We are grateful for the insightful and highly relevant question raised by Dr Malaviya1 concerning the 2017 European League Against Rheumatism/American College of Rheumatology classification criteria for adult and juvenile idiopathic inflammatory myopathies and their major subgroups. The question concerns autoantibodies, and in particular myositis-specific autoantibodies (MSAs), and why only the anti-Jo-1 autoantibody is included in the new classification criteria.. We understand the concern that was raised and we have discussed the limitation of having limited data on MSAs in our publication.2 This letter gives us a possibility to expand on this limitation and include some more explanations. Our study was initiated more than 10 years ago, and during the last decade we have seen a great advancement in the knowledge of autoantibodies specific for and associated with idiopathic inflammatory myopathies (IIM). This includes identification of several new MSAs, as well as advancement in methods used to ...
Cancer is a significant complication contributing to increased mortality in idiopathic inflammatory myopathies (IIMs), and the association between IIMs and cancer has been extensively reported. Myositis-specific autoantibodies (MSAs) can help to stratify patients into more homogeneous groups and may be used as a biomarker for cancer-associated myositis. In this study, we aimed to systematically define the cancer-associated MSAs in IIMs. Serum from 627 patients with IIMs was tested for MSAs. The cancer risk with different MSAs was estimated by standardized incidence ratio (SIR). Paraneoplastic manifestation, such as the close temporal relationship between myositis onset and cancer diagnoses in patients with different MSAs, was also evaluated. Compared with the general Chinese population, patients with IIMs and anti-transcriptional intermediary factor (TIF1)-γ antibodies (SIR = 17.28, 95% CI 11.94 to 24.14), anti-nuclear matrix protein (NXP2) antibodies (SIR = 8.14, 95% CI 1.63 to 23.86), or anti-SAE1
Cancer is a significant complication contributing to increased mortality in idiopathic inflammatory myopathies (IIMs), and the association between IIMs and cancer has been extensively reported. Myositis-specific autoantibodies (MSAs) can help to stratify patients into more homogeneous groups and may be used as a biomarker for cancer-associated myositis. In this study, we aimed to systematically define the cancer-associated MSAs in IIMs. Serum from 627 patients with IIMs was tested for MSAs. The cancer risk with different MSAs was estimated by standardized incidence ratio (SIR). Paraneoplastic manifestation, such as the close temporal relationship between myositis onset and cancer diagnoses in patients with different MSAs, was also evaluated. Compared with the general Chinese population, patients with IIMs and anti-transcriptional intermediary factor (TIF1)-γ antibodies (SIR = 17.28, 95% CI 11.94 to 24.14), anti-nuclear matrix protein (NXP2) antibodies (SIR = 8.14, 95% CI 1.63 to 23.86), or anti-SAE1
We welcome the comments from Meyer et al1 regarding our recent article which hypothesised a potential role for reactive oxygen species (ROS) as a mediator of muscle weakness induction in the idiopathic inflammatory myopathies (IIM).2 The focus of our article was specifically on the persistence of muscle weakness in the treated paucity or absence of inflammatory cell infiltrates, and the role that ROS may play as a mediator of this residual and non-inflammatory dysfunction.2 In our article we did not try to imply that the mechanisms of actions of immune cells and ROS generation are mutually exclusive, as clearly inflammatory cell infiltrations are a cause of muscle cell injury and thus weakness. In another recent, and related, review we suggest that inflammatory cell infiltration is in fact a secondary feature in IIM.3 We agree that there is likely an interaction between immune cell-mediated and ROS-mediated muscle dysfunction. The interesting beneficial effects of using ROS-targeted therapies ...
Rider LG, Werth VP, Huber AM, Alexanderson H, Rao AP, Ruperto N, Herbelin L, Barohn R, Isenberg D, Miller FW. Measures of adult and juvenile dermatomyositis, polymyositis, and inclusion body myositis: Physician and Patient/Parent Global Activity, Manual Muscle Testing (MMT), Health Assessment Questionnaire (HAQ)/Childhood Health Assessment Questionnaire (C-HAQ), Childhood Myositis Assessment Scale (CMAS), Myositis Disease Activity Assessment Tool (MDAAT), Disease Activity Score (DAS), Short Form 36 (SF-36), Child Health Questionnaire (CHQ), physician global damage, Myositis Damage Index (MDI), Quantitative Muscle Testing (QMT), Myositis Functional Index-2 (FI-2), Myositis Activities Profile (MAP), Inclusion Body Myositis Functional Rating Scale (IBMFRS), Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI), Cutaneous Assessment Tool (CAT), Dermatomyositis Skin Severity Index (DSSI), Skindex, and Dermatology Life Quality Index (DLQI). Arthritis Care Res (Hoboken). 2011 Nov;63 Suppl ...
