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Type D Lactic Acidosis

L-lactate And D-lactate - Clinical Significance Of The Difference

L-lactate And D-lactate - Clinical Significance Of The Difference

L-lactate and D-lactate - clinical significance of the difference L-lactate and D-lactate - clinical significance of the difference Modern blood gas analyzers often have incorporated sensor technology that allows measurement of plasma lactate concentration. In nature lactate exists in two isoforms: L-lactate and D-lactate. In all vertebrates, including humans, the L-lactate form is by far the most abundant and pathophysiologically significant, and it is this form that is specifically measured by the lactate sensors in blood gas analyzers and indeed all routine methods used to measure lactate in the clinical laboratory. The main focus of this brief review is physiological and pathological aspects that distinguish L-lactate and D-lactate. Consideration will be given to the very rare instance when measurement of blood D-lactate is clinically useful and just why the lactate sensor in blood gas analyzers is not useful in such rare circumstance. Lactate, the anion that results from dissociation of lactic acid, is an intracellular metabolite of glucose; specifically it is the end product of anaerobic glycolysis, the final step of which is conversion of pyruvate to lactate by the enzyme lactate dehydrogenase. In health around 1500 mmol of lactate is produced daily and so long as normal rate of metabolic disposal - principally by the liver and kidneys - is maintained, blood plasma concentration remains within the approximate reference range of 0.5-1.5 mmol/L [1]. Abnormal increase in plasma lactate (called hyperlactatemia) occurs if the rate of production exceeds the rate of disposal. If hyperlactatemia is sufficiently severe (plasma lactate >5.0 mmol/L), it is associated with acidosis (blood pH <7.35). The condition is then called lactic acidosis. There are many causes of hype Continue reading >>

D-lactic Acidosis: An Underrecognized Complication Of Short Bowel Syndrome

D-lactic Acidosis: An Underrecognized Complication Of Short Bowel Syndrome

D-Lactic Acidosis: An Underrecognized Complication of Short Bowel Syndrome Department of Medicine, Hartford Hospital, University of Connecticut School of Medicine, Hartford, CT 06102, USA Received 26 November 2014; Revised 28 March 2015; Accepted 8 April 2015 Copyright 2015 N. Gurukripa Kowlgi and Lovely Chhabra. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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. D-lactic acidosis (D-la) is a rare form of lactic acidosis seen mostly in patients with short bowel syndrome (SBS). Other conditions implicated are toxic ingestions of chemicals such as propylene glycol and rarely in patients with severe diabetic Continue reading >>

Lactic Acidosis: What You Need To Know

Lactic Acidosis: What You Need To Know

Lactic acidosis is a form of metabolic acidosis that begins in the kidneys. People with lactic acidosis have kidneys that are unable to remove excess acid from their body. If lactic acid builds up in the body more quickly than it can be removed, acidity levels in bodily fluids — such as blood — spike. This buildup of acid causes an imbalance in the body’s pH level, which should always be slightly alkaline instead of acidic. There are a few different types of acidosis. Lactic acid buildup occurs when there’s not enough oxygen in the muscles to break down glucose and glycogen. This is called anaerobic metabolism. There are two types of lactic acid: L-lactate and D-lactate. Most forms of lactic acidosis are caused by too much L-lactate. Lactic acidosis has many causes and can often be treated. But if left untreated, it may be life-threatening. The symptoms of lactic acidosis are typical of many health issues. If you experience any of these symptoms, you should contact your doctor immediately. Your doctor can help determine the root cause. Several symptoms of lactic acidosis represent a medical emergency: fruity-smelling breath (a possible indication of a serious complication of diabetes, called ketoacidosis) confusion jaundice (yellowing of the skin or the whites of the eyes) trouble breathing or shallow, rapid breathing If you know or suspect that you have lactic acidosis and have any of these symptoms, call 911 or go to an emergency room right away. Other lactic acidosis symptoms include: exhaustion or extreme fatigue muscle cramps or pain body weakness overall feelings of physical discomfort abdominal pain or discomfort diarrhea decrease in appetite headache rapid heart rate Lactic acidosis has a wide range of underlying causes, including carbon monoxide poisoni Continue reading >>

