Rituximab in refractory idiopathic inflammatory myopathies and antisynthetase syndrome: personal experience and review of the literature

Nalotto, Linda; Iaccarino, Leonardo; Zen, Margherita; Gatto, Mariele; Borella, Elisabetta; Domenighetti, Marta; Punzi, Leonardo; Doria, Andrea

doi:10.1007/s12026-013-8408-9

Cited by 46 publications

(37 citation statements)

References 57 publications

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“…On the other hand, dermatomyositis is marked by a complement-mediated microangiopathy, typically mediated by type I IFN phenotype and autoantibodies with distinct specificities 70,71 ; however, the exact mechanism involved in complement activation remains unclear. 72 Current biological treatments in polymyositis/dermatomyositis include blockade of cells and cytokines, including B-cells by rituximab, 73 T cells by abatacept and cytokines by anti-IL-1, anti-IL-6 or anti-IFNa monoclonal antibodies. 74 Autoantibodies to gal-3 were found more frequently in the sera of patients with polymyositis/dermatomyositis than in those with other autoimmune diseases, including RA, pSS, SSc and SLE.…”

Section: Polymyositis/dermatomyositismentioning

confidence: 99%

Galectin-3 in autoimmunity and autoimmune diseases

Oliveira

Gatto

Bassi

et al. 2015

Exp Biol Med (Maywood)

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143

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Galectin-3 (gal-3) is a b-galactoside-binding lectin, which regulates cell-cell and extracellular interactions during self/ non-self-antigen recognition and cellular activation, proliferation, differentiation, migration and apoptosis. It plays a significant role in cellular and tissue pathophysiology by organizing niches that drive inflammation and immune responses. Gal-3 has some therapeutic potential in several diseases, including chronic inflammatory disorders, cancer and autoimmune diseases. Gal-3 exerts a broad spectrum of functions which differs according to its intra-or extracellular localization. Recombinant gal-3 strategy has been used to identify potential mode of action of gal-3; however, exogenous gal-3 may not reproduce the functions of the endogenous gal-3. Notably, gal-3 induces monocyte-macrophage differentiation, interferes with dendritic cell fate decision, regulates apoptosis on T lymphocytes and inhibits B-lymphocyte differentiation into immunoglobulin secreting plasma cells. Considering the influence of these cell populations in the pathogenesis of several autoimmune diseases, gal-3 seems to play a role in development of autoimmunity. Gal-3 has been suggested as a potential therapeutic agent in patients affected with some autoimmune disorders. However, the precise role of gal-3 in driving the inflammatory process in autoimmune or immune-mediated disorders remains elusive. Here, we reviewed the involvement of gal-3 in cellular and tissue events during autoimmune and immune-mediated inflammatory diseases.

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Section: Polymyositis/dermatomyositismentioning

confidence: 99%

Galectin-3 in autoimmunity and autoimmune diseases

Oliveira

Gatto

Bassi

et al. 2015

Exp Biol Med (Maywood)

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143

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“…Em casos resistentes à terapêutica convencional tem sido usado rituximab com algum sucesso 12 . É mais frequente haver uma boa resposta à terapêutica a nível muscular, mas apesar do tratamento imunossupressor pode continuar a haver detioração pulmonar, sendo esta a principal causa de morbimortalidade 6 .…”

Section: Discussionunclassified

Doença pulmonar intersticial como primeir|a manifestação de síndrome anti-sintetase

Pires¹,

Sousa²,

Julião³

et al. 2014

Gal. Clin.

