DETECTION OF PLASMA TUMOR-NECROSIS-FACTOR, INTERLEUKIN-6, AND INTERLEUKIN-8 DURING THE JARISCH-HERXHEIMER REACTION OF RELAPSING FEVER

DETECTION OF PLASMA TUMOR-NECROSIS-FACTOR, INTERLEUKIN-6, AND INTERLEUKIN-8 DURING THE JARISCH-HERXHEIMER REACTION OF RELAPSING FEVER
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DOI:
10.1084/jem.175.5.1207
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发表时间:
1992-05-01
影响因子:
15.3
通讯作者:
GRIFFIN, GE
GRIFFIN, GE
中科院分区:
医学1区
文献类型:
--
作者:
NEGUSSIE, Y;REMICK, DG;GRIFFIN, GE

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Jarisch-Herxheimer反应(J-HR)是一种临床综合征,在第一次足够剂量的抗菌药物治疗莱姆病、梅毒和复发性发热等传染病后不久出现。之前试图确定可能导致死亡的这种反应的中介因素,但都没有成功。我们在埃塞俄比亚亚的斯亚贝巴进行了一项前瞻性试验,对17名接受青霉素治疗的患者进行了研究,以评估症状与血浆肿瘤坏死因子(TNF)、白介素6和8(IL-6和IL-8)水平的关系。17例患者中有14例(82%)出现典型的J-HR,包括体温升高(1.06+/-0.2℃),2小时达高峰,4小时白细胞减少(7.4+/-0.6×10(-3)个/mm~3),稍有下降,然后平均动脉压升高。青霉素作用后5+/-1h内,螺旋体从血液中清除。在J-HR期间没有死亡,但体质症状严重。少数患者入院时血浆肿瘤坏死因子、白介素6和-8水平升高,但这些细胞因子浓度比入院时分别升高7倍、6倍和4倍,这与观察到的J-HR的病理生理变化是一致的。在三名未患J-HR的患者中,未检测到血浆细胞因子水平升高。我们的结论是,青霉素治疗虱子传播的复发性发热的J-HR的严重病理生理变化与血浆肿瘤坏死因子、IL-6和-8浓度的一过性升高密切相关。
The Jarisch-Herxheimer Reaction (J-HR) is a clinical syndrome occurring soon after the first adequate dose of an antimicrobial drug to treat infectious diseases such as Lyme disease, syphilis, and relapsing fever. Previous attempts to identify factors mediating this reaction, that may cause death, have been unsuccessful. We conducted a prospective trial in Addis Ababa, Ethiopia on 17 patients treated with penicillin for proven louse-borne relapsing fever due to Borrelia recurrentis to evaluate the association of symptoms with plasma levels of tumor necrosis factor (TNF), interleukins 6, and 8 (IL-6 and -8). 14 of the 17 (82%) patients experienced a typical J-HR consisting of rigors, a rise in body temperature (1.06 +/- 0.2-degrees-C) peaking at 2 h, leukopenia (7.4 +/- 0.6 x 10(-3) cells/mm3) at 4 h, a slight decrease, and then rise of mean arterial blood pressure. Spirochetes were cleared from blood in 5 +/- 1 h after penicillin. There were no fatalities, but constitutional symptoms were severe during J-HR. Plasma TNF, IL-6, and -8 were raised in several patients on admission, but a seven-, six-, and fourfold elevation of these plasma cytokine concentrations over admission levels was detected, respectively, occurring in transient form coincidental with observed pathophysiological changes of J-HR. Elevated plasma cytokine levels were not detected in the three patients who did not suffer J-HR. We conclude that the severe pathophysiological changes characterizing the J-HR occurring on penicillin treatment of louse-borne relapsing fever are closely associated with transient elevation of plasma TNF, IL-6, and -8 concentrations.