Sepsis with liver dysfunction and coagulopathy predicts an inflammatory pattern of macrophage activation.
Sepsis with liver dysfunction and coagulopathy predicts an inflammatory pattern of macrophage activation.
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DOI:
10.1186/s40635-022-00433-y
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发表时间:
2022-02-21
影响因子:
3.5
通讯作者:
ProCESS Investigators
中科院分区:
文献类型:
--
作者:
Anderko RR;Gómez H;Canna SW;Shakoory B;Angus DC;Yealy DM;Huang DT;Kellum JA;Carcillo JA;ProCESS Investigators
Interleukin-1 receptor antagonists can reduce mortality in septic shock patients with hepatobiliary dysfunction and disseminated intravascular coagulation (HBD + DIC), an organ failure pattern with inflammatory features consistent with macrophage activation. Identification of clinical phenotypes in sepsis may allow for improved care. We aim to describe the occurrence of HBD + DIC in a contemporary cohort of patients with sepsis and determine the association of this phenotype with known macrophage activation syndrome (MAS) biomarkers and mortality. We performed a retrospective nested case–control study in adult septic shock patients with concurrent HBD + DIC and an equal number of age-matched controls, with comparative analyses of all-cause mortality and circulating biomarkers between the groups. Multiple logistic regression explored the effect of HBD + DIC on mortality and the discriminatory power of the measured biomarkers for HBD + DIC and mortality. Six percent of septic shock patients (n = 82/1341) had HBD + DIC, which was an independent risk factor for 90-day mortality (OR = 3.1, 95% CI 1.4–7.5, p = 0.008). Relative to sepsis controls, the HBD + DIC cohort had increased levels of 21 of the 26 biomarkers related to macrophage activation (p < 0.05). This panel was predictive of both HBD + DIC (sensitivity = 82%, specificity = 84%) and mortality (sensitivity = 92%, specificity = 90%). The HBD + DIC phenotype identified patients with high mortality and a molecular signature resembling that of MAS. These observations suggest trials of MAS-directed therapies are warranted. The online version contains supplementary material available at 10.1186/s40635-022-00433-y.
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影响因子:
27.4
作者:
Gabay C;Fautrel B;Rech J;Spertini F;Feist E;Kötter I;Hachulla E;Morel J;Schaeverbeke T;Hamidou MA;Martin T;Hellmich B;Lamprecht P;Schulze-Koops H;Courvoisier DS;Sleight A;Schiffrin EJ
通讯作者:
Schiffrin EJ
影响因子:
13.3
作者:
Fardet, Laurence;Galicier, Lionel;Hejblum, Gilles
通讯作者:
Hejblum, Gilles
影响因子:
6.5
作者:
AKASHI, K;HAYASHI, S;NIHO, Y
通讯作者:
NIHO, Y
DOI:
10.1016/s0889-8588(05)70521-9
发表时间:
1998-04-01
影响因子:
2.4
作者:
Janka, G;Imashuku, S;Henter, JI
通讯作者:
Henter, JI
影响因子:
3.3
作者:
Gómez H;Kellum JA
通讯作者:
Kellum JA