www.nature.com/articles/s41584-023-01033-0
  16. https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/1471-2474-13-103
  17. https://academic.oup.com/rheumatology/article/54/1/50/1840053
  18. https://pubmed.ncbi.nlm.nih.gov/28160487/
  19. https://www.sciencedirect.com/science/article/pii/S0049017225002343
  20. https://pubmed.ncbi.nlm.nih.gov/25530508/
  21. https://ard.bmj.com/content/annrheumdis/59/2/141.full.pdf
  22. https://academic.oup.com/rheumatology/article/56/5/802/2970098
  23. https://rarediseases.org/rare-diseases/sporadic-inclusion-body-myositis/
  24. https://www.nature.com/articles/s41598-024-71633-7
  25. https://www.neurology.org/doi/10.1212/WNL.0000000000012004
  26. https://pubmed.ncbi.nlm.nih.gov/29674613/
  27. https://www.rheumatic.theclinics.com/article/S0889-857X%2822%2900047-3/fulltext
  28. https://srjhs.org/scleroderma-dermatomyositis-overlap-syndrome/
  29. https://onlinelibrary.wiley.com/doi/10.1111/1756-185X.70084
  30. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2022.842586/full
  31. https://medlineplus.gov/genetics/condition/idiopathic-inflammatory-myopathy/
  32. https://www.ninds.nih.gov/sites/default/files/2025-05/inflammatory-myopathies.pdf
  33. https://www.myositis.org/about-myositis/types-of-myositis/inclusion-body-myositis/
  34. https://emedicine.medscape.com/article/759487-overview
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC9843184/
  36. https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2019.00739/full
  37. https://www.sciencedirect.com/science/article/abs/pii/S0385814609001059
  38. https://www.mayoclinic.org/diseases-conditions/polymyositis/symptoms-causes/syc-20353208
  39. https://www.ncbi.nlm.nih.gov/books/NBK558917/
  40. https://eyewiki.org/Dermatomyositis
  41. https://www.myositis.org/about-myositis/diagnosis/diagnostic-criteria/diagnostic-criteria-for-dermatomyositis/
  42. https://www.ninds.nih.gov/health-information/disorders/polymyositis
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC3676869/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC5394574/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC11278012/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC10497702/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC10373167/
  48. https://pubmed.ncbi.nlm.nih.gov/21336621/
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC10834225/
  50. https://pmc.ncbi.nlm.nih.gov/articles/PMC10924937/
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC4104537/
  52. https://www.ncbi.nlm.nih.gov/books/NBK6196/
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC6934928/
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC10017873/
  55. https://www.amboss.com/us/knowledge/idiopathic-inflammatory-myopathies/
  56. https://arupconsult.com/content/inflammatory-myopathies
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC5857275/
  58. https://acrjournals.onlinelibrary.wiley.com/doi/10.1002/art.40320
  59. https://radiopaedia.org/articles/amyopathic-dermatomyositis?lang=us
  60. https://www.ccjm.org/content/92/10/627
  61. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2021.783416/full
  62. https://emedicine.medscape.com/article/335925-overview
