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Terapêutica anti-TNF alfa no tratamento da artrite reumatoide
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Abstract(s)
A artrite reumatoide (AR) é uma doença autoimune inflamatória crónica, que tem como principal característica a inflamação das membranas sinoviais articulares, o que origina dor, inchaço, rigidez das articulações e limitação do movimento. A sua evolução causa deformação articular e, consequentemente, eventual incapacidade locomotora. Outros tecidos também podem ser afetados, como os pulmões, coração e olhos.
O diagnóstico e tratamento precoces são essenciais para abrandar a evolução da patologia. Estão disponíveis várias classes de fármacos que podem ser utilizadas no seu tratamento, porém apenas os fármacos modificadores do curso da doença (DMARDs, do inglês, Disease-modifying antirheumatic drugs) previnem a danificação articular e deformação. Estes são classificados como sintéticos/clássicos ou biológicos. Os DMARDs biológicos são fármacos mais recentes, que constituem uma alternativa à ausência de resposta aos fármacos clássicos verificada em alguns pacientes. Têm modos de ação que têm como objetivo diminuir a inflamação, através da inibição dos recetores de interleucina-6 (IL-6), da inibição dos fatores de necrose tumoral alfa (TNF-α), da depleção de linfócitos B e da inibição da co estimulação de células T.
Os TNF-α são citocinas que provocam a apoptose de células tumorais e estimulam a resposta inflamatória, pelo que a sua inibição diminui a inflamação sistémica. Os inibidores destas citocinas foram os primeiros DMARDs biológicos aprovados para o tratamento da artrite reumatoide. Atualmente estão aprovados cinco fármacos: etanercept, infliximab, adalimumab, certolizumab pegol e golimumab.
Nesta monografia apresentam-se capítulos introdutórios ao tema, incluindo as características da patologia, o diagnóstico, e o tratamento, entre outros. Segue-se a apresentação das características dos inibidores de TNF-α aprovados pela Agência Europeia dos Medicamentos (EMA) e das perspetivas futuras desta classe de fármacos no tratamento da artrite reumatoide.
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease, in which the main characteristic is inflammation of the synovial membranes, which causes pain, swelling, joint stiffness and limitation of movement. Its evolution causes joint deformation and, consequently, possible locomotor disability. Other tissues can also be affected, such as the lungs, heart and eyes. Early diagnosis and treatment are essential to slow down the evolution of the pathology. Several classes of drugs are available that can be used in its treatment, but only disease-modifying antirheumatic drugs (DMARDs) may prevent joint damage and deformation. These are classified as synthetic/classic or biological. Biological DMARDs are more recent drugs, which are an alternative to the non-response to classic drugs that happens in some patients. They act by mechanisms of action that aim to reduce inflammation, including interleukin-6 receptors blockade (IL-6), alpha tumor necrosis factors (TNF-α) blockade, depletion of B lymphocytes and T cell co-stimulation inhibition. TNF-α are cytokines that cause tumor cell apoptosis and stimulate the inflammatory response. Thus, their inhibition decreases systemic inflammation. Inhibitors of these cytokines were the first biologic DMARDs approved for the treatment of rheumatoid arthritis. Currently, five drugs are approved: etanercept, infliximab, adalimumab, certolizumab pegol and golimumab. This monograph contains introductory chapters to the subject, including the characteristics of the pathology, diagnosis, treatment, among others, and the presentation of the characteristics of TNF-α inhibitors approved by the European Medicines Agency (EMA) and the future perspectives of this class of drugs in the treatment of rheumatoid arthritis.
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease, in which the main characteristic is inflammation of the synovial membranes, which causes pain, swelling, joint stiffness and limitation of movement. Its evolution causes joint deformation and, consequently, possible locomotor disability. Other tissues can also be affected, such as the lungs, heart and eyes. Early diagnosis and treatment are essential to slow down the evolution of the pathology. Several classes of drugs are available that can be used in its treatment, but only disease-modifying antirheumatic drugs (DMARDs) may prevent joint damage and deformation. These are classified as synthetic/classic or biological. Biological DMARDs are more recent drugs, which are an alternative to the non-response to classic drugs that happens in some patients. They act by mechanisms of action that aim to reduce inflammation, including interleukin-6 receptors blockade (IL-6), alpha tumor necrosis factors (TNF-α) blockade, depletion of B lymphocytes and T cell co-stimulation inhibition. TNF-α are cytokines that cause tumor cell apoptosis and stimulate the inflammatory response. Thus, their inhibition decreases systemic inflammation. Inhibitors of these cytokines were the first biologic DMARDs approved for the treatment of rheumatoid arthritis. Currently, five drugs are approved: etanercept, infliximab, adalimumab, certolizumab pegol and golimumab. This monograph contains introductory chapters to the subject, including the characteristics of the pathology, diagnosis, treatment, among others, and the presentation of the characteristics of TNF-α inhibitors approved by the European Medicines Agency (EMA) and the future perspectives of this class of drugs in the treatment of rheumatoid arthritis.
Description
Keywords
Artrite reumatoide Inibidores dos tnf-? Tratamento Fisiopatologia Etiologia Medicamentos biológicos