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ResumoConsidera-se a presença do síndrome em pacientes com anticorpos antisintetase associados a duas das seguintes características, doença pulmonar intersticial, miopatia inflamatória e poliarterite inflamatória.Apresentamos o caso de um homem com diagnóstico efectuado há 13 anos, durante um internamento por "pneumonia", apresentando queixas de dispneia para esforços e cansaço fácil com 3 meses de evolução. Durante o internamento é identificada uma doença pulmonar intersticial e posteriormente surge um quadro de mialgias com elevação marcada das enzimas musculares. A electromiografia mostrou um padrão sugestivo de miopatia e identificou-se anticorpos anti-Jo-1, estabelecendo-se o diagnóstico de síndrome anti-sintetase. Sob terapêutica imunossupressora desde então, mantém seguimento em consulta externa, encontrando-se clinicamente bem.Palavras chave: síndrome antisintetasa; enfermedad pulmonar intersticial; miositis; anti-Jo-1. AbstractThe syndrome is generally considered present in patients with an antisynthetase antibody plus two of the following features, interstitial lung disease, inflammatory myopathy, and inflammatory polyarthritis.We report the case of a man with diagnosis made 13 years ago, during hospitalization for "pneumonia" with complaints of effort dyspnea and tiredness with 3 months of evolution. Non infectious interstititial lung disease was finally demonstrated and subsequently myalgia occurs with a marked elevation of muscle enzymes. Electromyography shows a pattern suggestive of myopathy and with identification of anti-Jo-1 the diagnosis of anti-synthetase syndrome is established. The patient is on immunosuppressive treatment since then, being followed at the outpatient clinic, without symptoms at the present moment.Keywords: anti-synthetase syndrome; interstitial lung disease; anti-Jo-1; myositis. IntroduçãoO síndrome anti-sintetase caracteriza-se pela associação de duas das seguintes características, doença pulmonar intersticial (DPI), miopatia inflamatória e poliarterite inflamatória com a presença de anticorpos anti-sintetase. Laboratorialmente é marcada pela presença de anticorpos anti-aminoacil-RNAt sintetase (anti-sintetase), sendo mais frequente o anti-Jo-1 1 . Trata-se de uma doença pouco comum, com uma prevalência de 1,5 por 100.000 habitantes 2 , tendo sido descrita em 1990 por Marguerie C, et al. Caso ClínicoApresentamos o caso de um homem, de 65 anos, não fumador, com antecedentes de hiperplasia benigna da próstata e doença coronária, que apresentava queixas de dor pré-cordial, cansaço fácil e dispneia para pequenos esforços com 3 meses de evolução associado nas duas ultiamas semanas a sudorese nocturna e tosse produtiva. Recorreu à consulta de Cardiologia (em Junho de 2000) tendo realizado prova de esforço e ecocardiograma que não mostraram alterações. Posteriormente recorreu ao Serviço de Urgência (SU), onde no estudo realizado se constatou a presença no RX de tórax de opacidades heterogéneas de ambas as bases e hipoxémia (pO 2 de 69,1mmHg) na gasimetria arterial. Este quadro f...

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“…Although many recent studies and case reports insist on the high rates of clinical response to rituximab [58][59][60], larger clinical trials aiming to address the benefit of rituximab as therapy in inflammatory myopathies are awaited. In particular, the relationship between response to rituximab and clinical and serological subsects of patients should be explored.…”

Section: Biological Therapiesmentioning

confidence: 99%

Idiopathic Inflammatory Myopathies: an Update on Classification and Treatment with Special Focus on Juvenile Forms

Pagnini

Vitale

Selmi

et al. 2015

Clinic Rev Allerg Immunol

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Juvenile inflammatory myopathies represent a heterogeneous group of rare and potentially fatal disorders of unknown aetiology, characterised by inflammation and proximal and symmetric muscle weakness. Beyond many similarities, specific clinical, laboratoristic and histopathologic features underlie different subsets with distinguishing demographic, prognostic and therapeutic peculiarities. Over time, several forms of inflammatory idiopathic myopathies have been described, including macrophagic myofascitis, immune-mediated necrozing myopathy and the spectrum of amyopathic dermatomyositis that include hypomyopathic dermatomyositis, inclusion body myositis and cancer-associated myositis occurring almost exclusively in adults. However, juvenile dermatomyositis is the most frequent in childhood, whereas polymyositis is relatively more frequent in adults. The aetiology is nowadays widely unclear; however, current theories contemplate a combination of environmental triggers, immune dysfunction and specific tissue responses involving muscle, skin and small vessels endothelium in genetically susceptible individuals. Myositis-specific autoantibodies, found almost exclusively in patients with myositis and myositis-associated autoantibodies, detectable both among patients with myositis and in subjects suffering from other autoimmune diseases, have an important clinical role because of their relation to specific clinical features, response to therapy and prognosis. The gold standard treatment for juvenile dermatomyositis is represented by corticosteroids, along with adjunctive steroid-sparing immunosuppressive therapies, which are used to counteract disease activity, prevent mortality, and reduce long-term disability. Further treatment approach such as biologic agents and autologous stem cell transplantation are emerging during the last years, in particular in patients difficult to treat and with poor prognosis. Therefore, a highly medical specialised approach is required for diagnosis and management of these conditions. This review comprehensively examines juvenile inflammatory myopathies focusing on clinical and laboratory classifications as well as on the current treatment approaches, referring in particular on biologic agents and latest therapeutic opportunities.

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Rituximab in refractory idiopathic inflammatory myopathies and antisynthetase syndrome: personal experience and review of the literature

Cited by 46 publications

References 57 publications

Galectin-3 in autoimmunity and autoimmune diseases

Galectin-3 in autoimmunity and autoimmune diseases

Doença pulmonar intersticial como primeir|a manifestação de síndrome anti-sintetase

Idiopathic Inflammatory Myopathies: an Update on Classification and Treatment with Special Focus on Juvenile Forms

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