Influence of an anti-tumor necrosis factor monoclonal antibody on cytokine levels in patients with sepsis

A pilot study of cerebral tissue oxygenation and postoperative cognitive dysfunction among patients undergoing coronary artery bypass grafting randomised to surgery with or without cardiopulmonary bypass*

“…There were no significant differences in any of these parameters between the two groups of patients. Median (IQR [range]) length of stay in ICU and in hospital was 1 (1-1 [1][2][3][4][5][6][7][8][9][10][11][12]) and 9 (6-12 ) days, respectively, in the CPB group, and 1 (1-1 [1][2][3][4][5][6][7][8]) and 8 (6-11 [4][5][6][7][8][9][10][11][12][13][14][15]) days for patients in the no-CPB group (p = 0.840 and p = 0.552, respectively).…”

“…Early postoperative cognitive tests were performed a median (IQR [range]) of 4 (4-6 [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]) days after surgery and compliance with tests was high. One patient who received CPB suffered a peri-operative stroke, and could not complete the tests at day 4, but was regarded as having early cognitive dysfunction.…”

“…Sceptics claim that postoperative cognitive dysfunction is a statistical aberration arising from methodological weaknesses, or from other temporary factors such as fatigue and lethargy caused by residual drug effects and the stress response to surgery [9]. If, however, one accepts that postoperative cognitive dysfunction exists and is the result of diffuse neuronal injury, then there are two possible conclusions.…”

Anti-IL-10 Therapeutic Strategy Using the Immunomodulator AS101 in Protecting Mice from Sepsis-Induced Death: Dependence on Timing of Immunomodulating Intervention

“…At present, it appears that this approach has not met with the expected successes. Sepsis-induced mortality was not significantly improved in any of the phase II/III studies that have been completed (15,16).…”

Desenvolvimento de anti-hTNFα terapêutico.

“…Apesar dos dados consistentes de proteção que vinham sendo obtidos em modelo experimental (BEUTLER; MILSARK; CERAMI, 1985;BAYSTON;COHEN, 1990;TRACEY et al, 1987), os resultados dos ensaios clínicos não foram satisfatórios. Embora tenha sido observada uma tendência na redução na taxa de mortalidade por choque com diminuição abrupta das concentrações elevadas de TNFα circulante, a diferença entre pacientes tratados com anti-TNFα e o grupo controle não foi significativa (ABRAHAM et al, 1995;DHAINAUT et al, 1995;FISHER et al, 1993). Partindo dos conhecimentos adquiridos, o anti-TNFα passou a ser testado como modulador em outras doenças inflamatórias e autoimunes, mostrando-se eficaz em modelo animal para o tratamento da AR (PIGUET et al, 1992;WILLIAMS;MAINI, 1992), e, progressivamente, conquistando espaço na pesquisa clínica reumatológica para diversas outras doenças.…”