Newsletter: D-lactic Acidosis

Newsletter: D-lactic Acidosis

AddthisShare | Facebook Twitter Pinterest Gmail var addthis_exclude = 'print, email'; D-Lactic Acidosis Craig Petersen RD, CNSC D-lactic acidosis, also referred to as D-lactate encephalopathy, is a rare neurological syndrome that can occur in individuals with short bowel syndrome (SBS) or following jejuno-ileal bypass surgery. A home parenteral or enteral nutrition (HPEN) consumer may develop the neurological symptoms—which can be quite striking—several months to years after the initial diagnosis of a malabsorption disorder. Misdiagnosis of D-lactic acidosis is common, as the neurologic symptoms are sometimes attributed to other causes. With proper diagnosis, D-lactic acidosis can be treated promptly and the symptoms will usually resolve within several hours to a few days. Symptoms Neurological symptoms associated with this syndrome typically present after the ingestion of enteral formula or food high in carbohydrates (either simple or complex) and include altered mental status, slurred speech, confusion, disorientation, difficulty concentrating, memory deficits, excessive sleepiness, weakness, abnormal gait, problems with muscle coordination, and even coma. Individuals with D-lactic acidosis often appear to be inebriated, or drunk, though they may not have consumed alcohol and alcohol is not detected in the blood. Behavior during episodes of D-lactic acidosis can be aggressive, hostile, or abusive. Neurological symptoms are episodic and may last from hours to days. They are accompanied by metabolic acidosis and elevation of plasma D-lactic acid (also referred to as D-lactate) concentration. Cause In D-lactic acidosis, carbohydrate that is not properly absorbed is fermented by an abnormal bacterial flora in the colon. This fermentation produces excessive amounts of Continue reading >>

Lactic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

Lactic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Lactate is a normal byproduct of glucose and amino acid metabolism. There are 2 main types of lactic acidosis: d-Lactic acidosis (d-lactate encephalopathy) is an unusual form of lactic acidosis. Type A lactic acidosis, the most serious form, occurs when lactic acid is overproduced in ischemic tissueas a byproduct of anaerobic generation of ATP during oxygen deficit. Overproduction typically occurs during global tissue hypoperfusion in hypovolemic, cardiac, or septic shock and is worsened by decreased lactate metabolism in the poorly perfused liver. It may also occur with primary hypoxia due to lung disease and with various hemoglobinopathies. Type B lactic acidosis occurs in states of normal global tissue perfusion (and hence ATP production) and is less ominous. Causes include local tissue hypoxia (eg, as with vigorous muscle use during exertion, seizures, hypothermic shivering), certain systemic and congenital conditions, cancer, and ingestion of certain drugs or toxins (see Table: Causes of Metabolic Acidosis ). Drugs include the nucleoside reverse transcriptase inhibitors and the biguanides phenformin and, less so, metformin; although phenformin has been removed from the market in most of the world, it is still available from China (including as a component of some Chinese proprietary medicines). Metabolism may be decreased due to hepatic insufficiency or thiamin deficiency. d-Lactic acidosis is an unusual form of lactic acidosis in which d-lactic acid, the product of bacterial carbohydrate metabolism in the colon of patients with jejunoileal bypass or intestinal resection, is systemically absorbed. It persists in circulation because human lactat Continue reading >>

Lactic Acidosis

Lactic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Description Lactic acidosis is a form of metabolic acidosis due to the inadequate clearance of lactic acid from the blood. Lactate is a byproduct of anaerobic respiration and is normally cleared from the blood by the liver, kidney and skeletal muscle. Lactic acidosis occurs when the body's buffering systems are overloaded and tends to cause a pH of ≤7.25 with plasma lactate ≥5 mmol/L. It is usually caused by a state of tissue hypoperfusion and/or hypoxia. This causes pyruvic acid to be preferentially converted to lactate during anaerobic respiration. Hyperlactataemia is defined as plasma lactate >2 mmol/L. Classification Cohen and Woods devised the following system in 1976 and it is still widely used:[1] Type A: lactic acidosis occurs with clinical evidence of tissue hypoperfusion or hypoxia. Type B: lactic acidosis occurs without clinical evidence of tissue hypoperfusion or hypoxia. It is further subdivided into: Type B1: due to underlying disease. Type B2: due to effects of drugs or toxins. Type B3: due to inborn or acquired errors of metabolism. Epidemiology The prevalence is very difficult to estimate, as it occurs in critically ill patients, who are not often suitable subjects for research. It is certainly a common occurrence in patients in high-dependency areas of hospitals.[2] The incidence of symptomatic hyperlactataemia appears to be rising as a consequence of the use of antiretroviral therapy to treat HIV infection. It appears to increase in those taking stavudine (d4T) regimens.[3] Causes of lactic acid Continue reading >>

Lactic Acidosis – Fatigued, Confused, Grumpy? This Might Be Why.

