Drug causes of metabolic acidosis are numerous and their mechanisms are diverse. Broadly, they can cause metabolic acidosis with either a normal anion gap (e.g. drug-induced renal tubular acidosis) or an elevated anion gap (e.g. drug-induced lactic acidosis or pyroglutamic acidosis). This review describes the drugs that can cause or contribute to metabolic acidosis during therapeutic use, the mechanisms by which this occurs, and how they may be identified in practice.
aNeurointensive Care Unit, St George's University Hospitals NHS Foundation Trust
bClinical Pharmacology, St George's University of London, London, UK
Correspondence to Andrew W. Hitchings, Senior Lecturer in Clinical Pharmacology and Consultant in Neurointensive Care, St George's University Hospitals NHS Foundation Trust and St George's University of London, Cranmer Terrace, London SW17 0RE, UK. Tel: +44 20 8725 5380; e-mail: firstname.lastname@example.org
Editor: R E Ferner, MSc, MD, FRCP, Director of the WestMidlands Centre for Adverse Drug Reaction Reporting and Consultant Physician at City Hospital, Birmingham, UK. Assistant Editor: Mr C Anton, MA, MEng. Editorial Board: Australia: Dr M Kennedy, Professor G M Shenfield, Denmark: Professor J S Schou; England: Dr J K Aronson,Dr A Hitchings; India: Professor N Gogtay; Netherlands: Professor C J van Boxtel, Dr B H Ch Stricker; New Zealand: Dr T Maling; Scotland: Dr D N Bateman; Wales: Professor P A Routledge.