Etanercept in the treatment of macrophage activation syndrome.

@article{Prahalad2001EtanerceptIT,
  title={Etanercept in the treatment of macrophage activation syndrome.},
  author={Sampath Prahalad and Kevin E. Bove and Duane Dickens and Daniel J. Lovell and Alexei A. Grom},
  journal={The Journal of rheumatology},
  year={2001},
  volume={28 9},
  pages={2120-4}
}
Macrophage activation syndrome (MAS), a recognized complication of systemic juvenile rheumatoid arthritis (sJRA), has been associated with significant morbidity and mortality. Dysregulation of macrophage-lymphocyte interactions leading to uncontrolled proliferation of highly activated macrophages and massive release of proinflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha) appears to be central to the pathogenesis of this syndrome. Until now the mainstay of therapy has been… CONTINUE READING

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Until now the mainstay of therapy has been corticosteroids and cyclosporin A. We describe a patient with MAS and sJRA successfully treated with the anti - TNF agent etanercept .
Until now the mainstay of therapy has been corticosteroids and cyclosporin A. We describe a patient with MAS and sJRA successfully treated with the anti - TNF agent etanercept .
Dysregulation of macrophage - lymphocyte interactions leading to uncontrolled proliferation of highly activated macrophages and massive release of proinflammatory cytokines including tumor necrosis factor - alpha ( TNF - alpha ) appears to be central to the pathogenesis of this syndrome .
Dysregulation of macrophage - lymphocyte interactions leading to uncontrolled proliferation of highly activated macrophages and massive release of proinflammatory cytokines including tumor necrosis factor - alpha ( TNF - alpha ) appears to be central to the pathogenesis of this syndrome .
Dysregulation of macrophage - lymphocyte interactions leading to uncontrolled proliferation of highly activated macrophages and massive release of proinflammatory cytokines including tumor necrosis factor - alpha ( TNF - alpha ) appears to be central to the pathogenesis of this syndrome .
Dysregulation of macrophage - lymphocyte interactions leading to uncontrolled proliferation of highly activated macrophages and massive release of proinflammatory cytokines including tumor necrosis factor - alpha ( TNF - alpha ) appears to be central to the pathogenesis of this syndrome .
Dysregulation of macrophage - lymphocyte interactions leading to uncontrolled proliferation of highly activated macrophages and massive release of proinflammatory cytokines including tumor necrosis factor - alpha ( TNF - alpha ) appears to be central to the pathogenesis of this syndrome .
Dysregulation of macrophage - lymphocyte interactions leading to uncontrolled proliferation of highly activated macrophages and massive release of proinflammatory cytokines including tumor necrosis factor - alpha ( TNF - alpha ) appears to be central to the pathogenesis of this syndrome .
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