PubMed · 3544325
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J Beurey, M Weber, C Jeandel, P Netter. [Argyria].. https://pubmed.ncbi.nlm.nih.gov/3544325/
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This was conducted to evaluate the analgesic effect of intravenous tenoxicam (non-steroidal anti-inflammatory drug) in the treatment of biliary colic pain and compared with spasmolytics. Thirtytwo patients (26 women, 6 men, mean age 47, range 38-55 years) with acute biliary colic were entered for study. They were allocated randomly to receive either tenoxicam 20 mg i.v. or hyoscine N-butylbromide 20 mg i.v. The patients recorded their pain severity on 5 point scale. The results showed that tenoxicam caused significant pain relief in 10 out of 16 patients at 30 min (mean pain score decreased from 2.75 +/- 0.93 to 0.49 +/- 0.51, p < 0.05) and in other 4 patients at 60 min (mean pain score decreased to 0.58 + 5.7, p < 0.05). None of these patients developed acute cholecystitis or pain relapse over a period of 24 h follow up. With use of hyoscine N-butylbromide, 7 out 16 patients had significant pain relief at 30 min (mean pain score decreased from 2.62 +/- 1.01 to 0.57 +/- 0.53, p < 0.05) and 3 other patients relieved at 60 min (mean pain score decreased to 0.66 +/- 0.57, p < 0.05). Four patients showed pain relapse within 24 h and needed pethidine-rescue treatment, two of them developed acute cholecystitis. Three out of 6 patients who showed no response to hyoscine N-butylbropmide and treated with 100 mg pethidine progressed to acute cholecystitis. We concluded that intravenous tenoxicam has rapid and prolong analgesic effects in the treatment of acute biliary colic as compared to hyoscine N-butylbroimde and it prevents the progression to acute cholecystitis.
We have analyzed the effects of IL-15, a growth factor with IL-2-like properties produced by dendritic and stromal cells, on 3 GM-CSF/IL-3-dependent AML cell lines: M-07e, UT-7 and TF-1. M-07e cells proliferated in response to IL-15, while UT-7 and TF-1 cells failed to respond. In addition, IL-15 supported long-term proliferation of M-07e cells, thus allowing selection of a subline (M-07SB), which displayed an enhanced sensitivity to IL-15. M-07e and M-07SB cells undergo apoptosis following 48-hr growth factor (GM-CSF or IL-15) starvation, as detected by cytofluorimetric analysis and DNA laddering. IL-15 (20 ng/ml) prevented apoptosis in both cell lines. M-07e and M-07SB expressed IL-2R beta, IL-2R gamma, Jak-1 and Jak-3 mRNA, while IL-15R alpha mRNA was undetectable. In contrast, IL-15R alpha was expressed in UT-7 and TF-1 cells, which lacked expression of IL-2R beta mRNA and, in the case of UT-7, also of Jak-3 mRNA. Accordingly, surface IL-2R beta protein was identified only in M-07e and M-07SB cells, by indirect immunofluorescence, while no expression of IL-2R alpha and IL-15R alpha was detected. Anti-IL-2R beta antibodies (10 microg/ml) efficiently blocked (90% inhibition) the proliferation and the anti-apoptotic effect induced by IL-15, while anti-GM-CSFR alpha antibodies had no effect. Anti-IL-2R gamma antibodies were less efficient at proliferation inhibition but synergized with suboptimal concentrations of anti-IL-2R beta antibodies. Our data suggest a role of IL-15 as an anti-apoptotic and mitogenic growth factor for a subset of myeloid leukemias expressing a functional IL-2R beta/gamma complex.
Cytogenetics is considered one of the most valuable prognostic determinants in acute myeloid leukemia (AML). However, many studies on which this assertion is based were limited by relatively small sample sizes or varying treatment approach, leading to conflicting data regarding the prognostic implications of specific cytogenetic abnormalities. The Medical Research Council (MRC) AML 10 trial, which included children and adults up to 55 years of age, not only affords the opportunity to determine the independent prognostic significance of pretreatment cytogenetics in the context of large patient groups receiving comparable therapy, but also to address their impact on the outcome of subsequent transplantation procedures performed in first complete remission (CR). On the basis of response to induction treatment, relapse risk, and overall survival, three prognostic groups could be defined by cytogenetic abnormalities detected at presentation in comparison with the outcome of patients with normal karyotype. AML associated with t(8;21), t(15;17) or inv(16) predicted a relatively favorable outcome. Whereas in patients lacking these favorable changes, the presence of a complex karyotype, -5, del(5q), -7, or abnormalities of 3q defined a group with relatively poor prognosis. The remaining group of patients including those with 11q23 abnormalities, +8, +21, +22, del(9q), del(7q) or other miscellaneous structural or numerical defects not encompassed by the favorable or adverse risk groups were found to have an intermediate prognosis. The presence of additional cytogenetic abnormalities did not modify the outcome of patients with favorable cytogenetics. Subgroup analysis demonstrated that the three cytogenetically defined prognostic groups retained their predictive value in the context of secondary as well as de novo AML, within the pediatric age group and furthermore were found to be a key determinant of outcome from autologous or allogeneic bone marrow transplantation (BMT) in first CR. This study highlights the importance of diagnostic cytogenetics as an independent prognostic factor in AML, providing the framework for a stratified treatment approach of this disease, which has been adopted in the current MRC AML 12 trial.