  63. https://www.myositis.org/about-myositis/complications/overlapping-autoimmune-diseases/
  64. https://www.ncbi.nlm.nih.gov/books/NBK559305/
  65. https://www.uptodate.com/contents/immune-mediated-necrotizing-myopathy
  66. https://www.mda.org/disease/inclusion-body-myositis
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC6277289/
  68. https://my.clevelandclinic.org/health/diseases/15700-inclusion-body-myositis
  69. https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2022.1020113/full
  70. https://bestpractice.bmj.com/topics/en-us/1018
  71. https://www.epocrates.com/online/diseases/1018/overlap-syndromes
  72. https://emedicine.medscape.com/article/1417215-overview
  73. https://www.jrd.or.kr/journal/view.html?doi=10.4078/jrd.2022.29.1.14
  74. https://pmc.ncbi.nlm.nih.gov/articles/PMC10331242/
  75. https://rmdopen.bmj.com/content/3/2/e000507
  76. https://pmc.ncbi.nlm.nih.gov/articles/PMC8412094/
  77. https://pmc.ncbi.nlm.nih.gov/articles/PMC8076669/
  78. https://pmc.ncbi.nlm.nih.gov/articles/PMC2493084/
  79. https://pmc.ncbi.nlm.nih.gov/articles/PMC3043460/
  80. https://pubmed.ncbi.nlm.nih.gov/11265425/
  81. https://pmc.ncbi.nlm.nih.gov/articles/PMC4762789/
  82. https://pmc.ncbi.nlm.nih.gov/articles/PMC11283853/
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC8047863/
  84. https://pubmed.ncbi.nlm.nih.gov/17333082/
  85. https://emedicine.medscape.com/article/1168167-clinical
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC2620635/
  87. https://pmc.ncbi.nlm.nih.gov/articles/PMC4515572/
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC65052/
  89. https://pmc.ncbi.nlm.nih.gov/articles/PMC7282149/
  90. https://www.sciencedirect.com/science/article/pii/S1016731519301952
  91. https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-024-03684-2
  92. https://jhoponline.com/issue-archive/2018-issues/jhop-december-2018-vol-8-no-4/review-of-pd-1-induced-myositis-and-a-case-of-pembrolizumab-induced-myositis-in-a-patient-with-metastatic-melanoma
  93. https://www.medlink.com/articles/alcoholic-myopathy
  94. https://pmc.ncbi.nlm.nih.gov/articles/PMC5513686/
  95. https://pmc.ncbi.nlm.nih.gov/articles/PMC10201226/
  96. https://pmc.ncbi.nlm.nih.gov/articles/PMC5612982/
  97. https://emedicine.medscape.com/article/1168167-treatment
  98. https://journals.asm.org/doi/10.1128/cmr.00001-08
  99. https://pubmed.ncbi.nlm.nih.gov/38494286/
  100. https://pubmed.ncbi.nlm.nih.gov/22075200/
  101. https://pmc.ncbi.nlm.nih.gov/articles/PMC7836281/
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC8604545/
  103. https://www.ncbi.nlm.nih.gov/books/NBK519513/
  104. https://pmc.ncbi.nlm.nih.gov/articles/PMC7364425/
  105. https://www.ncbi.nlm.nih.gov/books/NBK557731/
  106. https://pmc.ncbi.nlm.nih.gov/articles/PMC7711326/
  107. https://pubmed.ncbi.nlm.nih.gov/22018678/
  108. https://pmc.ncbi.nlm.nih.gov/articles/PMC8499436/
  109. https://pmc.ncbi.nlm.nih.gov/articles/PMC3388428/
  110. https://pubmed.ncbi.nlm.nih.gov/27726926/
  111. https://pmc.ncbi.nlm.nih.gov/articles/PMC11537714/
  112. https://pubmed.ncbi.nlm.nih.gov/39468967/
  113. https://pubmed.ncbi.nlm.nih.gov/24424174/
