Rovin Brad H, Tang Yuxiao, Sun Junfeng, Nagaraja Haikady N, Hackshaw Kevin V, Gray Linda, Rice Robert, Birmingham Daniel J, Yu Chack-Yung, Spetie Dan N, Aziz Amy, Hebert Lee A
Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210, USA.
Kidney Int. 2005 Aug;68(2):747-59. doi: 10.1111/j.1523-1755.2005.00453.x.
Active systemic lupus erythematosus (SLE) can cause fever. Steroids (glucocorticoids) suppress SLE fever; however, the extent to which steroid therapy affects SLE fever not previously been rigorously studied.
Study A is a prospective study of recurrently active SLE patients (N= 92, 60 renal SLE and 32 nonrenal SLE) who recorded daily oral evening temperatures while participating in a longitudinal study of risk factors for SLE flare. Study B is a retrospective study of consecutive febrile SLE patients (N= 22) who received steroids initially because SLE was suspected. At final analysis 11 had SLE fever and 11 had infection fever.
In study A during a mean follow-up of 13.2 +/- 8.1 months, 51 of the 92 patients experienced 73 SLE flares. In only one patient was SLE fever associated with SLE flare. In the other 50 patients who flared, there was no significant trend to develop fever prior to or at the onset of SLE flare. Prednisone, median dose 10 mg, was being received at 82% of the study visits at which an SLE flare was declared. In study B, prednisone 28 mg (range 20 to 40 mg) completely suppressed SLE fever, usually within 24 hours. In contrast, infection fever persisted despite prednisone 35 to 300 mg/day. Of those with infection fever, three developed fatal sepsis when high-dose steroid therapy was continued.
In SLE patients receiving prednisone at maintenance doses or greater, SLE fever is rare. When fever does develop, it is usually due to infection. Continuing high steroid dose steroid therapy in those with infection fever may increase the risk of severe sepsis.
活动性系统性红斑狼疮（SLE）可引起发热。类固醇（糖皮质激素）可抑制SLE发热；然而，类固醇治疗对SLE发热的影响程度此前尚未得到严格研究。
研究A是一项对复发性活动性SLE患者（n = 92，60例肾脏SLE和32例非肾脏SLE）的前瞻性研究，这些患者在参与SLE发作危险因素的纵向研究时记录每日口服夜间体温。研究B是一项对连续发热的SLE患者（n = 22）的回顾性研究，这些患者最初因怀疑患有SLE而接受类固醇治疗。在最终分析中，11例患有SLE发热，11例患有感染性发热。
在研究A中，平均随访13.2±8.1个月，92例患者中有51例经历了73次SLE发作。只有1例患者的SLE发热与SLE发作相关。在其他50例发作的患者中，在SLE发作之前或发作时没有明显的发热趋势。在宣布SLE发作的研究访视中，82%的患者正在接受泼尼松，中位剂量为10mg。在研究B中，泼尼松28mg（范围为20至40mg）通常在24小时内完全抑制SLE发热。相比之下，尽管每天使用35至300mg泼尼松，感染性发热仍持续存在。在患有感染性发热的患者中，有3例在继续高剂量类固醇治疗时发生了致命的败血症。
在接受维持剂量或更高剂量泼尼松治疗的SLE患者中，SLE发热很少见。当确实出现发热时，通常是由于感染。对患有感染性发热的患者继续进行高剂量类固醇治疗可能会增加严重败血症的风险。
