diabetestalk.net

Which Medications Are Associated With Hyperlactemia And Lactic Acidosis?

(pdf) Reported Survival With Severe Mixed Acidosis And Hyperlactemia After Toluene Poisoning

(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 >>

Investigation Of Risk Factors Affecting Lactate Levels In Japanese Patients Treated With Metformin

Investigation Of Risk Factors Affecting Lactate Levels In Japanese Patients Treated With Metformin

Investigation of Risk Factors Affecting Lactate Levels in Japanese Patients Treated with Metformin Department of Pharmacy, Mazda Hospital of Mazda Motor Corporation Department of Diabetes, Mazda Hospital of Mazda Motor Corporation Department of Diabetes, Mazda Hospital of Mazda Motor Corporation Volume 39 (2016) Issue 12 Pages 2022-2027 Released on J-STAGE: December 01, 2016 [Advance Publication] Released: - Received: June 27, 2016 Revised: - Accepted: October 02, 2016 Metformin is a biguanaide antidiabetic drug used worldwide, and its effectiveness and benefits have already been established. However, the safety of high doses of metformin in Japanese patients, especially in elderly patients with a decreased renal function, remains unclear. Among the side effects of metformin, lactate acidosis is the most problematic due to a high mortality rate. Therefore, we assessed plasma lactate levels in metformin-treated patients to identify independent risk factors for hyperlactemia. 290 outpatients receiving various doses of metformin at our hospital were enrolled between March and July 2014. Serum electrolytes, Cre (creatinine), BUN (blood urea nitrogen), UA (uric acid), HbA1c (hemoglobin A1c), and lactate levels were investigated. Lactate levels did not significantly differ between the elderly (75 years) and non-elderly (<75 years) groups. Patients in the elderly group had a significantly lower daily metformin dose and estimated glomerular filtration rate (eGFR), compared with the non-elderly group (both p<0.005). Between with and without hyperlactemia groups, no significant differences were observed in either Cre or age. On the other hand, patients with hyperlactemia had a significantly higher dose of metformin than those without hyperlactemia (p<0.05). In this study, we fou 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 >>

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 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 >>

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 >>

Haart-induced Lactic Acidosis

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 >>

Sepsis-associated Hyperlactatemia

Sepsis-associated Hyperlactatemia

Garcia-Alvarez et al. licensee BioMed Central Ltd.2014 There is overwhelming evidence that sepsis and septic shock are associated with hyperlactatemia (sepsis-associated hyperlactatemia (SAHL)). SAHL is a strong independent predictor of mortality and its presence and progression are widely appreciated by clinicians to define a very high-risk population. Until recently, the dominant paradigm has been that SAHL is a marker of tissue hypoxia. Accordingly, SAHL has been interpreted to indicate the presence of an `oxygen debt or `hypoperfusion, which leads to increased lactate generation via anaerobic glycolysis. In light of such interpretation of the meaning of SAHL, maneuvers to increase oxygen delivery have been proposed as its treatment. Moreover, lactate levels have been proposed as a method to evaluate the adequacy of resuscitation and the nature of the response to the initial treatment for sepsis. However, a large body of evidence has accumulated that strongly challenges such notions. Much evidence now supports the view that SAHL is not due only to tissue hypoxia or anaerobic glycolysis. Experimental and human studies all consistently support the view that SAHL is more logically explained by increased aerobic glycolysis secondary to activation of the stress response (adrenergic stimulation). More importantly, new evidence suggests that SAHL may actually serve to facilitate bioenergetic efficiency through an increase in lactate oxidation. In this sense, the characteristics of lactate production best fit the notion of an adaptive survival response that grows in intensity as disease severity increases. Clinicians need to be aware of these developments in our understanding of SAHL in order to approach patient management according to biological principles and to interpret Continue reading >>

Metformin-induced Lactic Acidosis (mila): A Case Report And Review Of Current Diagnostic Paradigm