Inflammatory myopathy (inflammatory muscle disease or myositis) is disease featuring weakness and inflammation of muscles and (in some types) muscle pain. The cause of much inflammatory myopathy is unknown (idiopathic), and such cases are classified according to their symptoms and signs and electromyography, MRI and laboratory findings. It can also be associated with underlying cancer. The main classes of idiopathic inflammatory myopathy are polymyositis (PM), dermatomyositis (DM), and inclusion-body myositis (IBM). There are a number of known causes of myopathy, and it is only once these have been ruled out that a clinician will assign an idiopathic inflammatory myopathy (IIM) syndrome to a case. The usual criteria for a diagnosis of PM are weakness in muscles of the head, neck, trunk, upper arms or upper legs; raised blood serum concentrations of some muscle enzymes such as creatine kinase; unhealthy muscle changes on electromyography; and biopsy findings of (i) muscle cell degeneration and ...
Hey there, good-looking and generous blog readers. Remember when we were a community? Did stupid memes and gave out goofy awards to one another? Donated blog space to spread the word about a rare condition? Harassed people on Twitter to text a vote for a bunch of kids in need? Time to see if that still can happen. On this ‪#‎GivingTuesday‬, please help the hundreds of children like my daughter, Lil Diva, who have the autoimmune disease Juvenile Myositis. The best way is to donate to Cure JM Foundation via the CrowdRise Holiday Challenge as our nonprofit tries to win $100,000 for disease research. To refresh your memory, Juvenile Myositis (JM) is a rare and life-threatening disease affecting one to five children in a million. LiL Diva was diagnosed with it 11 years ago at age 2. JM can affect virtually any system of the body, and there is no cure … yet. Cure JM Foundation is a nonprofit organization created and managed by families of children affected by Juvenile Myositis (JM) - the ...
Discussion. This is the first multicenter registry of inflammatory myopathies in the Community of Madrid, and it provides the most extensive compilation of data up to now. The registry was created for the purpose of retrospectively analyzing the clinical characteristics, comorbidities and complications of autoimmune inflammatory myopathies in a multicenter study of 12 hospitals in the Community of Madrid. We compared the clinical characteristics, analytical findings and prognosis in the different subgroups of autoimmune inflammatory myopathies.. The criteria of Tanimoto,9 published in 1995, have a greater specificity than those of Bohan and Peter.18,19 The only 2 cases that did not meet the criteria of Bohan and Peter, did conform to Tanimotos criteria, and corresponded to 2 patients with antisynthetase syndrome with elevated muscle enzymes, arthritis, general symptoms and interstitial lung disease in both cases, and mechanics hands in one.. Idiopathic inflammatory myopathies appear to be ...
TY - JOUR. T1 - International consensus on preliminary definitions of improvement in adult and juvenile myositis. AU - Rider, Lisa G.. AU - Giannini, Edward H.. AU - Brunner, Hermine I.. AU - Ruperto, Nicola. AU - James-Newton, Laura. AU - Reed, Ann M.. AU - Lachenbruch, Peter A.. AU - Miller, Frederick W.. PY - 2004/7. Y1 - 2004/7. N2 - Objective. To use a core set of outcome measures to develop preliminary definitions of improvement for adult and juvenile myositis as composite end points for therapeutic trials. Methods. Twenty-nine experts in the assessment of myositis achieved consensus on 102 adult and 102 juvenile paper patient profiles as clinically improved or not improved. Two hundred twenty-seven candidate definitions of improvement were developed using the experts consensus ratings as a gold standard and their judgment of clinically meaningful change in the core set of measures. Seventeen additional candidate definitions of improvement were developed from classification and regression ...
2017 (English)In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 76, 626-626 p.Article in journal, Meeting abstract (Other academic) Published ...
