ANTI-TUMOR NECROSIS FACTOR ALPHA BIOLOGIC THERAPY DOSE ADJUSTMENT NECESSITY IN PATIENTS WITH RHEUMATOID ARTHRITIS. A CASE PRESENTATION

L. Muflic, I. Ion
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Abstract

Rheumatoid arthritis is an inflammatory disease characterized by chronic joint erosive processes, affecting approximately 1% of the population. [1] The pathogenic mechanisms processes involve the activation of pro-inflammatory cytokines, including TNF alpha. [2] The purpose of this case presentation is to elucidate a possible correlation between the high level of blood TNF alpha and the apparent lack of response to biologic therapy directed against this molecule. A female patient, aged 55 years, diagnosed with rheumatoid arthritis in 2006, presents an increased inflammatory biological syndrome. The patient was being treated biologically (adalimumab, and two years of etanercept previously. One year ago, the patient presents the elevation values of the blood tests commonly used to monitor the status of patients with inflammatory rheumatoid arthritis up to 2.5-3 x than normal values. Initially, this increase is considered to be due to a respiratory seasonal condition. We continued monitoring the status, after subsequent remission of these respiratory disorders, and we observed the persistence of those elevated test, this time without an obvious possible causing comorbidity. We decided to evaluate the current patient status and we obtained the following information: Biological syndrome currently moderately exceeds the maximum normal values. ESR was 47 mm/h and CRP 1.5 than the normal value. TNF alpha value determined by immunochemical methods with detection by chemiluminescence (CLIA) is 67.2 pg / mL Biological confirmation by determining serum TNF alpha and increased observation that the current level may be one explanation for the possible reactivation of the disease prompted us to continue the study in patients receiving anti-TNF alpha biologic. This study is ongoing. We can imagine this correlation between the level of TNF alpha and the degree of disease activity at least in the case of a group of patients treated with biological drugs. If this could be demonstrated, then perhaps we can expect a change in the curative approach of these patients, meaning that dose adjustment can be considered depending on the level of TNF alpha, and why not, depending on other cytokines that may be included in future studies.
类风湿关节炎患者抗肿瘤坏死因子生物治疗剂量调整的必要性。案例展示
类风湿关节炎是一种以慢性关节侵蚀过程为特征的炎症性疾病,影响约1%的人口。[1]其致病机制涉及包括TNF α在内的促炎细胞因子的激活。[2]本病例报告的目的是阐明高水平血液TNF α与针对该分子的生物治疗明显缺乏反应之间的可能相关性。女性患者,55岁,2006年诊断为类风湿关节炎,炎症生物学综合征增加。患者此前正在接受生物治疗(阿达木单抗和2年依那西普)。一年前,患者通常用于监测炎症性类风湿关节炎患者状态的血液检查的升高值比正常值高2.5-3倍。最初,这种增加被认为是由于呼吸道季节性疾病。在这些呼吸系统疾病缓解后,我们继续监测状态,我们观察到这些升高的测试持续存在,这一次没有明显的可能引起合并症。我们决定评估当前患者的状态,我们获得了以下信息:生物学综合征目前中度超过最大正常值。ESR为47 mm/h, CRP高于正常值1.5。通过免疫化学方法和化学发光(CLIA)检测的TNF - α值为67.2 pg / mL,通过测定血清TNF - α的生物学证实,以及对当前水平可能是疾病可能再激活的一种解释的观察增加,促使我们继续在接受抗TNF - α生物制剂的患者中进行研究。这项研究正在进行中。我们可以想象TNF α水平与疾病活动程度之间的这种相关性,至少在一组接受生物药物治疗的患者中是这样。如果这可以被证明,那么也许我们可以期待这些患者的治疗方法的改变,这意味着剂量调整可以考虑取决于TNF α的水平,为什么不呢,取决于其他细胞因子可能包括在未来的研究中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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