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Metabolic Laboratory Data
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
So, let’s get back to measuring the BUN and understanding what it means. BUN is formed for ammonia disposal. Ammonia is produced by bacterial breakdown of dietary protein. Ammonia is also produced by amino acid catabolism to form glucose. Therefore, BUN can be viewed as an end product of protein/amino acid catabolism.
Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
Other sewer gases include carbon dioxide and methane which have little or no odor characteristics and have a saturated gas density approximately 1.5 and 0.6 times that of air, respectively. Methane is extremely flammable, has a wide explosive range, and a low flash point. These characteristics result in a substantial fire and explosion hazard. Ammonia has a distinct, strong odor with good warning characteristics which are present well before attaining toxic levels.
Metabolic Diseases
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Stephanie Grünewald, Alex Broomfield, Callum Wilson
Patients usually present in the neonatal period with lethargy, poor feeding, apnoea and encephalopathy. These symptoms reflect the toxic effects of ammonia on the brain and may be initially mistaken for signs of sepsis. Ammonia, the key diagnostic metabolite in the acute setting, is a respiratory stimulant and a respiratory alkalosis may be found early in the illness. Early treatment of hyperammonaemia determines the long-term outcome for the patients (Fig. 14.8).
Health care resource utilization in the management of patients with Arginase 1 Deficiency in the US: a retrospective, observational, claims database study
Published in Journal of Medical Economics, 2022
Aseel Bin Sawad, John Jackimiec, Mark Bechter, Michael Hull, Jason Yeaw, Yi Wang, George A. Diaz
Urea cycle disorders (UCDs) represent a group of inborn errors of metabolism, due to defects in one of the enzymes or transporters that are involved in the metabolism of amino acids and impair the detoxification of ammonia1. The most unique and least common among UCDs is Arginase 1 Deficiency (ARG1-D)2, an ultra-rare disorder that has been estimated to occur globally in approximately 1 in 357,000 live births with a population prevalence of 1 in 726,0003. ARG1-D is a distinct UCD caused by mutations in the ARG1 gene, which results in diminished or absent arginase 1 enzyme activity and subsequently, accumulation of arginine (hyperargininemia)1. Excessive levels of arginine lead to progressive neurologic manifestations, significant morbidity, and early mortality2,4,5. Although the clinical presentation of ARG1-D differs by patient, it typically presents in early childhood, with progressive and debilitating manifestations that include motor deficits (e.g. spasticity and difficulty walking), developmental delays, intellectual disabilities, and in some cases, seizures5–10. Excess ammonia in the blood (hyperammonemia) is usually less frequent and not as severe as in other UCDs1; however, episodes of symptomatic and even severe hyperammonemia may occur and can result in death4,6,8.
Hyperammonemia in acetaminophen toxicity
Published in Clinical Toxicology, 2022
Ryan T. Marino, Alexander M. Sidlak
We identified four main findings from our analysis: ammonia concentrations were significantly elevated, they could occur early in the course of toxicity, they were not useful in predicting the development of encephalopathy, and empiric treatment was often initiated, but benefits were unapparent. In this cohort of acetaminophen-induced hepatotoxicity, 59% [44/75] of patients had peak ammonia concentrations >100 µmol/L. Even in those patients with an acute overdose (<24 h), the median ammonia concentration on presentation was 71 µmol/L. The concentrations of ammonia in this subgroup were not statistically different than those of patients with delayed presentations. The lack of difference in median ammonia concentration between subgroups was likely due to the fact that the degree of toxicity mattered more than the timing of ingestion. Significant ingestions that lead to hepatotoxicity can likewise lead to early elevations in ammonia concentration.
Hyperammonemia in the setting of Roux-en-Y gastric bypass presenting with osmotic demyelination syndrome
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Carly Rosenberg, Michael Rhodes
The metabolism of ammonia is essentially linked to that of glutamate. Glutaminase initially cleaves glutamine in the gut into ammonia and glutamate. In the central nervous system, however, glutamine synthetase is responsible for catalyzing ammonia and glutamate into glutamine (Figure 3) [7]. Although the mechanism is not entirely understood, multiple studies have demonstrated the occurrence of astrocyte swelling and subsequent cerebral edema when exposed to ammonia [7,8]. The ‘Trojan Horse’ hypothesis proposed by Albrecht et al. [9] suggests that cerebral edema is in fact a consequence of both ammonia and glutamine. Ammonia is thought to induce glutamine production within the astrocyte by glutamine synthetase. However, excess glutamine as a result of excess ammonia is thought to be transported to the mitochondria where it is metabolized back to ammonia and glutamate by phosphate-activated glutaminase [7–9]. The accumulation of ammonia can lead to oxidative stress and thus swelling of astrocytes [7,9].