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      Drug-Induced Metabolic Acidosis

      review-article
      Author(s): 1 , 2 , 4 , 1 , a , 1 , 2 , 3
      Publication date (Electronic):
      Journal: F1000Research
      Publisher: F1000Research
      Keywords: metabolic, acidosis, drug-induced, MALA

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          Abstract

          Metabolic acidosis could emerge from diseases disrupting acid-base equilibrium or from drugs that induce similar derangements. Occurrences are usually accompanied by comorbid conditions of drug-induced metabolic acidosis, and clinical outcomes may range from mild to fatal. It is imperative that clinicians not only are fully aware of the list of drugs that may lead to metabolic acidosis but also understand the underlying pathogenic mechanisms. In this review, we categorized drug-induced metabolic acidosis in terms of pathophysiological mechanisms, as well as individual drugs’ characteristics.

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          Most cited references133

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          Metformin in patients with type 2 diabetes and kidney disease: a systematic review.

          Silvio E Inzucchi, Kasia Lipska, Helen Mayo … (2014)
          Metformin is widely viewed as the best initial pharmacological option to lower glucose concentrations in patients with type 2 diabetes mellitus. However, the drug is contraindicated in many individuals with impaired kidney function because of concerns of lactic acidosis.
          Article 0 comments Cited 189 times – based on 0 reviews     Review now
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            A review of the toxicity of HIV medications.

            Asa M Margolis, Harry Heverling, Paul A Pham … (2014)
            Antiretroviral therapy has changed human immunodeficiency virus (HIV) infection from a near-certainly fatal illness to one that can be managed chronically. More patients are taking antiretroviral drugs (ARVs) for longer periods of time, which naturally results in more observed toxicity. Overdose with ARVs is not commonly reported. The most serious overdose outcomes have been reported in neonates who were inadvertently administered supratherapeutic doses of HIV prophylaxis medications. Typical ARV regimens include a "backbone" of two nucleoside reverse transcriptase inhibitors (NRTI) and a "base" of either a protease inhibitor (PI) or nonnucleoside reverse transcriptase inhibitor. New classes of drugs called entry inhibitors and integrase inhibitors have also emerged. Older NRTIs were associated with mitochondrial toxicity, but this is less common in the newer drugs, emtricitabine, lamivudine, and tenofovir. Mitochondrial toxicity results from NRTI inhibition of a mitochondrial DNA polymerase. Mitochondrial toxicity manifests as myopathy, neuropathy, hepatic failure, and lactic acidosis. Routine lactate assessment in asymptomatic patients is not indicated. Lactate concentration should be obtained in patients taking NRTIs who have fatigue, nausea, vomiting, or vague abdominal pain. Mitochondrial toxicity can be fatal and is treated by supportive care and discontinuing NRTIs. Metabolic cofactors like thiamine, carnitine, and riboflavin may be helpful in managing mitochondrial toxicity. Lipodystrophy describes changes in fat distribution and lipid metabolism that have been attributed to both PIs and NRTIs. Lipodystrophy consists of loss of fat around the face (lipoatrophy), increase in truncal fat, and hypertriglyceridemia. There is no specific treatment of lipodystrophy. Clinicians should be able to recognize effects of chronic toxicity of ARVs, especially mitochondrial toxicity.
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              Propofol infusion syndrome.

              José Cardone, P Kam (2007)
              The clinical features of propofol infusion syndrome (PRIS) are acute refractory bradycardia leading to asystole, in the presence of one or more of the following: metabolic acidosis (base deficit > 10 mmol.l(-1)), rhabdomyolysis, hyperlipidaemia, and enlarged or fatty liver. There is an association between PRIS and propofol infusions at doses higher than 4 mg.kg(-1).h(-1) for greater than 48 h duration. Sixty-one patients with PRIS have been recorded in the literature, with deaths in 20 paediatric and 18 adult patients. Seven of these patients (four paediatric and three adult patients) developed PRIS during anaesthesia. It is proposed that the syndrome may be caused by either a direct mitochondrial respiratory chain inhibition or impaired mitochondrial fatty acid metabolism mediated by propofol. An early sign of cardiac instability associated with the syndrome is the development of right bundle branch block with convex-curved ('coved type') ST elevation in the right praecordial leads (V1 to V3) of the electrocardiogram. Predisposing factors include young age, severe critical illness of central nervous system or respiratory origin, exogenous catecholamine or glucocorticoid administration, inadequate carbohydrate intake and subclinical mitochondrial disease. Treatment options are limited. Haemodialysis or haemoperfusion with cardiorespiratory support has been the most successful treatment.
              Article 0 comments Cited 113 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): F1000Res
                Journal ID (iso-abbrev): F1000Res
                Journal ID (pmc): F1000Research
                Title: F1000Research
                Publisher: F1000Research (London, UK )
                ISSN (Electronic): 2046-1402
                Publication date (Electronic): 16 December 2015
                Publication date Collection: 2015
                Volume: 4
                Electronic Location Identifier: F1000 Faculty Rev-1460
                Affiliations
                [1 ]Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, 75390-8885, USA
                [2 ]Departments of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, 75390-8885, USA
                [3 ]Department of Physiology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, 75390-8885, USA
                [4 ]Baylor Family Medicine Residency at Garland, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, 75390-8885, USA
                Author notes

                Competing interests: The authors have no competing interests.

                Article
                DOI: 10.12688/f1000research.7006.1
                PMC ID: 4754009
                PubMed ID: 26918138
                SO-VID: 6b3c3db7-4804-4c99-9fb1-338040e1b845
                Copyright © Copyright: © 2015 Pham AQT et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date accepted : 15 December 2015
                Funding
                Funded by: National Institutes of Health
                Award ID: R01-DK092461
                Award ID: R01 DK081423
                Award ID: R01DK091392
                Award ID: U01-HL111146
                Funded by: O’Brien Kidney Research Center
                Award ID: P30 DK-079328
                The authors are supported by the National Institutes of Health (R01-DK092461, R01 DK081423, R01DK091392, U01-HL111146), the O’Brien Kidney Research Center (P30 DK-079328), and the Charles and Jane Pak Foundation.
                Categories
                Subject: Review
                Subject: Articles
                Subject: Antimicrobials & Drug Resistance
                Subject: Bacterial Infections
                Subject: Bone & Mineral Metabolism
                Subject: Cancer Therapeutics
                Subject: Cardiovascular Pharmacology
                Subject: Developmental & Pediatric Neurology
                Subject: Diabetes & Obesity
                Subject: Dialysis & Renal Transplantation
                Subject: Endocrine & Metabolic Pharmacology
                Subject: Epilepsy
                Subject: Gastrointestinal Pharmacology
                Subject: Hemodynamics, Vasc. Biology & Hypertension Sec. to Kidney Dis.
                Subject: HIV Infection & AIDS: Clinical
                Subject: Hypertension
                Subject: Mineral Metabolism & the Kidney
                Subject: Neuropharmacology & Psychopharmacology
                Subject: Pathophysiology of Chronic Kidney Disease (CKD)
                Subject: Pediatric Infectious Diseases
                Subject: Renal Function & Transport Physiology
                Subject: Renal Pharmacology
                Subject: Toxicology

                Keywords: metabolic,acidosis,drug-induced,mala
                Data availability:
                Keywords: metabolic, acidosis, drug-induced, mala

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