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| {{More citations needed|date=September 2009}} | | |
| | {{Infobox medical condition |
| | | name = Inclusion body myositis |
| | | synonyms = IBM |
| | | field = [[Rheumatology]], [[Neurology]] |
| | | symptoms = Progressive muscle weakness, difficulty swallowing |
| | | onset = Typically after age 50 |
| | | duration = Chronic |
| | | causes = Unknown, possibly [[autoimmune]] |
| | | risks = Age, male gender, genetic factors |
| | | diagnosis = [[Muscle biopsy]], [[Electromyography]], [[Blood test]] |
| | | differential = [[Polymyositis]], [[Dermatomyositis]], [[Amyotrophic lateral sclerosis]] |
| | | treatment = [[Physical therapy]], [[Occupational therapy]], supportive care |
| | | prognosis = Progressive, no cure |
| | | frequency = Rare |
| | }} |
| | {{Short description|A progressive muscle disorder}} |
| {{Infobox medical condition (new) | | {{Infobox medical condition (new) |
| | name = Inclusion body myositis | | | name = Inclusion body myositis |
| | synonyms = | | | synonyms = sIBM |
| | image = | | | image = |
| | caption = | | | caption = |
| | pronounce = | | | pronounce = |
| | field = [[Rheumatology]] | | | field = [[Rheumatology]], [[Neurology]], [[Neuromuscular medicine]] |
| | symptoms = | | | symptoms = Progressive [[muscle weakness]], muscle wasting |
| | complications = | | | complications = Mobility issues, difficulty swallowing ([[dysphagia]]) |
| | onset = | | | onset = Typically after age 45 |
| | duration = | | | duration = Chronic, lifelong |
| | types = | | | types = Sporadic inclusion body myositis (sIBM), Hereditary IBM |
| | causes = | | | causes = Unknown, possibly autoimmune and degenerative |
| | risks = | | | risks = Advanced age, genetic predisposition |
| | diagnosis = | | | diagnosis = [[Muscle biopsy]], clinical assessment, electromyography (EMG) |
| | differential = | | | differential = [[Deconditioning]], [[hereditary muscle diseases]], [[polymyositis]], [[dermatomyositis]] |
| | prevention = | | | prevention = None known |
| | treatment = | | | treatment = Supportive therapies (physical therapy, occupational therapy), symptomatic management |
| | medication = | | | medication = Immunotherapy generally ineffective; symptomatic medications as needed |
| | prognosis = | | | prognosis = Slowly progressive disability, typically non-fatal |
| | frequency = | | | frequency = 5-71 per 1,000,000 |
| | deaths = | | | deaths = Rarely directly fatal; associated complications can increase risk |
| }} | | }} |
| | | '''Inclusion body myositis''' ('''IBM'''), specifically '''sporadic inclusion body myositis''' ('''sIBM'''), is a chronic, slowly progressive inflammatory muscle disease characterized primarily by progressive [[muscle weakness]] and wasting. It predominantly affects older adults, typically beginning after the age of 45. |
| '''Inclusion body myositis''' ('''IBM''') [my-oh-SIGH-tis] (sometimes called sporadic inclusion body myositis, sIBM) is the most common [[Inflammatory myopathy|inflammatory muscle disease]] in older adults.<ref>{{cite journal|last1=Ahmed|first1=Mhoriam|last2=Machado|first2=Pedro M|last3=Miller|first3=Adrian|last4=Spicer|first4=Charlotte|last5=Herbelin|first5=Laura|last6=et|first6=al|title=Targeting protein homeostasis in sporadic inclusion body myositis|journal=Science Translational Medicine|date=March 23, 2016|volume=8|issue=331|pages=331ra41|doi=10.1126/scitranslmed.aad4583|pmid=27009270|pmc=5043094}}</ref> The disease is characterized by slowly progressive weakness and wasting of both proximal muscles (closest to the body's midline)and distal muscles (the limbs), most apparent in the [[finger]] [[flexor]]s and [[knee]] [[extensor]]s.<ref>{{cite journal|last1=Jackson|first1=CE|last2=Barohn|first2=RJ|last3=Gronseth|first3=G|last4=Pandya|first4=S|last5=Herbelin|first5=L|last6=and|first6=The Muscle Study Group|title=Inclusion body myositis functional rating scale: a reliable and valid measure of disease severity|journal=Muscle and Nerve|date=April 2008|volume=37|issue=4|pages=473–476|doi=10.1002/mus.20958|pmid=18236463}}</ref> IBM is often confused with an entirely different class of diseases, called [[Hereditary inclusion body myopathy|hereditary inclusion body myopathies]] (hIBM).