Lactic Acidosis Induced by Excessive Use of a Long-Acting Beta Agonist
Saho Katsumata1, Hirohisa Fujikawa2,1, Takashi Nakamura1
1Department of Internal Medicine, Suwa Central Hospital, Nagano, JPN.
Abstract:
Lactic acidosis is associated with poorer clinical outcomes in critical care. The causes of this condition are divided into two groups: type A (tissue hypoxia) and type B (metabolic abnormalities). Of these, drug-induced lactic acidosis is categorized as type B and is often overlooked due to clinicians' poor awareness. We herein report a rare case of drug-induced lactic acidosis due to excessive use of a long-acting beta agonist (LABA) in a patient with asthma-chronic obstructive pulmonary disease overlap exacerbation. He initially presented with markedly elevated lactate and metabolic acidosis with unknown etiology. A detailed medical interview revealed that he had inhaled a large amount of LABA on the day of admission, which led to our final diagnosis. The patient's respiratory status and lactate levels gradually improved with the appropriate use of inhalation therapy. While there have been many recent reports of lactic acidosis caused by short-acting beta agonists, our case suggests that excessive use of LABAs may also lead to lactic acidosis. Clinicians should be aware of the possibility that LABAs can cause lactic acidosis because poor awareness of the condition may lead to inappropriate patient care.
More Related Videos
06:45Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
Published on: October 4, 2021
09:31Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
Published on: November 5, 2016
Related Concept Videos
Antiasthma Drugs: β2-Adrenoceptor Agonists
One class of bronchodilators includes β2-adrenoceptor agonists. These agents target the β2-adrenoceptors located on bronchial smooth muscle cells. By stimulating these receptors, β2-agonists induce...
Muscle Recovery and Fatigue
Glucagon-like Receptor Agonists
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
Desensitization and Tachyphylaxis
Acute Respiratory Failure-III
Adrenergic Antagonists: ɑ and β-Receptor Blockers