  114. https://pmc.ncbi.nlm.nih.gov/articles/PMC4622906/
  115. https://pmc.ncbi.nlm.nih.gov/articles/PMC6245960/
  116. https://pubmed.ncbi.nlm.nih.gov/9812210/
  117. https://pmc.ncbi.nlm.nih.gov/articles/PMC3674618/
  118. https://pmc.ncbi.nlm.nih.gov/articles/PMC6927901/
  119. https://pmc.ncbi.nlm.nih.gov/articles/PMC11521033/
  120. https://pmc.ncbi.nlm.nih.gov/articles/PMC7388349/
  121. https://pmc.ncbi.nlm.nih.gov/articles/PMC10789353/
  122. https://pmc.ncbi.nlm.nih.gov/articles/PMC12322362/
  123. https://pmc.ncbi.nlm.nih.gov/articles/PMC10075366/
  124. https://pmc.ncbi.nlm.nih.gov/articles/PMC5828023/
  125. https://pmc.ncbi.nlm.nih.gov/articles/PMC4847327/
  126. https://pmc.ncbi.nlm.nih.gov/articles/PMC5836404/
  127. https://pmc.ncbi.nlm.nih.gov/articles/PMC2991777/
  128. https://pmc.ncbi.nlm.nih.gov/articles/PMC8412069/
  129. https://pmc.ncbi.nlm.nih.gov/articles/PMC4238868/
  130. https://pmc.ncbi.nlm.nih.gov/articles/PMC3681571/
  131. https://pmc.ncbi.nlm.nih.gov/articles/PMC4840953/
  132. https://pmc.ncbi.nlm.nih.gov/articles/PMC9178267/
  133. https://pmc.ncbi.nlm.nih.gov/articles/PMC6791565/
  134. https://www.ncbi.nlm.nih.gov/books/NBK563129/
  135. https://www.tandfonline.com/doi/full/10.2217/fmb.15.5
  136. https://academic.oup.com/cid/article/35/Supplement_1/S93/447283
  137. https://pmc.ncbi.nlm.nih.gov/articles/PMC11278868/
  138. https://www.uptodate.com/contents/rhabdomyolysis-clinical-manifestations-and-diagnosis
  139. https://pmc.ncbi.nlm.nih.gov/articles/PMC8061391/
  140. https://www.sciencedirect.com/science/article/pii/S1550413115003939
  141. https://journals.physiology.org/doi/abs/10.1152/ajpcell.00226.2006
  142. https://emedicine.medscape.com/article/335925-clinical
  143. https://pmc.ncbi.nlm.nih.gov/articles/PMC6263305/
  144. https://www.uptodate.com/contents/diagnosis-and-differential-diagnosis-of-dermatomyositis-and-polymyositis-in-adults
  145. https://www.ncbi.nlm.nih.gov/books/NBK436008/
  146. https://emedicine.medscape.com/article/1172746-clinical
  147. https://www.aafp.org/pubs/afp/issues/2020/0115/p95.html
  148. https://www.ncbi.nlm.nih.gov/books/NBK538200/
  149. https://pmc.ncbi.nlm.nih.gov/articles/PMC5736307/
  150. https://emedicine.medscape.com/article/335925-workup
  151. https://pmc.ncbi.nlm.nih.gov/articles/PMC6580360/
  152. https://www.sciencedirect.com/science/article/pii/S1568997219300096
  153. https://www.ncbi.nlm.nih.gov/books/NBK532860/
  154. https://pmc.ncbi.nlm.nih.gov/articles/PMC8412099/
  155. https://pmc.ncbi.nlm.nih.gov/articles/PMC10552815/
  156. https://pmc.ncbi.nlm.nih.gov/articles/PMC8951002/
  157. https://pn.bmj.com/content/20/5/385
  158. https://autoimmunhighlights.biomedcentral.com/articles/10.1007/s13317-014-0062-2
  159. https://pubmed.ncbi.nlm.nih.gov/18696397/
  160. https://www.nature.com/articles/s41584-023-01045-w
  161. https://pmc.ncbi.nlm.nih.gov/articles/PMC11611047/
  162. https://pmc.ncbi.nlm.nih.gov/articles/PMC6950531/
  163. https://pmc.ncbi.nlm.nih.gov/articles/PMC9398208/
  164. https://pmc.ncbi.nlm.nih.gov/articles/PMC12399281/
  165. https://pmc.ncbi.nlm.nih.gov/articles/PMC6299051/
  166. https://pmc.ncbi.nlm.nih.gov/articles/PMC10330909/
