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PTU-067 Hepatic steatosis in patients with autoimmune hepatitis—prevalence, progression and possible significance
  1. C Salmon1,
  2. B Hoeroldt2,
  3. A Dube3,
  4. E McFarlane1,
  5. D Gleeson1
  1. 1Department of Hepatology, Royal Hallamshire Hospital, Sheffield, UK
  2. 2Department of Gastroenterology, Rotherham General Hospital, Rotherham, UK
  3. 3Department of Histopathology, Royal Hallamshire Hospital, Sheffield, UK


Introduction A link between steatosis and Prednisolone therapy has been suggested, but is poorly documented. In chronic hepatitis C, steatosis has been linked with fibrosis progression. The prevalence and significance of steatosis in autoimmune hepatitis (AIH) are unclear.

Methods To assess the prevalence, progression and possible significance of steatosis in AIH. We studied 99 patients with AIH, 17 men, median age 48 (9–85) years, 31 probable, 68 definite by IAIHG criteria. We assessed steatosis (grade 1–3 and distribution), Ishak necro-inflammatory (NI) score and Ishak fibrosis score in paired liver biopsies: the initial diagnostic biopsy and a follow-up biopsy when in remission after median 25 (3–115) months Prednisolone.

Results 24 of the 99 patients had steatosis on the diagnostic biopsy (16 grade 1, 8 grade 2): 8 zone 1, 6 zone 2 and 12 zone 3. Patients with steatosis had lower NI scores than those without, (median 8 vs 13: p=0.003) but a similar prevalence of plasma cells (54.2% vs 64%) and rosettes (62.5% vs 60%). They were older (median 59 vs 45 years, p=0.001) and had a higher prevalence of diabetes (42% vs 12%, p=0.012) than those without steatosis but had similar body weight and BMI values. On follow-up biopsy, 46 of the 99 patients had steatosis, which had appeared or worsened in 31 patients. In six patients steatosis disappeared and 26 patients had developed new steatosis (7 zone 1, 6 zone 2, 24 zone 3). Steatosis grade worsened between diagnostic and follow-up biopsy (p<0.001). Worsening of steatosis was not related to gender, age, diabetes, or body weight or to duration, initial dose or maintenance dose of Prednisolone. Patients with worsening steatosis, compared to those with stable or improved steatosis, had similar falls in median NI score (12 to 3 and 13 to 3: p<0.001) between diagnostic and follow-up biopsy. However, they achieved no improvement in median fibrosis stage (3 to 3: NS), whereas in patients with stable or improving steatosis, median fibrosis score fell from 3 to 2 (p=0.004). In regression analysis worsening of steatosis was significantly associated with severity of fibrosis on follow-up biopsy: p=0.039.

Conclusion Steatosis is found in 1/4 of patients with AIH and is related to age and diabetes. Steatosis worsens in 1/3 of patients treated with Prednisolone, although an association with dose or duration of Prednisolone was not observed. Patients with worsening steatosis, despite reduction in inflammation, fail to achieve improvement in fibrosis, suggesting that steatosis progression might compromise long-term outcome in AIH.

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