title: Non-alcoholic fatty liver disease (NAFLD), insulin resistance and lipid profile in antiepileptic drug treatment.
abstract: OBJECTIVE
  Patients undergoing long-term treatment with valproic acid (VPA) are prone to develop different features of the metabolic syndrome (MS). The aim of the present study was to evaluate the occurrence of non-alcoholic fatty liver disease (NAFLD), insulin resistance (IR) and a pro-atherogenic lipid profile in patients undergoing VPA, carbamazepine (CBZ) and lamotrigine (LTG) monotherapy compared to healthy controls.
  
  
  METHODS
  Abdominal ultrasound as well as measurement of serum fasting insulin and glucose, serum lipids and liver function parameters were performed in VPA (n=23), CBZ (n=22) and LTG (n=23) treated non-diabetic and non-obese epileptic patients compared to healthy controls (n=16).
  
  
  RESULTS
  Ultrasound measurement demonstrated characteristics of fatty liver disease in 60.9% of VPA, in 22.7% of CBZ, in 8.7% of LTG treated patients and in 12.5% of the healthy controls, with highest level of steatosis seen in VPA treated patients. In addition, patients on VPA monotherapy showed a higher body-mass index (BMI) when compared to LTG treated patients and controls (p<or=0.049). Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and gamma-glutamyltransferase (gammaGT) were greatest in the CBZ group (p<or=0.043). Interestingly, serum fasting glucose, serum fasting insulin as well as the HOMA-IR did not differ significantly between groups.
  
  
  CONCLUSIONS
  In conclusion, VPA (and moderately CBZ) therapy is related to increased risk for ultrasonographic signs of fatty liver disease, emphasizing the importance of regular ultrasound measurements as well as monitoring of serum lipids and BMI during enzyme-modulating AED treatment.
authors.affiliation: Department of Neurology, Epilepsy Unit, Medical University Innsbruck, Innsbruck, Austria. gerhard.luef@i-med.ac.at
authors.forename: G
authors.initials: G
authors.lastname: Luef
authors.forename: M
authors.initials: M
authors.lastname: Rauchenzauner
authors.forename: M
authors.initials: M
authors.lastname: Waldmann
authors.forename: W
authors.initials: W
authors.lastname: Sturm
authors.forename: A
authors.initials: A
authors.lastname: Sandhofer
authors.forename: K
authors.initials: K
authors.lastname: Seppi
authors.forename: E
authors.initials: E
authors.lastname: Trinka
authors.forename: I
authors.initials: I
authors.lastname: Unterberger
authors.forename: C F
authors.initials: CF
authors.lastname: Ebenbichler
authors.forename: M
authors.initials: M
authors.lastname: Joannidis
authors.forename: G
authors.initials: G
authors.lastname: Walser
authors.forename: G
authors.initials: G
authors.lastname: Bauer
authors.forename: F
authors.initials: F
authors.lastname: Hoppichler
authors.forename: M
authors.initials: M
authors.lastname: Lechleitner
mesh_terms: D000005:Abdomen / Q000000981:diagnostic imaging; D000328:Adult; D000927:Anticonvulsants / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D001786:Blood Glucose / Q000187:drug effects; D015992:Body Mass Index; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004829:Epilepsy, Generalized / Q000188:drug therapy; D005234:Fatty Liver / Q000097:blood* / Q000139:chemically induced* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008055:Lipids / Q000097:blood*; D008111:Liver Function Tests; D008297:Male; D014463:Ultrasonography / Q000379:methods; D055815:Young Adult
chemical_list: D000927:Anticonvulsants; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008055:Lipids