<ref>[http://ibmmyositis.com/ IBMmyositis.com]</ref><ref>[https://cureibm.org/ cureibm.org]</ref> The "M" in hIBM is an abbreviation for "myopathy" while the "M" in IBM is an abbreviation for "myositis". These diseases should not be confused with each other. In IBM, two processes appear to occur in the muscles in parallel, one autoimmune and the other degenerative. Inflammation is evident from the invasion of muscle fibers by [[Lymphocyte|immune cells]]. Degeneration is characterized by the appearance of [[vacuole|holes]], deposits of [[Amyloid|abnormal proteins]], and filamentous inclusions in the muscle fibers.<ref>{{cite journal|last1=Machado|first1=P|last2=Dimachkie|first2=MM|last3=Bahron|first3=RJ|title=Sporadic Inclusion Body Myositis: new insights and potential therapy|journal=Current Opinion in Neurology|date=October 2014|volume=27|issue=5|pages=591–598|doi=10.1097/WCO.0000000000000129|pmid=25159931|pmc=4248565}}</ref> sIBM is a rare disease, with a prevalence ranging from 1 to 71 individuals per million.<ref>{{cite journal|last1=Machado|first1=P|last2=Brady|first2=S|last3=Hanna|first3=MG|title=Update in inclusion body myosities|journal=Current Opinion in Rheumatology|date=2013|volume=25|issue=763–771|pages=763–771|doi=10.1097/01.bor.0000434671.77891.9a|pmid=24067381|pmc=4196838|url=}}</ref><ref>{{cite web | url=http://rarediseases.org/rare-diseases/sporadic-inclusion-body-myositis/ | title=Sporadic Inclusion Body Myositis}}</ref> | | ==Signs and Symptoms== |
| | | Symptoms generally develop slowly and include: |
| Weakness comes on slowly (over months to years) in an asymmetric manner and progresses steadily, leading to severe weakness and wasting of arm and leg muscles. IBM is more common in men than women.<ref>{{cite web | url=http://patient.info/doctor/inclusion-body-myositis | title=Inclusion Body Myositis. IBM information; Age Related illness}}</ref> Patients may become unable to perform [[activities of daily living]] and most require assistive devices within 5 to 10 years of symptom onset.<ref>{{cite web | url=http://www.ibmfoundation.org/index.php/understanding-ibm | title=Understanding IBM}}</ref> sIBM is not considered a [[wiktionary:fatal|fatal]] disorder, but the risk of serious injury due to falls is increased. Death in IBM is sometimes related to [[malnutrition]] and [[respiration (physiology)|respiratory]] failure.<ref>{{cite journal|last1=Cox|first1=FM|last2=Titulaer|first2=MJ|last3=Sont|first3=JK|last4=Wintzen|first4=AR|last5=et|first5=al|title=A 12-year follow-up in sporadic inclusion body myositis: an end stage with major disabilities|journal=Brain|date=November 1, 2011|volume=134|issue=11|pages=3167–3175|doi=10.1093/brain/awr217|pmid=21908393}}</ref> There is no effective treatment for the disease.
| | * Progressive weakness in the forearms, wrists, thighs, and muscles controlling finger flexion |
| | | * Difficulty swallowing ([[dysphagia]]) |
| ==Signs and symptoms== | | * Gradual muscle atrophy, especially in the quadriceps and forearm muscles |
| How sIBM affects individuals is quite variable as is the age of onset (which generally varies from the forties upwards). Because sIBM affects different people in different ways and at different rates, there is no "textbook case."
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| Eventually, sIBM results in general, progressive muscle weakness. The [[quadriceps]] and forearm muscles are usually affected early on. Common early symptoms include frequent tripping and falling, weakness going up stairs and trouble manipulating the fingers (including difficulty with tasks such as turning doorknobs or gripping keys). [[Foot drop]] in one or both feet has been a symptom of IBM and advanced stages of [[polymyositis]] (PM).
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| During the course of the illness, the patient's mobility is progressively restricted as it becomes hard for him or her to bend down, reach for things, walk quickly and so on. Many patients say they have balance problems and fall easily, as the muscles cannot compensate for an off-balanced posture. Because sIBM makes the leg muscles weak and unstable, patients are very vulnerable to serious injury from tripping or falling down. Although pain has not been traditionally part of the "textbook" description, many patients report severe muscle pain, especially in the thighs.