Lactic Acidosis – Fatigued, Confused, Grumpy? This Might Be Why.

Many people with gut issues suffer from cogitative issues and body-wide symptoms, along with the gastrointestinal hell they’re going through. One of the reasons is often high levels of D-lactic acid. A few definitions acidosis – an abnormal decrease in pH levels. If systemic this is usually only a tenth of a pH level, or so, high. lactic acid (lactate) – an organic compound formed from fermentation, as well as by humans during normal metabolism and exercise. There are two main types discussed here D-lactic acid and L-lactic acid (two mirror-image isomers), DL-lactic acid is a mixture of the two in equal amounts. See Wikipedia for more information on D&L chirality prefixes. L-lactic acid – the type produced in the human body and the primary type found in the human diet. This form is easy for the body and rarely accumulates at a rate higher than the bodies ability to remove it. Short term acidosis is possible from l-lactic acid with extended strenuous exercise, but is usually cleared within a few hours. Acidosis can also occur with organ failure and other illness. D-lactic acid – this type is mostly foreign to the body and difficult to remove. It can easily build up, when it does this is called lactic acidosis. This article will refer it to as d-lactic acidosis to distinguish Lactate – In this context – the conjugate base of lactic acid, the two terms are used interchangeably. Lactic acid actually isn’t the real culprit that causes the fatigue, brain fog, etc. (see below for symptoms). When lactic acid is formed in the body (by us during exercise, or by bacteria) hydrogen ions are formed, hydrogen ions lower the pH (make it acidic), hydrogen is the true culprit. Excess hydrogen causes problems of its own, but the increased systemic acidity is what causes m Continue reading >>

Lactic Acidosis - Cancer Therapy Advisor

Lactic Acidosis - Cancer Therapy Advisor

Hyperlactatemia, anion gap metabolic acidosis, strong ion gap metabolic acidosis Tissue hypoperfusion, ischemia, anaerobic metabolism, shock, acid-base disorders Lactic acidosis associated with critical illness is commonly a byproduct of a much larger problem. In 1976 Cohen and Woods classified lactic acidosis based on etiology. Type A is due to clinical evidence of tissue hypoperfusion. Type B occurs in the absence of clinical evidence of tissue hypoperfusion. Type B is further divided into subgroups B1 - underlying disease/physiologic state; B2 - medication or toxin; and B3 - inborn errors of metabolism. In critically ill patients, lactic acidosis is typically associated with increased lactate production (hypoperfusion, mitochondrial dysfunction), and/or decreased metabolism/clearance. Approximately 1400 mmol of lactic acid is produced daily. The kidneys metabolize up to 30% with no significant elimination. The liver is very efficient in lactate metabolism and elimination and serum lactate levels should remain in the normal range until about 75% of hepatic function is lost. The clinical features of lactic acidosis are similar to other forms of metabolic acidoses. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Other clinical features are related to the underlying cause of lactic acidosis, such as signs of hypoperfusion. Hyperventilaton (rapid shallow or Kussmaul respirations). Seizure (generalized seizures can cause a transient lactic acidosis). Signs of hypovolemia (dry mucous membranes, decreased capillary refill, skin tenting, oliguria). Abdominal pain (especially with mesenteric ischemia). There may only be subtle clinical findings, therefore one needs to have a high suspicion in clinically relevent situations (e.g. i Continue reading >>

D-lactic Acidosis. A Review Of Clinical Presentation, Biochemical Features, And Pathophysiologic Mechanisms.

D-lactic Acidosis. A Review Of Clinical Presentation, Biochemical Features, And Pathophysiologic Mechanisms.

