Dexamethasone and tocilizumab treatment considerably reduces the value of C-reactive protein and procalcitonin to detect secondary bacterial infections in COVID-19 patients.
Dexamethasone and tocilizumab treatment considerably reduces the value of C-reactive protein and procalcitonin to detect secondary bacterial infections in COVID-19 patients.
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DOI：
10.1186/s13054-021-03717-z
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发表时间：
2021-08-05
期刊：
影响因子：
--
通讯作者：
Pickkers P
中科院分区：
文献类型：
--
作者：
Kooistra EJ;van Berkel M;van Kempen NF;van Latum CRM;Bruse N;Frenzel T;van den Berg MJW;Schouten JA;Kox M;Pickkers P
降钙素原（PCT）和C反应蛋白（CRP）先前被证明对检测重症COVID-19患者的继发感染具有价值。然而，自从免疫调节治疗的引入，这些生物标志物的价值尚不清楚。我们研究了接受地塞米松联合或不联合托珠单抗治疗的重症COVID-19患者的PCT和CRP动力学，并评估了这些生物标志物检测继发性细菌感染的价值。在这项前瞻性研究中，190名重症COVID-19患者被分为三个治疗组：无地塞米松、无托珠单抗（D−T−）、地塞米松、无托珠单抗（D+T−）和地塞米松和托珠单抗（D+T+）。在地塞米松治疗的最后一天对齐PCT和CRP的系列数据，并在地塞米松停药前6天和停药后10天之间分析这些生物标志物的动力学。此外，将D+T−和D+T+组再分为继发性感染和非继发性感染组，以分析PCT和CRP动力学的差异，并计算这些生物标志物对继发性感染发生的检测准确性。地塞米松停药后，PCT和CRP水平反弹，D+T−组最明显。发生继发性感染后，D+T−组中未观察到PCT和CRP水平显著升高（分别为p = 0.052和p = 0.08）。尽管D+T+组发生继发性感染的患者PCT水平显著升高（p = 0.0003），但这种升高仅在感染后第2天开始明显。CRP水平在D+T+组中仍然受到抑制。PCT和CRP水平的受试者工作曲线分析得出的曲线下面积分别为0.52和0.55，均显著低于未接受免疫调节药物治疗的COVID-19患者组（分别为0.80和0.76，组间差异的p值分别为0.001和0.02）。在重症COVID-19患者中停用地塞米松会导致PCT和CRP水平反弹性升高，与继发性细菌感染的发生无关。此外，地塞米松和托珠单抗的免疫调节治疗显著降低了PCT和CRP检测COVID-19患者继发感染的价值。在线版本包含补充材料，可通过10.1186/s13054-021-03717-z获得。
Procalcitonin (PCT) and C-reactive protein (CRP) were previously shown to have value for the detection of secondary infections in critically ill COVID-19 patients. However, since the introduction of immunomodulatory therapy, the value of these biomarkers is unclear. We investigated PCT and CRP kinetics in critically ill COVID-19 patients treated with dexamethasone with or without tocilizumab, and assessed the value of these biomarkers to detect secondary bacterial infections. In this prospective study, 190 critically ill COVID-19 patients were divided into three treatment groups: no dexamethasone, no tocilizumab (D−T−), dexamethasone, no tocilizumab (D+T−), and dexamethasone and tocilizumab (D+T+). Serial data of PCT and CRP were aligned on the last day of dexamethasone treatment, and kinetics of these biomarkers were analyzed between 6 days prior to cessation of dexamethasone and 10 days afterwards. Furthermore, the D+T− and D+T+ groups were subdivided into secondary infection and no-secondary infection groups to analyze differences in PCT and CRP kinetics and calculate detection accuracy of these biomarkers for the occurrence of a secondary infection. Following cessation of dexamethasone, there was a rebound in PCT and CRP levels, most pronounced in the D+T− group. Upon occurrence of a secondary infection, no significant increase in PCT and CRP levels was observed in the D+T− group (p = 0.052 and p = 0.08, respectively). Although PCT levels increased significantly in patients of the D+T+ group who developed a secondary infection (p = 0.0003), this rise was only apparent from day 2 post-infection onwards. CRP levels remained suppressed in the D+T+ group. Receiver operating curve analysis of PCT and CRP levels yielded area under the curves of 0.52 and 0.55, respectively, which are both markedly lower than those found in the group of COVID-19 patients not treated with immunomodulatory drugs (0.80 and 0.76, respectively, with p values for differences between groups of 0.001 and 0.02, respectively). Cessation of dexamethasone in critically ill COVID-19 patients results in a rebound increase in PCT and CRP levels unrelated to the occurrence of secondary bacterial infections. Furthermore, immunomodulatory treatment with dexamethasone and tocilizumab considerably reduces the value of PCT and CRP for detection of secondary infections in COVID-19 patients. The online version contains supplementary material available at 10.1186/s13054-021-03717-z.
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作者：
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DOI：
10.1164/rccm.200205-446oc
发表时间：
2003-02-15
影响因子：
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作者：
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通讯作者：
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