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      New insights into the treatment of myositis

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          Abstract

          The myositis syndromes include polymyositis, dermatomyositis (DM), necrotizing myopathy, inclusion body myositis (IBM), antisynthetase syndrome and overlap syndromes with myositis. These syndromes mostly occur in middle-aged patients, while juvenile DM occurs in children and adolescents. Patients mostly show a subacute weakness and myalgia in the upper and lower limbs, the diagnosis is based upon these clinical findings in combination with muscle biopsy results and specific serum autoantibodies. In recent years, research achieved a better understanding about the molecular mechanism underlying the myositis syndromes, as well as disease progress and extramuscular organ manifestations, such as interstitial lung disease and association with neoplasias. Treatment mainly consists of glucocorticosteroids and immunosuppressants. IBM is usually refractory to treatments. This review provides an overview of the current standards of treatment and new treatment options like monoclonal antibodies and new molecular therapies and their first results from clinical trials.

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          A controlled trial of high-dose intravenous immune globulin infusions as treatment for dermatomyositis.

          Joshua Stein, Dennis Otero, A Soueidan … (1993)
          Dermatomyositis is a clinically distinct myopathy characterized by rash and a complement-mediated microangiopathy that results in the destruction of muscle fibers. In some patients the condition becomes resistant to therapy and causes severe physical disabilities. We conducted a double-blind, placebo-controlled study of 15 patients (age, 18 to 55 years) with biopsy-proved, treatment-resistant dermatomyositis. The patients continued to receive prednisone (mean daily dose, 25 mg) and were randomly assigned to receive one infusion of immune globulin (2 g per kilogram of body weight) or placebo per month for three months, with the option of crossing over to the alternative therapy for three more months. Clinical response was gauged by assessing muscle strength, neuromuscular symptoms, and changes in the rash. Changes in immune-mediated muscle abnormalities were determined by repeated muscle biopsies. The eight patients assigned to immune globulin had a significant improvement in sores of muscle strength (P < 0.018) and neuromuscular symptoms (P < 0.035), whereas the seven patients assigned to placebo did not. With crossovers a total of 12 patients received immune globulin. Of these, nine with severe disabilities had a major improvement to nearly normal function. Their mean muscle-strength scores increased from 74.5 to 84.7, and their neuromuscular symptoms improved. Two of the other three patients had mild improvement, and one had no change in his condition. Of 11 placebo-treated patients, none had a major improvement, 3 had mild improvement, 3 had no change in their condition, and 5 had worsening of their condition. Repeated biopsies in five patients of muscles whose strength improved to almost normal showed an increase in muscle-fiber diameter (P < 0.04), an increase in the number and a decrease in the diameter of capillaries (P < 0.01), resolution of complement deposits on capillaries, and a reduction in the expression of intercellular adhesion molecule 1 and major-histocompatibility-complex class I antigens. High-dose intravenous immune globulin is a safe and effective treatment for refractory dermatomyositis.
          Article 0 comments Cited 134 times – based on 0 reviews     Review now
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            Mycophenolate mofetil improves lung function in connective tissue disease-associated interstitial lung disease.

            M. Krishnamoorthy, Mikel Olson, Laurie Frankel … (2013)
            Small series suggest mycophenolate mofetil (MMF) is well tolerated and may be an effective therapy for connective tissue disease-associated interstitial lung disease (CTD-ILD). We examined the tolerability and longitudinal changes in pulmonary physiology in a large and diverse cohort of patients with CTD-ILD treated with MMF. We identified consecutive patients evaluated at our center between January 2008 and January 2011 and prescribed MMF for CTD-ILD. We assessed safety and tolerability of MMF and used longitudinal data analyses to examine changes in pulmonary physiology over time, before and after initiation of MMF. We identified 125 subjects treated with MMF for a median 897 days. MMF was discontinued in 13 subjects. MMF was associated with significant improvements in estimated percentage of predicted forced vital capacity (FVC%) from MMF initiation to 52, 104, and 156 weeks (4.9% ± 1.9%, p = 0.01; 6.1% ± 1.8%, p = 0.0008; and 7.3% ± 2.6%, p = 0.004, respectively); and in estimated percentage predicted diffusing capacity (DLCO%) from MMF initiation to 52 and 104 weeks (6.3% ± 2.8%, p = 0.02; 7.1% ± 2.8%, p = 0.01). In the subgroup without usual interstitial pneumonia (UIP)-pattern injury, MMF significantly improved FVC% and DLCO%, and in the subgroup with UIP-pattern injury, MMF was associated with stability in FVC% and DLCO%. In a large diverse cohort of CTD-ILD, MMF was well tolerated and had a low rate of discontinuation. Treatment with MMF was associated with either stable or improved pulmonary physiology over a median 2.5 years of followup. MMF appears to be a promising therapy for the spectrum of CTD-ILD.
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              An antibody blocking activin type II receptors induces strong skeletal muscle hypertrophy and protects from atrophy.