D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms. Department of Medicine, Mount Sinai Medical Center, New York, New York 10029, USA. Medicine (Baltimore). 1998 Mar;77(2):73-82. 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. Continue reading >>

Lactic Acidosis Clinical Presentation: History, Physical Examination

Lactic Acidosis Clinical Presentation: History, Physical Examination

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... The onset of acidosis may be rapid (ie, within minutes to hours) or progressive (ie, over a period of several days). Lactic acidosis frequently occurs during strenuous exercise in healthy people, bearing no consequence. However, development of lactic acidosis in disease states is ominous, often indicating a critical illness of recent onset. Therefore, a careful history should be obtained to evaluate the underlying pathophysiologic cause of shock that contributed to lactic acidosis. Furthermore, a detailed history of ingestion of various prescription drugs or toxins from the patient or a collateral history from the patient's family should be obtained. The clinical signs and symptoms associated with lactic acidosis are highly dependent on the underlying etiology. No distinctive features are specific for hyperlactatemia. Lactate acidosis is present in patients who are critically ill from hypovolemic, septic, or cardiogenic shock. Lactate acidosis always should be suspected in the presence of elevated anion gap metabolic acidosis. Lactic acidosis is a serious complication of antiretroviral therapy. A history of antiretroviral treatment should be obtained. Children who have a relatively mild form of congenital lactic acidosis may develop firmament metabolic acidosis during an acute illness such as respiratory infection. These patients have a deficiency in the activity of pyruvate dehydrogenase, and the stress-induced increases in the glycolytic rate may result in severe metabolic acidosis. D-lactic acidosis, a unique form of lactic acidosis, can occur in patients with jejunoileal bypass or small bowel resection causing short bowel syndrome. In these settings, the glucose and car Continue reading >>

Both L- And D-lactate Contribute To Metabolic Acidosis In Diarrheic Calves

Both L- And D-lactate Contribute To Metabolic Acidosis In Diarrheic Calves

Both L- and D-Lactate Contribute to Metabolic Acidosis in Diarrheic Calves College of Pharmacy and Nutrition, University of Saskatchewan, SK, S7N 5C9, Canada Search for other works by this author on: Western College of Veterinary Medicine, University of Saskatchewan, SK, S7N 5C9, Canada Search for other works by this author on: Western College of Veterinary Medicine, University of Saskatchewan, SK, S7N 5C9, Canada Search for other works by this author on: College of Pharmacy and Nutrition, University of Saskatchewan, SK, S7N 5C9, Canada To whom correspondence should be addressed. E-mail: [email protected] Search for other works by this author on: The Journal of Nutrition, Volume 131, Issue 8, 1 August 2001, Pages 21282131, Olutosin O. Omole, Germain Nappert, Jonathan M. Naylor, Gordon A. Zello; Both L- and D-Lactate Contribute to Metabolic Acidosis in Diarrheic Calves, The Journal of Nutrition, Volume 131, Issue 8, 1 August 2001, Pages 21282131, Diarrhea in neonates is often complicated by metabolic acidosis. We used blood gas analysis and HPLC to determine whether bacterial fermentation might contribute to acidosis in diarrheic calves. Diarrheic calves (n = 21) had significantly lower pH, PCO2, HCO3 and a higher anion gap than healthy calves (n = 21). Serum concentrations (mean SD, mmol/L) of DL-,L- and D-lactate were also significantly higher in diarrheic (8.9 5.1, 4.1 3.4 and 5.2 5.7) than in healthy calves (1.7 1.2, 2.0 1.1 and too low to quantify). D- and L-lactate accounted for 64% anion gap increase in diarrheic calves. Fecal D- and L-lactate concentrations were also significantly higher in diarrheic calves (9.4 3.0 and 11.9 2.7 mmol/L) than healthy calves (1.1 0.1 and 1.6 0.1 mmol/L). The elevated concentrations of serum and fecal D-lactate suggest gut bacter Continue reading >>

