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Original Article

SAF score and mortality in NAFLD after up to 41 years of follow-up

, , , , , & show all
Pages 87-91 | Received 06 Jul 2016, Accepted 25 Aug 2016, Published online: 10 Sep 2016
 

Abstract

Background and aims: A new score for the histological severity of nonalcoholic fatty liver disease (NAFLD), called SAF (Steatosis, Activity and Fibrosis) has been developed. We aimed to evaluate the impact of this score on overall mortality.

Methods: We used data from 139 patients with biopsy-proven NAFLD. All biopsies were graded according to the SAF scoring system and disease severity was classified as mild, moderate or severe. Causes of death were extracted from a national, population-based register. A Cox regression model, adjusted for sex, body mass index (BMI) and diabetes mellitus type 2, was applied.

Results: At baseline 35 patients presented with mild or moderate disease respectively, and 69 patients with severe disease. During follow-up (median 25.3 years, range 1.7–40.8) 74 patients died, 11 in the mild group (31%), 18 in the moderate group (51%) and 45 in the severe group (65%), p = .002. Compared to patients with mild disease, patients with moderate disease did not have a significant increase in overall mortality (HR 1.83, 95%CI 0.89–3.77, p = .10). Patients with severe disease had a significant increase in mortality (HR 2.65, 95%CI 1.19–5.93, p = .017). However, when adjusting for fibrosis stage, significance was lost (HR 1.85, 95%CI 0.76–4.54, p = .18). NASH, defined as per the FLIP algorithm, was not associated with mortality compared to not having NASH (HR 1.46, 95%CI 0.74–2.90, p = .28).

Conclusions: After adjustment for fibrosis, the SAF score was not associated with increased mortality in NAFLD. This finding should be corroborated in larger cohorts with similar follow-up time.

Disclosure statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

Funding

HH was supported by grants from the Stockholm County Council (ALF projects 20140329 and 20150403) and from the Royal Swedish Academy of Sciences Foundations (project ME2015-0011).

PS was supported by grants from the Swedish Society of Medicine (Gastroenterology Fund), Ruth and Richard Julins Fund and the Stockholm City Council (ALF project 2015403).

RH was supported by grants from the Swedish Cancer Foundation and King Gustaf V:s and Queen Victorias Freemason’s Foundation.

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