              Estelle Lach-Trifilieff, Jerome Feige, Sophie Brachat … (2014)
              The myostatin/activin type II receptor (ActRII) pathway has been identified to be critical in regulating skeletal muscle size. Several other ligands, including GDF11 and the activins, signal through this pathway, suggesting that the ActRII receptors are major regulatory nodes in the regulation of muscle mass. We have developed a novel, human anti-ActRII antibody (bimagrumab, or BYM338) to prevent binding of ligands to the receptors and thus inhibit downstream signaling. BYM338 enhances differentiation of primary human skeletal myoblasts and counteracts the inhibition of differentiation induced by myostatin or activin A. BYM338 prevents myostatin- or activin A-induced atrophy through inhibition of Smad2/3 phosphorylation, thus sparing the myosin heavy chain from degradation. BYM338 dramatically increases skeletal muscle mass in mice, beyond sole inhibition of myostatin, detected by comparing the antibody with a myostatin inhibitor. A mouse version of the antibody induces enhanced muscle hypertrophy in myostatin mutant mice, further confirming a beneficial effect on muscle growth beyond myostatin inhibition alone through blockade of ActRII ligands. BYM338 protects muscles from glucocorticoid-induced atrophy and weakness via prevention of muscle and tetanic force losses. These data highlight the compelling therapeutic potential of BYM338 for the treatment of skeletal muscle atrophy and weakness in multiple settings.
              Article 0 comments Cited 119 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Stefanie Glaubitz
                Rachel Zeng
                Jens Schmidt:
                ORCID: https://orcid.org/0000-0002-5589-2371
                Journal
                Journal ID (nlm-ta): Ther Adv Musculoskelet Dis
                Journal ID (iso-abbrev): Ther Adv Musculoskelet Dis
                Journal ID (publisher-id): TAB
                Journal ID (hwp): sptab
                Title: Therapeutic Advances in Musculoskeletal Disease
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Print): 1759-720X
                ISSN (Electronic): 1759-7218
                Publication date (Electronic): 8 January 2020
                Publication date Collection: 2020
                Volume: 12
                Electronic Location Identifier: 1759720X19886494
                Affiliations
                [1-1759720X19886494]Department of Neurology, Muscle Immunobiology Group, Neuromuscular Center, University Medical Center Göttingen, Göttingen, Germany
                [2-1759720X19886494]Department of Neurology, Muscle Immunobiology Group, Neuromuscular Center, University Medical Center Göttingen, Göttingen, Germany
                [3-1759720X19886494]Department of Neurology, Muscle Immunobiology Group, Neuromuscular Center, University Medical Center Göttingen, Robert-Koch-Sr. 40, 37075 Göttingen, Germany
                Author notes
                Author information
                https://orcid.org/0000-0002-5589-2371
                Article
                Publisher ID: 10.1177_1759720X19886494
                DOI: 10.1177/1759720X19886494
                PMC ID: 6950531
                PubMed ID: 31949477
                SO-VID: 848589bd-d5ad-4279-8ae1-ebb6a56919af
                Copyright © © The Author(s), 2020
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 4 July 2019
                Date accepted : 10 October 2019
                Categories
                Subject: Review
                Custom metadata
                cover-date January-December 2020
                typesetter ts1

                Keywords: myositis,polymyositis,dermatomyositis,inclusion body myositis,necrotizing myopathy,antisynthetase syndrome,overlap syndrome
                Data availability:
                Keywords: myositis, polymyositis, dermatomyositis, inclusion body myositis, necrotizing myopathy, antisynthetase syndrome, overlap syndrome

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