Stockman A, Zilko P J, Major G A, Tait B D, Property D N, Mathews J D, Hannah M C, McCluskey J, Muirden K D
J Rheumatol. 1986 Apr;13(2):269-73.
In a 3-centre study involving 144 patients with rheumatoid arthritis (RA), a relationship between side effects from D-penicillamine and HLA antigens, allotypic markers of the IgG heavy chain (Gm) and allotypes of complement components Bf, C4A and C4B was sought. There was a significant association between proteinuria induced by D-penicillamine and the antigens DR3 and B8. However, the presence of DR2 seemed to protect against the development of proteinuria. Thrombocytopenia from D-penicillamine was significantly associated with HLA-A1 and DR4; 15 of 23 patients who possessed both antigens developed thrombocytopenia (p less than 0.001 uncorrected, approximate relative risk (RR) = 5.5). A null complement allele located at the C4B locus (C4BQO) was also associated with thrombocytopenia from D-penicillamine (p less than 0.005, RR = 17.3). Our study confirms the findings from other series which indicate that there is a genetic predisposition for the development of proteinuria from D-penicillamine in RA and suggests that this may also be the case in D-penicillamine induced thrombocytopenia.
在一项涉及144例类风湿性关节炎（RA）患者的3中心研究中，探寻了青霉胺的副作用与HLA抗原、IgG重链（Gm）的同种异型标记以及补体成分Bf、C4A和C4B的同种异型之间的关系。青霉胺诱导的蛋白尿与抗原DR3和B8之间存在显著关联。然而，DR2的存在似乎可预防蛋白尿的发生。青霉胺所致的血小板减少与HLA - A1和DR4显著相关；23例同时拥有这两种抗原的患者中有15例发生了血小板减少（未校正p值小于0.001，近似相对风险（RR）= 5.5）。位于C4B位点的无效补体等位基因（C4BQO）也与青霉胺所致的血小板减少相关（p值小于0.005，RR = 17.3）。我们的研究证实了其他系列研究的结果，即类风湿性关节炎患者中存在对青霉胺诱导蛋白尿发生的遗传易感性，并表明青霉胺诱导的血小板减少可能也是如此。
