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Lactic Acidosis Mechanism

Lactic Acidosis | Md Nexus

Lactic Acidosis | Md Nexus

Cohen-Woods Classification of Lactic Acidosis Type A: due to decreased perfusion or oxygenation However, these may cause type A lactic acidosis in some cases Type B2: due to medication or intoxication Type B3: due to inborn error of metabolism Mitochondrial Encephalomyopathy + Lactic Acidosis + Stroke-Like Episodes (MELAS) Tumors May Benefit from Acidosis: acidic microenvironment is critical for tumorigenesis, angiogenesis, and metastasis Physiology: decreased lactate clearance (with severe liver metastases)+ increased glycolytic activity of tumor (Warburg Effect) + tissue tumor hypoxia Treatment: bicarbonate administration may increase lactic acid production Tumor Lysis Syndrome (see Tumor Lysis Syndrome , [[Tumor Lysis Syndrome]]) Anaphylaxis (see Anaphylaxis , [[Anaphylaxis]]) Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Congestive Heart Failure (CHF)/Cardiogenic Shock (see Congestive Heart Failure , [[Congestive Heart Failure]] and Cardiogenic Shock , [[Cardiogenic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Hemorrhagic Shock (see Hemorrhagic Shock , [[Hemorrhagic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Hypovolemic Shock (see Hypovolemic Shock , [[Hypovolemic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Sepsis (see Sepsis , [[Sepsis]]): common etiology of lactic acidosis Physiology: decreased lactate clearance (likely due to inhibition of pyruvate dehydrogenase + epinephrine-induced 2-adrene Continue reading >>

Type B Lactic Acidosis: A Rare But Life Threatening Hematologic Emergency. A Case Illustration And Brief Review

Type B Lactic Acidosis: A Rare But Life Threatening Hematologic Emergency. A Case Illustration And Brief Review

Type B lactic acidosis: a rare but life threatening hematologic emergency. A case illustration and brief review Wederson M Claudino ,* Ajoy Dias ,* William Tse ,* and Vivek R Sharma * Division of Hematology and Medical Oncology, James Graham Brown Cancer Center, University of Louisville Health Sciences Center, Louisville, Kentucky, USA Address correspondence to: Dr. Vivek R Sharma, Division of Hematology and Medical Oncology, James Graham Brown Cancer Center, 529 South Jackson Street, Louisville, Kentucky 40202, USA. E-mail: [email protected] Major strides have been made in improving the treatment of medical emergencies associated with malignancies. Nonetheless, metabolic emergencies in cancer patients can often times be life-threatening. Type B lactic acidosis is a rare but potentially fatal paraneoplastic phenomenon that has been described in association with hematologic and solid malignancies and portends a poor prognosis if not rapidly recognized and treated. It is believed that this occurs as a result of cancer cells switching their glucose metabolism from an oxidative oxygen- dependent pathway towards a glycolytic phenotype, also known as the Warburg effect. Though rare, it is important to consider this entity in the differential diagnosis of type B lactic acidosis since prompt identification and treatment may help improve outcomes in this otherwise fatal process. We present a case of type B lactic acidosis in a patient with chronic lymphocytic leukemia along with a brief review of the literature. Keywords: Lactic acidosis, malignancy, hematologic emergency Otto Warburg was a German physiologist awarded a Nobel Prize in 1931 for his pioneering work with respiratory enzymes [ 1 ]. Later on, his continued investigations led to the discovery that canc Continue reading >>

Cancer-associated Type B Lactic Acidosis

Cancer-associated Type B Lactic Acidosis

Posted on September 12, 2013 by AJKDblog in Commentary // 0 Comments Fig 2 Sia et al , National Kidney Foundation. Lactic acidosis is an acid-base disturbance commonly seen in hospitalized patients. Most cases of lactic acidosis are due to hypoperfusion (type A lactic acidosis), which results in higher anaerobic lactate production and decreased lactate clearance due to hepatic or kidney dysfunction. Type B lactic acidosis is not associated with tissue hypoperfusion and can be seen in the setting of patients with various cancers, typically hematologic, as well as those taking certain medications such as metformin, linezolid, and propofol. Because type B lactic acidosis occurs less commonly, lack of familiarity with this diagnosis may delay appropriate management and contribute to poorer outcomes. In the September issue of AJKD, Sia and colleagues discuss a patient with multiple myeloma refractory to two autologous stem cell transplants who presented with progressive dyspnea and was initially found to have severe metabolic acidosis with a markedly elevated serum lactate level. A diagnosis of type B lactic acidosis was made on the basis of hemodynamic stability and no other identifiable causes for type A lactic acidosis. The patient was found to have recurrent myeloma with 52% plasma cells in his bone marrow biopsy. In spite of the initiation of multiple chemotherapeutic agents and intravenous bicarbonate, his lactic acidosis worsened, necessitating renal replacement therapy. Unfortunately, this measure was not effective at reversing his clinical decline, and the patient died on hospital day 14. This teaching case highlights the importance of recognizing type B lactic acidosis and implementing prompt treatment. Sia and colleagues present an informative discussion on the p Continue reading >>

