Lactic Acidosis In Diabetes
Evgenideion Hospital and Research Laboratory Christeas Hall Athens, Greece Evgenideion Hospital and Research Laboratory Christeas Hall Athens, Greece Evgenideion Hospital and Research Laboratory Christeas Hall Athens, Greece Evgenideion Hospital and Research Laboratory Christeas Hall Athens, Greece Please review our Terms and Conditions of Use and check box below to share full-text version of article. I have read and accept the Wiley Online Library Terms and Conditions of Use. Use the link below to share a full-text version of this article with your friends and colleagues. Learn more. Lactic acidosis occurs when there is an imbalance between production and clearance of lactate. Lactic acidosis due to hypoxia is classified as Type A. Hyperlactemia without tissue hypoxia is referred to as Type B lactic acidosis. Metforminassociated lactic acidosis is uncommon but carries a high mortality rate. It is not usually due to the drug but to predisposing conditions such as severe liver, renal, or cardiac disease. The clinical presentation is that of metabolic acidosis. The diagnosis is based in the presence of low arterial pH together with increased blood lactate levels. Metforminassociated lactic acidosis can be prevented through awareness of the risk factors. Metformin should be immediately discontinued in every patient presenting with lactic acidosis. Effective management of the predisposing disease and hemodialysis techniques together with efforts to maintain cardiac output, blood pressure, oxygenation, and renal perfusion are the mainstay of therapy. Continue reading >>
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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 >>
Fasting Plasma Lactate Concentrations In Ambulatory Elderly Patients With Type 2 Diabetes Receiving Metformin Therapy: A Retrospective Cross-sectional Study - Sciencedirect
Volume 73, Issue 12 , December 2010, Pages 617-622 Fasting Plasma Lactate Concentrations in Ambulatory Elderly Patients With Type 2 Diabetes Receiving Metformin Therapy: A Retrospective Cross-sectional Study Author links open overlay panel Yi-ChunLinab Liang-YuLinac Huei-FangWangd Hong-DaLinab Metformin is a worldwide accepted biguanide antidiabetic agent, and its effectiveness and benefit have already been well established. Among the side effects of metformin, lactate acidosis is the most problematic because of a high mortality rate, which impedes its use in clinical practice, especially in elderly patients with type 2 diabetes. Aging is associated with a decreased renal function and increasing comorbidities, but few data are available regarding plasma lactate levels in this unique population. In this study, we assessed fasting plasma lactate levels in ambulatory, elderly Taiwanese patients with type 2 diabetes, who were taking the drug, metformin, to identify independent risk factors for hyperlactemia in this group. Sixty-six ambulatory type 2 diabetic patients, > 80 years of age (mean, 83.6 years; range, 80-90 years), receiving metformin therapy, were enrolled, from January 2005 to September 2009, in the Diabetes Case Management Program. A further 79 younger patients (also type 2 diabetics on metformin) served as controls (mean age, 59.9 years; range, 37-79 years). Fasting serum electrolytes, creatinine, bicarbonate, glycated hemoglobin, plasma glucose and lactate levels were determined. Lactate levels did not differ between the elderly and control groups (13.2 +/ 5.2 mg/dL and 13.5 +/ 4.8 mg/dL, respectively). None of the patients fulfilled the lactic acidosis criteria. Patients in the elderly group had a significantly lower daily metformin dose, higher creatinine Continue reading >>
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Lactic Acidosis
Background In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [1, 2] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [3] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentation and Differentials.) The causes of lactic acidosis are listed in the chart below. Go to Acute Lactic Ac Continue reading >>
Hyperlactatemia And Antiretroviral Therapy: The Swiss Hiv Cohort Study
