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Pyruvate carboxylase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
In the complex form, severe neonatal lactic acidosis is the presenting feature [22, 23]. The initial acidosis may be fatal and many patients have died by three months of age. Most have hepatomegaly. Metabolic acidosis may lead to dehydration, coma, shock, and apnea. This disorder has now been observed in North American, Egyptian, and Saudi Arabian patients [9, 20, 24–26].
Respiratory Medicine
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Colin Wallis, Helen Spencer, Sam Sonnappa
Non-pulmonary causes: Congenital heart disease.Sepsis.Severe metabolic acidosis.
Clinical Manifestation of Mitochondrial Disorders in Childhood
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Ketogenic diet can stimulate fatty acid metabolism, provides an alternative energy source and supplements intermediates missing in PDHC (coenzyme A of Krebs cycle) (Gano et al., 2014). In patients with milder forms of the disease, some treatment effects were observed after fast carbohydrates restriction (improved muscle weakness and dystonic disorder) (Debray et al., 2006). A very small number of about 5% patients with mutations in the PDHA1 gene are thiamine-responsive, however, initial therapy with thiamine (50 mg/kg/day) may be indicated especially for those presenting with a dystonic disorder. Dichloroacetate has been used but significant side effects, such as peripheral neuropathy, may limit effectiveness. The benefit of treatment combination of high dose of thiamine and biotin has been established in some patients with thiamine transporters deficiency (SLC19A3) (Subramanian et al., 2006). Metabolic acidosis can be partially compensated using alkalinisation therapy.
Serum anion gap at admission predicts all-cause mortality in critically ill patients with cerebral infarction: evidence from the MIMIC-III database
Published in Biomarkers, 2020
Xuefang Liu, Yanlin Feng, Xinyu Zhu, Ying Shi, Manting Lin, Xiaoyan Song, Jiancheng Tu, Enwu Yuan
The serum anion gap (AG) is a mathematical derivation parameter calculated from the difference between cation and anion concentrations (Glasmacher and Stones 2016, Torrente 2017). The equation, AG = [Na+ (mmol/L) + K+ (mmol/L)] − [Cl− (mmol/L) + HCO3− (mmol/L)], was widely used. AG reflects the unmeasured anion concentration. In clinical practice, it has been regarded as a parameter to evaluate the acid-base status and helps to identify various forms of metabolic acidosis. Recent studies have shown that levels of AG were linked to prognosis for coronary artery disease (CAD) (Yang et al. 2017), sepsis (Mohr et al. 2018), acute kidney injury (AKI) (Cheng et al. 2020) and chronic kidney disease (CKD) (Abramowitz et al. 2012). Disturbances in brain metabolism occur, once there are instabilities in cerebral blood flow (CBF), causing shifts in ion concentrations. Research revealed that acid/base balance in the systemic circulation responded rapidly to the ischaemic event in the brain (Martha et al. 2018), suggesting that AG could be a potential biomarker for cerebral infarction.
Electrolyte and acid-base disorders in cancer patients and its impact on clinical outcomes: evidence from a real-world study in China
Published in Renal Failure, 2020
Yang Li, Xiaohong Chen, Ziyan Shen, Yimei Wang, Jiachang Hu, Jiarui Xu, Bo Shen, Xiaoqiang Ding
All of the eligible participants had received sodium, potassium and chloride tests. Of them, about two-thirds measured the level of magnesium and phosphorus (n = 16,940). Acid-base level was measured in 3,484 patients (13.5%) in the format of arterial blood gas analysis who were usually in critical status. Totally 15,000 patients (58.0%) were recognized with at least one category of electrolyte and acid-base abnormalities. Hypocalcemia (27.8%) was the most common electrolyte disorder (Figure 2(a)), followed by hypophosphatemia (26.7%), hypochloremia (24.4%) and hyponatremia (22.5%). The incidence of simple metabolic acidosis (MAC) and metabolic alkalosis (MAL) was 12.8% and 22.1% respectively. Patients with dual metabolic acid-base disorders (MAC + MAL) accounted for 30.2% (Figure 2(b)).
Approach to the patient presenting with metabolic acidosis
Published in Acta Clinica Belgica, 2019
Jill Vanmassenhove, Norbert Lameire
This article covers the following topics regarding metabolic acidosis: How to define and diagnose metabolic acidosis.How to differentiate high anion gap metabolic acidosis vs non anion gap metabolic acidosis and how to recognize mixed acid base disturbances.How to be aware of the potential caveats of the several diagnostic tools.