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Journal of Clinical Anesthesia Aug 2024
Topics: Humans; Hypoglycemic Agents; Acidosis; Perioperative Period; Respiratory Aspiration; Perioperative Care
PubMed: 38460414
DOI: 10.1016/j.jclinane.2024.111416 -
Critical Care and Resuscitation :... Mar 2022To assess the incidence and impact of metabolic acidosis in Indigenous and non-Indigenous patients Retrospective study. Adult intensive care units (ICUs) from...
To assess the incidence and impact of metabolic acidosis in Indigenous and non-Indigenous patients Retrospective study. Adult intensive care units (ICUs) from Australia and New Zealand. Patients aged 16 years or older admitted to an Australian or New Zealand ICU in one of 195 contributing ICUs between January 2019 and December 2020 who had metabolic acidosis, defined as pH < 7.30, base excess (BE) < 4 mEq/L and PaCO ≤ 45 mmHg. The primary outcome was the prevalence of metabolic acidosis. Secondary outcomes included ICU length of stay, hospital length of stay, receipt of renal replacement therapy (RRT), major adverse kidney events at 30 days (MAKE30), and hospital mortality. Overall, 248 563 patients underwent analysis, with 11 537 (4.6%) in the Indigenous group and 237 026 (95.4%) in the non-Indigenous group. The prevalence of metabolic acidosis was higher in Indigenous patients (9.3% 6.1%; < 0.001). Indigenous patients with metabolic acidosis received RRT more often (28.2% 22.0%; < 0.001), but hospital mortality was similar between the groups (25.8% in Indigenous 25.8% in non-Indigenous; = 0.971). Critically ill Indigenous ICU patients are more likely to have a metabolic acidosis in the first 24 hours of their ICU admission, and more often received RRT during their ICU admission compared with non-Indigenous patients. However, hospital mortality was similar between the groups.
PubMed: 38046846
DOI: 10.51893/2022.1.OA2 -
Pediatric Nephrology (Berlin, Germany) Aug 2023
Topics: Infant, Newborn; Humans; Acidosis; Weight Loss
PubMed: 36598596
DOI: 10.1007/s00467-022-05845-2 -
Pediatric Nephrology (Berlin, Germany) Aug 2023
Topics: Infant, Newborn; Humans; Acidosis; Weight Loss
PubMed: 36598597
DOI: 10.1007/s00467-022-05847-0 -
Acta Neurologica Taiwanica Dec 2023Myalgia (also called muscle pain or muscle ache) is a symptom associated with many diseases, including fibromyalgia, neurodegenerative diseases, degenerative spine...
Myalgia (also called muscle pain or muscle ache) is a symptom associated with many diseases, including fibromyalgia, neurodegenerative diseases, degenerative spine diseases, etc. Myalgia is a major medical problem affecting 60~85% of the population (lifetime prevalence). However, our understanding of chronic myalgia is still limited and effective treatment for intractable myalgia like fibromyalgia is still lacking. Although multifactorial, one known source of muscle pain is tissue acidosis. Experimental muscle pain can be induced by the intramuscular infusion of a buffered acidic solution in humans. As well, animal studies have revealed that acidic infusion activates chemosensitive nociceptors via the proton-sensing ion channels and receptors. Intriguingly, acid signaling in muscle afferents is promiscuous and could be either pro-nociceptive or antinociceptive, so we have coined the term sngception to describe the somatosensory function of acid sensation. Recent single-cell RNAseq studies have shown proton-sensing ion channels and receptors are expressed in all subpopulations of the somatosensory neurons, including nociceptors and non-nociceptive mechanoreceptors. Here, we address how the acid signaling is integrated in muscle afferents and why muscle pain can be chronic and intractable in mouse models of fibromyalgia. Besides acidosis, we have recently found oxidative stress can be another factor to activate proton-sensing ion channels and thus trigger fibromyalgia-like pain in mice. Together, understanding how the acid signaling works in muscle afferents will provide novel therapeutic strategies for myalgia.
Topics: Humans; Mice; Animals; Myalgia; Fibromyalgia; Protons; Ion Channels; Acidosis
PubMed: 37967833
DOI: No ID Found -
Clinical Medicine (London, England) Mar 2024This review concerns the rare, acquired, usually iatrogenic, high-anion-gap metabolic acidosis, pyroglutamic acidosis. Pyroglutamate is a derivative of the amino acid... (Review)
Review
This review concerns the rare, acquired, usually iatrogenic, high-anion-gap metabolic acidosis, pyroglutamic acidosis. Pyroglutamate is a derivative of the amino acid glutamate, and is an intermediate in the 'glutathione cycle', by which glutathione is continuously synthesized and broken down. The vast majority of pyroglutamic acidosis cases occur in patients on regular, therapeutic doses of paracetamol. In about a third of cases, flucloxacillin is co-prescribed. In addition, the patients are almost always seriously unwell in other ways, typically with under-nourishment of some form. Paracetamol, with underlying disorders, conspires to divert the glutathione cycle, leading to the overproduction of pyroglutamate. Hypokalaemia is seen in about a third of cases. Once the diagnosis is suspected, it is simple to stop the paracetamol and change the antibiotic (if flucloxacillin is present), pending biochemistry. N-acetyl-cysteine can be given, but while the biochemical justification is compelling, the clinical evidence base is anecdotal.
