Which medications cause lactic acidosis and hyperlactatemia?
Mar 14, 2015 · Hyperlactatemia due to drug treatment is a complication in which of the following conditions? a. Salt-losing tubulopathy b. Cirrhosis c. AIDS d. Isonatremic dehydration Answer: c
What is hyperlactatemia with acidosis?
A total of 286 patients experienced medication-induced lactate level elevations, from which 59 unique medications were identified. The most commonly identified agents were epinephrine and albuterol. Medication-induced lactate level elevation was classified as lactic acidosis (64.0%), hyperlactatemia (31.1%), or not specified (4.9%).
What is the prevalence of medication-induced hyperlactatemia in the US?
Hyperlactatemia due to drug treatment is a complication in which of the following conditions? a. Salt-losing tubulopathy b. Cirrhosis c. AIDS d. Isonatremic dehydration
Is hyperlactatemia associated with NRTI therapy?
Oct 06, 2016 · Late onset hyperlactatemia occurs in the absence of any evidence of global or regional tissue hypoxia. The mechanism of late onset hyperlactatemia is not understood. Hyperlactatemia is a common accompaniment to treatment with β 2-agonists such as epinephrine. Epinephrine-induced hyperlactatemia is thought to be due to accelerated aerobic …
What causes Hyperlactatemia?
Hyperlactatemia develops when the rate at which lactate is released from peripheral tissue cells to circulation exceeds the rate at which it is removed from circulation by liver and kidneys. Both increased lactate production and decreased lactate removal/metabolism can be causative.
What is Hyperlactatemia and acidosis?
Hyperlactatemia is defined as a persistent, mild to moderate (2-4 mmol/L) increase in blood lactate concentration without metabolic acidosis, whereas lactic acidosis is characterized by persistently increased blood lactate levels (usually >5 mmol/L) in association with metabolic acidosis.Sep 11, 2020
What drugs cause lactic acidosis?
Drugs such as metformin, linezolid, propofol, intravenous epinephrine, inhaled beta agonists (eg, albuterol), and nucleoside reverse transcriptase inhibitors (NRTIs), which are used for treatment of human immunodeficiency virus (HIV), have been linked to lactic acidosis.Jul 29, 2020
What is lactic acidosis symptoms?
The symptoms of lactic acidosis include abdominal or stomach discomfort, decreased appetite, diarrhea, fast, shallow breathing, a general feeling of discomfort, muscle pain or cramping, and unusual sleepiness, tiredness, or weakness. If you have any symptoms of lactic acidosis, get emergency medical help right away.
What does Hyperlactatemia mean?
Hyperlactatemia is defined as a lactate measurement > 2 mmol/L, and is common in critical illness (4). Lactate should not be regarded as toxic or harmful by itself. Although frequently used to diagnose in adequate tissue oxygenation, other processes not related to tissue oxygen at ion may increase lactate levels (4).
How do you treat Hyperlactatemia?
Venous hyperlactatemia was considered at > 2.2 mmol/l. Treatment consisted of a daily vitamin regime of L-carnitine, thiamine, vitamin B6, hydroxicobalamine, and vitamin C; any glucose intake was discontinued.
What medications cause lactic acidosis and Hyperlactatemia?
The most commonly identified agents were epinephrine and albuterol.
What happens in lactic acidosis?
In people with lactic acidosis, problems with the liver (and sometimes with the kidneys) make these organs unable to remove extra acid from their bodies. If lactate builds up in the body faster than it can be removed, acid levels spike in bodily fluids like blood.
What causes increased lactic acid?
The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization.
What are 3 symptoms of lactic acid build up?
Muscle ache, burning, rapid breathing, nausea, stomach pain: If you've experienced the unpleasant feeling of lactic acidosis, you likely remember it. Lactic acidosis caused by intense exercise is usually temporary. It happens when too much acid builds up in your bloodstream.Jan 17, 2022
What happens if your lactic acid is too high?
Higher-than-normal lactic acid levels can lead to a condition called lactic acidosis. If it's severe enough, it can upset your body's pH balance, which indicates the level of acid in your blood. Lactic acidosis can lead to these symptoms: muscle weakness.Aug 20, 2021
How is metformin induced lactic acidosis treated?
Treatment of the lactic acidosis induced by metformin is based on the use of supportive general measures; in severe cases, procedures of extrarrenal purification like hemodialysis or continuous hemodiafiltration have been successfully used. Metformin is the main biguanide, widely used in diabetes mellitus treatment.
What are the factors that contribute to hyperlactatemia?
Other predisposing factors to hyperlactatemia and lactate acidosis include age, obesity, and ethanol intake. Age is thought to result in cumulative oxidative damage to mitochondria and therefore predisposes patients to mitochondrial dysfunction.
Is hyperlactatemia a marker of hypoperfusion?
Two important paradigms have framed current understanding of hyperlactatemia in this setting. The first is that lactate is a marker of tissue hypoperfusion and thus of oxygen debt. The second concept is that hyperlactatemia is an ominous sign. This is a conception that has been rightfully ingrained in the psyche of clinicians based on data that originated in Weil's seminal work but that has stood the test of time in demonstrating a clear association between elevated lactate levels and worse outcome. The wide embrace of these two concepts has reduced the understanding of lactate to that of being an “evil” molecule, and a marker of tissue hypoxia and anaerobic metabolism. This chapter proposes to provide the reader with a different perspective, providing evidence that lactate is not just a “waste” product of anaerobiosis, but rather a key player in intermediary metabolism and energy homeostasis, that lactate is crucial for intercellular and interorgan cooperation, substrate distribution, and perhaps adaptation to injury, and thus that hyperlactatemia cannot be an exclusive reflection of tissue hypoxia.
