Acetaminophen, like conventional NSAIDs, may reduce synovitis in osteoarthritic knees
Acetaminophen, like conventional NSAIDs, may reduce synovitis in osteoarthritic knees
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DOI：
10.1093/rheumatology/kel100
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发表时间：
2006-11-01
期刊：
影响因子：
5.5
通讯作者：
Buckwalter, Kenneth A.
中科院分区：
文献类型：
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作者：
Brandt, Kenneth D.;Mazzuca, Steven A.;Buckwalter, Kenneth A.
目的：确定使用非甾体抗炎药（NSAIDs）和对乙酰氨基酚（ACET）治疗有症状的膝关节骨关节炎（OA）患者在多大程度上能减少磁共振成像（MRI）所量化的关节积液总量和滑膜组织体积。
方法：连续性初步研究纳入膝关节OA患者，分别使用NSAIDs（n = 10）或ACET治疗，在西安大略大学和麦克马斯特大学疼痛量表评分达到25分中的15分的患者接受1.5T MRI检查。在轴位短T1反转恢复图像中对积液进行量化；为测量滑膜组织体积，在静脉注射钆造影剂3分钟后获取脂肪抑制的T1加权轴位图像。在初次MRI检查后，患者恢复使用常规止痛药物，直至膝关节疼痛严重程度恢复至基线水平，再次测量疼痛程度并重复MRI检查。
结果：停药后服用ACET和NSAIDs的受试者疼痛严重程度相似。重新使用ACET使疼痛评分均值降低50%（P = 1.7×10⁻¹²），与重新使用NSAIDs后的情况相当（49%，P = 6.0×10⁻⁷）。两种药物停药引发膝关节疼痛发作期间测量的平均关节积液总量相当（ACET为16.9 ml，NSAID为16.2 ml；P = 0.884）。重新使用ACET（-4.5 ml，P = 0.009）和NSAID（-3.3 ml，P = 0.013）后，平均关节积液总量均显著减少；两种药物之间的差异无统计学意义。滑膜体积分析得出相似结果。
结论：尽管这些数据未设对照且来自小样本，但表明ACET对膝关节OA患者可能具有显著的抗炎作用，与NSAIDs的效果相当，可能是通过对神经源性炎症产生影响。关节疼痛是OA的临床特征，也是患者最常寻求医疗帮助的原因。由于许多OA患者使用NSAIDs后症状改善，人们普遍认为OA疼痛是由滑膜炎症引起的。然而，OA疼痛的起源众多，可能因患者而异，在同一患者中，每次就诊情况也可能不同。尽管关节软骨通常是该疾病最明显病理变化的部位，但它无神经分布，因此不是关节疼痛的来源。然而，除滑膜外，软骨下骨、关节囊、骨赘、半月板、韧带、关节周围肌腱、附着点和滑囊都含有伤害性神经末梢，化学或物理介质对其刺激可能是OA疼痛的基础。
Objective. To determine the extent to which treatment of patients with symptomatic knee osteoarthritis (OA) with non-steroidal anti-inflammatory drugs (NSAIDs) and acetaminophen (ACET) reduces total effusion volume and synovial tissue volume, as quantified by magnetic resonance imaging (MRI).Methods. Sequential pilot studies used subjects whose knee OA was treated with NSAIDs (n=10) or with ACET = 15 of 25 on the Western Ontario and McMaster Universities' pain scale underwent 1.5T MRI. Effusion was quantified in axial short tau inversion recovery images; to measure synovial tissue volume, fat-suppressed T1-weighted axial images were obtained 3 min after i.v. injection of gadolinium contrast. After the initial MRI examination, patients resumed their customary pain medications until the severity of knee pain returned to baseline, when pain was again measured and the MRI was repeated.Results. Pain severity after washout was similar in subjects taking ACET and NSAIDs. Reinstitution of ACET resulted in a 50% decrease in the mean of pain scores (P=1.7 x 10(-12)) that was comparable with that seen after the reinstitution of NSAID (49%, P=6.0 x 10(-7)). The mean total effusion volume measured during the flare of knee pain induced by the withdrawal of the two drugs was comparable (ACET 16.9 ml, NSAID 16.2 ml; P=0.884). Significant decreases in mean total effusion volume were observed after reinstitution of both ACET (-4.5 ml, P=0.009) and NSAID (-3.3 ml, P=0.013); the difference between drugs was not significant. Analyses of synovial volume yielded similar results.Conclusion. While uncontrolled and derived from small samples, these data suggest that ACET may have a significant anti-inflammatory effect in patients with knee OA, comparable with that achieved with NSAIDs, possibly through an effect on neurogenic inflammation. Joint pain is the clinical feature of OA that most often leads the affected individual to seek medical attention. Because many patients with OA improve symptomatically with the use of NSAIDs, it has been widely assumed that the pain of OA is due to synovial inflammation. However, the origins of OA pain are numerous and may vary from patient to patient and, within the same subject, from visit to visit. Although the articular cartilage is usually the site of the most obvious pathological changes in this disease, it is aneural and, therefore, is not the source of joint pain. However, in addition to the synovium, the subchondral bone, joint capsule, osteophytes, menisci, ligaments, periarticular tendons, entheses and bursae all contain nociceptive nerve endings, stimulation of which by chemical or physical mediators may be a basis for OA pain.