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Diabetic Ketoacidosis
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Laboratory assessment of DKA includes testing for increased production of ketone bodies: ß-hydroxybutyric acid, acetoacetic acid, and acetone. The latter two are detectable in blood or urine by the semiquantitative nitroprusside test. This test fails to detect ß-hydroxybutyric acid, which is important because it is the predominant ketone in DKA, produced more than acetoacetic acid by a factor of 7–10. For this reason, the direct assay for ß-hydroxybutyric acid is preferred.
The patient with acute endocrine problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
A metabolic condition associated with an accumulation of ketone bodies. Ketones (acetoacetic acid and beta hydroxybutyrate) result from the breakdown of free fatty acids and deamination of amino acids. Ketones can be smelt on the breath (like fruit or nail polish remover) due to acetone (from acetoacetic acid).
Basic Concepts of Acid–Base Physiology
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The majority of the non-volatile or metabolic acids are derived from protein metabolism, primarily metabolism of exogenous protein in the form of methionine and phosphoproteins. Sulphuric acid is formed from sulphur-containing amino acids such as cysteine and methionine. Hydrochloric acid is formed from the degradation of lysine, arginine and histidine. Phosphoric acid is formed by the hydrolysis of phosphoproteins. A person consuming 100 g of protein a day produces about 1.1 mol of hydrogen ions during the conversion of protein nitrogen to urea. About 1500 mmol/day of lactic acid is produced by normal anaerobic metabolism of glucose and glycogen processes in the red blood cells, skin and skeletal muscle. The lactate is oxidized in the liver to regenerate bicarbonate. Excess lactic acid in the plasma indicates a diminished supply of oxygen to tissues. Acetoacetic acid and β-hydroxybutyric acid are produced by the metabolism of triglycerides during fasting. Acetoacetic acid and hydroxybutyric acids, in excess of normal amounts (e.g. in diabetic ketoacidosis), are excreted by the kidneys. Acetoacetic acid can be decarboxylated to acetone, which is excreted via the lungs and the kidneys. About 30 mmol of bicarbonate is lost in the faeces via the gastrointestinal tract, and this is equivalent to an acid load to the body.
Enrichment of sulphate-reducers and depletion of butyrate-producers may be hyperglycaemia signatures in the diabetic oral microbiome
Published in Journal of Oral Microbiology, 2022
Camilla Pedrosa Vieira Lima, Daniela Corrêa Grisi, Maria Do Carmo Machado Guimarães, Loise Pedrosa Salles, Paula de Castro Kruly, Thuy Do, Luiz Gustavo Dos Anjos Borges, Naile Dame-Teixeira
A growing body of literature recognizes the importance of salivary glucose as a biomarker of blood glucose levels [9–12]. Salivary glucose may be accountable for reducing the pH of the oral cavity, since oral bacteria can use glucose as a substrate in fermentative pathways, releasing acids as final metabolites. If these changes in the availability of metabolic substrates linger, the so-called ‘dynamic stability stage’ of the oral microbiome can be lost [13]. The acidification would facilitate acidogenic bacterial growth, shifting the ecological balance of the microbiota [8,14]. Furthermore, individuals with uncontrolled DM frequently present ketoacidosis increasing the ketone bodies (acetone, acetoacetic acid, and β-hydroxybutyric acid) in blood and urine [15], and probably in saliva. The potentially altered pH [4] can represent a selective pressure over the diabetic oral microbiome. If the pH-balance of the microbial community is disrupted by severe environmental pressures, the microbiome may collapse into an ‘acidogenic stage’ (increase in the acidogenic microorganisms) that initiates dental caries or into an ‘’inflammatory stage” (increase of inflammophilic anaerobic microorganisms) leading to periodontitis [13].
High anion gap metabolic acidosis induced by cumulation of ketones, L- and D-lactate, 5-oxoproline and acute renal failure
Published in Acta Clinica Belgica, 2018
Laura Heireman, Boris Mahieu, Mark Helbert, Wim Uyttenbroeck, Jan Stroobants, Marian Piqueur
In addition, acute renal failure is associated with acidosis due to accumulation of organic acids (HAGMA component) and decreased ammonia production (normal anion gap metabolic acidosis or NAGMA component). Nevertheless, serum bicarbonate levels usually remain >15 mmol/L and the anion gap does not exceed 20 mmol/L [10]. Diabetic ketoacidosis is caused by overproduction of ketones, such as β-hydroxybutyric acid and acetoacetic acid. Ketones circulate in the anionic form, leading to the development of HAGMA [12]. D-lactate-induced HAGMA may occur in patients with a history of short bowel syndrome because unabsorbed carbohydrates act as a substrate for colonic bacteria to form D-lactic acid, which is then absorbed in the gut [13]. Accumulation of L-lactate caused by the increased anaerobic metabolism associated with tissue hypoxia may also induce HAGMA [14]. Tissue hypoxia may be induced by the circulatory disturbances associated with sepsis [14].
The role of the clinical laboratory in diagnosing acid–base disorders
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
Ketoacidosis, a frequent cause of metabolic acidosis, is associated with an accumulation of ketone bodies. The most common cause of ketoacidosis is diabetic ketoacidosis. Less frequent causes are fasting ketosis, alcoholic ketoacidosis, and salicylate poisoning. The term “ketone bodies” refers to three molecules. The first is acetoacetate, which accumulates during fatty acid metabolism under low carbohydrate conditions. The second is beta-hydroxybutyric acid, which is formed from reduction of acetoacetate in the mitochondria. These two predominant ketone bodies are energy-rich compounds that transport energy from the liver to other tissues. The third is acetone, which is generated by spontaneous decarboxylation of acetoacetate and is responsible for the sweet odor on the breath of individuals with ketoacidosis. During periods of glucose deficiency, ketone bodies play a key role in sparing glucose utilization to provide the brain with an alternative source of energy. Acetoacetic acid is the only true ketoacid, but in ketoacidosis, beta-hydroxybutyric acid is the most important “ketone” because it results from the reduction of acetoacetic acid by NADH. Beta-hydroxybutyric acid is a hydroxyacid but not a true ketoacid. Acetone, the least abundant ketone body is formed from the decarboxylation of acetic acid. Acetone is a ketone but not an acid. Ketone bodies are produced by the liver and are always present in the blood [110,114,193–197]. Their levels increase during fasting and prolonged exercise. They are also found in the blood of neonates and pregnant women because physiological ketosis occurs quite readily in the neonatal period and during pregnancy [193].