THE SYNOVIAL PROSTAGLANDIN SYSTEM IN CHRONIC INFLAMMATORY ARTHRITIS - DIFFERENTIAL-EFFECTS OF STEROIDAL AND NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
THE SYNOVIAL PROSTAGLANDIN SYSTEM IN CHRONIC INFLAMMATORY ARTHRITIS - DIFFERENTIAL-EFFECTS OF STEROIDAL AND NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
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DOI：
10.1111/j.1476-5381.1981.tb08743.x
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发表时间：
1981-01-01
影响因子：
7.3
通讯作者：
PUGLIESE, F
中科院分区：
文献类型：
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作者：
BOMBARDIERI, S;CATTANI, P;PUGLIESE, F
1本研究旨在描述类风湿性关节炎或银屑病关节炎患者滑液中花生四烯酸代谢产物的谱，并比较6α-甲基强的松龙（6-MeP：4-8 mg/天）或吲哚洛芬（1.2 g/天）短期治疗后其浓度的变化，吲哚洛芬是一种非甾体抗炎药，具有证实的滑液前列腺素抑制作用。2采用放射免疫分析法测定23例患者关节液中前列腺素E2（PGE 2）、血栓素B2（TX B2）、6-酮-PGF 1 α和PGF 2 α的含量，并对提取的免疫反应物进行薄层层析分析。3PGE_2和TXB_2在未经治疗的患者中占总免疫反应性的60%以上。在滑液中检测到的不同花生四烯酸代谢物之间不存在任何恒定比率，这与这些化合物的异质细胞来源一致。4吲哚洛芬治疗与滑膜前列腺素和血栓素浓度的一致降低相关，范围从6-酮-PGF 1 α的36%到PGE 2的90%。5相反，6-MeP引起不同的代谢产物通过环氧合酶途径的相反的变化。因此，6-MeP后6-keto-PGF 1 α浓度降低35%，PGF 2 α浓度升高30%，而PGE 2和TXB 2无变化。6虽然6-MeP不能降低滑膜PGE 2和TXB 2水平的机制尚不确定，但本研究的结果清楚地表明，治疗剂量的甾体和非甾体抗炎药引起花生四烯酸代谢的明显变化，这可能与其特定的治疗作用和副作用有关。
1 The present study was undertaken to characterize the spectrum of arachidonic acid metabolites present in synovial effusions of patients with rheumatoid or psoriatic arthritis, and to compare changes in their concentration following a short-term treatment with 6α-methyl-prednisolone (6-MeP: 4-8 mg/day) or indoprofen (1.2 g/day), a nonsteroidal anti-inflammatory agent with proven synovial prostaglandin inhibitory effect. 2 Measurements of prostaglandin E2 (PGE2), thromboxane (TX) B2, 6-keto-PGF1α and PGF2α were performed by radioimmunoassay techniques in synovial effusions obtained from 23 patients, and validated by thin-layer chromatographic analysis of the extracted immunoreactivity. 3 PGE2 and TXB2 accounted for more than 60% of the total immunoreactivity in untreated patients. The absence of any constant ratio between the different arachidonic acid metabolites detected in synovial fluid is consistent with a heterogeneous cellular origin of these compounds. 4 Indoprofen treatment was associated with a consistent reduction of synovial prostaglandin and thromboxane concentrations, ranging from 36% in the case of 6-keto-PGF1α to 90% in the case of PGE2. 5 In contrast, 6-MeP caused opposite changes on different metabolites originating via the cyclo-oxygenase pathway. Thus, 6-keto-PGF1α concentrations were reduced by 35%, PGF2α concentrations were increased by 30%, while PGE2 and TXB2 were unchanged following 6-MeP. 6 Although the mechanism(s) underlying the failure of 6-MeP to reduce synovial PGE2 and TXB2 levels are uncertain, the results of the present study clearly indicate that therapeutic doses of steroidal and nonsteroidal anti-inflammatory drugs cause quite distinct changes in arachidonic acid metabolism, which might be relevant to their specific therapeutic actions and side-effects.