Overview Autoantibodies FAQs Resources Myositis may be idiopathic or caused by conditions such as microbial infections, drugs, or injury leading to inflammation and damage in the muscles. Idiopathic inflammatory myopathies (IIM) are a rare and heterogeneous group of autoimmune diseases characterized by acute, subacute, or chronic mus
Idiopathic inflammatory myopathies (IIM) are a great concern in acquired muscle illnesses. An appropriate and rapid diagnosis is necessary, because morbidity and mortality are high and as a specific treatment is needed (corticosteroids, immunosuppressant, and biotherapies).. Currently the use of muscle MRI in departments managing IIM is common. In absence of recommendations fixing their place in the diagnostic phase, the practices observed are extremely heterogeneous. Some systematically order a muscle MRI for patients suspected to suffer from IIM, others hold this examination for patients selected according to non defined criteria, and others sometimes use MRI to follow-up patients. This practices diversity well reflects the lack of data in the literature, making it impossible to appreciate the real contribution of this test. The results published in the great majority of studies are obtained with patients whose IIM diagnosis is already established. The diagnostic accuracy of muscle MRI in ...
(HealthDay)-Ultrasonography findings seem to correlate well with the disease activity of idiopathic inflammatory myopathies (IIMs), and may be a useful tool for patient evaluation, according to a study published online ...
REVIEW KAREN RENDT, MD Department of Rheumatic and Immunologic Diseases, Cleveland Clinic Inflammatory myopathies: Narrowing the differential diagnosis ■ A B S T R AC T weakW ness, the first step is to with distinguish HEN A PATIENT PRESENTS Muscle weakness is a feature of numerous conditions, but the muscle weakness of inflammatory myopathies, especially polymyositis and dermatomyositis, is easy to differentiate by specific clinical, laboratory, electromyographic, and histological features. ■ KEY POINTS Diagnostic criteria currently include proximal muscle weakness, increased creatine kinase, abnormal (myopathic) electromyogram, typical histologic appearance on muscle biopsy, and cutaneous abnormalities typical of dermatomyositis. A muscle biopsy specimen demonstrating typical histologic features in the absence of metabolic myopathy, infection, or drug effect establishes the diagnosis of polymyositis. Numerous prescription and over-the-counter drugs, notably the statins, are associated with ...
ABSTRACT: This review summarizes the previous and current literature on the immunogenetics of idiopathic inflammatory myopathy (IIM) and updates the research progress that has been made over the past decade. A substantial part of the genetic risk for developing adult- and juvenile-onset IIM lies within the major histocompatibility complex (MHC), and a tight relationship exists between individual human leukocyte antigen alleles and specific serological subtypes, which in turn dictate clinical disease phenotypes. Multiple genetic regions outside of the MHC are increasingly being identified in conferring IIM disease susceptibility. We are still challenged with the task of studying a serologically and clinically heterogeneous disorder that is rarer by orders of magnitude than the likes of rheumatoid arthritis. An ongoing and internationally coordinated IIM genome-wide association study may provide further insights into IIM immunogenetics. ...
Polymyositis, dermatomyositis and related disorders, also known as the idiopathic inflammatory myopathies (IIM), are an uncommon, heterogeneous group of diseases. This is an omnibus protocol designed to continue our description of this rare group of diseases, further delineate important groups of patients, and obtain useful material for further study of immunological abnormalities, pathogenesis and etiology of IIM. Often the diagnosis of an IIM can be confused with other illness (such as adult-onset dystrophies), and therefore, we will be evaluating patients with other illnesses (who are referred with a preliminary diagnosis of an IIM). Patients evaluated with IIM will receive (with informed consent) the best standard therapies available and consideration for entry into any therapeutic protocols. MRI will be performed on healthy volunteers to help develop a mathematical method for quantitating edema of muscle MRI in patients. MRI/PET will be performed on some patients and on healthy volunteers ...