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| When present, [[dysphagia|difficulty swallowing (dysphagia)]] is a progressive condition in those with inclusion body myositis and often leads to death from [[aspiration pneumonia]]. Dysphagia is present in 40 to 85% of IBM cases.<ref name="pmid18936555">{{cite journal |vauthors=Oh TH, Brumfield KA, Hoskin TL, Kasperbauer JL, Basford JR |title=Dysphagia in inclusion body myositis: clinical features, management, and clinical outcome |journal=Am J Phys Med Rehabil |volume=87 |issue=11 |pages=883–9 |year=2008 |pmid=18936555 |doi=10.1097/PHM.0b013e31818a50e2 }}</ref>
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| IBM can also result in diminished capacity for aerobic exercise. This decline is most likely a consequence of the sedentary lifestyle that is often associated with the symptoms of IBM (i.e. progressive muscle weakness, decreased mobility, and increased level of fatigue). Therefore, one focus of treatment should be the improvement of aerobic capacity.<ref>{{cite journal |vauthors=Johnson LG, Collier KE, Edwards DJ, etal |title=Improvement in aerobic capacity after an exercise program in sporadic inclusion body myositis |journal=J Clin Neuromuscul Dis |volume=10 |issue=4 |pages=178–84 |date=June 2009 |pmid=19494728 |doi=10.1097/CND.0b013e3181a23c86 |url=https://semanticscholar.org/paper/50cff0d0e651d5297b000c798ee6ad3c872434a1 }}</ref>
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| Patients with sIBM usually eventually need to resort to a cane or a walker and in most cases, a wheelchair eventually becomes a necessity.
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| "The progressive course of s-IBM leads slowly to severe disability. Finger functions can become very impaired, such as for manipulating pens, keys, buttons, and zippers, pulling handles, and firmly grasping handshakes. Arising from a chair becomes difficult. Walking becomes more precarious. Sudden falls, sometimes resulting in major injury to the skull or other bones, can occur, even from walking on minimally-irregular ground or from other minor imbalances outside or in the home, due to weakness of quadriceps and gluteus muscles depriving the patient of automatic posture maintenance. A foot-drop can increase the likelihood of tripping. [[Dysphagia]] can occur, usually caused by upper esophageal constriction that often can be symptomatically improved, for several months to years, by bougie dilation per a GI or ENT physician. Respiratory muscle weakness can sometimes eventuate."<ref name="pmid16432144">{{cite journal |vauthors=Askanas V, Engel WK |title=Inclusion-body myositis: a myodegenerative conformational disorder associated with Abeta, protein misfolding, and proteasome inhibition |journal=Neurology |volume=66 |issue=2 Suppl 1 | pages = S39–S48 |year=2006 |pmid=16432144 |doi=10.1212/01.wnl.0000192128.13875.1e}}</ref>
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| ==Causes== | | ==Causes== |
| The cause of IBM is unknown. IBM likely results from the interaction of a number of genetic and environmental factors.<ref name="General Information About IBM">{{cite web|title=Inclusion Body Myositis (IBM)|url=http://ibmmyositis.com/aboutibm1old.htm|accessdate=7 May 2017}}</ref> | | The exact [[cause]] of IBM remains unknown. The condition is thought to involve both autoimmune and degenerative processes, possibly influenced by genetic factors. |
| | | ==Risk Factors== |
| There are two major theories about how sIBM is caused. One hypothesis suggests that the inflammation-immune reaction, caused by an unknown trigger – likely an undiscovered virus or an autoimmune disorder– is the primary cause of sIBM and that the degeneration of muscle fibers and protein abnormalities are secondary features.<ref name="pmid16932602">{{cite journal |author=Dalakas MC |title=Sporadic inclusion body myositis--diagnosis, pathogenesis and therapeutic strategies |journal=Nat Clin Pract Neurol |volume=2 |issue=8 |pages=437–447 |year=2006 |pmid=16932602 |doi=10.1038/ncpneuro0261|url=https://zenodo.org/record/1233387 }}</ref> Despite the arguments "in favor of an adaptive immune response in sIBM, a purely autoimmune hypothesis for sIBM is untenable because of the disease's resistance to most immunotherapy."<ref>{{EMedicine|article|1172746|Inclusion Body Myositis}}</ref>
| | Factors increasing the likelihood of developing IBM include: |
| | | * Advanced age, typically over 45 |
| The second school of thought advocates the theory that sIBM is a degenerative disorder related to aging of the muscle fibers and that abnormal, potentially pathogenic protein accumulations in myofibrils play a key causative role in sIBM (apparently before the immune system comes into play). This hypothesis emphasizes the abnormal intracellular accumulation of many proteins, protein aggregation and misfolding, [[proteosome]] inhibition, and [[endoplasmic reticulum]] (ER) stress.<ref name="pmid16432144"/>
| | * Genetic susceptibility |
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| One review discusses the "limitations in the beta-amyloid-mediated theory of IBM myofiber injury."<ref name="pmid19080758">{{cite journal |author=Greenberg SA. |title=Inclusion body myositis: review of recent literature |journal=Curr Neurol Neurosci Rep |volume=9 |issue=1 |pages=83–89 |year=2009 |pmid=19080758 |doi=10.1007/s11910-009-0013-x }}</ref>