Hyperlactatemia and Antiretroviral Therapy: The Swiss HIV Cohort Study University Hospitals of Lausanne, Swiss HIV Cohort Study Data Center University Hospitals of Lausanne, Geneva, Hospitals of St. Gallen University Hospitals of Lausanne, St. Gallen University Hospitals of Lausanne, Swiss HIV Cohort Study Data Center Medical Research Council Health Services Research Collaboration, Department of Social Medicine, University of Bristol University Hospitals of Lausanne, Swiss HIV Cohort Study Data Center University Hospitals of Lausanne, Swiss HIV Cohort Study Data Center Reprints or correspondence: Dr. A. Telenti, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland ( [email protected] ). Search for other works by this author on: Clinical Infectious Diseases, Volume 33, Issue 11, 1 December 2001, Pages 19311937, K. Boubaker, M. Flepp, P. Sudre, H. Furrer, A. Haensel, B. Hirschel, K. Boggian, J.-P. Chave, E. Bernasconi, M. Egger, M. Opravil, M. Rickenbach, P. Francioli, A. Telenti, Swiss HIV Cohort Study; Hyperlactatemia and Antiretroviral Therapy: The Swiss HIV Cohort Study, Clinical Infectious Diseases, Volume 33, Issue 11, 1 December 2001, Pages 19311937, The prevalence, clinical presentation, and risk factors for hyperlactatemia among patients receiving antiretroviral therapy was determined during a 1-month period for patients in the Swiss HIV Cohort Study. Overall, 73 (8.3%) of 880 patients presented an increase in serum lactate of >1.1 times the upper normal limit (UNL). For 9 patients (1%), lactate elevation was moderate or severe (>2.2 times the UNL). Patients who presented with hyperlactatemia were more likely to be receiving stavudine with or without didanosine (odds ratio, 2.7; 95% confidence interval, 1.54.8), as compared with patie Continue reading >>
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Haart-induced Lactic Acidosis
Nucleoside Reverse Transcriptase Inhibitors are associated with hyperlactemia and lactic acidosis NRTI also cause pancreatitis, myopathy, peripheral neuropathy, anemia, neutropenia, hepatic toxicity [1] Specifically didanosine (ddI) and stavudine (d4T) These medicines are no longer first-line agents in the US and Europe, but are in low-middle income countries Adverse effects of NRTI is by way of mitochondrial toxicity. NRTI inhibit human DNA polymerase gamma, a key enzyme for mitochondrial replication. Impaired electron transport chain, leading to leakage of electrons and increased production of reactive oxygen species. [2] Variable onset of mitochondrial toxicity, and not at any set point in NRTI use. [2] Use of stavudine and didanosine containing regimens Additional studies cite a CD4 count less than 500 as a risk factor. [4] Age, as the risk of hyperlactemia increases 50% with every 10 years of aging Associated with dyslipidemia and insulin resistance [5] Since the symptoms are non-specific, most patients present with advanced symptoms and the more serious lactic acidosis. [3] Creatinine clearance, as renal failure is a significant risk factor for the development of lactic acidosis from hyperlactemia. . [7] Liver Function Test, as hepatic dysfunction precludes oxidation of lactate, thus resulting in elevated lactate levels in the blood Anecdotal evidence to support Riboflavin (50mg/day), and/or thiamine (100mg BID) [8] Stop all anti-retrovirals until lactate normalization [2] Consider antioixidant supplementation to reduce oxidative stress and hyperlactemia [9] Lee WM, Dienstag JL. Lee W.M., Dienstag J.L. Lee, William M., and Jules L. Dienstag.Toxic and Drug-Induced Hepatitis. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. Kasper D, Fauci A, Hauser Continue reading >>
(pdf) Reported Survival With Severe Mixed Acidosis And Hyperlactemia After Toluene Poisoning
Lactic acidosis is a recognized complication of the inhalant abuse such as toluene, especially in patients with renal insufciency. We report a case of severe metabolic acidosis and hyperlactemia due to toluene snifng. The favorable outcome, despite extremely poor clinical symptoms, signs, laboratory and radiological ndings, was unexpected. Specic aspects of the clinical course are addressed. Toluene snifng should be considered in evaluating sever metabolic acidosis. Favorable outcome could be achieved with early diagnosis and proper interventions. Key words: Lactic acidosis, toluene, hyperlactemia Reported survival with severe mixed acidosis and unstable with sinus tachycardia (heart rate of 120 beats per minute) and hypotension (blood pressure was 90/45 mmHg) on inotropic medications norepinephrine started at 10 microgram/min. He required an FIO2 of 80% to maintain his oxygen saturation above 90%. He had bilateral coarse crepitations on chest auscultation. Abdominal examinations were unremarkable. Initial arterial blood gases interpretations showed severe mixed acidosis with pH 6.5 (7.35-7.45). His arterial lactate was 16 mmol/L, his CBC was normal, he had a serum creatinine of 211 mmol/L, urea was 50 mmol/L and cardiac enzymes were normal. Toxicology screen was negative for alcohol, salicylates and acetaminophen. Chest radiographs were obtained which showed diffuse bilateral inltrates [Figure 1]. Compute tomography (CT) of the abdomen and chest showed a small stone in the left kidney and bilateral consolidative changes of both lungs. ECG was normal except for sinus tachycardia. Left ventricular (LV) function was good on echocardiography and chamber sizes were of normal dimensions. Patient received supportive treatment with invasive hemodynamic monitoring, intravenous Continue reading >>