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 >>

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

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 >>

Etiology And Therapeutic Approach To Elevated Lactate

Etiology And Therapeutic Approach To Elevated Lactate

Etiology and therapeutic approach to elevated lactate aResearch Center for Emergency Medicine, Aarhus University Hospital, Denmark bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States dDepartment of Anesthesia Critical Care, Beth Israel Deaconess Medical Center, Boston, MA, United States bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States aResearch Center for Emergency Medicine, Aarhus University Hospital, Denmark bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States dDepartment of Anesthesia Critical Care, Beth Israel Deaconess Medical Center, Boston, MA, United States Corresponding author: Michael W. Donnino Beth Israel Deaconess Medical Center One Deaconess Road, W/CC 2 Boston, Boston, MA 02215 Phone: 617-754-2450 Fax: 617-754-2350 [email protected] The publisher's final edited version of this article is available at Mayo Clin Proc See other articles in PMC that cite the published article. Lactate levels are commonly evaluated in acutely ill patients. Although most commonly used in the context of evaluating shock, lactate can be elevated for many reasons. While tissue hypoperfusion is probably the most common cause of elevation 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 >>

Emdocs.net Emergency Medicine Educationlactate In Sepsis: Pearls & Pitfalls - Emdocs.net - Emergency Medicine Education

Emdocs.net Emergency Medicine Educationlactate In Sepsis: Pearls & Pitfalls - Emdocs.net - Emergency Medicine Education

Author: Erik Hofmann, MS, MD (EM Resident Physician, LAC + USC Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF) A 56 year-old female with a past medical history of recurrent urinary tract infections and hyperlipidemia presents with 1 week of suprapubic pain and fever. The patient states that she has been having progressively worsening suprapubic pain, sharp, constant, and radiating to the right flank. She has had subjective fever over the past 3 days and burning with urination for the past week. The patient states that the burning with urination is similar to her prior episodes of UTI, but that she has never had pain like this. The patient took ibuprofen 400 mg PO Q4 hours but it only provided temporary relief. Vital signs include a temperature of 101.2, HR 100, BP 132/80, RR 16, and SaO2 100% on room air. Positive physical exam findings include CVT. Blood cultures, lactate, CBC, urine analysis, urine culture and chem 7 are drawn within 3 hours of presenting to the ED. Significant laboratory results include WBC 15K and a lactate of 3.0 mmol/L. Urinalysis demonstrates pyuria, moderate blood, and positive leukocyte esterase. The patient is started on ceftriaxone 1g IV Q24 hours and 2L of crystalloid. A second lactate drawn within 6 hours of presenting to the ED is 2.55 mmol/L. Question: Where should you send this patient? Most of our pyruvate and lactate is generated via a redox-coupled interconversion catalyzed by lactate dehydrogenase (LDH) during anaerobic glycolysis. NADH is oxidized to NAD when pyruvate is converted to lactate producing protons in the process. LDH is a tetramer with five isoforms that is composed of various combinat Continue reading >>

Investigation Of Risk Factors Affecting Lactate Levels In Japanese Patients Treated With Metformin

Investigation Of Risk Factors Affecting Lactate Levels In Japanese Patients Treated With Metformin

Investigation of Risk Factors Affecting Lactate Levels in Japanese Patients Treated with Metformin Department of Pharmacy, Mazda Hospital of Mazda Motor Corporation Department of Diabetes, Mazda Hospital of Mazda Motor Corporation Department of Diabetes, Mazda Hospital of Mazda Motor Corporation Volume 39 (2016) Issue 12 Pages 2022-2027 Released on J-STAGE: December 01, 2016 [Advance Publication] Released: - Received: June 27, 2016 Revised: - Accepted: October 02, 2016 Metformin is a biguanaide antidiabetic drug used worldwide, and its effectiveness and benefits have already been established. However, the safety of high doses of metformin in Japanese patients, especially in elderly patients with a decreased renal function, remains unclear. Among the side effects of metformin, lactate acidosis is the most problematic due to a high mortality rate. Therefore, we assessed plasma lactate levels in metformin-treated patients to identify independent risk factors for hyperlactemia. 290 outpatients receiving various doses of metformin at our hospital were enrolled between March and July 2014. Serum electrolytes, Cre (creatinine), BUN (blood urea nitrogen), UA (uric acid), HbA1c (hemoglobin A1c), and lactate levels were investigated. Lactate levels did not significantly differ between the elderly (75 years) and non-elderly (<75 years) groups. Patients in the elderly group had a significantly lower daily metformin dose and estimated glomerular filtration rate (eGFR), compared with the non-elderly group (both p<0.005). Between with and without hyperlactemia groups, no significant differences were observed in either Cre or age. On the other hand, patients with hyperlactemia had a significantly higher dose of metformin than those without hyperlactemia (p<0.05). In this study, we fou Continue reading >>

More in ketosis