β Agonist–induced lactic acidosis, an evidence-based approach to a critical question

Pourmand, Ali; Dorwart, Kelsey; Mazer‐Amirshahi, Maryann; Nasser, Sigrid; Shokoohi, Hamid

doi:10.1016/j.ajem.2015.12.085

Cited by 3 publications

(5 citation statements)

References 16 publications

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“…β2‐agonist‐induced hyperlactatemia is believed to be a type B lactic acidosis and is a described physiologic response in both adults and children 3 . The hyperlactatemia can occur regardless of the route of β2‐agonist delivery, 7 is dose‐related, 12 occurs more often in asthmatics than healthy controls, 3,5 and is reversible after discontinuation of β2‐agonists 13 . There are mixed data on the impact of this lactic acidosis on mortality 2,6 …”

Section: Discussionmentioning

confidence: 99%

“…However, it was previously proposed to be a type A lactic acidosis in healthy participants receiving β2‐agonists, and there should be limited anaerobic metabolism. Furthermore, in controlled situations (mechanical ventilation, induction of labor), β2‐agonist lactic acidosis can occur in the absence of clinical hypoxia or failure of oxygenation 7 . Recent hypotheses suggest that β2‐receptor activation stimulates lactic acid production in skeletal muscle and adipose tissue by altering aerobic glycolysis, gluconeogenesis, pyruvate metabolism, or free fatty acid production 8 .…”

Section: Discussionmentioning

confidence: 99%

“…It has been suggested that patients in a physiologic abnormal state (such as respiratory distress) enter a hyperadrenergic state that exacerbates the chemical effects of β2‐agonists 8 . This may be worsened by exogenous steroids or epinephrine concomitantly administered with β2‐agonists for asthma or chronic obstructive pulmonary disease 7 . As we performed this study in healthy volunteers, the mild changes in lactic acid suggest that physiologic stress may be needed to exacerbate the underlying chemical changes responsible for a more profound lactic acidosis.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, in controlled situations (mechanical ventilation, induction of labor), β2-agonist lactic acidosis can occur in the absence of clinical hypoxia or failure of oxygenation. 7 Recent hypotheses suggest that β2-receptor activation stimulates lactic acid production in skeletal muscle and adipose tissue by altering aerobic glycolysis, gluconeogenesis, pyruvate metabolism, or free fatty acid production. 8 Dodda and Spiro suggest 2 primary mechanisms in a published case summary.…”

Section: Lactic Acidosis Is Classified Into 2 Categories Typementioning

confidence: 99%

“…5 The phenomenon of hyperlactatemia after receiving β2-agonists is well documented in case reports, trials of healthy volunteers, and symptomatic patients in both emergency departments and intensive care units. 3,[5][6][7] Several mechanisms have been proposed; however, the exact mechanism remains controversial. 8 It was originally proposed to be related to the work of breathing of patients with respiratory distress.…”

mentioning

confidence: 99%

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Effects of Continuous Albuterol Inhalation on Serum Metabolome in Healthy Subjects: More Than Just Lactic Acid

Nowadly

Liao

Rose

2020

The Journal of Clinical Pharma

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Treatment with β2-agonists may cause elevated lactic acid, the end product of anaerobic metabolism of glucose. It has been proposed that lactic acidosis associated with β2-agonists is caused by changes to direct biochemical impacts on glycolysis, gluconeogenesis, pyruvate metabolism, and free fatty acid production. However, much remains unknown, and there is a paucity of evidence regarding the underlying chemical changes associated with this lactic acidosis. The goal of our study was to investigate the impact of 1 hour of continuous albuterol on the untargeted serum metabolome of healthy subjects. Twenty-four healthy participants received 7.5 mg of continuous albuterol for 1 hour. Baseline, 1-hour, and 2-hour lactic acid levels were drawn. Samples obtained at baseline and 1 hour were sent for untargeted metabolomic profiling. Participants had a baseline lactic acid of 1.45 ± 0.46 mmol/L. On average, lactate levels increased 0.33 ± 0.67 mmol/L after 1 hour (P = .02) and remained elevated at 2 hours (0.32 ± 0.72 mmol/L, P = .02), although there was overlap in lactate levels across times. For metabolomic analysis, fatty acids, organic acids, and sugars were elevated, and amino acids were reduced. Lactic acid and pyruvic acid metabolites, however, did not significantly change (after false discovery rate adjustment). In healthy participants, continuous albuterol alters the serum metabolome, but this change may not be clinically significant. The data support recent hypotheses that β2-receptor activation stimulates lactic acid production, altering aerobic glycolysis, gluconeogenesis, and free fatty acid production.

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