Speerstra F, van de Putte L B, Rasker J J, Reekers P, Vandenbroucke J P
Scand J Rheumatol. 1984;13(4):363-8. doi: 10.3109/03009748409111310.
We studied patients with rheumatoid arthritis who have been treated with aurothioglucose (Au) and subsequently with D-penicillamine (DP), and who developed drug-induced proteinuria, over a 10-year period. Twelve patients developed Au-induced and 19 DP-induced proteinuria. Of the 12 patients with Au-induced proteinuria, only 2 (17%) developed DP-induced proteinuria, indicating a slightly increased risk as compared with the overall incidence (9.3%) of this reaction in 168 DP-treated patients. In addition, only a minority (2 out of 19, 10.6%) of patients with DP-induced proteinuria had previous Au-induced proteinuria. These data may indicate that different mechanisms are operative in Au and DP-induced proteinuria, as is also suggested by the finding that HLA-DR3 was present more frequently in the latter (50%) than in the former (21%). A history of previous Au-induced proteinuria is insufficient reason to deny these patients the benefits of subsequent treatment with DP.
我们对类风湿性关节炎患者进行了为期10年的研究，这些患者先后接受了金硫葡萄糖（Au）和随后的青霉胺（DP）治疗，并出现了药物性蛋白尿。12例患者出现了Au诱导的蛋白尿，19例患者出现了DP诱导的蛋白尿。在12例Au诱导蛋白尿的患者中，只有2例（17%）出现了DP诱导的蛋白尿，与168例接受DP治疗患者中该反应的总体发生率（9.3%）相比，风险略有增加。此外，在19例DP诱导蛋白尿的患者中，只有少数（2例，10.6%）曾有Au诱导的蛋白尿。这些数据可能表明，Au和DP诱导蛋白尿的机制不同，这也由以下发现所提示：HLA-DR3在后者（50%）中比在前者（21%）中更频繁出现。既往有Au诱导蛋白尿的病史并不是拒绝这些患者后续接受DP治疗益处的充分理由。