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| Dalakas (2006) suggested that a chain of events causes IBM—some sort of virus, likely a [[retrovirus]], triggers the cloning of [[T cells]]. These T cells appear to be driven by specific [[antigen]]s to invade muscle fibers. In people with sIBM, the muscle cells display “flags” telling the immune system that they are infected or damaged (the muscles ubiquitously express MHC class I antigens) and this immune process leads to the death of muscle cells. The chronic stimulation of these antigens also causes stress inside the muscle cell in the [[endoplasmic reticulum]] (ER) and this ER stress may be enough to cause a self-sustaining T cell response (even after a virus has dissipated). In addition, this ER stress may cause the misfolding of protein. The ER is in charge of processing and folding molecules carrying antigens. In IBM, muscle fibers are overloaded with these [[major histocompatibility complex]] (MHC) molecules that carry the antigen protein pieces, leading to more ER stress and more protein misfolding.<ref name="pmid16932602"/>
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| A self-sustaining T cell response would make sIBM a type of autoimmune disorder. When studied carefully, it has not been impossible to detect an ongoing viral infection in the muscles. One theory is that a chronic viral infection might be the initial triggering factor setting IBM in motion. There have been a handful of IBM cases—approximately 15—that have shown clear evidence of a virus called [[HTLV-1]]. The HTLV-1 virus can cause [[leukemia]], but in most cases lies dormant and most people end up being lifelong carriers of the virus. One review says that the best evidence points towards a connection with some type of retrovirus and that a retroviral infection combined with immune recognition of the retrovirus is enough to trigger the inflammation process.<ref name="pmid16932602"/>
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| * [[amyloid]] protein
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| * The hypothesis that [[beta amyloid]] protein is key to IBM has been supported in a mouse model using an Aβ vaccine that was found to be effective against inclusion body myositis in mouse models. Although this vaccine is likely not safe for human use, it still shows that attacking Aβ has efficacy in mice against IBM.<ref>{{cite journal |title=Immunization with amyloid-β attenuates inclusion body myositis-like myopathology and motor impairment in a transgenic mouse model |vauthors=Kitazawa M, Vasilevko V, Cribbs DH, LaFerla FM |journal=The Journal of Neuroscience |date=13 May 2009 |volume=29 |issue=19 |pages=6132–41 |lay-url=http://today.uci.edu/news/nr_ibmimmunization_090513.php |quote=Inclusion body myositis...features include T-cell mediated inflammatory infiltrates and aberrant accumulations of proteins, including amyloid-β (Aβ), tau, ubiquitinated proteins, apolipoprotein E, and β-synuclein in skeletal muscle. ... active immunization markedly reduces intracellular Aβ deposits and attenuates the motor impairment compared with untreated mice...Aβ oligomers contribute to the myopathy process as they were significantly reduced in the affected skeletal muscle from immunized mice. In addition, the anti-Aβ antibodies produced in the immunized mice blocked the toxicity of the Aβ oligomers in vitro, providing a possible key mechanism for the functional recovery. |doi=10.1523/JNEUROSCI.1150-09.2009 |pmid=19439591 |pmc=3049190}}</ref> | |
| * Following up on earlier leads, the Greenberg group report finding that the protein TDP-43 is a very prominent and highly sensitive and specific feature of IBM. This protein is normally found within the nucleus but in IBM is found in the cytoplasm of the cell. This important advance should help develop a new screening technique for IBM and may provide clues in terms of a therapeutic approach<ref>{{cite journal |title=Sarcoplasmic redistribution of nuclear TDP-43 in inclusion body myositis |author=Salajegheh, M, Pinkus, JL, Taylor, JP, Amato, AA, Nazareno, R, Baloh, RH, Greenberg, SA. |journal=Muscle Nerve |year=2009 |volume=40 |issue=1 |pages=19–31 |doi=10.1002/mus.21386 |pmid=19533646 |pmc=2700211}}</ref> | |
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| ===Genetics===
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| sIBM is not inherited and is not passed on to the children of IBM patients. There are genetic features that do not directly cause IBM but that appear to predispose a person to getting IBM — having this particular combination of genes increases one's susceptibility to getting IBM. Some 67% of IBM patients have a particular combination of [[human leukocyte antigen]] genes in a section of the 8.1 ancestral haplotype in the center of the MHC class II region. sIBM is not passed on from generation to generation, although the susceptibility region of genes may be.<ref name="pmid16932602"/>
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| There are also several rare forms of hereditary inclusion body myopathy that are linked to specific genetic defects and that are passed on from generation to generation. Since these forms do not show features of muscle inflammation, they are classified as myopathies rather than forms of myositis. Because they do not display inflammation as a primary symptom, they may in fact be similar, but different diseases to sporadic inclusion body myositis. There are several different types, each inherited in different ways. See [[hereditary inclusion body myopathy]].