Topics: Humans; Pyrrolidonecarboxylic Acid; Acetaminophen; Acidosis; Floxacillin; Anti-Bacterial Agents
PubMed: 38431210
DOI: 10.1016/j.clinme.2024.100030 -
International Journal of Molecular... Mar 2024MELAS syndrome, characterized by mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes, represents a devastating mitochondrial disease, with... (Review)
Review
MELAS syndrome, characterized by mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes, represents a devastating mitochondrial disease, with the stroke-like episodes being its primary manifestation. Arginine supplementation has been used and recommended as a treatment for these acute attacks; however, insufficient evidence exists to support this treatment for MELAS. The mechanisms underlying the effect of arginine on MELAS pathophysiology remain unclear, although it is hypothesized that arginine could increase nitric oxide availability and, consequently, enhance blood supply to the brain. A more comprehensive understanding of these mechanisms is necessary to improve treatment strategies, such as dose and regimen adjustments; identify which patients could benefit the most; and establish potential markers for follow-up. This review aims to analyze the existing evidence concerning the mechanisms through which arginine supplementation impacts MELAS pathophysiology and provide the current scenario and perspectives for future investigations.
Topics: Humans; MELAS Syndrome; Acidosis, Lactic; Arginine; Stroke; Dietary Supplements
PubMed: 38612442
DOI: 10.3390/ijms25073629 -
The Journal of Biological Chemistry Dec 2023Pyruvate dehydrogenase (PDH) is the rate-limiting enzyme for glucose oxidation that links glycolysis-derived pyruvate with the tricarboxylic acid (TCA) cycle. Although...
Pyruvate dehydrogenase (PDH) is the rate-limiting enzyme for glucose oxidation that links glycolysis-derived pyruvate with the tricarboxylic acid (TCA) cycle. Although skeletal muscle is a significant site for glucose oxidation and is closely linked with metabolic flexibility, the importance of muscle PDH during rest and exercise has yet to be fully elucidated. Here, we demonstrate that mice with muscle-specific deletion of PDH exhibit rapid weight loss and suffer from severe lactic acidosis, ultimately leading to early mortality under low-fat diet provision. Furthermore, loss of muscle PDH induces adaptive anaplerotic compensation by increasing pyruvate-alanine cycling and glutaminolysis. Interestingly, high-fat diet supplementation effectively abolishes early mortality and rescues the overt metabolic phenotype induced by muscle PDH deficiency. Despite increased reliance on fatty acid oxidation during high-fat diet provision, loss of muscle PDH worsens exercise performance and induces lactic acidosis. These observations illustrate the importance of muscle PDH in maintaining metabolic flexibility and preventing the development of metabolic disorders.
Topics: Animals; Mice; Acidosis, Lactic; Glucose; Muscle, Skeletal; Pyruvate Dehydrogenase Complex; Pyruvic Acid; Glutamine; Alanine; Gene Deletion; Diet; Mortality, Premature
PubMed: 37865313
DOI: 10.1016/j.jbc.2023.105375 -
Metabolites Oct 2023Pneumonia is a common clinical disease in the neonatal period and poses a serious risk to infant health. Therefore, the understanding of molecular mechanisms is of great...
Pneumonia is a common clinical disease in the neonatal period and poses a serious risk to infant health. Therefore, the understanding of molecular mechanisms is of great importance for the development of methods for the rapid and accurate identification, classification and staging, and even disease diagnosis and therapy of pneumonia. In this study, a nontargeted metabonomic method was developed and applied for the analysis of serum samples collected from 20 cases in the pneumonia control group (PN) and 20 and 10 cases of pneumonia patients with metabolic acidosis (MA) and myocardial damage (MD), respectively, with the help of ultrahigh-performance liquid chromatography-high-resolution mass spectrometry (UPLC-HRMS). The results showed that compared with the pneumonia group, 23 and 21 differential metabolites were identified in pneumonia with two complications. They showed high sensitivity and specificity, with the area under the curve (ROC) of the receiver operating characteristic curve (ROC) larger than 0.7 for each differential molecule. There were 14 metabolites and three metabolic pathways of sphingolipid metabolism, porphyrin and chlorophyll metabolism, and glycerophospholipid metabolism existing in both groups of PN and MA, and PN and MD, all involving significant changes in pathways closely related to amino acid metabolism disorders, abnormal cell apoptosis, and inflammatory responses. These findings of molecular mechanisms should help a lot to fully understand and even treat the complications of pneumonia in infants.
PubMed: 37999214
DOI: 10.3390/metabo13111118 -
Kidney360 Jun 2024
Randomized Controlled Trial
Topics: Humans; Hyperkalemia; Renal Insufficiency, Chronic; Acidosis; Silicates; Male
PubMed: 38622759
DOI: 10.34067/KID.0000000000000446