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Which Medications Are Associated With Hyperlactemia And Lactic Acidosis?

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 >>

Lactate And Lactic Acidosis

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 >>

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

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 >>

The Riddle Of Hyperlactatemia

The Riddle Of Hyperlactatemia

A recent observational study in a large cohort of critically ill patients confirms the association between hyperlactatemia and mortality. The mechanisms regulating the rates of lactate production and clearance in critical illness remain poorly understood. During exercise, hyperlactatemia clearly results from an imbalance between oxygen delivery and energy requirements. In critically ill patients, the genesis of hyperlactatemia is significantly more complex. Possible mechanisms include regional hypoperfusion, an inflammation-induced upregulation of the glycolitic flux, alterations in lactate-clearing mechanisms, and increases in the work of breathing. Understanding how these complex processes interact to produce elevations in lactate continues to be an important area of research. LactateCritical IllnessBlood LactateLactate ProductionBlood Lactate Level The lack of a reliable indicator to assess cellular hypoxia and monitor the effectiveness of therapeutic interventions remains a major challenge in critical care medicine. In a study published in the previous issue of Critical Care, Khosravani and colleagues [ 1 ] further illustrated the independent association between mortality and blood lactate levels. They noted an independent association between mortality and blood lactate levels of above 2.0 mmol/L. Their study is important for several reasons. First, the authors cast a wide net by including all adult intensive care unit admissions (n = 13,932) occurring during a 3-year period in a well-defined patient population of 1.2 million. Over 12,000 patients had at least one lactate determination during their first 24 hours. Of these, 36% had a lactate concentration of greater than 2.0 mmol/L (the authors' definition of hyperlactatemia) and another 4% developed hyperlactatemi Continue reading >>

Fatal Type-b Lactic Acidosis In Association With Hiv Associated Lymphoma - A Case Report With Review Of Literature

Fatal Type-b Lactic Acidosis In Association With Hiv Associated Lymphoma - A Case Report With Review Of Literature

Fatal Type-B Lactic Acidosis in Association with HIV Associated Lymphoma - A Case Report with Review of Literature Asif Salim, Sara Chinthu, Shobhana Nayak Rao * and Pradeep Shenoy M Department of Nephrology, K.S. Hegde Medical Academy, Medical Sciences Complex, Derlakatte, Mangalore 575013, Karnataka, India Associate Professor and Head, Department of Nephrology, K.S. Hegde Medical Academy, Derlakatte, Mangalore 575013, Karnataka, India Received date: June 27, 2017; Accepted date: June 27, 2017; Published date: July 24, 2017 Citation: Salim A, Chinthu S, Rao SN, Shenoy PM (2017) Fatal Type-B Lactic Acidosis in Association with HIV Associated Lymphoma- A Case Report with Review of Literature. Jour Ren Med Vol.1. No.2: 8. Visit for more related articles at Journal of Renal Medicine Hyperlactemia is defined as whole blood lactate levels > 2 mmol/L. Type-B lactic acidosis refers to conditions wherein overproduction of lactate is not related to reduction in tissue oxygen. The occurrence of severe lactic acidosis in malignancies is a rare and often pre-terminal complication. We present two HIV positive patients with type-B lactic acidosis as a pre-terminal event after being diagnosed with non Hodgkins lymphoma. The first patient, a 45-year-old male, HIV positive since 2012 on therapy admitted with h/o of pedal edema, generalized weakness and decreased appetite 1 week duration. Abdominal ultrasound scan revealed bilateral moderate hydro-ureteronephrosis with large left pleural effusion, cytology revealed malignant serous lymphoma confirmed by supraclavicular lymph node biopsy. Before initiation of chemotherapy, his general condition rapidly worsened with onset of lactic acidosis (10 mmol/L) and he expired. The second patient, a 59-year-old male presented with acute hematemesi Continue reading >>

Fasting Plasma Lactate Concentrations In Ambulatory Elderly Patients With Type 2 Diabetes Receiving Metformin Therapy: A Retrospective Cross-sectional Study - Sciencedirect

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 >>

Lactic Acidosis

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 >>

Lactic Acidosis: Background, Etiology, Epidemiology

Lactic Acidosis: Background, Etiology, Epidemiology

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... 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 Presentationand Differe Continue reading >>