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| A 2007 review concluded there is no indication that the genes responsible for the familial or hereditary conditions are involved in sIBM.<ref name="pmid17366591">{{cite journal |vauthors=Needham M, Mastaglia FL, Garlepp MJ |title=Genetics of inclusion-body myositis |journal=Muscle Nerve |volume=35 |issue=5 |pages=549–561 |year=2007 |pmid=17366591 |doi=10.1002/mus.20766}}</ref>
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| ==Diagnosis== | | ==Diagnosis== |
| Elevated [[creatine kinase]] (CK) levels in the blood (at most ~10 times normal) are typical in sIBM but affected individuals can also present with normal CK levels. [[Electromyography]] (EMG) studies usually display abnormalities such as increased insertional activity and short duration motor unit potentials. Muscle biopsy may display several common findings including; inflammatory cells invading muscle cells, vacuolar degeneration, inclusions or plaques of abnormal proteins. sIBM is a challenge to the pathologist and even with a biopsy, diagnosis can be ambiguous.
| | Diagnosis typically involves: |
| | | * Clinical evaluation and detailed patient history |
| A diagnosis of inclusion body myositis was historically dependent on muscle biopsy results. Antibodies to cytoplasmic 5'-nucleotidase (cN1A; NT5C1A) have been strongly associated with the condition. In the clinical context of a classic history and positive antibodies, a muscle biopsy might be unnecessary.
| | * [[Electromyography]] (EMG) to assess muscle activity |
| | | * [[Muscle biopsy]] revealing characteristic inclusions and inflammation |
| ===Differential diagnosis===
| | Differential diagnosis should consider: |
| IBM is often initially misdiagnosed as [[polymyositis]]. A course of [[prednisone]] is typically completed with no improvement and eventually sIBM is confirmed. sIBM weakness comes on over months or years and progresses steadily, whereas polymyositis has an onset of weeks or months. Other forms of muscular dystrophy (e.g. limb girdle) must be considered as well.
| | * [[Deconditioning]] |
| | | * [[Hereditary muscle diseases]] |
| ===Classification===
| | * [[Polymyositis]] |
| * The common type is sIBM; it strikes individuals apparently at random.<ref>{{cite journal |vauthors=Karpati G, O'Ferrall EK | date = Jan 2009 | title = Sporadic inclusion body myositis: Pathogenic considerations| url = | journal = Ann Neurol | volume = 65 | issue = 1| pages = 7–11 | doi=10.1002/ana.21622| pmid = 19194875 }}</ref> | | * [[Dermatomyositis]] |
| * There is a type that has been observed in multiple siblings in the same generation in several families, termed ''familial inflammatory sIBM'', but it is not passed on from generation to generation.<ref name="pmid16932602" /> | |
| * There are also several very rare forms of ''hereditary inclusion body myopathy'' (hIBM) that are linked to specific genetic defects and that are passed on from generation to generation, each inherited in different ways.<ref>{{cite journal |author1=Broccolini A. |author2=Mirabella M. | year = 2014 | title = Hereditary inclusion-body myopathies | url = | journal = Biochim. Biophys. Acta | volume = 1852| issue = 4| pages = 644–650| doi = 10.1016/j.bbadis.2014.08.007 | pmid=25149037}}</ref>
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| ==Treatment== | | ==Treatment== |
| There is no standard course of treatment to slow or stop the progression of the disease. sIBM patients do not reliably respond to the anti-inflammatory, immunosuppressant, or immunomodulatory medications. Management is symptomatic. Prevention of falls is an important consideration. [[Exercise therapy for idiopathic inflammatory myopathies|Specialized exercise therapy]] may supplement treatment to enhance quality of life. Physical therapy is recommended to teach the patient a home exercise program, to teach how to compensate during mobility-gait training with an assistive device, transfers and bed mobility. | | There is currently no curative treatment for IBM. Management primarily includes: |
| | | * Physical therapy and occupational therapy to maintain mobility and functionality |
| ==Other related disorders== | | * Supportive interventions such as speech therapy for dysphagia |
| When sIBM was originally described, the major feature noted was muscle inflammation. Two other disorders were also known to display muscle inflammation, and sIBM was classified along with them. They are [[dermatomyositis]] (DM) and [[polymyositis]] (PM) and all three illnesses were called [[idiopathic]] (of unknown origin) myositis or inflammatory myopathies.