Lactic Acidosis - Statpearls - Ncbi Bookshelf

Lactic Acidosis - Statpearls - Ncbi Bookshelf

Christopher D. Foucher1; Robert E. Tubben2. 2 McLaren Greater Lansing/ Michigan State Lactic acid is produced in physiologically normal processes, andasa common finding in disease states. When increased production is comorbid with decreased clearance, the severity of the clinical course escalates. Importantly, the effects of severely elevated levels of lactic acid can have profound hemodynamic consequences and can lead to death. Serum lactate levels can be both a marker for risk as well as a therapeutic target. The higher the level and the longer the time to normalization of elevated serum lactate, the greater the risk of death. Lactic acid is normally produced in excess by about 20 mmol/kg/day, which enters the bloodstream. It is then metabolized mostly via the liver and the kidney. Some tissues can use lactate as a substrate and oxidize it to carbon dioxide (C02) and water, but only the liver and kidney have the necessary enzymes to utilize lactate for the process of gluconeogenesis. The tissues which normally produce excess lactic acid include the skin, red cells, brain tissue, muscle, and the gastrointestinal (GI) tract. During heavy exercise, it is the skeletal muscles which produce the most excess circulating lactate, which normalizes in the absence of impaired hepatic metabolism. In general, elevated lactate can be the result of increased production, decreased clearance, or both. Pyruvate production as a result of glycolysis gets shunted into two main metabolic pathways. Under aerobic conditions, it enters the citric acid cycle after having been converted to acetyl-CoA by pyruvate dehydrogenase, and a series of reactions occur to form ATP and NADH, which goes on to the process of oxidative phosphorylation which produces the majority of ATP in a cell. However, un Continue reading >>

Lactic Acidosis And Beta Agonist Therapy In Asthma

Lactic Acidosis And Beta Agonist Therapy In Asthma

Lactic Acidosis and Beta Agonist Therapy in Asthma A 45 y/o male with moderate persistent asthma presents with wheezing and cough following a viral URI. He is tachypneic and has diffuse wheezing. PEFR is 250 (>50% below his normal). Initial ABG is 7.46/33/70 on room air with a lactate of 2.0 mmol/L. He receives IV steroids and 4 rounds of albuterol nebulizers. On repeat evaluation, his work of breathing and wheezing have improved and his PEFR is now >300. He is completed alert and oriented with a BP of 118/70 and a HR of 110. Repeat ABG shows 7.35/35/100 on room air; however, his lactate is now 7 mmol/L. QUESTION: Is the rise in his lactate expected following beta-agonist therapy? A simple respiratory alkalosis is the most common acid-base disorder in acute asthma.[1]However, lactic acidosis is frequently identified especially in cases of severe asthma.[2-4]Possible causes of lactic acidosis in asthma include: Tissue hypoxia due to hypoxemia and the decrease in venous return caused by elevated intrinsic PEEP Relative hepatic ischemia and impaired lactate clearance due to venous congestion Increased respiratory muscle work against constricted upper airways Wait, -agonist therapy can cause an elevated lactate? How? Causes of lactic acidosis can be organized into two categories: [5-6] Type A: Secondary to tissue hypoxia (shock, cardiac arrest) Type B: Lactic acidosis without hypoxia.This can occur through several mechanisms including: Impaired pyruvate dehydrogenase activity (thiamine deficiency) Medication-induced mitochondrial dysfunction (antiretroviral therapy, linezolid, propofol, etc) Impaired conversion of lactate to glucose (hepatic dysfunction) Lactic acidosis caused by -agonist therapy is a type B lactic acidosis. The exact mechanism for the rise in lactate leve Continue reading >>

