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Abstract Background Alactic base excess (ABE) is a novel biomarker to evaluate the renal capability of handling acid-base disturbances, which has been found to be associated with adverse prognosis of sepsis and shock patients. This study aimed to evaluate the association between ABE and the risk of in-hospital mortality in patients with acute myocardial infarction (AMI). Methods This retrospective cohort study collected AMI patients’ clinical data from the Medical Information Mart for Intensive Care (MIMIC)-IV database. The outcome was in-hospital mortality after intensive care unit (ICU) admission. Univariate and multivariate Cox proportional hazards models were performed to assess the association of ABE with in-hospital mortality in AMI patients, with hazard ratios (HRs) and 95% confidence intervals (CI). To further explore the association, subgroup analyses were performed based on age, AKI, eGFR, sepsis, and AMI subtypes. Results Of the total 2779 AMI patients, 502 died in hospital. Negative ABE (HR = 1.26, 95%CI: 1.02–1.56) (neutral ABE as reference) was associated with a higher risk of in-hospital mortality in AMI patients, but not in positive ABE (P = 0.378). Subgroup analyses showed that negative ABE was significantly associated with a higher risk of in-hospital mortality in AMI patients aged>65 years (HR = 1.46, 95%CI: 1.13–1.89), with eGFR

Background: Alactic base excess (ABE) is a novel biomarker to evaluate the renal capability of handling acid-base disturbances, which has been found to be associated with adverse prognosis of sepsis and shock patients. This study aimed to evaluate the association between ABE and the risk of in-hospital mortality in patients with acute myocardial infarction (AMI). Methods: This retrospective cohort study collected AMI patients' clinical data from the Medical Information Mart for Intensive Care (MIMIC)-IV database. The outcome was in-hospital mortality after intensive care unit (ICU) admission. Univariate and multivariate Cox proportional hazards models were performed to assess the association of ABE with in-hospital mortality in AMI patients, with hazard ratios (HRs) and 95% confidence intervals (CI). To further explore the association, subgroup analyses were performed based on age, AKI, eGFR, sepsis, and AMI subtypes. Results: Of the total 2779 AMI patients, 502 died in hospital. Negative ABE (HR = 1.26, 95%CI: 1.02–1.56) (neutral ABE as reference) was associated with a higher risk of in-hospital mortality in AMI patients, but not in positive ABE (P = 0.378). Subgroup analyses showed that negative ABE was significantly associated with a higher risk of in-hospital mortality in AMI patients aged>65 years (HR = 1.46, 95%CI: 1.13–1.89), with eGFR<60 (HR = 1.35, 95%CI: 1.05–1.74), with AKI (HR = 1.32, 95%CI: 1.06–1.64), with ST-segment elevation acute myocardial infarction (STEMI) subtype (HR = 1.79, 95%CI: 1.18–2.72), and without sepsis (HR = 1.29, 95%CI: 1.01–1.64). Conclusion: Negative ABE was significantly associated with in-hospital mortality in patients with AMI. [ABSTRACT FROM AUTHOR]

Inspired by the Stewart-Figge acid–base approach, Gattinoni et al. recently introduced a new internal milieu parameter known as alactic base excess (ABE). The authors defined ABE as the sum of lactate and standard base excess. In the context of sepsis, ABE has been proposed as a valuable marker to discern between metabolic acidosis resulting from the accumulation of lactate and the retention of fixed acids, which can occur in cases of renal failure. Multiple studies have demonstrated that a negative ABE value (<−3 mmol/L) represents an early marker of renal dysfunction, and significantly correlates with higher mortality rates in septic patients. In conclusion, ABE is a simple and useful parameter that can be used to better interpret a patient's acid–base status, assess renal function, and general prognosis in sepsis. By incorporating ABE into clinical practice, healthcare professionals can enhance their understanding of the complex acid–base imbalances in their patients and tailor more individualized, effective treatment plans. [ABSTRACT FROM AUTHOR]

Abstract Background Alactic base excess (ABE) is a novel biomarker that estimates the renal capability of handling acid–base alterations during the sepsis. Hence, the aim of this study was to evaluate the use of ABE to predict the renal replacement therapy (RRT) in patients with septic shock. Methods A total of 164 patients admitted to the intensive care units with a diagnosis of septic shock according to the third international consensus on sepsis and septic shock (Sepsis-3) were included. This study was retrospective, single center, and conducted between January 1, 2016, and December 31, 2020. The individuals were stratified in patients who did [n = 68] or did not [n = 96] receive the RRT. The diagnostic performed of the variables for the classification into patients who required RRT was evaluated by receiver operating characteristic (ROC) analysis and area under curve (AUC) was calculated. Univariate and multivariate logistic regression models were used to identify risk factors for RRT. Results The median age of the patients was 59 years and female sex (51.8%) predominated. ABE (odds ratio [OR] 1.2270, [95% confidence interval [CI] 1.0453–1.4403], p = 0.0124) and urea (OR 1.0114, [95% CI 1.0053–1.0176], p = 0.0002) were associated with risk of RRT. HCO3− (OR 0.6967, [95% CI 0.5771–0.8410], p = 0.0002) was a protective factor of RRT. ABE (AUC = 0.649, p 75 mg/dL, respectively. Conclusion Although HCO3− is associated with low risk, ABE and urea are independent risk factors for RRT in the patients with septic shock.

