Walker S E, Jacobson J D
Department of Internal Medicine, University of Missouri, Columbia, USA.
Rheum Dis Clin North Am. 2000 Nov;26(4):713-36. doi: 10.1016/s0889-857x(05)70166-6.
PRL is capable of influencing immune responses and is a cytokine in all likelihood. Circulating PRL is elevated in a number of autoimmune diseases, and about 20% of SLE patients are hyperprolactinemic. The serum PRL concentration often does not reflect disease activity in SLE. The PRL-suppressing drug bromocriptine has been reported to benefit small numbers of patients with reactive arthritis and inflammatory eye disease, and bromocriptine may be beneficial in treating SLE. In NZB/NZW mice, bromocriptine was beneficial and prolonged life. Bromocriptine therapy favorably modified disease in human SLE. In a preliminary open-label study, SLE patients treated with bromocriptine for 6 months had significant improvement in disease activity. These responses were corroborated by masted therapeutic studies. Daily treatment with low-dose bromocriptine prevented lupus flares, and bromocriptine was as effective as hydroxychloroquine in treating active nonorgan-threatening disease. The reports of the efficacy of bromocriptine treatment of SLE are encouraging. Additional studies may confirm the findings reported in this review and may lead to further use of hormonal modification to treat lupus and other autoimmune diseases. For the present, it is important to understand that treatment with dopamine agonists such as bromocriptine is experimental and best confined to therapeutic trials. In the experience of the authors, bromocriptine should not be relied on to treat severe life-threatening autoimmune disease. If bromocriptine is used to treat SLE and is then discontinued, the patient should be observed carefully for rebound hyperprolactinemia and the development of a lupus flare. GnRH is produced by lymphocytes and exerts immunomodulatory actions. Thus, GnRH resembles a cytokine. GnRH can be shown to exert gender-restricted immune actions in vitro and in vivo. The authors' preliminary observations are consistent with the possibility that gender-related differences in expression of the GnRH receptor or in GnRH signal transducers may contribute to gender-related differences in immune responsiveness to GnRH. These differences in G proteins may contribute to the gender-related differences in immunity and expression of autoimmune disease.
催乳素（PRL）能够影响免疫反应，很可能是一种细胞因子。在多种自身免疫性疾病中，循环中的PRL水平会升高，约20%的系统性红斑狼疮（SLE）患者存在高催乳素血症。血清PRL浓度通常不能反映SLE的疾病活动情况。据报道，抑制PRL的药物溴隐亭对少数反应性关节炎和炎性眼病患者有益，且溴隐亭可能对治疗SLE有益。在新西兰黑/新西兰白（NZB/NZW）小鼠中，溴隐亭有益且能延长寿命。溴隐亭疗法对人类SLE的疾病有良好改善作用。在一项初步的开放标签研究中，接受溴隐亭治疗6个月的SLE患者疾病活动度有显著改善。这些反应在后续的大规模治疗研究中得到了证实。每日用低剂量溴隐亭治疗可预防狼疮发作，且溴隐亭在治疗非器官威胁性的活动性疾病方面与羟氯喹一样有效。关于溴隐亭治疗SLE疗效的报道令人鼓舞。更多研究可能会证实本综述中报道的发现，并可能导致进一步利用激素调节来治疗狼疮和其他自身免疫性疾病。目前，重要的是要明白，使用多巴胺激动剂如溴隐亭进行治疗是试验性的，最好仅限于治疗试验。根据作者的经验，不应依赖溴隐亭来治疗严重危及生命的自身免疫性疾病。如果使用溴隐亭治疗SLE，然后停药，应仔细观察患者是否出现反弹性高催乳素血症和狼疮发作。促性腺激素释放激素（GnRH）由淋巴细胞产生并发挥免疫调节作用。因此，GnRH类似于一种细胞因子。GnRH在体外和体内均可表现出性别受限的免疫作用。作者的初步观察结果与以下可能性一致，即GnRH受体表达或GnRH信号转导器中的性别相关差异可能导致对GnRH免疫反应性的性别相关差异。G蛋白的这些差异可能导致免疫方面的性别相关差异以及自身免疫性疾病的表达差异。