What is elevated lactate?
An elevated blood lactate concentration (hyperlactatemia) is a typical finding during exercise and in critical illness, most notably sepsis, cardiogenic shock, cardiac surgery, and liver failure. In essentially all situations of severe disease-related physiologic stress, an elevated blood lactate concentration has been demonstrated reproducibly and consistently to be an independent predictor of mortality.94–98 More than 50 years ago Dr Weil's group demonstrated an exponential increase in the mortality of critically ill patients with increasing blood lactate concentrations. 99,100 More recent studies suggest that the mortality increases linearly above a lactate concentration of 1.4 mmol/L and that this association is independent of organ dysfunction or the presence of shock. 94,101–103 Stress hyperlactemia, similar to stress hyperglycemia, is a marker of illness severity and a beneficial adaptive evolutionary response.
Does ethanol cause fatty liver?
Ethanol has been shown to induce ultrastructural changes in hepatic mitochondria and to induce fatty liver.
Does linezolid cause hyperlactatemia?
Hyperlactatemia and metabolic acidosis are adverse effects of linezolid that could be related to its capacity for inter fering with mitochondrial function. A 63-year-old woman developed an optic neuropathy, encephalopathy, skeletal myopathy, lactic acidosis, and renal failure after taking linezolid for 4 months (123AE).
What is metabolic acidosis?
Abstract Metabolic acidosis is a disorder frequently encountered in emergency medicine and intensive care medicine. As literature has been enriched with new data concerning the management of metabolic acidosis, the French Intensive Care Society (Société de Réanimation de Langue Française [SRLF]) and the French Emergency Medicine Society (Société Française de Médecine d’Urgence [SFMU]) have developed formalized recommendations from experts using the GRADE methodology. The fields of diagnostic strategy, patient assessment, and referral and therapeutic management were addressed and 29 recommendations were made: 4 recommendations were strong (Grade 1), 10 were weak (Grade 2), and 15 were experts’ opinions. A strong agreement from voting participants was obtained for all recommendations. The application of Henderson–Hasselbalch and Stewart methods for the diagnosis of the metabolic acidosis mechanism is discussed and a diagnostic algorithm is proposed. The use of ketosis and venous and capillary lactatemia is also treated. The value of pH, lactatemia, and its kinetics for the referral of patients in pre-hospital and emergency departments is considered. Finally, the modalities of insulin therapy during diabetic ketoacidosis, the indications for sodium bicarbonate infusion and extra-renal purification as well as the modalities of mechanical ventilation during severe metabolic acidosis are addressed in therapeutic management.
Is ascorbate cytotoxic to dogs?
Background: High-dose, pharmacological ascorbate ( P-AscH −) is preferentially cytotoxic to human cancer cells in vitro . Investigations on the efficacy of P-AscH− as an adjuvant treatment for multiple human cancers are on-going, but has yet to be formally investigated in dogs. The primary objectives of this study were to determine the pharmacokinetic (PK) profile of P-AscH− in healthy Beagle dogs and the effects of P-AscH− on canine osteosarcoma cells in vitro. Methods: Eight purpose-bred, healthy, spayed female Beagle dogs, between 20 and 21 months old, and 8–10 kg were administered two doses of P-AscH− (550 or 2,200 mg/kg) via intravenous infusion over 6 h, on separate days. Plasma ascorbate concentrations were measured at 12 time points during and after infusion for PK analysis using nonlinear mixed-effects (NLME) and non-compartmental analysis (NCA). Clonogenic assays were performed on 2 canine osteosarcoma cell lines (D-17 and OSCA-8) and canine primary dermal fibroblasts after exposure to high concentrations of ascorbate (75 pmoles/cell). Results: Plasma ascorbate levels in the dogs peaked at approximately 10 mM following 2,200 mg/kg and returned to baseline 6–8 h after dosing. Minor adverse effects were seen in two dogs. Ascorbate (75 pmoles/cell) significantly decreased survival in both the osteosarcoma cell lines (D-17 63% SD 0.010, P = 0.005; OSCA-8 50% SD 0.086, P = 0.026), compared to normal fibroblasts (27% SD 0.056). Conclusions: Pharmacological ascorbate is preferentially cytotoxic to canine-derived cancer cells. High levels of ascorbate can be safely administered to dogs. Further studies are needed to determine the effects of P-AscH− on canine patients.
Is lactate a stereoisomer?
Lactate occurs in two stereoisomers or enantiomers: L-lactate and D-lactate (Fig. 5.1). L-lactate is the predominant stereoisomer in healthy subjects. D-lactate is usually synthesized from bacteria. In clinical laboratories, only L-lactate (simply lactate) is measured.
Can mitochondrial toxicity be transmitted during pregnancy?
In the context of pregnancy, mitochondrial toxicity may be manifested and exclusively restricted to the carrying mother (maternal toxicity) or may be trans lated into the embryo (fetal toxicity). This chapter describes the mechanisms of action and potential secondary mitochondrial effects of drugs currently used in clinical practice during pregnancy in an attempt to increase awareness and caution about their management. In case of human pregnancies, novel approaches based on in silico modeling and system pharmacology, aimed to design and predict on-target and off-target effects of a drug before administration, should be considered in order to maximize its therapeutic action and minimize its toxic consequences. During pregnancy, acute disorders, such as migraine or infectious diseases, may require short-term treatment with potential mitochondrial toxic medication. Although mitochondrial toxicity is widely documented in nonpregnant adults, little information is known within the context of human pregnancy, particularly in terms of in utero exposure.