RESUMO
The most common types of chronic inflammatory arthritis are rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis. In order to assess the activity of these diseases and tailor therapy, several outcome measures have been developed. They include composite scores based on clinical findings, biochemical markers and patient questionnaires. This article discusses the most commonly used outcome measures and looks at their limitations in quantifying the complex clinical features of different types of inflammatory arthritis, focusing in particular on rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis.
Assuntos
Artrite Psoriásica , Artrite Reumatoide , Gerenciamento Clínico , Avaliação de Resultados em Cuidados de Saúde/métodos , Espondilite Anquilosante , Artrite Psoriásica/fisiopatologia , Artrite Psoriásica/terapia , Artrite Reumatoide/fisiopatologia , Artrite Reumatoide/terapia , Humanos , Projetos de Pesquisa , Índice de Gravidade de Doença , Espondilite Anquilosante/fisiopatologia , Espondilite Anquilosante/terapia , Avaliação de Sintomas/métodosAssuntos
Complicações na Gravidez/diagnóstico , Doença de Still de Início Tardio/diagnóstico , Adulto , Anti-Inflamatórios/uso terapêutico , Feminino , Humanos , Imunoglobulinas Intravenosas/uso terapêutico , Inflamação/diagnóstico , Inflamação/tratamento farmacológico , Inflamação/imunologia , Metilprednisolona/uso terapêutico , Gravidez , Complicações na Gravidez/tratamento farmacológico , Complicações na Gravidez/imunologia , Doença de Still de Início Tardio/tratamento farmacológico , Doença de Still de Início Tardio/imunologiaRESUMO
Despite often knowing the aetiology of sepsis and its clinical course there has not been the anticipated advances in treatment strategies. Cytokines are influential mediators of immune/inflammatory reactions and in patients with sepsis high circulating levels are implicated in the onset and perpetuation of organ failure. Antagonising the activities of pro-inflammatory cytokines enhances survival in animal models of sepsis but, so far, such a therapeutic strategy has not improved patient outcome. This article addresses the questions of why encouraging laboratory findings have failed to be translated into successful treatments of critically ill patients and whether modifying cytokine activity still remains a promising avenue for therapeutic advance in severe sepsis. In pursuing this task we have selected reports that we believe provide an incisive, critical and balanced view of the topic.
