• Journal of Korean Neurosurgical Society
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• v.56 no.2
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• pp.135-140
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• 2014

Objective : Propofol and volatile anesthesia have been associated with metabolic acidosis induced by increased lactate. This study was designed to evaluate changes in pH, base excess (BE), and lactate in response to different anesthetic agents and to characterize propofol infusion-associated lactic acidosis. Methods : The medical records of patients undergoing neurosurgical anesthesia between January 2005 and September 2012 were examined. Patients were divided into 2 groups : those who received propofol (total intravenous anesthesia, TIVA) and those who received sevoflurane (balanced inhalation anesthesia, BIA) anesthesia. Propensity analysis was performed (1 : 1 match, n=47), and the characteristics of the patients who developed severe acidosis were recorded. Results : In the matched TIVA and BIA groups, the incidence of metabolic acidosis (11% vs. 13%, p=1) and base excess (p>0.05) were similar. All patients in the TIVA group who developed severe acidosis did so within 4 hours of the initiation of propofol infusion, and these patients improved when propofol was discontinued. Conclusions : The incidence of metabolic acidosis was similar during neurosurgical anesthesia with propofol or sevoflurane. In addition, severe acidosis associated with propofol infusion appears to be reversible when propofol is discontinued.

• Biomedical Science Letters
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• v.21 no.4
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• pp.241-247
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• 2015

Lactate and ketone bodies are considered biological markers for ketosis and several inherited metabolic disorders. In the current study, the specific ratios of lactate and ketone bodies as analytical tools for differential diagnosis of various lactic acidosis were devised. The study included a protein precipitation step following tert-butyldimethylsilyl derivatisation. Total run time was approximately 30 min including sample preparation and GS/MS analysis. The limits of detection were below 0.1 pg/mL over the targeted 4 analytes. The calibration curve was linear over the concentration range of $0.001{\sim}250{\mu}g/mL$ for pyruvate, beta-hydroxybutyrate, and acetoacetate ($R^2$ > 0.99). Inter-day accuracy and precision were 87.7~94.8% with RSD of 2.5~5.7% at 2 levels. Absolute recoveries (%) of target analytes were 87.0~98.4%. The method was validated for the quantification of lactate and ketone bodies for differentiation of lactic acidosis.

• Asian-Australasian Journal of Animal Sciences
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• v.2 no.3
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• pp.346-348
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• 1989

• Proceedings of the KSMRM Conference
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• 2000.11a
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• pp.59-59
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• 2000

• Neonatal Medicine
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• v.17 no.2
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• pp.254-261
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• 2010

Little is known about neonatal mitochondrial disease, though mitochondrial metabolic disorders may often present in the neonatal period because of the high energy requirement of neonate. In newborn period, common presentations are not specific and the disease course may be rapid and fatal. In this study, we report three cases of neonatal mitochondrial disease. The first case was strongly suspected because of sudden seizure and mental change with severe lactic acidosis, and multiorgan failure. Plasma lactate/pyruvate (L/P) ratio was increased to 55.6 with marked lactic aciduria and increased plasma alanin up to 2,237 nmol/mL. In the second patient, a peritoneal dialysis was performed for acute adrenal and renal failure, but metabolic acidosis persisted. Plasma L/P ratio was increased to 23.9, and MRC I (mitochondrial respiratory chain defect) was diagnosed through the enzymatic analysis of the muscles. The third case showed repetitive episode of lactic acidosis during the first two months of life, hypotonia, failure to thrive and feeding difficulties. We found markedly increased cerebrospinal fluid L/P ratio up to 57 though plasma L/P ratio(19.4) was borderline with increased plasma lactate. The lactate peak was prominent in brain magnetic resonance spectroscopy (MRS). MRC II was confirmed through muscle biopsy. Plasma lactate level and lactate peak of brain MRS were normalized after conservative treatment.

• Food Science and Biotechnology
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• v.15 no.6
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• pp.948-953
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• 2006

The D-form of lactic acid is frequently detected in fermented foods, and an excessive dietary intake of D-lactic acid may induce metabolic stress in both infants and patients. This work was carried out to determine the prevailing microorganisms relevant to the accumulation of D-lactic acid in kimchi. Leuconostoc (Leuc.) mesenteroides and Leuc. citreum primarily synthesized D-lactate with a small quantity of L-form. Leuc. gelidum and Leuc. inhae evidenced patterns similar to this. Lactobacillus (Lb.) plantarum and Lb. brevis were shown to convert glucose into a balanced mixture of D-/L-lactic acid, whereas Lb. casei principally synthesized L-lactic acid and a very small quantity of D-lactic acid. When kimchi was incubated at 8 or $22^{\circ}C$, D-lactic acid was over-produced than L-form. Leuconostoc was determined as the primary producer between the initial to mid-phase of fermentation and Lb. plantarum or Lb. brevis seemed to boost D-lactic acid content during later stage of acid accumulation.

• Food Science and Biotechnology
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• v.14 no.1
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• pp.64-67
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• 2005

Commercial kimchi and sauerkraut were analyzed for their D- and L-lactic acid contents. Ranges of D- and L-lactic acid contents in commercial kimchi were 17-57 (38.51 mean) and 25-87 (64.47 mean) mM, respectively. Ratio of D-lactic acid on L-lactic acid (D/L) was 0.50-0.80 (0.60 mean). Ranges of D- and L-lactic acid contents in commercial sauerkraut were 68.96-103.62 (88.97 mean) and 74.46-82.26 (78.91 mean) mM, respectively, with D/L of 0.90-1.26 (1.13 mean). Results reveal kimchi and sauerkraut contained a significant amount of D-lactic acid, with sauerkraut showing a higher content than kimchi, while L-lactic acid contents were not significantly different.

• Proceedings of the PSK Conference
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• 2000.04a
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• pp.201.2-202
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• 2000

• Journal of Genetic Medicine
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• v.16 no.1
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• pp.31-38
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• 2019

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a maternally inherited mitochondrial disorder of which m.3243A>G is the most commonly associated mutation, resulting in an inability to meet the energy requirements of various organs. MELAS poses a diagnostic challenge owing to its multiple organ involvement and great clinical variability due to its heteroplasmic nature. We report three cases from a family who were initially misdiagnosed with myasthenia gravis or undiagnosed. Although there is no optimal consensus treatment approach for patients with MELAS because of the disease's heterogeneity, our 21-year-long therapy regimen of ${\text\tiny{L}}-arginine$, ${\text\tiny{L}}-carnitine$, and coenzyme Q10 supplementation combined with dietary management appeared to provide noticeable protection from the symptoms and complications. Prompt early diagnosis is important, as optimal multidisciplinary management and early intervention may improve outcomes.

• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.2
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• pp.165-171
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• 2018

An overdose of antihypertensive agents, such calcium channel blockers (CCBs) and angiotensin II receptor blocker (ARBs), and the antihyperglycemic agent, metformin, leads to hypotension and lactic acidosis, respectively. A 40-year-old hypertensive and diabetic man with hyperlipidemia and a weight of 110 kg presented to the emergency room with vomiting, dizziness, and hypotension following an attempted drug overdose suicide with combined CCBs, ARBs, 3-hydroxy-3-methylglutaryl-coemzyme A reductase inhibitors, and metformins. A conventional medical treatment initially administered proved ineffective. The treatment was then changed to simultaneous extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT), which was effective. This shows that simultaneous ECMO and CRRT can be an effective treatment protocol in cases of ineffective conventional medical therapy for hypotension and lactic acidosis due to an overdose of antihypertensive agents and metformin, respectively.