Materials and Methods: レ4 consecutive patients with a diagnosis of fatty
liver disease who underwent a baseline TE examination between 2007 and 2010 at our Centre were genotyped for PNPLA3 rs734809 C/G, and investigated with a second TE examination at least 24 months apart. TE was considered reliable if >10 valid measurements were obtained, with selleck kinase inhibitor a success rate >65% and an interquartile range <30% of the result. Significant fibrosis was excluded by LSM <5.8 kPa as previously reported (Wong et al, Hepatology 2010). Results: Eleven (4%) patients had unsuccessful TE, 163 (108 men, 55 females) were included, 72% nonalcoholic fatty liver disease, 18% alcoholic liver disease, Talazoparib datasheet 19% diabetics, 34% with arterial hypertension, median age 52 yrs (range 18-73), BMI 27.5 kq/mq (range 1941), baseline LSM 6.3 kPa (range 2.5-63.9) and follow-up LSM 5.9 kPa (range 3.3-53.2), and interval between LSMs 41 months (range 24-76). At baseline 66 (41%) patients had LSM <5.8 kPa, 55% of them being PNPLA3 wild type compared to 34% of those with LSM >5.8 kPa (p=0.01).48 (29%) patients had both baseline and follow-up LSM <5.8 kPa, showing significantly lower baseline BMI (p<0.0001), higher baseline serum HDL (p=0.019) and lower triglycerides (p<0.0001) with respect to all other
patients. By multivariate logistic regression analysis PNPLA3 wild type (p=0.002, OR 3.1, 95%CI 2.1-11.5-6.4) and baseline triglycerides <120 mg/dl (p<0.0001, OR 4.4, 95%CI 2.1-9.1) independently predicted baseline LSM <5.8 kPa, conversely, BMI <29 kg/mq (p=0.003, OR 5.1, 95%CI 1.7-14.9) and triglycerides <120 mg/dl (p<0.0001, OR 4.6, 95%CI 2.1-10) independently predicted both baseline and follow-up LSM <5.8 for kPa. Conclusions:
Among patients with fatty liver, wild type PNPLA3 homozygosity and low serum triglycerides are independently associated with normal liver stiffness at presentation, but only the latter and being non-obese independently predict that they will maintain it during the follow-up. These results emphasize the role of modifiable risk factors in the progression of fatty liver. Disclosures: Mario Pirisi – Advisory Committees or Review Panels: Merck; Speaking and Teaching: Gilead, Bristol-Myers-Squibb The following people have nothing to disclose: Cristina Rigamonti, Michela E. Burlone, Miriam Gravellone, Andrea Magri, Rosalba Minisini, Cosimo Colletta Non-alcoholic fatty liver disease (NAFLD) has a complex natural history; only a fraction of patients progress to cirrhosis and its complications. Using paired biopsies one may detect gradual changes in fibrosis and other features prior to clinical cirrhosis.