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Manosalva C, Quiroga J, Hidalgo AI, Alarcón P, Ansoleaga N, Hidalgo MA, Burgos RA. Role of Lactate in Inflammatory Processes: Friend or Foe. Front Immunol 2022; 12:808799. [PMID: 35095895 PMCID: PMC8795514 DOI: 10.3389/fimmu.2021.808799] [Citation(s) in RCA: 100] [Impact Index Per Article: 33.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/04/2021] [Accepted: 12/23/2021] [Indexed: 12/13/2022] Open
Abstract
During an inflammatory process, shift in the cellular metabolism associated with an increase in extracellular acidification are well-known features. This pH drop in the inflamed tissue is largely attributed to the presence of lactate by an increase in glycolysis. In recent years, evidence has accumulated describing the role of lactate in inflammatory processes; however, there are differences as to whether lactate can currently be considered a pro- or anti-inflammatory mediator. Herein, we review these recent advances on the pleiotropic effects of lactate on the inflammatory process. Taken together, the evidence suggests that lactate could exert differential effects depending on the metabolic status, cell type in which the effects of lactate are studied, and the pathological process analyzed. Additionally, various targets, including post-translational modifications, G-protein coupled receptor and transcription factor activation such as NF-κB and HIF-1, allow lactate to modulate signaling pathways that control the expression of cytokines, chemokines, adhesion molecules, and several enzymes associated with immune response and metabolism. Altogether, this would explain its varied effects on inflammatory processes beyond its well-known role as a waste product of metabolism.
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Affiliation(s)
- Carolina Manosalva
- Faculty of Sciences, Institute of Pharmacy, Universidad Austral de Chile, Valdivia, Chile
| | - John Quiroga
- Laboratory of Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile
- Graduate School, Faculty of Veterinary Sciences, Universidad Austral de Chile, Valdivia, Chile
| | - Alejandra I. Hidalgo
- Laboratory of Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile
| | - Pablo Alarcón
- Laboratory of Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile
| | - Nicolás Ansoleaga
- Laboratory of Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile
- Graduate School, Faculty of Veterinary Sciences, Universidad Austral de Chile, Valdivia, Chile
| | - María Angélica Hidalgo
- Laboratory of Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile
| | - Rafael Agustín Burgos
- Laboratory of Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile
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Weemaes M, Hiele M, Vermeersch P. High anion gap metabolic acidosis caused by D-lactate: mind the time of blood collection. Biochem Med (Zagreb) 2020; 30:011001. [PMID: 31839728 PMCID: PMC6904971 DOI: 10.11613/bm.2020.011001] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/02/2019] [Accepted: 10/20/2019] [Indexed: 11/06/2022] Open
Abstract
Introduction D-lactic acidosis is an uncommon cause of high anion gap acidosis. Materials and methods A 35-year old woman was admitted to the emergency room with somnolence, drowsiness, dizziness, incoherent speech and drunk appearance. Her past medical history included a Roux-en-Y bypass. Point-of-care venous blood analysis revealed a high anion gap acidosis. Based on the clinical presentation, routine laboratory results and negative toxicology screening, D-lactate and 5-oxoprolinuria were considered as the most likely causes of the high anion gap acidosis. Urine organic acid analysis revealed increased lactate, but no 5-oxoproline. Plasma D-lactate was < 1.0 mmol/L and could not confirm D-lactic acidosis. What happened Further investigation revealed that the blood sample for D-lactate was drawn 12 hours after admission, which might explain the false-negative result. Data regarding the half-life of D-lactate are, however, scarce. During a second admission, one month later, D-lactic acidosis could be confirmed with an anion gap of 40.7 mmol/L and a D-lactate of 21.0 mmol/L measured in a sample collected at the time of admission. Main lesson The time of blood collection is of utmost importance to establish the diagnosis of D-lactic acidosis due to the fast clearance of D-lactate in the human body.
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Affiliation(s)
- Matthias Weemaes
- Clinical Department of Laboratory Medicine, UZ Leuven, Leuven, Belgium
| | - Martin Hiele
- Clinical Department of Gastroenterology, UZ Leuven, Leuven, Belgium
| | - Pieter Vermeersch
- Clinical Department of Laboratory Medicine, UZ Leuven, Leuven, Belgium.,Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium
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Bianchetti DGAM, Amelio GS, Lava SAG, Bianchetti MG, Simonetti GD, Agostoni C, Fossali EF, Milani GP. D-lactic acidosis in humans: systematic literature review. Pediatr Nephrol 2018; 33:673-681. [PMID: 29218437 DOI: 10.1007/s00467-017-3844-8] [Citation(s) in RCA: 37] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/11/2017] [Revised: 10/31/2017] [Accepted: 11/03/2017] [Indexed: 12/18/2022]
Abstract
BACKGROUND D-lactic acidosis is an uncommon and challenging form of metabolic acidosis that may develop in short bowel syndrome. It has been documented exclusively in case reports and small case series. METHODS We performed a review of the literature in the National Library of Medicine and Excerpta Medica databases. RESULTS We identified 84 original reports published between 1977 and 2017. D-lactic acidosis was observed in 98 individuals ranging in age from 7 months to 86 years with short bowel syndrome. The clinical presentation included Kussmaul breathing, confusion, slurred speech, and gait disturbances. Furthermore, among 99 consecutive patients with short bowel syndrome, 21 reported having episodes with symptoms consistent with D-lactic acidosis. In addition, D-lactic acid might also contribute to acidosis in diabetes mellitus. Finally, abnormally high D-lactic acid was documented after administration or ingestion of large amounts of propylene glycol, as paraneoplastic phenomenon and perhaps also in a so far poorly characterized inherited inborn error of metabolism. CONCLUSIONS In humans with short bowel syndrome (or carbohydrate malabsorption), D-lactic acidosis is likely rather common and under-recognized. This condition should be included in the differential diagnosis of unexplained high-gap metabolic acidosis where the anion causing the acidosis is not known. Furthermore, diabetic acidosis might be caused by accumulation of both ketone bodies and D-lactic acid. Finally, there are endogenous sources of D-lactic acid in subjects with propylene glycol intoxication.
