title: Hepatic steatosis and disease activity in subjects with psoriatic arthritis receiving tumor necrosis factor-α blockers.
abstract: OBJECTIVE
  Little is known about tumor necrosis factor-α (TNF-α) blockers, disease activity, and liver steatosis (hepatic steatosis; HS) in subjects with psoriatic arthritis (PsA). We prospectively evaluated changes in HS during treatment with TNF-α blockers.
  
  
  METHODS
  In 48 patients with PsA who had evidence of HS before the beginning of TNF-α blocker treatment, an ultrasound followup examination was performed after a 12-month treatment period with TNF-α blockers. All subjects were stratified according to minimal disease activity (MDA) or not (n-MDA), during treatment with TNF-α blockers. Changes in grade of HS were evaluated in parallel in 42 controls with HS and without PsA.
  
  
  RESULTS
  At baseline, no significant difference in HS score was found between PsA subjects and controls (HS scores 1.46 ± 0.65 vs 1.62 ± 0.66, respectively; p = 0.249). At 12-month followup, a worsening HS score was found in 20 (41.7%) patients with PsA and in 6 (14.3%) controls (p = 0.005). Overall, the grade of HS worsening was higher in patients with PsA (0.37 ± 0.70) than in controls (0.09 ± 0.43; p = 0.028). A significantly lower prevalence of worsening HS was found among patients with PsA with MDA, compared with n-MDA subjects (16.7% vs 66.7%, respectively; p = 0.001). Laboratory measures of liver function behaved similarly. The risk of worsening HS in patients with PsA who had MDA was similar to that in controls (HR 1.20, 95% CI 0.34-4.33, p = 0.77), and higher in patients who did not have MDA (HR 4.46, 95% CI 1.73-11.47, p = 0.001, regression analysis).
  
  
  CONCLUSIONS
  Compared with patients with MDA, those with active disease after 12-month treatment with TNF-α blockers exhibited significantly higher incidence of worsening liver steatosis.
authors.affiliation: Department of Clinical and Experimental Medicine, Regional Reference Centre for Coagulation Disorders, Rheumatology Research Unit, Psoriatic Arthritis Clinic, Federico II University, Naples, Italy. dario.diminno@hotmail.it
authors.forename: Matteo Nicola Dario
authors.initials: MN
authors.lastname: Di Minno
authors.forename: Salvatore
authors.initials: S
authors.lastname: Iervolino
authors.forename: Rosario
authors.initials: R
authors.lastname: Peluso
authors.forename: Anna
authors.initials: A
authors.lastname: Russolillo
authors.forename: Roberta
authors.initials: R
authors.lastname: Lupoli
authors.forename: Raffaele
authors.initials: R
authors.lastname: Scarpa
authors.forename: Giovanni
authors.initials: G
authors.lastname: Di Minno
authors.forename: Giovanni
authors.initials: G
authors.lastname: Tarantino
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000009:adverse effects; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage / Q000009:adverse effects; D018501:Antirheumatic Agents / Q000008:administration & dosage / Q000009:adverse effects*; D015535:Arthritis, Psoriatic / Q000188:drug therapy* / Q000453:epidemiology; D000068800:Etanercept; D005234:Fatty Liver / Q000139:chemically induced* / Q000000981:diagnostic imaging / Q000453:epidemiology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000009:adverse effects; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000008:administration & dosage; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014463:Ultrasonography
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept