When a child presents with high-anion gap metabolic acidosis, the pediatrician can proceed with confidence by recalling some basic principles. Defects of organic acid, pyruvate, and ketone body metabolism that present with acute acidosis are reviewed. Flowcharts for identifying the underlying cause and initiating life-saving therapy are provided. By evaluating electrolytes, blood sugar, lactate, ammonia, and urine ketones, the provider can determine the likelihood of an inborn error of metabolism. Freezing serum, plasma, and urine samples during the acute presentation for definitive diagnostic testing at the provider's convenience aids in the differential diagnosis.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.pcl.2017.11.003 | DOI Listing |
Intensive Care Med Exp
January 2025
Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, O&N1 Box 503, 3000, Louvain, Belgium.
Background: Sepsis-induced cardiomyopathy (SICM) often occurs in the acute phase of sepsis and is associated with increased mortality due to cardiac dysfunction. The pathogenesis remains poorly understood, and no specific treatments are available. Although SICM is considered reversible, emerging evidence suggests potential long-term sequelae.
View Article and Find Full Text PDFCommun Biol
December 2024
Precision Cardiovascular Laboratory, The University of Sydney, Sydney, NSW, Australia.
Front Nutr
December 2024
State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang, Jiangxi, China.
Introduction: Hyperuricemia (HUA) is a metabolic disease caused by purine metabolism disorders in the body. Lactic acid bacteria (LAB) and their fermentation broth have the potential to alleviate hyperuricemia, but the potential mechanism of action is still unclear.
Methods: The LAB with high inhibitory activity against xanthine oxidase (XOD) were screened out.
J Clin Invest
December 2024
Division of Nutritional Science and Obesity Medicine, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Despite the impressive clinical benefits and widespread adoption of sodium glucose cotransporter 2 inhibitors (SGLT2i) to treat all classes of heart failure, their cardiovascular mechanisms of action are poorly understood. Proposed mechanisms range broadly and include enhanced ketogenesis, where the mild ketosis associated with SGLT2i use is presumed to be beneficial. However, in this issue of the JCI, carefully conducted metabolic flux studies by Goedeke et al.
View Article and Find Full Text PDFJ Clin Invest
December 2024
Department of Internal Medicine (Endocrinology), Yale School of Medicine, New Haven Connecticut, USA.
Previous studies highlight the potential for sodium-glucose cotransporter type 2 (SGLT2) inhibitors (SGLT2i) to exert cardioprotective effects in heart failure by increasing plasma ketones and shifting myocardial fuel utilization toward ketone oxidation. However, SGLT2i have multiple in vivo effects and the differential impact of SGLT2i treatment and ketone supplementation on cardiac metabolism remains unclear. Here, using gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) methodology combined with infusions of [13C6]glucose or [13C4]βOHB, we demonstrate that acute SGLT2 inhibition with dapagliflozin shifts relative rates of myocardial mitochondrial metabolism toward ketone oxidation, decreasing pyruvate oxidation with little effect on fatty acid oxidation in awake rats.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!