| | Immunotherapy typically has limited or no benefit in IBM patients. |
| | | ==Prognosis== |
| It appears that sIBM and polymyositis share some features, especially the initial sequence of immune system activation, however, polmyositis comes on over weeks or months, does not display the subsequent muscle degeneration and protein abnormalities as seen in IBM, and as well, polymyositis tends to respond well to treatments, IBM does not. IBM is often confused with (misdiagnosed as) polymyositis. Polymyositis that does not respond to treatment is likely IBM.<ref>[http://www.myositis.org/your-myositis-community/live-discussions/406-when-myositis-doesnt-respond-to-treatment When myositis doesn't respond to treatment] Retrieved 20 April 2015.</ref>
| | IBM progresses slowly, causing increasing disability but rarely affecting life expectancy directly. However, complications such as severe swallowing difficulties can contribute to health risks. |
| | | ==Epidemiology== |
| [[Dermatomyositis]] shares a number of similar physical symptoms and histopathological traits as polymyositis, but exhibits a skin rash not seen in polymyositis or sIBM. It may have different root causes unrelated to either polymyositis or sIBM. | | IBM is a relatively rare condition, with prevalence estimates ranging from 5 to 71 cases per million people worldwide, making it one of the most common inflammatory muscle diseases in adults over 50. |
| | | ==Prevention== |
| Mutations in [[valosin-containing protein]] (VCP) cause [[multisystem proteinopathy]] (MSP), which can present (among others) as a rare form of inclusion body myopathy.
| | No known preventive measures exist for inclusion body myositis. |
| | | ==Related pages== |
| ==References==
| | * [[Inflammatory myopathy]] |
| {{Reflist}}
| | * [[Autoimmune disease]] |
| | | * [[Muscle biopsy]] |
| == External links ==
| | * [[Neurodegenerative disease]] |
| {{Medical resources
| |
| | DiseasesDB = 30691
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| | ICD10 = {{ICD10|M60.8}}
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| | ICD9 = {{ICD9|359.71}}
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| | ICDO =
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| | OMIM = 147421
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| | MedlinePlus =
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| | eMedicineSubj = neuro
| |
| | eMedicineTopic = 422
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| | MeshID = D018979
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| | Orphanet = 611
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| | GeneReviewsNBK = NBK1262
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| | GeneReviewsName = Inclusion Body Myopathy 2
| |
| }}
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| *[https://www.ncbi.nlm.nih.gov/books/NBK1262/ GeneReview/NIH/UW entry on Inclusion Body Myopathy 2] | |
| {{Systemic connective tissue disorders}} | | {{Systemic connective tissue disorders}} |
| {{Myopathy}} | | {{Myopathy}} |
|
| |
| {{DEFAULTSORT:Inclusion Body Myositis}} | | {{DEFAULTSORT:Inclusion Body Myositis}} |
| [[Category:Systemic connective tissue disorders]] | | [[Category:Systemic connective tissue disorders]] |
| [[Category:Muscular disorders]] | | [[Category:Muscular disorders]] |
| [[Category:Inflammations]] | | [[Category:Inflammations]] |
| <gallery>
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| File:Affected_quadriceps_(rectus_femoris)_in_IBM.png|Affected quadriceps (rectus femoris) in IBM
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| File:Inclusion_body_myositis_arms.png|Inclusion body myositis arms
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| File:Inclusion_body_myositis_histology.jpg|Inclusion body myositis histology
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| File:Inclusion_body_myositis_MRI.jpg|Inclusion body myositis MRI
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| </gallery>
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