... is the inflammation of the muscles as a result of injury, infection, certain medicines, chronic disease or exercise. Some of the persistent or chronic forms are idiopathic inflammatory myopathies, meaning that the cause is not known. This is the forum for discussing anything related to Myositis
Polymyositis (PM) is an inflammatory muscle disease of unknown etiology. PM, dermatomyositis (DM), and inclusion body myositis are the major members of a group of syndromes called the idiopathic inflammatory myopathies. In much of the literature, PM and DM are grouped as one disease. However, DM is not simply PM with the addition of a rash. Each disease has characteristic clinical differences, histopathologic findings, and immune markers. No strictly defined diagnostic criteria for PM or DM
Myositis-specific autoantibodies (MSAs) are found in almost half the patients with an idiopathic inflammatory myopathy (IIM). Several clinical and epidemiological studies have suggested that MSAs are associated with specific clinical characteristics. Some of these associations are well-defined and are of clinical significance ( eg, anti-Jo-1 and the anti-synthetase syndrome), others are less well established and can cause unnecessary anxiety for both patients and physicians ( eg, anti-SRP and cardiac involvement). In this review, an overview is given of the various MSAs, their biochemical background, their clinical usefulness, and the promises they hold for a better understanding of IIM ...
ABSTRACTIn recent years, antisynthetase syndrome has been recognized as an important cause of autoimmune inflammatory myopathy in a subset of patients with polymyositis and dermatomyositis. It is associated with serum antibodies to aminoacyl-transfer RNA synthetases and is characterized by a constellation of manifestations, including fever, myositis, interstitial lung disease,
Kevin McKeever discusses his daughters battle with juvenile myositis, the Cure JM Foundation, and their goal of never letting another child suffer from the disease. Read more →. ...
Thighs subcutaneous and myofascial signal abnormalities were detected in 8/43 (18.6%) and in 12/43 (27.9%) patients respectively. WB-MRI revealed inflammatory involvement of myofascial and subcutaneous areas other than the thigh in 8/43 (18.6%) and 10/43 (23.2%) patients, respectively Concordance between WB and thigh MRI scores in the evaluation of myofascial and subcutaneous tissue was moderate (myofascial scores rs = 0.59, subcutaneous scores rs = 0.69). Although concordance in detecting muscle inflammation between thigh and WB-MRI muscle scores was excellent (rs = 0.97), two patients with negative thigh-MRI showed muscle signal abnormalities in muscle groups different from the thigh. Inter-reader agreement was excellent for both thigh-MRI and WB-MRI scores (ICC 0.96 and 0.98 respectively). Both scores showed excellent correlations with clinical measures of disease activity (Manual Muscle Test (MMT) rs = -0.82, Childhood Myositis Assessment Scale (CMAS) rs = -0.83 for thigh-MRI; MMT rs = ...
The field of autoantibodies related to immune-mediated inflammatory myopathies has expanded in recent years and there is now a host of antibodies that have relevance to these myopathies. The 1975 Bohan and Peter criteria for the classification of immune-mediated inflammatory myopathies do not reflect many newer insights, and several newer classification schemes exist, but none enjoy uniform acceptance.12 Some controversy remains as to the pathophysiology behind dermatomyositis, but this disease is probably the most consistently defined. Conversely, polymyositis has several varied definitions, and in the Bohan and Peter criteria it was not delineated from inclusion body myopathy (IBM). The antisynthetase syndrome associated with antibodies described in this section does not cleanly sort under either the dermato- or polymyositis labels. The inflammatory myopathies associated with SRP and 200/100 antibodies do not even necessarily have the inflammatory muscle infiltrates that we traditionally ...
Some types of autoimmune disease attack the muscles of the body. The "myositis-specific antibodies" (MSA) can assist in the diagnosis of polymyositis and dermatomyositis in those patients who have the diseases. About 50% of patients with polymyositis or dermatomyositis have specific MSA or myositis associated antibodies (MAA). MSA are almost never found in patients without myositis, even if they have other muscle diseases of autoimmune diseases. This means that when the physicians examination and initial testing suggest the possibility of polymyositis or dermatomyositis, a positive test for an MSA can be strong supporting evidence for the diagnosis.. For a long time the testing for these antibodies was only available in research studies, but it is now possible to obtain this testing clinically. The Myositis Profile* performed at the OMRF Clinical Immunology Laboratory includes tests for 12 of the MSAs and MAAs. Additional antibodies may be detectable using this profile. Dr. Ira Targoff is the ...