  167. https://pmc.ncbi.nlm.nih.gov/articles/PMC11409827/
  168. https://pmc.ncbi.nlm.nih.gov/articles/PMC7955788/
  169. https://pubmed.ncbi.nlm.nih.gov/39843353/
  170. https://clinicaltrials.gov/study/NCT06536166
  171. https://pmc.ncbi.nlm.nih.gov/articles/PMC6299050/
  172. https://www.myositis.org/wp-content/uploads/2018/01/PhysiciansGuide.pdf
  173. https://www.myositis.org/wp-content/uploads/2018/01/Myositis-and-Exercise-Part-1-PT-and-OT-Final.pdf
  174. https://www.the-rheumatologist.org/article/occupational-therapy-can-benefit-rheumatology-patients/
  175. https://pmc.ncbi.nlm.nih.gov/articles/PMC4234135/
  176. https://www.myositis.org/wp-content/uploads/2018/07/Nutrition-and-Myositis-Peterson.pdf
  177. https://www.hss.edu/health-library/conditions-and-treatments/nutrition-supplements-reduce-medication-side-effects-myositis
  178. https://pmc.ncbi.nlm.nih.gov/articles/PMC7120298/
  179. https://www.pulmonaryfibrosis.org/docs/default-source/programs/educational-materials/fact-sheets-english/pf-series---myositis-ild.pdf
  180. https://ufhealth.org/conditions-and-treatments/myositis-interstitial-lung-disease-center
  181. https://www.niehs.nih.gov/research/resources/imacs/diseaseactivity
  182. https://pmc.ncbi.nlm.nih.gov/articles/PMC6702032/
  183. https://www.niehs.nih.gov/sites/default/files/2025-05/myositis_disease_activity_assessment_tool_2009_pdfat_508.pdf
  184. https://pmc.ncbi.nlm.nih.gov/articles/PMC4959629/
  185. https://pubmed.ncbi.nlm.nih.gov/37945774/
  186. https://academic.oup.com/rheumatology/article/61/5/1760/6555980
  187. https://pmc.ncbi.nlm.nih.gov/articles/PMC10149065/
  188. https://www.hopkinsmedicine.org/inhealth/myositis
  189. https://www.niehs.nih.gov/research/resources/imacs/patientoutcome
  190. https://pmc.ncbi.nlm.nih.gov/articles/PMC6397434/
  191. https://pmc.ncbi.nlm.nih.gov/articles/PMC2077543/
  192. https://www.sciencedirect.com/science/article/pii/S1297319X25000946
  193. https://journals.lww.com/neur/fulltext/2010/58010/effect_of_early_treatment_in_polymyositis_and.12.aspx
  194. https://pmc.ncbi.nlm.nih.gov/articles/PMC6065613/
  195. https://onlinelibrary.wiley.com/doi/10.1002/acr2.11751
  196. https://journals.sagepub.com/doi/10.1177/1759720X20936822
  197. https://pmc.ncbi.nlm.nih.gov/articles/PMC11050089/
  198. https://www.clinexprheumatol.org/article.asp?a=22220
  199. https://acrjournals.onlinelibrary.wiley.com/doi/10.1002/acr.24993
  200. https://pmc.ncbi.nlm.nih.gov/articles/PMC10815524/
  201. https://www.orpha.net/en/disease/detail/611
  202. https://www.sciencedirect.com/science/article/abs/pii/S0049017219301362
  203. https://pmc.ncbi.nlm.nih.gov/articles/PMC9204871/
  204. https://www.myositis.org/blog/patient-reported-quality-of-life-study-results/
  205. https://pmc.ncbi.nlm.nih.gov/articles/PMC12291288/
  206. https://www.rheumatologyadvisor.com/reports/pain-burden-in-iims-linked-to-impaired-qol/
  207. https://www.cell.com/cell/fulltext/S0092-8674%2824%2900701-3
  208. https://pmc.ncbi.nlm.nih.gov/articles/PMC6558048/
  209. https://www.myositis.org/blog/protect-yourself-this-flu-season/
  210. https://pmc.ncbi.nlm.nih.gov/articles/PMC5754739/
Add your contribution
Related Hubs
User Avatar
No comments yet.