Metformin-induced Lactic Acidosis (mila): A Case Report And Review Of Current Diagnostic Paradigm
Get rights and content A new diagnostic paradigm has been proposed to better categorize causes of Metformin-Associated Lactic Acidosis (MALA). The diagnostic criteria defines a link between Metformin and lactic acidosis if lactate is >5mmol/L, Ph<7.35 and Metformin assay >5mg/L. Metformin assays are not readily available in emergency departments including nationwide Veterans Affairs Hospitals; thereby making this proposed classification tool difficult to use in todays clinical practice. We describe a case report of a 45-year-old male, who took twice the amount of Metformin prescribed and presented with Metformin-induced lactic acidosis. According to the new criterion, our case would be classified as Lactic Acidosis in Metformin-Treated Patients (LAMT). However, the term LAMT does not distinguish between a septic patient taking Metformin with lactic acidosis, and a patient who ingested toxic amounts of Metformin and has lactic acidosis (in absence of Metformin assay). Our case highlights the importance of medication reconciliation done on arrival to emergency department. Timing and dosing of Metformin in patients who present to the emergency department with lactic acidosis may cinch the diagnosis of Metformin-Induced Lactic Acidosis (MILA) in the absence of a Metformin assay but in the right clinical context. Choose an option to locate/access this article: Check if you have access through your login credentials or your institution. Continue reading >>
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Recoverable, Record-high Lactic Acidosis In A Patient With Glycogen Storage Disease Type 1: A Mixed Type A And Type B Lactate Disorder
Recoverable, Record-High Lactic Acidosis in a Patient with Glycogen Storage Disease Type 1: A Mixed Type A and Type B Lactate Disorder 1Department of Medicine, Hadassah Hebrew University Hospital, Mt. Scopus, Jerusalem, Israel 2Department of Pediatrics, Hadassah Hebrew University Hospital, Mt. Scopus, Jerusalem, Israel 3Department of Critical Care Unit, Hadassah Hebrew University Hospital, Mt. Scopus, Jerusalem, Israel Received 25 September 2016; Accepted 2 November 2016 Copyright 2016 Yonatan Oster et al. 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. A 17-year-old patient with GSD type 1a (von Gierke disease) was hospitalized with an extremely elevated serum lactate following an intercurrent infection and interruption of his frequent intake of carbohydrates. The patient developed shock, oliguric renal failure, and cardiorespiratory failure requiring mechanical ventilation and inotropes. At the peak of metabolic decompensation and clinical instability, serum lactate reached a level of 47.6 mmol/L which was accompanied by a severe anion gap metabolic acidosis with a pH of 6.8 and bicarbonate of 4 meq/L. The patient was stabilized with massive infusions of sodium bicarbonate (45 meq/h) and glucose and recovered without the need for dialysis. This patient illustrates pathophysiologic mechanisms involved in the development of extreme mixed type A and type B lactic acidemia, reflecting altered metabolic pathways in GSD type 1, combined with tissue hypoperfusion. The rationale for the specific interventions in this case is outlined. Lactic acidosis is an anion gap metabolic acidosis that results from lactate Continue reading >>
Causes Of Lactic Acidosis
INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>
Lactic Acidosis
hyperlactaemia: a level from 2 to 5 mmol/L normal production is 20 mmols/kg/day, enters the circulation and undergoes hepatic and renal metabolism (Cori cycle) all tissues can produce lactate under anaerobic conditions lactic acid has a pK value of about 4 so it is fully dissociated into lactate and H+ at body pH (i.e. it is a strong ion) during heavy exercise, the skeletal muscles contribute most of the much increased circulating lactate during pregnancy, the placenta is an important producer of lactate (can pass to fetus as well) major source in sepsis and ARDS is the lung lactate is metabolised predominantly in the liver (60%) and kidney (30%) the heart can also use lactate for ATP production 50% is converted into glucose (gluconeogenesis) and 50% into CO2 and water (citric acid cycle) this results in no net acid accumulation but requires aerobic metabolism the small amount of lactate that is renally filtered (180mmol/day) is fully reabsorbed (ii) impaired