Necrotizing fasciitis and myositis are devastating infections characterized by high mortality. Group A streptococcus (GAS) is a common cause of these infections, but the molecular pathogenesis is poorly understood. We report a genome-wide analysis using serotype M1 and M28 strains that identified GAS genes contributing to necrotizing myositis in nonhuman primates (NHP), a clinically relevant model. Using transposon-directed insertion-site sequencing (TraDIS), we identified 126 and 116 GAS genes required for infection by serotype M1 and M28 organisms, respectively. For both M1 and M28 strains, more than 25% of the GAS genes required for necrotizing myositis encode known or putative transporters. Thirteen GAS transporters contributed to both M1 and M28 strain fitness in NHP myositis, including putative importers for amino acids, carbohydrates, and vitamins and exporters for toxins, quorum-sensing peptides, and uncharacterized molecules. Targeted deletion of genes encoding 5 transporters confirmed ...
Necrotizing fasciitis and myositis are devastating infections characterized by high mortality. Group A streptococcus (GAS) is a common cause of these infections, but the molecular pathogenesis is poorly understood. We report a genome-wide analysis using serotype M1 and M28 strains that identified GAS genes contributing to necrotizing myositis in nonhuman primates (NHP), a clinically relevant model. Using transposon-directed insertion-site sequencing (TraDIS), we identified 126 and 116 GAS genes required for infection by serotype M1 and M28 organisms, respectively. For both M1 and M28 strains, more than 25% of the GAS genes required for necrotizing myositis encode known or putative transporters. Thirteen GAS transporters contributed to both M1 and M28 strain fitness in NHP myositis, including putative importers for amino acids, carbohydrates, and vitamins and exporters for toxins, quorum-sensing peptides, and uncharacterized molecules. Targeted deletion of genes encoding 5 transporters confirmed ...
Walk Strong to Cure JM™ is Cure JMs signature National Walk Program. Families, friends and communities come together to support children, teens, and young adults fighting Juvenile Myositis.. Walk Strong to Cure JM™ events help to raise awareness of Juvenile Myositis and and raise funds for JM research and programs. They provide an opportunity for JM families to meet other JM families in their community while enjoying an array of fun activities for all ages.. Since 2016, Walk Strong™ events have raised hundreds of thousands of dollars for Juvenile Myositis research and programs.. Be part of the movement!. The following Walk Strong to Cure JM™ events are scheduled for the remainder of 2017 and 2018:. ...
Acquired non-inflammatory myopathy (ANIM) is a neurological disorder primarily affecting skeletal muscle, most commonly in the limbs of humans, resulting in a weakness or dysfunction in the muscle. A myopathy refers to a problem or abnormality with the myofibrils, which compose muscle tissue. In general, non-inflammatory myopathies are a grouping of muscular diseases not induced by an autoimmune-mediated inflammatory pathway. These muscular diseases usually arise from a pathology within the muscle tissue itself rather than the nerves innervating that tissue. ANIM has a wide spectrum of causes which include drugs and toxins, nutritional imbalances, acquired metabolic dysfunctions such as an acquired defect in protein structure, and infections. Acquired non-inflammatory myopathy is a different diagnosis than inflammatory myopathy. Inflammatory myopathies are a direct result of some type of autoimmune mediated pathway whereas ANIM is not the result of a dysfunction of the immune system. In ...
In addition to self-limited myotoxicity, statins have recently been shown to trigger an immune-mediated necrotizing myopathy (IMNM), which is distinguished from polymyositis (PM) and dermatomyositis (DM) by the absence of primary inflammation on muscle biopsy. Previously, we have shown that patients with statin-associated necrotizing myopathy express an autoantibody targeting 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the pharmacological target of statins (1,2). We conducted a case-control study to characterize the comorbidities and detailed individual statin history and to investigate the possible clinical associations that could contribute to the development of anti-HMGCR-positive myopathy in statin-treated patients.. Within our longitudinal cohort, we identified 58 anti-HMGCR-positive statin-exposed myositis patients and 37 comparator myositis patients who were exposed to a statin and were anti-HMGCR negative. All patients met the Bohan and Peter criteria for PM or DM (3,4). Of note, ...
Created to raise public awareness of Juvenile Myositis and to fund research for a cure for JM, including Juvenile Dermatomyositis and Juvenile Polymyositis. Find disease details, news stories, research, and a message board. ...
