Autoantibody profiles in the sera of European patients with myositis

Brouwer, R.; Hengstman, G.J.D.; Egberts, W.T.M. Vree; Ehrfeld, H.; Božič, Borut; Ghirardello, Anna; Gröndal, Gerður; Hietarinta, M.; Isenberg, David; Kalden, Joachim R.; Lundberg, Ingrid E.; Moutsopoulos, H. M.; Roux‐Lombard, Pascale; Vencovský, Jiří; Wikman, Anna-Lis; Seelig, H. P.; Engelen, B.G.M. van; Venrooij, W.J.W. van

doi:10.1136/ard.60.2.116

Cited by 352 publications

(224 citation statements)

References 48 publications

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“…For a control IFN␣ inducer, ultraviolet-inactivated herpes simplex virus type 1 (HSV-1) was prepared and used as described previously (15). The cell cultures were incubated for 20 hours at 37°C in 7% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti–Jo‐1 or anti–Ro 52/anti–Ro 60 autoantibodies

Eloranta

Helmers

Ulfgren

et al. 2007

Arthritis & Rheumatism

164

128

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Objective. To investigate type I interferon (IFN) system activation and its correlation with autoantibodies and organ manifestations in polymyositis (PM), dermatomyositis (DM), and inclusion body myositis.Methods. Sera from 30 patients and 16 healthy controls, or purified IgG, were combined with material released from necrotized cells to stimulate Conclusion. Immune complexes containing antiJo-1 or anti-Ro 52/anti-Ro 60 autoantibodies and RNA may act as endogenous IFN␣ inducers that activate IFN␣ production in PDCs. These PDCs could be of importance for inducing myositis, whereas in DM patients without autoantibodies the presence of MX-1 protein in capillaries suggests another cellular IFN␣ source and induction mechanism. Consequently, the type I IFN system may be of importance in both PM and DM, but via different pathways.The idiopathic inflammatory myopathies polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM) are characterized by symmetric, proximal muscle weakness and decreased muscle endurance. Other organs are frequently involved, such as skin in DM and lungs in PM and DM. Shared classic histopathologic features are the presence of inflammatory cell infiltrates in skeletal muscle tissue, dominated by T cells and macrophages, and regenerating and degenerating muscle fibers (1). Another characteristic feature is the presence of autoantibodies, of which anti-histidyltransfer RNA synthetase (anti-HisRS or anti-Jo-1) is one of the most frequent (2). This autoantibody is considered myositis specific and is associated with a distinctive clinical phenotype, the so-called antisynthetase syndrome, which is characterized by myositis, Raynaud's phenomenon, interstitial lung disease (ILD),

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Section: Methodsmentioning

confidence: 99%

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti–Jo‐1 or anti–Ro 52/anti–Ro 60 autoantibodies

Eloranta

Helmers

Ulfgren

et al. 2007

Arthritis & Rheumatism

164

128

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“…A recent systematic review of IIM epidemiology estimated an incidence of 7.98 per million/year and a prevalence of 14/ 100,000 (10). The prevalence of antisynthetase antibodies ranges from 20-40% in patients with IIM (11,12). Presenting symptoms in antisynthetase syndrome most commonly include myalgia (in 86% of patients), arthritis, or arthralgia (in 69%) and shortness of breath (in 64%) (13).…”

Section: Discussionmentioning

confidence: 99%

Respiratory Distress and Nephropathy in a Young Male With Small‐Joint Polyarthritis