Metformin And Fatal Lactic Acidosis

Metformin And Fatal Lactic Acidosis

Publications Published: July 1998 Information on this subject has been updated. Read the most recent information. Dr P Pillans,former Medical Assessor, Centre for Adverse Reactions Monitoring (CARM), Dunedin Metformin is a useful anti-hyperglycaemic agent but significant mortality is associated with drug-induced lactic acidosis. Significant renal and hepatic disease, alcoholism and conditions associated with hypoxia (eg. cardiac and pulmonary disease, surgery) are contraindications to the use of metformin. Other risk factors for metformin-induced lactic acidosis are sepsis, dehydration, high dosages and increasing age. Metformin remains a major reported cause of drug-associated mortality in New Zealand. Of the 12 cases of lactic acidosis associated with metformin reported to CARM since 1977, 2 occurred in the last year and 8 cases had a fatal outcome. Metformin useful but small risk of potentially fatal lactic acidosis Metformin is a useful therapeutic agent for obese non-insulin dependent diabetics and those whose glycaemia cannot be controlled by sulphonylurea monotherapy. Lactic acidosis is an uncommon but potentially fatal adverse effect. The reported frequency of lactic acidosis is 0.06 per 1000 patient-years, mostly in patients with predisposing factors.1 Examples of metformin-induced lactic acidosis cases reported to CARM include: A 69-year-old man, with renal and cardiac disease, was prescribed metformin due to failing glycaemic control on glibenclamide monotherapy. He was well for six weeks, then developed lactic acidosis and died within 3 days. Post-surgical lactic acidosis caused the death of a 70-year-old man whose metformin was not withdrawn at the time of surgery. A 56-year-old woman, with no predisposing disease, died from lactic acidosis following major 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 >>

Lactic Acidosis | Definition Of Lactic Acidosis By Medical Dictionary

Lactic Acidosis | Definition Of Lactic Acidosis By Medical Dictionary

Lactic acidosis | definition of lactic acidosis by Medical dictionary 1. the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH. 2. a pathologic condition resulting from this process, characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biologic activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. adj., adj acidotic. Acidosis usually occurs secondary to some underlying disease process; the two major types, distinguished according to cause, are metabolic acidosis and respiratory acidosis (see accompanying table). In mild cases the symptoms may be overlooked; in severe cases symptoms are more obvious and may include muscle twitching, involuntary movement, cardiac arrhythmias, disorientation, and coma. In general, treatment consists of intravenous or oral administration of sodium bicarbonate or sodium lactate solutions and correction of the underlying cause of the imbalance. Many cases of severe acidosis can be prevented by careful monitoring of patients whose primary illness predisposes them to respiratory problems or metabolic derangements that can cause increased levels of acidity or decreased bicarbonate levels. Such care includes effective teaching of self-care to the diabetic so that the disease remains under control. Patients receiving intravenous therapy, especially those having a fluid deficit, and those with biliary or intestinal intubation should be watched closely for early signs of acidosis. Others predisposed to acidosis are patients with shock, hyperthyroidism, advanced circulatory failure, renal failure, 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 >>

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Abstract Although metformin has become a drug of choice for the treatment of type 2 diabetes mellitus, some patients may not receive it owing to the risk of lactic acidosis. Metformin, along with other drugs in the biguanide class, increases plasma lactate levels in a plasma concentration-dependent manner by inhibiting mitochondrial respiration predominantly in the liver. Elevated plasma metformin concentrations (as occur in individuals with renal impairment) and a secondary event or condition that further disrupts lactate production or clearance (e.g., cirrhosis, sepsis, or hypoperfusion), are typically necessary to cause metformin-associated lactic acidosis (MALA). As these secondary events may be unpredictable and the mortality rate for MALA approaches 50%, metformin has been contraindicated in moderate and severe renal impairment since its FDA approval in patients with normal renal function or mild renal insufficiency to minimize the potential for toxic metformin levels and MALA. However, the reported incidence of lactic acidosis in clinical practice has proved to be very low (< 10 cases per 100,000 patient-years). Several groups have suggested that current renal function cutoffs for metformin are too conservative, thus depriving a substantial number of type 2 diabetes patients from the potential benefit of metformin therapy. On the other hand, the success of metformin as the first-line diabetes therapy may be a direct consequence of conservative labeling, the absence of which could have led to excess patient risk and eventual withdrawal from the market, as happened with earlier biguanide therapies. An investigational delayed-release metformin currently under development could potentially provide a treatment option for patients with renal impairment pending the resu Continue reading >>