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Affiliation(s)
- Davide G A M Bianchetti
- Pediatric Department of Southern Switzerland, Bellinzona, and Università della Svizzera Italiana, Lugano, Switzerland
| | - Giacomo S Amelio
- Pediatric Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico and Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy
| | - Sebastiano A G Lava
- Department of Pediatrics, University Children's Hospital of Bern, Inselspital, Bern, Switzerland
| | - Mario G Bianchetti
- Pediatric Department of Southern Switzerland, Bellinzona, and Università della Svizzera Italiana, Lugano, Switzerland.
| | - Giacomo D Simonetti
- Pediatric Department of Southern Switzerland, Bellinzona, and Università della Svizzera Italiana, Lugano, Switzerland
| | - Carlo Agostoni
- Pediatric Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico and Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy
| | - Emilio F Fossali
- Pediatric Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico and Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy
| | - Gregorio P Milani
- Pediatric Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico and Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy
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Zafar A, Khatri IA. An overview of complications affecting the Central Nervous System following bariatric surgery. ACTA ACUST UNITED AC 2018; 23:4-12. [PMID: 29455214 PMCID: PMC6751905 DOI: 10.17712/nsj.2018.1.20170316] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
Bariatric surgery has been considered as an effective treatment for morbid obesity. Apart from procedures related complications, a broad spectrum of neurological disorders affecting any part of neuraxis has been reported following BS. Central nervous system complications, although less common than peripheral nervous system complications, carry significant morbidity and potential mortality. Encephalopathy, behavioral and psychiatric disorders, myelopathy and optic neuropathy are the most frequently reported CNS complications. Early detection and prompt management may improve or completely reverse these neurological complications. It is essential that the treating physicians must be aware of their clinical manifestations and management, so early diagnosis and treatment can prevent patients from suffering significant neurological deficits and even death. This review discusses the clinical manifestations of these complications in detail which will help concerned physician in earlier recognition and hence prevent the delay in specific treatment.
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Affiliation(s)
- Azra Zafar
- Department of Neurology, College of Medicine, Imam Abdulrahman Bin Faisal University, Dammam, Kingdom of Saudi Arabia. E-mail:
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Wallis A, Ball M, McKechnie S, Butt H, Lewis DP, Bruck D. Examining clinical similarities between myalgic encephalomyelitis/chronic fatigue syndrome and D-lactic acidosis: a systematic review. J Transl Med 2017; 15:129. [PMID: 28592308 PMCID: PMC5463382 DOI: 10.1186/s12967-017-1229-1] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/08/2017] [Accepted: 05/30/2017] [Indexed: 12/18/2022] Open
Abstract
BACKGROUND The pursuit for clarity in diagnostic and treatment pathways for the complex, chronic condition of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) continues. This systematic review raises a novel question to explore possible overlapping aetiology in two distinct conditions. Similar neurocognitive symptoms and evidence of D-lactate producing bacteria in ME/CFS raise questions about shared mechanisms with the acute condition of D-lactic acidosis (D-la). METHODS D-la case reports published between 1965 and March 2016 were reviewed for episodes describing both neurological symptoms and high D-lactate levels. Fifty-nine D-la episodes were included in the qualitative synthesis comparing D-la symptoms with ME/CFS diagnostic criteria. A narrative review of D-la mechanisms and relevance for ME/CFS was provided. RESULTS The majority of neurological disturbances reported in D-la episodes overlapped with ME/CFS symptoms. Of these, the most frequently reported D-la symptoms were motor disturbances that appear more prominent during severe presentations of ME/CFS. Both patient groups shared a history of gastrointestinal abnormalities and evidence of bacterial dysbiosis, although only preliminary evidence supported the role of lactate-producing bacteria in ME/CFS. LIMITATIONS Interpretation of results are constrained by both the breadth of symptoms included in ME/CFS diagnostic criteria and the conservative methodology used for D-la symptom classification. Several pathophysiological mechanisms in ME/CFS were not examined. CONCLUSIONS Shared symptomatology and underlying microbiota-gut-brain interactions raise the possibility of a continuum of acute (D-la) versus chronic (ME/CFS) presentations related to D-lactate absorption. Measurement of D-lactate in ME/CFS is needed to effectively evaluate whether subclinical D-lactate levels affect neurological symptoms in this clinical population.
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Affiliation(s)
- Amy Wallis
- Psychology Department, College of Health and Biomedicine, Victoria University, PO Box 14428, Melbourne, VIC 8001 Australia
| | - Michelle Ball
- Psychology Department, College of Health and Biomedicine, Victoria University, PO Box 14428, Melbourne, VIC 8001 Australia
| | - Sandra McKechnie
- College of Engineering & Science, Victoria University, Melbourne, VIC Australia
| | - Henry Butt
- Bioscreen Yarraville (Aust) Pty Ltd, Melbourne, VIC Australia
| | | | - Dorothy Bruck
- Psychology Department, College of Health and Biomedicine, Victoria University, PO Box 14428, Melbourne, VIC 8001 Australia
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Abstract
Lactic acidosis is an etiologically and biochemically heterogeneous disorder that is due to the overproduc tion of lactic acid or the underutilization of lactate. It occurs with disorders in which tissue oxygenation is impaired (Type A) and with disorders in which it is not (Type B). Lactic acidosis is an anion-gap metabolic acidosis in which the lactate concentration is greater than or equal to 5 mM and the systemic pH is less than 7.30. Treatment is largely empiric and generally unsatis factory. The use of sodium bicarbonate in lactic acidosis is currently controversial. The adverse effects of bicar bonate and the beneficial effects of dichloroacetate in experimental models of lactic acidosis are reviewed.
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Affiliation(s)
- Robert A. Kreisberg
- University of South Alabama College of Medicine, 2451 Fillingim St, Mobile, AL 36617
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Abstract
Obesity has attained pandemic proportions, and bariatric surgery is increasingly being employed resulting in turn to more neurological complications which must be recognized and managed. Neurological complications may result from mechanical or inflammatory mechanisms but primarily result from micro-nutritional deficiencies. Vitamin B12, thiamine, and copper constitute the most frequent deficiencies. Neurological complications may occur at reasonably predictable times after bariatric surgery and are associated with the type of surgery used. During the early post-operative period, compressive or stretch peripheral nerve injury, rhabdomyolysis, Wernicke's encephalopathy, and inflammatory polyradiculoneuropathy may occur. Late complications ensue after months to years and include combined system degeneration (vitamin B12 deficiency) and hypocupric myelopathy. Bariatric surgery patients require careful nutritional follow-up with routine monitoring of micronutrients at 6 weeks and 3, 6, and 12 months post-operatively and then annually after surgery and multivitamin supplementation for life. Sustained vigilance for common and rare neurological complications is essential.
