RESUMO
Psoriasis is a chronic inflammatory condition that often requires life-long treatment. Conventional therapies have not fully met the needs of psoriatic patients, because of limited efficacy, adverse effects with cumulative use, and patient inconvenience. In the past decade, biologic immunotherapies have become accepted treatments for psoriasis as a result of perceived efficacy and safety on the part of patients and practitioners. However, most data on these medications come from relatively limited short-term trials. In this review, we will focus on the available long-term data on the efficacy of the biologic agents. We will emphasize the strengths and weakness of the available data of the biologic agents that are Food and Drug Administration (FDA)-approved for the treatment of moderate to severe psoriasis (alefacept, efalizumab,* etanercept, infliximab, and adalimumab), with the inclusion of a newer agent currently under FDA evaluation (ustekinumab).
Assuntos
Produtos Biológicos/uso terapêutico , Fármacos Dermatológicos/uso terapêutico , Psoríase/tratamento farmacológico , Produtos Biológicos/efeitos adversos , Terapia Biológica/métodos , Fármacos Dermatológicos/efeitos adversos , Aprovação de Drogas , Humanos , Índice de Gravidade de Doença , Estados Unidos , United States Food and Drug AdministrationRESUMO
Psoriasis is a common, chronic, inflammatory skin disease that can have a significant impact on the quality of life of those who are afflicted. Recent advances in the understanding of the pathophysiology of psoriasis have led to the development of new, genetically engineered, targeted therapies for this disease. Among the most successful strategies for treatment has been the use of biologic immunotherapies targeting tumor necrosis factor alpha (TNF). Recent research has evaluated the efficacy and safety of a new anti-TNF agent, adalimumab. Adalimumab is a human monoclonal antibody that is approved by the US Food and Drug Administration (FDA) and the European Medicines Agency (EMEA) for the treatment of rheumatoid arthritis and psoriatic arthritis. Recently released data from large, randomized clinical trials suggests that adalimumab has significant efficacy for the treatment of chronic plaque psoriasis and is well tolerated. Thus, adalimumab seems to be a promising therapeutic approach for patients who suffer from moderate to severe plaque psoriasis.
RESUMO
UNLABELLED: The use of pancuronium in fast-track cardiac surgical patients may be associated with delays in clinical recovery. Our objective in this study was to evaluate the incidence and severity of residual neuromuscular blockade after cardiac surgery in patients randomized to receive either pancuronium (0.08-0.1 mg/kg) or rocuronium (0.6-0.8 mg/kg). Eighty-two patients undergoing cardiopulmonary bypass were randomized to a pancuronium (n = 41) or rocuronium (n = 41) group. Intraoperative and postoperative management was standardized. In the intensive care unit, train-of-four (TOF) ratios were measured each hour until weaning off ventilatory support was initiated. Neuromuscular blockade was not reversed. After tracheal extubation, patients were examined for signs and symptoms of residual paresis. When weaning of ventilatory support was initiated, significant neuromuscular blockade was present in the pancuronium subjects (TOF ratio: median, 0.14; range, 0.00-1.11) compared with the rocuronium subjects (TOF ratio: median, 0.99; range, 0.87-1.21) (P < 0.05). Patients in the rocuronium group were more likely to be free of signs and symptoms of residual paresis than patients in the pancuronium group. Our findings suggest that the use of longer-acting muscle relaxants in cardiac surgical patients is associated not only with impaired neuromuscular recovery, but also with signs and symptoms of residual muscle weakness in the early postoperative period. IMPLICATIONS: The use of long-acting muscle relaxants in fast-track cardiac surgical patients is associated with significant residual neuromuscular block in the intensive care unit, including signs and symptoms of residual paresis.