Causes Of Lactic Acidosis

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 >>

Mala: Metformin-associated Lactic Acidosis

Mala: Metformin-associated Lactic Acidosis

By Charles W. O’Connell, MD Introduction Metformin is a first-line agent for type 2 diabetes mellitus often used as monotherapy or in combination with oral diabetic medications. It is a member of the biguanide class and its main intended effect is expressed by the inhibition of hepatic gluconeogenesis. In addition, metformin increases insulin sensitivity, enhances peripheral glucose utilization and decreases glucose uptake in the gastrointestinal tract. Phenformin, a previously used biguanide, as withdrawn from the market in the 1970’s due its association with numerous cases of lactic acidosis. Metformin is currently used extensively in the management of diabetes and is the most commonly prescribed biguanide worldwide. The therapeutic dosage of metformin ranges from 850 mg to a maximum of 3000 mg daily and is typically divided into twice daily dosing. It is primarily used in the treatment of diabetes but has been used in other conditions associated with insulin resistance such as polycystic ovarian syndrome. MALA is a rare but well reported event that occurs with both therapeutic use and overdose states. Case presentation A 22-year-old female presents to the Emergency Department after being found alongside a suicide note by her family. She was thought to have taken an unknown, but large amount of her husband’s metformin. She arrives at the ED nearly 10 hours after ingestion. She was agitated, but conversant. She reports having nausea and vague feelings of being unwell and is very distraught over the state of her critically ill husband. She has some self-inflicted superficial lacerations over her left anterior forearm. Her vital assigns upon arrival were: T 98.9 degrees Fahrenheit, HR initially 140 bpm which improved to 110 bpm soon after arrival, BP 100/50, RR 22, 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 >>

Albuterol-induced Lactic Acidosis | Anesthesiology | Asa Publications

Albuterol-induced Lactic Acidosis | Anesthesiology | Asa Publications

*Assistant Professor, Outcomes Research Institute and Department of Anesthesiology, University of Louisville. Anesthesia Consultant, Anesthesiology Associates of Tallahassee, P.A. Professor of Anesthesiology and Neurosurgery, Associate Professor for Education, Department of Anesthesiology, University of Florida. Received from the Outcomes Research Institute and Department of Anesthesiology, University of Louisville, Louisville, Kentucky; and the Department of Anesthesiology and Neurosurgery, University of Florida, Gainesville, Florida. Anesthesiology 8 2003, Vol.99, 505-506. doi: Anesthesiology 8 2003, Vol.99, 505-506. doi: EdwinB. Liem, StephenC. Mnookin, MichaelE. Mahla; Albuterol-induced Lactic Acidosis. Anesthesiology 2003;99(2):505-506. 2018 American Society of Anesthesiologists You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account LACTIC acidosis occurring in association with -2 agonist treatments such as salbutamol, 1,2 ritodrine, 3 meta-proterenol, 4 and albuterol 5 has been reported, and its mechanism remains poorly understood. Lactic acidosis in the setting of severe asthma has been attributed to the production of lactate by overworked respiratory muscles. 6 However, the increased work of breathing seems an unlikely factor in patients who are anesthetized, paralyzed, and mechanically ventilated, and this phenomenon has not been previously reported in anesthetized patients. We report a case of severe lactic acidosis in a patient undergoing thoracoscopic sympathectomy under general anesthesia who received repeated albuterol nebulizer treatments for bronchospasm. A 39-yr-old white woman was scheduled for thoracoscopic sympathectomy at the University of Florida, Sh Continue reading >>

Does Linezolid Cause Lactic Acidosis By Inhibiting Mitochondrial Protein Synthesis?

Does Linezolid Cause Lactic Acidosis By Inhibiting Mitochondrial Protein Synthesis?

Does Linezolid Cause Lactic Acidosis by Inhibiting Mitochondrial Protein Synthesis? Department of Neurology, Columbia University College of Physicians and Surgeons Reprints or correspondence: Dr. Michio Hirano, Columbia University Medical Center, 630 W 168th St., P&S 4-443, New York, NY 10032 ( [email protected] ). Search for other works by this author on: Department of Neurology, Columbia University College of Physicians and Surgeons Infectious Diseases, Department of Internal Medicine, Indiana University Medical Center Division of Molecular Medicine, Health Research, New York State Department of Health Division of Molecular Medicine, Health Research, New York State Department of Health Division of Molecular Medicine, Health Research, New York State Department of Health Clinical Infectious Diseases, Volume 40, Issue 12, 15 June 2005, Pages e113e116, Michio Hirano, Lluis Palenzuela, Noah M. Hahn, Robert P. Nelson, Janet N. Arno, Carol Schobert, Robert Bethel, Lisa A. Ostrowski, Manjuli R. Sharma, Partha P. Datta, Rajendra K. Agrawal, Jennifer E. Schwartz; Does Linezolid Cause Lactic Acidosis by Inhibiting Mitochondrial Protein Synthesis?, Clinical Infectious Diseases, Volume 40, Issue 12, 15 June 2005, Pages e113e116, Linezolid, an oxazolidinone antibiotic, inhibits bacterial protein synthesis by binding to 23S ribosomal RNA (rRNA). We studied 3 patients who experienced lactic acidosis while receiving linezolid therapy. The toxicity may have been caused by linezolid binding to mitochondrial 16S rRNA. Genetic polymorphisms may have contributed to the toxicity in 2 patients. Linezolid (Zyvox; Pfizer) is the first commercially available oxazolidinone antibacterial agent and is effective against gram-positive organisms, including bacterial strains that are resistant to met Continue reading >>

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