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D-lactic acidosis: an underrecognized complication of short bowel syndrome. Gastroenterol Res Pract 2015; 2015:476215. [PMID: 25977687 PMCID: PMC4421027 DOI: 10.1155/2015/476215] [Citation(s) in RCA: 103] [Impact Index Per Article: 10.3] [Reference Citation Analysis] [Abstract] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/26/2014] [Revised: 03/28/2015] [Accepted: 04/08/2015] [Indexed: 12/15/2022] Open
Abstract
D-lactic acidosis or D-lactate encephalopathy is a rare condition that occurs primarily in individuals who have a history of short bowel syndrome. The unabsorbed carbohydrates act as a substrate for colonic bacteria to form D-lactic acid among other organic acids. The acidic pH generated as a result of D-lactate production further propagates production of D-lactic acid, hence giving rise to a vicious cycle. D-lactic acid accumulation in the blood can cause neurologic symptoms such as delirium, ataxia, and slurred speech. Diagnosis is made by a combination of clinical and laboratory data including special assays for D-lactate. Treatment includes correcting the acidosis and decreasing substrate for D-lactate such as carbohydrates in meals. In addition, antibiotics can be used to clear colonic flora. Although newer techniques for diagnosis and treatment are being developed, clinical diagnosis still holds paramount importance, as there can be many confounders in the diagnosis as will be discussed subsequently.
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Abstract
Bariatric surgery has been increasingly employed to manage morbid obesity. Approximately 150000 bariatric procedures are performed in the US annually. Neurologic complications arise in as many as 5% of individuals having this surgery. Although the etiology of some of these complications remains obscure, the majority are the consequence of vitamin (most commonly thiamine and vitamin B12) or mineral (most commonly copper) deficiency and familiarity with these disorders is essential. Their rapid diagnosis and appropriate treatment is essential to avoid long-term, irreversible consequences including, in some instances, death.
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Affiliation(s)
- Joseph R Berger
- Department of Neurology, University of Kentucky College of Medicine, Lexington, KY, USA.
| | - Divya Singhal
- Department of Neurology, University of Kentucky College of Medicine, Lexington, KY, USA
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Increased circulating D-lactate levels predict risk of mortality after hemorrhage and surgical trauma in baboons. Shock 2012; 37:473-7. [PMID: 22266971 DOI: 10.1097/shk.0b013e318249cb96] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/12/2023]
Abstract
Patients with hemorrhagic shock and/or trauma are at risk of developing colonic ischemia associated with bacterial translocation that may lead to multiple organ failure and death. Intestinal ischemia is difficult to diagnose noninvasively. The present retrospective study was designed to determine whether circulating plasma D-lactate is associated with mortality in a clinically relevant two-hit model in baboons. Hemorrhagic shock was induced in anesthetized baboons (n = 24) by controlled bleeding (mean arterial pressure, 40 mmHg), base excess (maximum -5 mmol/L), and time (maximum 3 h). To mimic clinical setting more closely, all animals underwent a surgical trauma after resuscitation including midshaft osteotomy stabilized with reamed femoral interlocking nailing and were followed for 7 days. Hemorrhagic shock/surgical trauma resulted in 66% mortality by day 7. In nonsurvivor (n = 16) hemorrhagic shock/surgical trauma baboons, circulating D-lactate levels were significantly increased (2-fold) at 24 h compared with survivors (n = 8), whereas the early increase during hemorrhage and resuscitation declined during the early postresuscitation phase with no difference between survivors and nonsurvivors. Moreover, D-lactate levels remained elevated in the nonsurvival group until death, whereas it decreased to baseline in survivors. Prediction of death (receiver operating characteristic test) by D-lactate was accurate with an area under the curve (days 1-3 after trauma) of 0.85 (95% confidence interval, 0.72-0.93). The optimal D-lactate cutoff value of 25.34 μg/mL produced sensitivity of 73% to 99% and specificity of 50% to 83%. Our data suggest that elevation of plasma D-lactate after 24 h predicts an increased risk of mortality after hemorrhage and trauma.
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Abstract
Optimal functioning of the central and peripheral nervous system is dependent on a constant supply of appropriate nutrients. The first section of this review discusses neurologic manifestations related to deficiency of key nutrients such as vitamin B(12), folate, copper, vitamin E, thiamine, and others. The second section addresses neurologic complications related to bariatric surgery. The third sections includes neurologic presentations caused by nutrient deficiencies in the setting of alcoholism. The concluding section addresses neurologic deficiency diseases that have a geographic predilection.
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Affiliation(s)
- Neeraj Kumar
- Department of Neurology, Mayo Clinic College of Medicine, Mayo Clinic, 200 First Street, SW, Rochester, MN 55905, USA.
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Abstract
OBJECTIVE To review the clinical essentials of Wernicke encephalopathy (WE) after bariatric surgery. SUMMARY BACKGROUND DATA An estimated 205,000 bariatric surgical procedures were performed in the United States in 2007. Such procedures may potentially lead to severe nutritional complications. METHODS Literature searches were performed in Medline, Embase, and abstract collections. Inclusion criteria were WE after bariatric surgery, diagnosed by the presence of two or more of the following signs: mental status changes, eye movement abnormalities, cerebellar dysfunction, and dietary deficiency. RESULTS Of 104 reported cases of WE after bariatric surgery, 84 cases were included. Gastric bypass or a restrictive procedure had been performed in 80 cases (95%). Admission to hospital for WE occurred within 6 months of surgery in 79 cases (94%). Frequent vomiting was a risk factor in 76 cases (90%) and had lasted for a median of 21 days at admission. Intravenous glucose administration without thiamine was a risk factor in 15 cases (18%). Brain magnetic resonance imaging identified lesions characteristic of WE in 14 of 30 cases (47%). Incomplete recovery was observed in 41 cases (49%); memory deficits and gait difficulties were frequent sequela. The recent increase in the use of bariatric surgery in the United States was associated with an increase in reported WE cases. CONCLUSIONS The number of WE cases after bariatric surgery is substantially higher than previously reported. Surgeons, allied health providers, and patients need to be aware of the predisposing factors and symptoms to prevent and optimize the management of this condition.