hepatic metabolism of lactate (large capacity to clear) clinically there is often a combination of the above to produce a persistent lactic acidosis anaerobic muscular activity (sprinting, generalised convulsions) tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia) reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning) Type B No Evidence of Inadequate Tissue Oxygen Delivery once documented the cause must be found and treated appropriately D lactate is isomer of lactate produced by intestinal bacterial and not by humans it is not detected on standard lactate assays a bed side test may be able to be developed to help with diagnosis of mesenteric ischaemia venous samples are equivalent to arterial in clinical practice do not need to take off tourniq Continue reading >>
Lactate And Lactic Acidosis
The integrity and function of all cells depend on an adequate supply of oxygen. Severe acute illness is frequently associated with inadequate tissue perfusion and/or reduced amount of oxygen in blood (hypoxemia) leading to tissue hypoxia. If not reversed, tissue hypoxia can rapidly progress to multiorgan failure and death. For this reason a major imperative of critical care is to monitor tissue oxygenation so that timely intervention directed at restoring an adequate supply of oxygen can be implemented. Measurement of blood lactate concentration has traditionally been used to monitor tissue oxygenation, a utility based on the wisdom gleaned over 50 years ago that cells deprived of adequate oxygen produce excessive quantities of lactate. The real-time monitoring of blood lactate concentration necessary in a critical care setting was only made possible by the development of electrode-based lactate biosensors around a decade ago. These biosensors are now incorporated into modern blood gas analyzers and other point-of-care analytical instruments, allowing lactate measurement by non-laboratory staff on a drop (100 L) of blood within a minute or two. Whilst blood lactate concentration is invariably raised in those with significant tissue hypoxia, it can also be raised in a number of conditions not associated with tissue hypoxia. Very often patients with raised blood lactate concentration (hyperlactatemia) also have a reduced blood pH (acidosis). The combination of hyperlactatemia and acidosis is called lactic acidosis. This is the most common cause of metabolic acidosis. The focus of this article is the causes and clinical significance of hyperlactatemia and lactic acidosis. The article begins with a brief overview of normal lactate metabolism. Normal lactate production and Continue reading >>
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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 >>
Risk Factors Of Post-operative Severe Hyperlactatemia And Lactic Acidosis Following Laparoscopic Resection For Pheochromocytoma
Risk factors of post-operative severe hyperlactatemia and lactic acidosis following laparoscopic resection for pheochromocytoma Scientific Reportsvolume7, Articlenumber:403 (2017) Severe hyperlactatemia (SH)/lactic acidosis (LA) after laparoscopic resection of pheochromocytoma is an infrequently reported complication. The study aims to investigate the incidence of this complication and to determine the clinical risk factors. Patients who underwent laparoscopic resection for pheochromocytoma between 2011 and 2014 at Peking Union Medical College Hospital were enrolled. LA was defined as pH < 7.35, bicarbonate <20 mmol/L, and serum lactate 5 mmol/L; SH as lactate 5 mmol/L; and moderate hyperlactatemia (MH) as lactate 2.55.0 mmol/L without evidence of acidosis (pH > 7.35 and/or bicarbonate >20 mmol/L). Data concerning patient demographics, clinical history, and laboratory results were collected and statistical analyses were performed. Out of 145 patients, 59 (40.7%) developed post-operative hyperlactatemia. The incidences of MH and SH/LA were 25.5% and 15.2%, respectively. Multivariate analysis demonstrated that body mass index (BMI) (odds ratio [OR], 1.204; 95% confidence interval [CI], 1.0161.426), 24-hour urine epinephrine concentration (OR, 1.012; 95% CI, 1.0021.022), and tumor size (OR, 1.571; 95% CI, 1.1022.240) were independent predictors of post-operative SH/LA. The data show that post-operative SH/LA is not a rare complication after pheochromocytoma resection and may be closely associated with higher BMI, larger tumor size, and higher levels of urine epinephrine. Pheochromocytoma is a rare, catecholamine-producing neuroendocrine tumor originating from chromaffin cells of the adrenal medulla 1 . Cardinal manifestations of pheochromocytoma include episodic hypertens Continue reading >>
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 >>