Introduction: Gattinoni et al. have recently introduced a new parameter: the “alactic base excess” (ABE). ABE is equivalent to the number of strong acids, other than lactate, which are present in the plasma in abnormal concentrations, negative ABE being associated with higher mortality in sepsis. Hemoperfusion (HPF) is an extracorporeal procedure that involves the passage of blood through an adsorption cartridge, where solutes are removed by direct binding to the sorbent material. Then, it was decided to explore the influence of HPF on negative ABE value in sepsis. Materials and methods: Basal values of ABE, standard base excess (SBE), and lactate (mean, standard deviation [SD]) were obtained. The difference between these parameter values before and after four sessions of HPF (HA330) (delta value) was evaluated. Student’s t-test and Wilcoxon test were applied. Results: From 32 patients (age: 57±13) suffering from respiratory insufficiency secondary to COVID-19 who were treated with HPF in the critical care unit of Clinica de la Mujer, Bogotá (Colombia), 6 patients presented with metabolic acidosis with negative ABE value (‒2.7±1) with negative SBE (‒4.7±1) and high lactate serum value (2±0.7 mmol/L). Delta ABE, SBE, and lactate were: 7.7 (p = 0.005), 6.1 (p = 0.003), and 1.6 (p = NS), respectively. Thus, negative ABE was significantly reversed by HPF, since SBE value turned positive without significant change in lactate. Conclusion: Negative alactic parameter was significantly reversed by HPF in septic patients. It is necessary to carry out evaluations in larger groups to estimate their impact on clinical outcomes.

Base excess (BE) and lactate concentration may predict mortality in critically ill patients. However, the predictive values of alactic BE (aBE; the sum of BE and lactate), or a combination of BE and lactate are unknown. The study aimed to investigate whether BE, lactate, and aBE measured on admission to ICU may predict the 28-day mortality for patients undergoing any form of shock. In 143 consecutive adults, arterial BE, lactate, and aBE were measured upon ICU admission. Receiver Operating Curve (ROC) characteristics and Cox proportional hazard regression models (adjusted to age, gender, forms of shock, and presence of severe renal failure) were then used to investigate any association between these parameters and 28-day mortality. aBE < −3.63 mmol/L was found to be associated with a hazard ratio of 3.19 (HR; 95% confidence interval (CI): 1.62–6.27) for mortality. Risk of death was higher for BE < −9.5 mmol/L (HR: 4.22; 95% CI: 2.21–8.05), particularly at lactate concentrations > 4.5 mmol/L (HR: 4.62; 95% CI: 2.56–8.33). A 15.71% mortality rate was found for the combined condition of BE > cut-off and lactate < cut-off. When BE was below but lactate above their respective cut-offs, the mortality rate increased to 78.91%. The Cox regression model demonstrated that the predictive values of BE and lactate were mutually independent and additive. The 28-day mortality in shock patients admitted to ICU can be predicted by aBE, but BE and lactate deliver greater prognostic value, particularly when combined. The clinical value of our findings deserves further prospective evaluation. [ABSTRACT FROM AUTHOR]

Purpose: Alactic base excess (ABE) is a novel biomarker defined as the sum of lactate and standard base excess and estimates the renal capability of handling acid-base disturbances in sepsis. The objective of this study is to see if ABE is an independent predictor of mortality in septic patients with and without renal dysfunction., Materials and Methods: We retrospectively studied 1178 patients with sepsis and septic shock. Patients were divided according to ABE values: 1) negative ABE (<-3 mmol/L); 2) neutral ABE (≥ - 3 and < 4 mmol/L); and 3) positive ABE (≥4 mmol/L). The effect of ABE on mortality was evaluated using Cox regression weight by inverse probability weighting (IPWT) analysis after propensity score assessment. Additionally, we performed a stratified analysis in patients with GFR > 60 mL/min/1.73 m2., Results: Negative ABE patients had higher mortality than patients with neutral ABE (adjusted HR 1.43; 95%CI 1.02-2.01). Also, in patients with GFR > 60 mL/min/1.73 m2 (n = 493), we observed higher mortality in patients with negative ABE (adjusted HR 2.43; 95%CI 1.07-5.53)., Conclusions: Negative ABE is an independent predictor of in-hospital mortality in septic patients with and without renal dysfunction., Competing Interests: Declaration of Competing Interest Authors declare no conflicts of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)