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Gibbs ME, Hertz L. Inhibition of astrocytic energy metabolism by D-lactate exposure impairs memory. Neurochem Int 2007; 52:1012-8. [PMID: 18063442 DOI: 10.1016/j.neuint.2007.10.014] [Citation(s) in RCA: 45] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/09/2007] [Revised: 09/21/2007] [Accepted: 10/19/2007] [Indexed: 11/17/2022]
Abstract
Bead discrimination learning in day-old chicken was inhibited by bilateral injection into the intermediate medial mesopallium (IMM), a homolog of the mammalian brain cortex, of the poorly metabolized enantiomer of L-lactate, D-lactate. The window of vulnerability extended from 10 min before training to 20 min after training. Unilateral injection 10 min before training inhibited only in the left IMM, whereas 10 min after training injection was only inhibitory if made into the right hemisphere. The pre-training administration caused memory loss from the earliest time tested whereas memory was maintained for another 20 min when D-lactate was injected 10 min post-training. The ability of acetate, an astrocyte-specific substrate, injected into the IMM to counteract the inhibitory effect was tested. Following D-lactate injection 10 min before training, rescue of memory immediately after training was achieved by acetate as long as aspartate, an oxaloacetate precursor, was also present. This suggests that pyruvate carboxylation is necessary for net synthesis of glutamate, which is known to occur at this time [Gibbs, M.E., Lloyd, H.G.E., Santa, T., Hertz, L., 2007. Glycogen is a preferred glutamate precursor during learning in 1-day-old chick: biochemical and behavioral evidence. J. Neurosci. Res., 85, 3326-3333]. However, acetate alone rescued memory 20 min post-training (following d-lactate injection 10 min after training), indicating that pyruvate at this time is used for energy production, consistent with memory inhibition by dinitrophenol. These findings suggest that D-lactate acts by inhibiting uptake of L-lactate into astrocytes (an extracellular effect) or metabolism of pyruvate in astrocytic mitochondria (an intracellular effect). An apparent lag phase between the administration of d-lactate and its inhibition of learning favors the latter possibility. Thus, under the present experimental conditions D-lactate acts as an astrocytic metabolic inhibitor rather than as an inhibitor of neuronal L-lactate uptake, as has occasionally been suggested. Analogously, a rare reversible neurological syndrome with memory deficits, D-lactate encephalopathy, may mainly or exclusively be due to astrocytic malfunction.
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Affiliation(s)
- Marie E Gibbs
- Department of Anatomy and Developmental Biology, Monash University, Clayton 3800, Australia
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Abstract
Optimal functioning of the central and peripheral nervous system is dependent on appropriate nutrients. Neurologic consequences of nutritional deficiencies are not restricted to underdeveloped countries. Multiple nutritional deficiencies can coexist. Obesity is of particular concern in the developed world. The rising rate of bariatric surgery are accompanied by neurologic complications related to nutrient deficiencies. Prognosis depends on prompt recognition and institution of appropriate therapy. This review discusses peripheral nervous system manifestations related to the deficiency of key nutrients, neurologic complications associated with bariatric surgery, and conditions that have a geographic significance associated with bariatric surgery and certain conditions that have a geographic predilection.
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Affiliation(s)
- Neeraj Kumar
- Department of Neurology, Mayo Clinic, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
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Collange O, Veber B, Tamion F, Lavoine A, Plissonnier D, Dureuil B. [Interest of D-lactate as a colic hypoperfusion marker during aortic abdominal aneurysm surgery]. ACTA ACUST UNITED AC 2006; 25:940-6. [PMID: 16891085 DOI: 10.1016/j.annfar.2006.03.040] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/15/2004] [Accepted: 03/10/2006] [Indexed: 12/22/2022]
Abstract
OBJECTIVE D-lactate is the dextrogyre form of the lactate usually measured in intensive care. Its bacterial origin should make it a marker of translocation during gut ischemia. The aim was to test D-lactate as a postoperative marker of colic hypoperfusion measured during aortic surgery. STUDY DESIGN Prospective observational cohort study. PATIENTS AND MEASUREMENTS Patients operated for abdominal aortic aneurysm. Two groups were stratified on inferior mesenteric arterial residual pressure (IMArP) measured during the surgery: Colic hypoperfusion during surgery (CHs) group: patients with an IMArP < 40 mmHg. CONTROL GROUP patients with an IMArP > or = 40 mmHg. Baseline data such as age, duration of aortic clamping and severity score (IGS II) were collected. The D-lactate was measured in postoperative at admission time in ICU and then daily. D-lactate(max) defined the maximum value of D-lactate for one patient. MAIN RESULTS Twenty-nine patients were included, 23 in the control group and 6 in the CHs group. Groups were comparable at baseline. D-lactate(max) was significantly higher in the CHs group (median: 0.13 mmol/l; min-max: 0.03-0.9 mmol/l) than in the control group (0.03; 0-0.26 mmol/l, p=0.007). CONCLUSION D-lactate could be postoperative marker of colic hypoperfusion measured during surgery for abdominal aortic aneurysm.
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Affiliation(s)
- O Collange
- Département d'anesthésie-réanimation, hôpital Charles-Nicolle, CHU de Rouen, 76031 Rouen, France.
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Abstract
D-lactic acidosis, also referred to as D-lactate encephalopathy, is a rare neurologic syndrome that occurs in individuals with short bowel syndrome or following jejuno-ileal bypass surgery. Symptoms typically present after the ingestion of high-carbohydrate feedings. Neurologic symptoms include altered mental status, slurred speech, and ataxia, with patients often appearing drunk. Onset of neurologic symptoms is accompanied by metabolic acidosis and elevation of plasma D-lactate concentration. In these patients, malabsorbed carbohydrate is fermented by an abnormal bacterial flora in the colon, which produces excessive amounts of D-lactate. High amounts of D-lactate are absorbed into the circulation, resulting in an elevated concentration of D-lactate in the blood. Development of neurologic symptoms has been attributed to D-lactate, but it is unclear if this is the cause or whether other factors are responsible. This review examines the pathophysiology of the production and accumulation of D-lactate while exploring the potential factors contributing to the development of neurologic manifestations. Methods of diagnosis and treatment are reviewed. Areas requiring further investigation are identified.
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Affiliation(s)
- Craig Petersen
- University of California, Davis, Medical Center, Sacramento, CA 95817, USA.