Korsten

Konig

Müller

et al. 2016

Arthritis Care & Research

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History of the present illness. A 27-year-old man presented to our department with a 4-week history of worsening fatigue, malaise, and painful swelling of his wrists and finger joints. He further complained of new-onset progressive dyspnea with nonproductive cough, subfebrile temperatures, and proximal muscle weakness in his lower extremities in the last 10 days. Except for the arthritis, he had not experienced these symptoms in the past. Two months prior to admission, he was seen for the first time by a rheumatologist. At that time, he reported severe pain and stiffness in his hands, particularly at night, but no breathing or muscle difficulties. Laboratory tests at the rheumatologist's office showed increased C-reactive protein (CRP) levels and high-titer anti-cyclic citrullinated peptide (CCP) antibodies. Plain radiographs demonstrated an erosion at the fifth metatarsal head of his right foot. He was diagnosed with rheumatoid arthritis (RA) and started on oral methotrexate (MTX) and prednisone. Medical historyThe patient reported having intermittent arthralgias in his hands, elbows, and hips for the past 3 years. He had been treated with nonsteroidal antiinflammatory drugs and oral glucocorticoids as needed by his primary care provider. In the last couple of months, he increasingly experienced painful arthritis in his hands. After being diagnosed with RA, oral treatment with MTX 15 mg weekly and prednisone 50 mg daily (followed by slow tapering) was initiated, along with prophylactic pantoprazole (40 mg daily) and folic acid (5 mg weekly). He was adherent to the therapy and denied taking over-the-counter drugs or supplements. There were no other medical or surgical illnesses.Social and family history. He used to work as a gardener. His social history was negative for smoking and alcohol abuse. He denied recent travel or contact with someone with similar symptoms. His grandmother had a diagnosis of RA, but his family history was otherwise negative for autoimmune or pulmonary disorders. Review of systems.There was no history of photosensitivity, rash, sicca symptoms, Raynaud's phenomenon, back pain, hemoptysis, dysphagia, or diarrhea.Physical examination. On admission, his temperature was 37.08C, blood pressure 130/80 mm Hg, pulse 105 beats per minute, respiratory rate 24 breaths per minute, and oxygen saturation of 95% while breathing ambient air. There was no lymphadenopathy, jaundice, or cyanosis. Auscultation of the lung revealed fine bibasilar crackles. Cardiac (except tachycardia), abdominal, and neurologic examinations were unremarkable. His wrists, metacarpophalangeal, and proximal interphalangeal joints of both hands were swollen and tender with limited range of motion. There was isolated weakness of the thigh muscles (4/5), but no muscle wasting or fasciculations.Laboratory tests and imaging. Initial workup showed a hemoglobin level of 14.5 gm/dl (normal range [NR] 13.5-17.5), white blood cell count of 13.3 3 10 3 /ml (NR 4-11 3 10 3 ), and platelets of 273 3 10 3 /ml (NR 150-350 3 10 3 ). The differe...

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“…However, plasmaapheresis is already done for almost 3 years and is still continued without any side eVects. According to Hengstman et al [9,13], treatment for myositis may be done for years.…”

Section: Discussionmentioning

confidence: 99%

“…DiVuse alveolar damage is reported to have the worst prognosis and bronchiolitis obliterans organizing pneumonia (BOOP/COP) has the most favorable prognosis [10,15,19]. Anti-SRP antibodies, which are mainly polymyositis speciWc, may also be found in dermatomyositis or systemic sclerosis [5,9,13]. In a recent report, Suzuki et al [20] suggest to classify SRP positive myositis as a particular form of polymyositis.…”

Section: Discussionmentioning

confidence: 99%

Signal recognition particle (SRP) positive myositis in a patient with cryptogenic organizing pneumonia (COP)

et al. 2009

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We report of a 46-year-old female patient with cryptogen organizing pneumonia preceeding the rare SRP positive necrotising myositis without cardiac involvement and no sign of dysphagia. Myositis showed full regression without oral immune suppression but with extracorporeal treatment, performed as a combined therapy of plasmaexchange and immunoadsorption. After 33-month of treatment, anti-SRP antibodies were not detectable any more.

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Autoantibody profiles in the sera of European patients with myositis

Cited by 352 publications

References 48 publications

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti–Jo‐1 or anti–Ro 52/anti–Ro 60 autoantibodies

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti–Jo‐1 or anti–Ro 52/anti–Ro 60 autoantibodies

Respiratory Distress and Nephropathy in a Young Male With Small‐Joint Polyarthritis

Signal recognition particle (SRP) positive myositis in a patient with cryptogenic organizing pneumonia (COP)

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