title: Prevalence and risk factors for liver biochemical abnormalities in Canadian patients with systemic lupus erythematosus.
abstract: OBJECTIVE
  To determine the prevalence of abnormal liver enzymes in patients with systemic lupus erythematosus (SLE) and whether further investigations were done, and the differences in SLE-related and/or metabolic factors in patients with and without liver biochemical abnormalities.
  
  
  METHODS
  Patients from the University of Toronto Lupus Clinic who met at least 4 of the American College of Rheumatology classification criteria for SLE and had 1.5 times the upper limit for aspartate transaminase or alanine transaminase on 2 consecutive visits within a 2-year period were matched with controls for age, sex, and SLE duration. Demographic, clinical, and laboratory data were extracted at the time of the first appearance of liver enzyme abnormality for the cases and at the reference point for the controls.
  
  
  RESULTS
  From the 1533 patients reviewed, 134 (8.7%) met the inclusion criteria. Thirty of these patients were evaluated by a hepatologist, 75 had imaging studies (41 were done specifically for liver investigation), and 13 had liver biopsies. Results based on these investigations showed 31 fatty livers, 35 cases of drug-induced hepatotoxicity, 10 autoimmune etiologies, and 3 cases of viral hepatitis. Compared to controls, cases were higher in body mass index, anti-dsDNA antibody, prevalence of hypertension, antiphospholipid syndrome, and use of immunosuppressive medication, especially azathioprine and methotrexate; they were lower in IgM.
  
  
  CONCLUSIONS
  Metabolic abnormalities such as obesity and hypertension and hepatotoxic effects of medication used to treat SLE may contribute more than SLE-related factors to liver biochemical abnormalities in patients with SLE.
authors.affiliation: Division of Health Care and Outcome Research, Toronto Western Research Institute, Toronto, Ontario, Canada.
authors.forename: Darryl
authors.initials: D
authors.lastname: Huang
authors.forename: Elaheh
authors.initials: E
authors.lastname: Aghdassi
authors.forename: Jiandong
authors.initials: J
authors.lastname: Su
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Mosko
authors.forename: Gideon M
authors.initials: GM
authors.lastname: Hirschfield
authors.forename: Dafna D
authors.initials: DD
authors.lastname: Gladman
authors.forename: Murray B
authors.initials: MB
authors.lastname: Urowitz
authors.forename: Paul R
authors.initials: PR
authors.lastname: Fortin
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000032:analysis; D057134:Antibodies, Neutralizing / Q000097:blood; D016736:Antiphospholipid Syndrome / Q000453:epidemiology; D001219:Aspartate Aminotransferases / Q000032:analysis; D001327:Autoimmune Diseases / Q000201:enzymology / Q000453:epidemiology; D001379:Azathioprine / Q000627:therapeutic use; D015992:Body Mass Index; D002170:Canada / Q000453:epidemiology; D004247:DNA / Q000276:immunology; D005234:Fatty Liver / Q000139:chemically induced / Q000201:enzymology / Q000453:epidemiology / Q000821:virology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000453:epidemiology; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008099:Liver / Q000201:enzymology* / Q000821:virology; D008180:Lupus Erythematosus, Systemic / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000453:epidemiology* / Q000378:metabolism*; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D015995:Prevalence; D012307:Risk Factors; D012720:Severity of Illness Index; D014463:Ultrasonography
chemical_list: D057134:Antibodies, Neutralizing; D007166:Immunosuppressive Agents; D004247:DNA; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001379:Azathioprine; D008727:Methotrexate