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Abstract
Lactic acidosis is frequently encountered in the intensive care unit. It occurs when there is an imbalance between production and clearance of lactate. Although lactic acidosis is often associated with a high anion gap and is generally defined as a lactate level >5 mmol/L and a serum pH <7.35, the presence of hypoalbuminemia may mask the anion gap and concomitant alkalosis may raise the pH. The causes of lactic acidosis are traditionally divided into impaired tissue oxygenation (Type A) and disorders in which tissue oxygenation is maintained (Type B). Lactate level is often used as a prognostic indicator and may be predictive of a favorable outcome if it normalizes within 48 hours. The routine measurement of serum lactate, however, should not determine therapeutic interventions. Unfortunately, treatment options remain limited and should be aimed at discontinuation of any offending drugs, treatment of the underlying pathology, and maintenance of organ perfusion. The mainstay of therapy of lactic acidosis remains prevention.
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Affiliation(s)
- Pamela J Fall
- Section of Nephrology, Hypertension and Transplantation, Department of Medicine, Medical College of Georgia, Augusta 30912, USA
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19
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Abstract
D-lactate is normally present in the blood of mammals at nanomolar concentrations due to methylglyoxal metabolism; millimolar d-lactate concentrations can arise due to excess gastrointestinal microbial production. Grain overload in ruminants, short-bowel syndrome in humans, and diarrhea in calves can all result in profound D-lactic acidemia, with remarkably similar neurological manifestations. In the past, D-lactate was thought to be excreted mainly in the urine, and metabolized slowly by the enzyme d-alpha-hydroxy acid dehydrogenase. More recent studies reported that mammals have a relatively high capacity for D-lactate metabolism and identified a putative mammalian D-lactate dehydrogenase. A growing body of literature is also emerging describing subclinical elevation of D-lactate as an indicator of sepsis and trauma. This article describes advances in the understanding of D-lactate metabolism, D-lactic acidosis in ruminants and humans, and subclinical elevation of d-lactate.
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Gentile A, Sconza S, Lorenz I, Otranto G, Rademacher G, Famigli-Bergamini P, Klee W. d-Lactic Acidosis in Calves as a Consequence of Experimentally Induced Ruminal Acidosis. ACTA ACUST UNITED AC 2004; 51:64-70. [PMID: 15153075 DOI: 10.1111/j.1439-0442.2004.00600.x] [Citation(s) in RCA: 40] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/29/2022]
Abstract
In order to test the hypothesis that ruminal drinking in calves can lead to D-lactic metabolic acidosis, ruminal acidosis was induced in nine calves by intraruminal application of untreated whole milk via a stomach tube. The amount of the daily force-fed liquid was 3 x 1 l. The experimental design called for an end of intraruminal applications if two or more of the following signs were observed: severe depression, estimated degree of dehydration >10%, absence of sucking reflex, lack of appetite for two consecutive feedings, severe metabolic acidosis with calculated Actual Base Excess (ABE) <-15 mmol/l. The procedure was scheduled to be discontinued on the 17th day of experiment. The onset of ruminal acidification occurred rapidly, and mean pH value fell from 6.70 (+/-0.48) to 4.90 (+/-0.38) after the first application. The following days the pH values varied between 4 and 5. Rumen acidity was characterized biochemically by a significant increase in both isomers of lactic acid. The effects of the intraruminal administration on the calves were detrimental; eight of nine calves showed an acute disease process. According to the pre-established clinical standard, seven of nine calves were removed from the intraruminal feeding schedule. All but one of the calves developed severe systemic acidosis. The increase in anion gap demonstrated the net acid load. In all the calves D-lactate levels were found to show a significant and rapid increase. On the contrary, L-lactate never deviated from physiological levels. These observations confirm that, in young calves as in adult cattle, ruminal acidosis may lead to a clinically manifested D-lactic metabolic acidosis.
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Affiliation(s)
- A Gentile
- Veterinary Clinical Department, Faculty of Veterinary Medicine, University of Bologna, via Tolara di Sopra 50, 40064 Ozzano Emilia, Bologna, Italy
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21
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Abstract
There are two common types of adult patient with a short bowel, those with jejunum in continuity with a functioning colon and those with a jejunostomy. Both groups have potential problems of undernutrition, but this is a greater problem in those without a colon, as they do not derive energy from anaerobic bacterial fermentation of carbohydrate to short chain fatty acids in the colon. Patients with a jejunostomy have major problems of dehydration, sodium and magnesium depletion all due to a large volume of stomal output. Both types of patient have lost at least 60 cm of terminal ileum and so will become deficient of vitamin B12. Both groups have a high prevalence of gallstones (45%) resulting from periods of biliary stasis. Patients with a retained colon have a 25% chance of developing calcium oxalate renal stones and they may have problems with D (-) lactic acidosis. The survival of patients with a short bowel, even if they need long-term parenteral nutrition, is good.
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Affiliation(s)
- J M Nightingale
- Gastroenterology Centre, Leicester Royal Infirmary, United Kingdom.
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22
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Haschke-Becher E, Baumgartner M, Bachmann C. Assay of D-lactate in urine of infants and children with reference values taking into account data below detection limit. Clin Chim Acta 2000; 298:99-109. [PMID: 10876007 DOI: 10.1016/s0009-8981(00)00272-2] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/18/2022]
Abstract
Accumulation of D-lactic acid produced by intestinal bacteria such as streptococci and lactobacilli has been extensively studied in ruminants [1-4]. In humans an increased production of D-lactate by intestinal bacteria under pathological conditions such as the short bowel syndrome can cause metabolic acidosis [5-8]. Since the lactate assays routinely used only measure L-lactate we developed a sensitive method of D-lactate quantification and established reference values in spot urines of infants and children (0 to 4 years of age). The enzymatic method with fluorimetric quantification of NADH is linear up to 2 mmol/l. It has a detection limit of 3.4 micromol/l. Among structurally related organic acids an interference was found only for L-lactate and DL-2-hydroxybutyrate at concentrations which are way beyond their physiological excretion. One hundred and sixty five spot urines of healthy Swiss (S), Austrian (A), German (G) and Chilean (CHI) infants aged from 0 to 4 years were analyzed. The distribution of the data is close to a lognormal one. Values below the detection limit were simulated and age groups were formed. In all populations D-lactate excretion was found highest during the first year of life; it declines with age during infancy and remains stable from 2.5 to 4 years of age. We show that D-lactate is excreted physiologically by healthy infants and children below 4 years of age and present reference values for D-lactate excretion which show some differences between the populations tested.