Myositis (my-o-SY-tis) is a rare type of autoimmune disease that inflames and weakens muscle fibers. Autoimmune diseases occur when the bodys own immune system attacks itself. In the case of myositis, the immune system attacks healthy muscle tissue, which results in inflammation, swelling, pain, and eventual weakness. When there is no skin involvement, it is called polymyositis. When there is skin involvement, it is called dermatomyositis.
TY - JOUR. T1 - The myositis clinical phenotype associated with anti-Zo autoantibodies. T2 - a case series of nine UK patients. AU - Tansley, Sarah L. AU - Betteridge, Zoe. AU - Lu, Hui. AU - Davies, Emma. AU - Rothwell, Simon. AU - New, Paul P. AU - Chinoy, Hector. AU - Gordon, Patrick. AU - Gunawardena, Harsha. AU - Lloyd, Mark. AU - Stratton, Richard. AU - Cooper, Robert. AU - McHugh, Neil J. N1 - © The Author(s) 2019. Published by Oxford University Press on behalf of the British Society for Rheumatology.. PY - 2019/10/26. Y1 - 2019/10/26. N2 - OBJECTIVES: It has been over 10 years since the first report of autoantibodies directed against phenylalanyl tRNA synthetase (anti-Zo) in a patient with features of the anti-synthetase syndrome. In that time no further cases have been published. Here we aim to characterize more fully the clinical phenotype of anti-Zo-associated myositis by describing the clinical features of nine patients.METHODS: Anti-Zo was identified by protein-immunoprecipitation ...
Can anyone throw light on another issue I am interested in, related to myositis of skeletal muscle - thighs, buttocks, and sometimes lower legs? Is exercise of the muscles that give rise to...
Corbus Pharmaceuticals will host Jerry Williams, the Founder and President of MSU, Heather Spadaccini, Jerrys friend and part-time caregiver, and author, Emily A. Filmore, a Co-Founding Director and Current Board Advisor for MSU to share their personal myositis journeys with employees on May 29, 2018.
Walk Strong to Cure JM - wrote - We are walking in the Walk Strong to Cure JM to find a cure for Juvenile Myositis! Juvenile Myositis (JM) is a life-threatening disease which causes the bodys own immune system to attack healthy cells and tissues. It can cause pain, weakness, inability to walk and disfigurement. It can affect virtually any system of the body, the heart, lungs, skin, muscles, and more. But with support from friends and family like you, were getting closer to better treatments and a cure. Last year, we were able to fund research at 10 prestigious research institutions, helping to advance JM research at an unprecedented pace - including important JM research we are funding right here at Lurie Childrens! Your gift now will keep that momentum going. Every donation goes straight to Cure JM, and over 91% of all funds raised go directly to research. Can we count on you to help today?
Thank you, SBPRA, for this nice Press Release for the CureJM Fundraiser! Lets find a cure! Noted Author Sherrill S. Cannon Joins the Fight to Find a Cure for Juvenile Myositis (JM) - Raising Funds for The Cure JM Foundation Juvenile Myositis is a group of rare and life-threatening autoimmune conditions that affect over 17,000…
Proliferative myositis (PM) is a rare benign inflammatory myopathy. It is sometimes classified as a subtype of a pseudosarcomatous proliferative soft-tissue lesion. Epidemiology Thought to commonly occur in middle-aged adults (around 50 years),...
To the Editor:. We read with interest the recent letter by Nagashima, et al1, who suggested that destructive/erosive arthropathy in anti-Jo-1-positive patients with dermatomyositis (DM) sine myositis is another disease subset, classifiable as DM sine myositis overlapping with rheumatoid arthritis (RA). Moreover, the authors state that anticyclic citrullinated peptide antibodies (anti-CCP) are useful for distinguishing subluxing from destructive arthropathy in this setting. We describe our experience on the topic.. We have followed 12 anti-Jo-1-positive patients (8 women, 4 men, ages 46-78 yrs) with antisynthetase syndrome (Table 1). The disease spectrum is characterized by the occurrence of cutaneous findings in all cases ("mechanics hands"), interstitial lung involvement in all cases (by chest high resolution computed tomography, pulmonary function tests, and DLCO), myositis (8/12 patients; muscle biopsy), and arthritis (11/12 patients; clinical observation). All arthritis patients satisfied ...
