Abstract
IntroductionThere is a complex interplay between changes in acid–base components and inflammation. This manuscript aims to explore associations between plasma cytokines and chemokines and acid–base status on admission to intensive care.MethodsWe conducted a prospective cohort study in a 13-bed ICU in a tertiary-care center in Brazil. 87 unselected patients admitted to the ICU during a 2-year period were included. We measured multiple inflammatory mediators in plasma using multiplex assays and evaluated the association between mediator concentrations and acid–base variables using a variety of statistical modeling approaches, including generalized linear models, multiadaptive regression splines and principal component analysis.ResultsWe found a positive association between strong ion gap (SIG) and plasma concentrations of interleukin (IL)6, 8, 10 and tumor necrosis factor (TNF); whereas albumin was negatively associated with IL6, IL7, IL8, IL10, TNF and interferon (IFN)α. Apparent strong ion difference (SIDa) was negatively associated with IL10 and IL17. A principal component analysis including SAPS 3 indicated that the association between acid–base components and inflammatory status was largely independent of illness severity, with both increased SIG and decreased SIDa (both drivers of acidosis) associated with increased inflammation.ConclusionAcid–base variables (especially increased SIG, decreased albumin and decreased SIDa) on admission to ICU are associated with immunological activation. These findings should encourage new research into the effects of acid–base status on inflammation.
Highlights
There is a complex interplay between changes in acid–base components and inflammation
Evidence from cell culture [14] and intact animals [15] show that acidosis increases inflammation, it is unknown if a specific change in acid-base status in humans is associated with changes in inflammatory response
apparent strong ion difference (SIDa) was negatively associated with plasma IL10 and IL17 whereas strong ion gap (SIG) was positively associated with IL6, IL8, IL10 and TNFα
Summary
There is a complex interplay between changes in acid–base components and inflammation. Cytokine release is induced by a variety of signals, including those derived from pathogens (for example, endotoxin), or those related to tissue damage (for example, complement activation, ischemia-reperfusion injury and oxidative stress) [3]. Evidence from cell culture [14] and intact animals [15] show that acidosis increases inflammation, it is unknown if a specific change in acid-base status (for example, increase in SIG or decrease in weak acids such as albumin) in humans is associated with changes in inflammatory response. No study hitherto has evaluated the association between acid-base abnormalities (for example high SIG, low albumin) in critically ill humans and inflammatory mediator expression
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