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Affiliation(s)
- E Haschke-Becher
- Laboratoire Central de Chimie Clinique, Centre Hospitalier Universitaire Vaudois, Bugnon 46, CH-1011, Lausanne, Switzerland.
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23
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Abstract
In this report, we describe a 50-year-old woman with a short bowel who had recurrent episodes of weakness, ataxia, slurred speech, confusion, and nausea. D-Lactic acidosis was diagnosed on the basis of a D-lactate level of 8.2 mmol/L (normal, 0 to 0.25) obtained during an episode of confusion. D-Lactic acidosis is a potentially fatal clinical condition seen in patients with a short small intestine and an intact colon. Excessive production of D-lactate by abnormal bowel flora overwhelms normal metabolism of D-lactate and leads to an accumulation of this enantiomer in the blood. This disorder provides insight into the role of intestinal flora in human metabolism and demonstrates the manner in which altered intestinal flora can produce disease in humans. Increased awareness of D-lactic acidosis is necessary for prompt and appropriate treatment. The pathophysiology and treatment of D-lactic acidosis are reviewed.
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Affiliation(s)
- A Vella
- Department of Internal Medicine, Mayo Clinic Rochester, Minnesota 55905, USA
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24
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Uribarri J, Oh MS, Carroll HJ. D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms. Medicine (Baltimore) 1998; 77:73-82. [PMID: 9556700 DOI: 10.1097/00005792-199803000-00001] [Citation(s) in RCA: 190] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023] Open
Abstract
This report describes a case of d-lactic acidosis observed by the authors and then reviews all case reports of d-lactic acidosis in the literature in order to define its clinical and biochemical features and pathogenetic mechanisms. The report also reviews the literature on metabolism of d-lactic acid in humans. The clinical presentation of d-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The diagnosis should be considered in a patient who presents with metabolic acidosis and high serum anion gap, normal lactate level, negative Acetest, short bowel syndrome or other forms of malabsorption, and characteristic neurologic findings. Development of the syndrome requires the following conditions 1) carbohydrate malabsorption with increased delivery of nutrients to the colon, 2) colonic bacterial flora of a type that produces d-lactic acid, 3) ingestion of large amounts of carbohydrate, 4) diminished colonic motility, allowing time for nutrients in the colon to undergo bacterial fermentation, and 5) impaired d-lactate metabolism. In contrast to the initial assumption that d-lactic acid is not metabolized by humans, analysis of published data shows a substantial rate of metabolism of d-lactate by normal humans. Estimates based on these data suggest that impaired metabolism of d-lactate is almost a prerequisite for the development of the syndrome.
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Affiliation(s)
- J Uribarri
- Department of Medicine, Mount Sinai Medical Center, New York, New York 10029, USA
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25
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Bongaerts GP, Tolboom JJ, Naber AH, Sperl WJ, Severijnen RS, Bakkeren JA, Willems JL. Role of bacteria in the pathogenesis of short bowel syndrome-associated D-lactic acidemia. Microb Pathog 1997; 22:285-93. [PMID: 9160298 DOI: 10.1006/mpat.1996.0122] [Citation(s) in RCA: 70] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
Previously, we have demonstrated that short bowel syndrome (SBS) patients suffer daily from D-lactic acidemia; in these patients rather high amounts of (bacterial) D-lactate emerge in blood and urine with a circadian rhythm. The aim of this study was to establish the microbial basis of D-lactic acidemia in SBS. Therefore, faecal flora of (young and adult) SBS-patients was analysed qualitatively and quantitatively, and compared to that of controls. The isolated bacterial species were screened for massive D- and/or L-lactate production after in vitro growth. After introduction of oral feeding in SBS-infants shortly after the resection, lactobacilli increased from < or = 1% up to 60 +/- 5% of the faecal flora within 2-3 weeks. In the faeces of patients with oral feeding the lactate producers Lactobacillus acidophilus and Lactobacillus fermentum were the major resident bacteria (each with 10(10)-10(12) cfu/g faeces). During active growth in vitro these lactobacilli produced massive amounts of D- and L-lactic acid from glucose. Use of oral antibiotics in two SBS-children did not reduce the total numbers of lactobacilli, but caused shifts within the intestinal populations of at least lactobacilli. It is concluded that the strongly reduced intestinal capacity for carbohydrate absorption and the oral consumption of easily fermentable carbohydrates form the physiological basis for D-lactic acidemia in SBS, and that the fermentative D-lactate production by intestinal bacteria, especially the abundant, resident lactobacilli, forms its microbial basis. In these patients the antimicrobial and therapeutic effects of antibiotics are unpredictable.
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Affiliation(s)
- G P Bongaerts
- Department of Medical Microbiology, University Hospital Nijmegen Sint Radboud, The Netherlands
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26
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Caldarini MI, Pons S, D'Agostino D, DePaula JA, Greco G, Negri G, Ascione A, Bustos D. Abnormal fecal flora in a patient with short bowel syndrome. An in vitro study on effect of pH on D-lactic acid production. Dig Dis Sci 1996; 41:1649-52. [PMID: 8769294 DOI: 10.1007/bf02087915] [Citation(s) in RCA: 34] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Abstract
D-Lactic acidosis associated with encephalopathy is a clinical condition that occurs in patients with short bowel syndrome. We studied the fecal flora and the composition of fecal water of a child who developed this unusual disorder. Bacteriological studies showed that the patient's stool contained a marked predominance of gram-positive anaerobes. Two strains were identified, Lactobacillus plantarum and Lactobacillus salivarius, as the main bacteria isolated. Fecal water showed pH 4.8 and total lactic acid (sum of L- and D-lactic acids) was the principal organic anion found in the feces. We also incubated the patient's stool in a continuous culture with a view to determining the effect of the pH on the production of volatile fatty acids (VFA) and L- and D-lactic acids. The culture was maintained at pH 5.0, 5.5, 6.0, and 6.5 for four consecutive periods of four days each. We then studied the culture for a further four days at pH 5.0 once again. This study showed that with the progressive rise of the pH from 5.0 to 6.5 L- and D-lactic acids decreased and VFA production increased. D-Lactic acid formation was inhibited at pH 6.5, but when the culture was returned to pH 5.0, it increased to a high level again. These results suggest that the pH plays an important role in the ecological changes in the colonic bacteria that result in D-lactic acid production.