side or another which might have suggested a unilateral intracranial process, and there does not seem to be an obvious corticospinal pattern of weakness where the flexors of the arm are weaker than the extensors and the extensors of the legs are weaker than the flexors. Moving down the motor fiber pathway, now that we think its less likely to be in the brain or spine, could it be a radiculopathy as the nerves exit the spinal column? Probably not given the widespread distribution of the weakness. Could it be the nerves themselves? Sure, a symmetric progressive polyneuropathy, and something like CIDP or one of its variants, might be possible were the weakness is more distal than proximal. But her weakness is very very proximal. So already I am thinking about disorders which preferentially affect the shoulders and hip flexor muscle groups and the neuromuscular junction, conditions like myasthenia gravis, dermatomyositis, and polymyositis. If her symptoms had not come on so abruptly and progressed ...
Myositis means inflammation of the muscles, and is another autoimmune disorder sometimes associated with lupus. I suffer with this condition too. It is often debilitating and I tend to struggle more with the myositis than I do with lupus. Symptoms of myositis may include muscle weakness, muscle pain, rashes, difficulty swallowing, muscle wasting and generally feeling unwell and tired. At times, my myositis has been so bad that I have been unable to lift my head off my pillow, or lift my arm to do my hair. I regularly struggle with climbing stairs, sitting down and getting up off a chair, swallowing, getting into and out of the bath, and generally getting out and about. It is usually diagnosed through a combination of medical history and tests, which include EMG, muscle biopsy, MRI, CT scans and blood tests checking your muscle enzymes (e.g. Creatinine Kinase) and other inflammatory markers. Myositis is usually treated with steroids and immune-suppressants, similar to lupus. I am one of the ...
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Doctors may use a physical exam, lab tests, imaging tests and a muscle biopsy to diagnose myositis. There is no cure for these diseases, but you can treat the symptoms. Polymyositis and dermatomyositis are first treated with high doses of a corticosteroid. Other options include medications, physical therapy, exercise, heat therapy, assistive devices, and rest.. NIH: National Institute of Neurological Disorders and Stroke. ...
Results Anti-HMGCR antibodies were observed in 2.7% (37/1379 patients) of the UKMYONET database. The predominant reported clinical diagnoses in these patients were polymyositis (21/37) and statin associated myositis (7/37). A positive anti-HMGCR antibody was associated with: HLA-DRB1*11 (53.8% vs 9.9% in anti-HMGCR negative patients, p=0.01), previous statin exposure (31.4% vs 28.6% p=0.032), and higher median peak-creatine kinase (6945.5U/L vs 1159.0U/L, p=0.001). The frequency of anti-HMGCR antibody positivity in the UK appears lower than that seen in other international cohorts (although this may be dependent on the type of patients targeted for collection). ...
PubMed journal article A Comprehensive Overview on Myositis-Specific Antibodies: New and Old Biomarkers in Idiopathic Inflammatory Myopath were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.
Background: The antisynthetase (AS) syndrome is characterized by fever, non-erosive arthritis, inflammatory myopathy, interstitial lung disease, cutaneous involvement, and antibody specificity. Cardiac involvement is extremely rare; we present one of two cases of AS syndrome-associated myocarditis from our institution.. Clinical Case: A 51 year old woman with history of inflammatory arthritis and hypothyroidism presented with 6 months of increasing fatigue, bilateral proximal muscle weakness, leg edema, dyspnea, and orthopnea. Physical examination revealed a Caucasian woman, markedly dyspneic while speaking, with signs of acute decompensated heart failure (HF) including elevated jugular venous pulse, bilateral rales, S3 gallop, and massive peripheral edema with bilateral proximal upper and lower extremity weakness.. Diagnostic Testing: Her muscle weakness was concerning for myopathy along with new HF symptoms. Laboratory studies revealed elevations of serum creatine kinase, aldolase, and cardiac ...
Infectious myositis is an acute, subacute, or chronic infection of skeletal muscle. Once considered a tropical disease, it is now seen in temperate climates as well, particularly with the emergence of HIV infection.
I picked this up from Twitter - Myositis Support in the USA and Idera are hosting a video chat session about a Phase 2 trial for Ideras drug IMO-8400 for treatment of DM. Background to the drug and...
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