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

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 >>

Case 25 Hyperlactemia

Case 25 Hyperlactemia

In this case, an 18-year-old male presents to the emergency department with status asthmaticus. He subsequently developed hyperlactemia during the first 8h of his hospitalization. This chapter reviews causes of hyperlactemia, including specific discussions on propofol infusion syndrome, toxic alcohol-related hyperlactemia, clenbuterol exposure, and mitochondrial toxins. HyperlactemiaTheophyllineAlbuterolCyanide toxicity This is a preview of subscription content, log in to check access Boyd JH, Walley KR. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Curr Opin Crit Care. 2008;14:37983. CrossRef PubMed Google Scholar Bray RJ. Propofol infusion syndrome in children. Paediatr Anesthe. 1998;8:4919. CrossRef Google Scholar Chasiotis D, Sahlin K, Hultman E. Regulation of glycogenolysis in human muscle in response to epinephrine infusion. J Appl Physiol Respir Environ Exerc Physiol. 1983;54(1):4550. PubMed Google Scholar Daubert GP, Mabasa VH, Leung VW, et al. Acute clenbuterol overdose resulting in supraventricular tachycardia and atrial fibrillation. J Med Toxicol. 2007;3:5660. CrossRef PubMed PubMedCentral Google Scholar Dodda V, Spiro P. Can albuterol be blamed for lactic acidosis? Respir Care. 2012;57(12):21158. PubMed Google Scholar Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000;117(1):2607. CrossRef PubMed Google Scholar Hoffman RJ, Hoffman RS, Freyberg CL, et al. Clenbuterol ingestion causing prolonged tachycardia, hypokalemia, and hypophosphatemia with confirmation by quantitative levels. J Toxicol Clin Toxicol. 2001;39:339044. CrossRef Google Scholar Hoffman RS, Kirrane BM, Marcus SM, Clenbuterol Study Investigators. A descriptive study of an outbreak of clenbuterol-containing heroin. Ann Continue reading >>

The Phantom Of Metformin-induced Lactic Acidosis In End-stage Renal Disease Patients: Time To Reconsider With Peritoneal Dialysis Treatment

The Phantom Of Metformin-induced Lactic Acidosis In End-stage Renal Disease Patients: Time To Reconsider With Peritoneal Dialysis Treatment

1Department of Internal Medicine, Nephrology Division, King Fahd Hospital of the University, University of Dammam, Saudi Arabia 2Department of Electrical Engineering, Queens University, Kingston, Ontario, Canada Correspondence to: Abdullah K. Al-Hwiesh, King Fahd Hospital of the University, Department of Internal Medicine, Nephrology Division, Al-Khobar, Saudi Arabia. ahwiesh{at}uod.edu.sa, dralhwiesh{at}yahoo.com Objective: Metformin continues to be the safest and most widely used antidiabetic drug. In spite of its well-known benefits; metformin use in end-stage renal disease (ESRD) patients is still restricted. Little has been reported about the effect of peritoneal dialysis (PD) on metformin clearance and the phantom of lactic acidosis deprives ESRD patients from metformin therapeutic advantages. Peritoneal dialysis is probably a safeguard against lactic acidosis, and it is likely that using this drug would be feasible in this group of patients. Material and methods: The study was conducted on 83 PD patients with type 2 diabetes mellitus. All patients were on automated PD (APD). Metformin was administered in a dose of 500 1,000 mg daily. Patients were monitored for glycemic control. Plasma lactic acid and plasma metformin levels were monitored on a scheduled basis. Peritoneal fluid metformin levels were measured. In addition, the relation between plasma metformin and plasma lactate was studied. Results: Mean fasting blood sugar (FBS) was 10.9 0.5 and 7.8 0.7, and mean hemoglobin A1-C (HgA1C) was 8.2 0.8 and 6.4 1.1 at the beginning and end of the study, respectively (p < 0.001). The mean body mass index (BMI) was 29.1 4.1 and 27.3 4.5 at the beginning and at the end of the study, respectively (p < 0.001). The overall mean plasma lactate level across all blood sample 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

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 >>

Hyperlactemia Induction Modes Affect The Lactate Minimum Power And Physiological Responses In Cycling

Hyperlactemia Induction Modes Affect The Lactate Minimum Power And Physiological Responses In Cycling

The lactate minimum test (LMT) is considered a valid procedure for estimating the maximal lactate steady-state intensity (MLSS) in a single-session test ( 2,17 ), being the only single session that estimates MLSS using a direct physiological criterion to identify the maximal blood lactate production-removal equilibrium ( 10 ). Lactate minimum intensity (LMI) represents the exercise intensity at which the minimum lactate value is reached in the lactate-intensity relationship. Thus, it is crucial to know the main factors that can affect the lactate-intensity relationship and could therefore alter the LMI determination ( 6,23 ). Despite factors such as muscle glycogen stores ( 31 ) and the duration of exercise stages during the incremental exercise (IE) phase (i.e., between 3 and 5 minutes) ( 22,31 ) not affecting the LMI determination, Carter et al. ( 6 ) and Ribeiro et al. ( 23 ) related that LMI is modified by the initial exercise intensity and by the recovery mode (i.e., active recovery vs. passive recovery) after the hyperlactemia induction phase, respectively. In both studies ( 6,23 ), the experimental manipulation (i.e., initial exercise intensity and recovery mode) modified the blood lactate response at the start of the IE phase and affected the lactate-intensity relationship during the test. In addition to the aforementioned findings, in which the blood lactate behavior at the start of the IE phase seems to alter the lactate-intensity relationship and consequently the LMI determination, more attention should be focused on the hyperlactemia induction mode. In an isolated study, Smith et al. ( 30 ) related, in 8 endurance-trained competitive cyclists, that different induction modes did not modify the LMI, inducing hyperlactemia using a ramp incremental test and all Continue reading >>

Hyperlactatemia And Antiretroviral Therapy: The Swiss Hiv Cohort Study

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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