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Affiliation(s)
- M I Caldarini
- Departamento de Bioquímica Clínica. Facultad de Farmacia y Bioquímica, Buenos Aires, Argentina
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27
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Halperin ML, Kamel KS. D-lactic acidosis: turning sugar into acids in the gastrointestinal tract. Kidney Int 1996; 49:1-8. [PMID: 8770942 DOI: 10.1038/ki.1996.1] [Citation(s) in RCA: 79] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Affiliation(s)
- M L Halperin
- Renal Division, St. Michael's Hospital, Toronto, Ontario, Canada
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28
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Abstract
D-Lactic acidosis is seen in patients with intestinal bypass or short bowels in whom colonic produced D-lactate accumulates. An intestinal bypassed patient with D-lactic acidosis had higher fecal D-lactate (122.4 mmol/liter) and L-lactate (90.1 mmol/liter) than described before in humans. D-Lactate fluctuated between 0.5 and 3.1 mmol/liter in plasma (normal < 0.1 mmol/liter) and between 1.1 and 52.8 mmol/liter in urine (normal < 0.7 mmol/liter) within a few hours, indicating that the human organism do metabolize and excrete D-lactate. The patient with D-lactic acidosis had a 10-fold increased DL-lactate production from glucose in fecal homogenates compared to 14 healthy controls and a patient with intestinal bypass, who did not have D-lactic acidosis. A 67% carbohydrate (starch)-enriched diet resulted in a minor elevation of fecal and plasma lactate, whereas 50 + 100 + 150 g of ingested lactose increased D-lactate in feces (84.0 mmol/liter) and plasma (2.3 mmol/liter) considerably in the patient with D-lactic acidosis. Intestinal prolongation (22 cm ileum) had a temporary effect on fecal and plasma D-lactate, but intestinal continuity was reestablished 26 months later because D-lactic acidosis recurred (plasma 8.6 mmol/liter, urine 101.3 mmol/liter). Large amounts of lactulose (160 g/day) to 12 normal individuals increased D-lactate to 13.6 +/- 3.5 mmol/liter in feces, but never increased D-lactate in plasma or urine. The in vitro fermentation of glucose in fecal homogenates increased DL-lactate, which disappeared after complete metabolization of the glucose. L-Lactate was converted to D-lactate and vice versa, and both were degraded to the short-chain fatty acids acetate, propionate, and butyrate. An infrequent, but elevated ability of the colonic flora to produce lactate may be a prerequisite for D-lactic acidosis to occur and may explain why the syndrome is so seldom seen even in patients with intestinal bypass or short bowels. The suggestion that D-lactate is not metabolized and hence accumulates is probably not valid.
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Affiliation(s)
- H Hove
- Department of Medicine A, Rigshospitalet, University of Copenhagen, Denmark
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29
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Bustos D, Pons S, Pernas JC, Gonzalez H, Caldarini MI, Ogawa K, De Paula JA. Fecal lactate and short bowel syndrome. Dig Dis Sci 1994; 39:2315-9. [PMID: 7956597 DOI: 10.1007/bf02087644] [Citation(s) in RCA: 28] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
In patients with short bowel syndrome (SBS), the carbohydrate overload to the colon may disturb the normal pattern of colonic fermentation with production of D-lactic acid and subsequent development of a metabolic D-lactic acidosis. We measured D-lactic acid in blood, urine, and feces, as well as the composition of fecal water and fecal reducing substances from 11 patients with SBS, comparing the results with those from normal subjects. The fecal water from patients with SBS was characterized by low pH, potassium, and volatile fatty acids, high osmotic gap, and high concentration of L- and D-lactic acid. Five of 11 had abnormal amounts of fecal reducing substances. Fecal D-lactic acid was increased in nine of 11 patients. However, none of these patients showed D-lactic acid in urine, and only one had a very low concentration in plasma. These results show that D-lactic acid was overproduced in the colon of most of the patients with SBS. However, other factors such as absorption or impaired D-lactic acid metabolism may be necessary for a plasmatic increase of D-lactic acid.
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Affiliation(s)
- D Bustos
- Instituto de Gastroenterologia Dr. Jorge Perez Companc, Buenos Aires, Argentina
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30
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Affiliation(s)
- A Spital
- Department of Medicine, Genesee Hospital, Rochester, NY 14607
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31
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Gurevitch J, Sela B, Jonas A, Golan H, Yahav Y, Passwell JH. D-lactic acidosis: a treatable encephalopathy in pediatric patients. Acta Paediatr 1993; 82:119-21. [PMID: 8453209 DOI: 10.1111/j.1651-2227.1993.tb12538.x] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/30/2023]
Abstract
A 20-month old infant, who had short bowel syndrome following extensive surgery for a mid gut volvulus, developed hyperchloremic acidosis, with a large anion gap after enteral feeding was instituted. The organic acidosis was at least partly due to an increased concentration of D-lactic acid. This patient, as did five other pediatric patients, presented with a typical encephalopathy syndrome. Early recognition of this syndrome and treatment with an intestinal antibiotic and discontinuation of enteral feeding enabled prompt correction of the hyperchloremic acidosis and a rapid clinical recovery.
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Affiliation(s)
- J Gurevitch
- Department of Pediatrics, Sheba Medical Center, Tel Hashomer, Israel
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32
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Mayne AJ, Handy DJ, Preece MA, George RH, Booth IW. Dietary management of D-lactic acidosis in short bowel syndrome. Arch Dis Child 1990; 65:229-31. [PMID: 2317072 PMCID: PMC1792240 DOI: 10.1136/adc.65.2.229] [Citation(s) in RCA: 43] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
Manipulation of carbohydrate intake was used to treat severe, recurrent D-lactic acidosis in a patient with short bowel syndrome. Dietary carbohydrate composition was determined after assessment of D-lactic acid production from various carbohydrate substrates by faecal flora in vitro. This approach may be preferable to repeated courses of antibiotics.
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Affiliation(s)
- A J Mayne
- Institute of Child Health, University of Birmingham
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33
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Abstract
Although intestinal bypass procedures are no longer performed, important lessons have been learned concerning clinical arthritides resulting from bacterial overgrowth and immune complex deposition. This information is of considerable value in patients who present with the clinical picture of intestinal bypass arthritis on the basis of other bowel abnormalities. Furthermore, the pathogenetic mechanisms involving bacterial overgrowth, release of bacterial antigens, and immune complex deposition may be pertinent to many types of inflammatory arthritis.