D-lactic Acidosis: A Personal Experience

D-lactic Acidosis: A Personal Experience

We began the roller coaster ride called short bowel syndrome (SBS) in 2007. When my daughter Ally was four years old, she lost all but twenty-five centimeters of her small intestine due to a mid-gut volvulus. Her colon remained intact. Early on I joined various social media sites, as well as the Oley Foundation. Thankfully, I read of others experiences where their child acted drunk due to D-lactic acidosis, so when Ally first had symptoms I was aware of this disorder. We didnt begin having significant D-lactic issues until 2013. Ally had had a colostomy reversed and we later found out that she had nerve damage resulting in poor colonic motility. It was the perfect storm for D-lactic acidosis: very short small intestine, high amounts of enteral carbs to keep her off parenteral nutrition (PN), and poor colonic motility. Her symptoms have ranged from mildly blurred vision to a comatose-like sleep state. Specifically, over the years Ally has experienced slurred speech, incoherent speech, inability to walk, out-of-character anger or silliness, deep sleep that goes on for hours to days, academic decline, and hall All during one of her sleepy episodes of D-Lactic ucinations. She was exceptionally good at coloring, but in a D-lactic episode she would scribble and would think it was beautiful. At the worst of her D-lactic episodes, she could not remember the six to eight hours a day that she had spent in an episode. At best she would be a little cranky and maybe take a long nap. We say shes either a happy drunk, an angry drunk, or a sleepy drunk. We went about six months with Ally having D-lactic episodes about four to five times per week and without successful treatment. The usual antibiotics did not help. While the effects would go away and there were no lingering neurologica Continue reading >>

Human Metabolome Database: Showing Metabocard For D-lactic Acid (hmdb0001311)

Human Metabolome Database: Showing Metabocard For D-lactic Acid (hmdb0001311)

You are using an unsupported browser. Please upgrade your browser to a newer version to get the best experience on Human Metabolome Database. Showing metabocard for D-Lactic acid (HMDB0001311) Lactic acid is an organic acid. It is a chiral molecule, consisting of two optical isomers, L-lactic acid and D-lactic acid, with the L-isomer being the most common in living organisms. Lactic acid plays a role in several biochemical processes and is produced in the muscles during intense activity. D-Lactic acid is the end product of the enzyme glyoxalase II (or hydroxyacyl-glutathione hydrolase) (EC 3.1.2.6), which converts the intermediate substrate S-lactoyl-glutathione to reduced glutathione and D-lactate (OMIM: 138790 ). Structure for HMDB0001311 (D-Lactic acid) This compound belongs to the class of organic compounds known as alpha hydroxy acids and derivatives. These are organic compounds containing a carboxylic acid substituted with a hydroxyl group on the adjacent carbon. Pyruvate Decarboxylase E1 Component Deficiency (PDHE1 Deficiency) McLellan AC, Phillips SA, Thornalley PJ: Fluorimetric assay of D-lactate. Anal Biochem. 1992 Oct;206(1):12-6. [ PubMed:1456422 ] Fukushima T, Iizuka H, Yokota A, Suzuki T, Ohno C, Kono Y, Nishikiori M, Seki A, Ichiba H, Watanabe Y, Hongo S, Utsunomiya M, Nakatani M, Sadamoto K, Yoshio T: Quantitative analyses of schizophrenia-associated metabolites in serum: serum D-lactate levels are negatively correlated with gamma-glutamylcysteine in medicated schizophrenia patients. PLoS One. 2014 Jul 8;9(7):e101652. doi: 10.1371/journal.pone.0101652. eCollection 2014. [ PubMed:25004141 ] Duran M, Van Biervliet JP, Kamerling JP, Wadman SK: D-lactic aciduria, an inborn error of metabolism? Clin Chim Acta. 1977 Feb 1;74(3):297-300. [ PubMed:832430 ] D-La Continue reading >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Dlac - Clinical: D-lactate, Plasma

Dlac - Clinical: D-lactate, Plasma

An adjunct to urine D-lactate (preferred), in the diagnosis of D-lactate acidosis DLAU / D-Lactate, Urine is the preferred specimen for D-lactate determinations. Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test D-lactate is produced by bacteria residing in the colon when carbohydrates are not completely absorbed in the small intestine. When large amounts of D-lactate are present, individuals can experience metabolic acidosis, altered mental status (from drowsiness to coma), and a variety of other neurologic symptoms, particularly dysarthria and ataxia. D-lactic acidosis is typically observed in patients with a malabsorptive disorder, such as short-bowel syndrome, or, following a jejunoileal bypass. In addition, healthy children presenting with gastroenteritis may also develop the critical presentation of D-lactic acidosis. Routine lactic acid determinations in blood will not reveal abnormalities because most lactic acid assays measure only L-lactate. Accordingly, D-lactate analysis must be specifically requested (eg, DLAC / D-Lactate, Plasma). However, as D-lactate is readily excreted in urine, DLAU / D-Lactate, Urine is the preferred specimen for D-lactate determinations. Continue reading >>

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