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34
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Abstract
An understanding of the pathophysiology of lactic acidosis is crucial in facilitating the optimal care of critically ill patients. The relevant biochemistry of lactic acidosis is reviewed, and the more controversial aspects relating to the genesis of the acidosis are highlighted. The current system of classification of lactic acidosis divides etiologies on the basis of the presence or absence of clinical signs of tissue hypoperfusion. Several types of lactic acidosis in which clinical evidence of tissue hypoperfusion is lacking demonstrate hemodynamic evidence of occult hypoperfusion. The diagnostic and therapeutic implications of this observation are discussed. Current diagnostic criteria for lactic acidosis include a pH less than 7.35 and blood lactate concentration greater than 5 to 6 mM/L. An important issue relates to the implications of lactate values that are greater than normal but below this diagnostic range. The use of the oxygen flux test may be valuable in the diagnosis of occult tissue hypoperfusion in patients with low-grade elevations in lactate levels. The current therapy for lactic acidosis involves addressing the primary cause and supportive management. The use of bicarbonate in the therapy for lactic acidosis is controversial due to potential adverse effects on cardiac function. The specifics of this controversy are outlined, and newer therapeutic alternatives are reviewed. The use of blood lactate concentration as a prognostic index may be more useful in patients with shock than without shock.
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Affiliation(s)
- B A Mizock
- Division of Critical Care Medicine, Chicago Medical School, Illinois
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35
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Karton MA, Rettmer R, Lipkin EW, Ott SM, Chait A. D-lactate and metabolic bone disease in patients receiving long-term parenteral nutrition. JPEN J Parenter Enteral Nutr 1989; 13:132-5. [PMID: 2496243 DOI: 10.1177/0148607189013002132] [Citation(s) in RCA: 20] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
D-lactate accumulates in some patients with malabsorption who continue oral intake of carbohydrate leading to a clinical syndrome of acidosis and encephalopathy. To assess the possibility that D-lactate contributes to acidosis and/or metabolic bone disease in patients with malabsorption receiving long-term parenteral nutrition yet maintaining oral intake, D-lactate levels in serum and urine were measured in 14 long-term parenteral nutrition subjects (average duration of support 74 months) and 27 control subjects. Significant elevations in both serum and urine D-lactate were found in only two parenteral nutrition subjects. Both subjects with elevated D-lactate levels had bone pain, x-ray evidence of fractures, and biopsy evidence of osteomalacia. These studies suggest that D-lactate accumulation may be a heretofore unappreciated metabolic abnormality associated with metabolic bone disease and acidosis in patients with malabsorption who are supported by long-term parenteral nutrition.
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Affiliation(s)
- M A Karton
- Department of Medicine, University of Washington, Seattle 98195
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36
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Karton M, Rettmer RL, Lipkin EW. Effect of parenteral nutrition and enteral feeding on D-lactic acidosis in a patient with short bowel. JPEN J Parenter Enteral Nutr 1987; 11:586-9. [PMID: 3123729 DOI: 10.1177/0148607187011006586] [Citation(s) in RCA: 25] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
D-Lactic acid can accumulate in blood in some patients with intestinal failure, leading to a clinical syndrome of severe acidosis and encephalopathy. The possible impact of parenteral nutrition on its clinical course has not been established. One patient with a severe short-bowel syndrome supported by long-term parenteral nutrition who suffered repeated episodes of ataxia and disorientation associated with elevated serum levels of D-lactate was studied. Results demonstrated no impact of glucose- vs lipid-based parenteral nutrition formulations on total acid production or serum D-lactic acid levels, increased serum D-lactate levels during administration of neomycin, but prompt resolution of both acidosis and clinical symptoms with discontinuation of oral intake. This study confirms the findings of other investigators that D-lactic acidosis may be a significant, heretofore unappreciated complication in patients with severe short-bowel syndrome, and that prompt resolution may be effected with abrupt discontinuation of oral intake. Furthermore, the present study suggests neither a detrimental nor a beneficial effect of parenteral nutrition on this syndrome.
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Affiliation(s)
- M Karton
- Department of Medicine, University of Washington, Seattle 98195
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37
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38
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Abstract
Although D-lactate is not a product of human intermediary metabolism, absorption of D-lactate produced by abnormal intestinal bacteria can cause systemic acidosis in patients who have undergone gastrointestinal surgery, particularly jejunoileal bypass. In order to learn more about the prevalence of D-lactate encephalopathy, its occurrence in other disorders, and how well D-lactate concentration correlates with clinical symptoms, serum D-lactate levels were determined in several specific populations. D-lactate was undetectable (less than 0.5 mmol/liter) in 72 healthy volunteers and 57 obese persons. In 33 patients who had jejunoileal bypass, 16 reported symptoms consistent with D-lactate encephalopathy since surgery. Nine of these 16 had D-lactate levels greater than 0.5 mmol/liter (range 0.7 to 11.5 mmol/liter). Levels of D-lactate fluctuated over time, and in two patients, markedly elevated levels correlated with an encephalopathy accompanied by hyperchloremic metabolic acidosis and elevated anion gap. In 470 randomly chosen hospitalized patients, D-lactate level greater than 0.5 mmol/liter was found in 13 (2.8 percent), and 60 percent of these had a history of gastrointestinal surgery or disease. It is concluded that elevated serum D-lactate levels are relatively common in patients with jejunoileal bypass, and although more rare, occur in other gastrointestinal disorders as well. The symptoms of D-lactate encephalopathy are quite sensitive, but not necessarily specific for this disorder.
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39
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Ramakrishnan T, Stokes P. Beneficial effects of fasting and low carbohydrate diet in D-lactic acidosis associated with short-bowel syndrome. JPEN J Parenter Enteral Nutr 1985; 9:361-3. [PMID: 4009922 DOI: 10.1177/0148607185009003361] [Citation(s) in RCA: 19] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
Abstract
A case of D-lactic acidosis in an 18-yr-old man with a short bowel is reported. The diagnosis, suspected on clinical grounds, was confirmed by serum and urine levels of D-lactate. Our studies revealed that an ad libitum diet was associated with elevated D-lactate levels and "nothing per oral" and 10% carbohydrate diet regimens caused a drop in D-lactate levels. We recommend npo and low carbohydrate diet as preferred alternatives to antibiotics in some patients with D-lactic acidosis. The literature is reviewed.
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