Effects of roux-en-y gastric bypass and sleeve gastrectomy on non-alcoholic fatty liver disease: A 12-month follow-up study with paired liver biopsies

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Roux-en-Y gastric bypass (RYGB) improves, and can sometimes resolve, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) but data based on histologi-cal assessment for the efficacy of sleeve gastrectomy (SG) in resolving NAFLD are sparse. Conse-quently, we aimed to compare the efficacy of RYGB vs. SG on NAFLD 12 months after surgery. In a prospective cohort study, 40 patients with obesity underwent bariatric surgery (16 RYGB and 24 SG). During surgery, a liver biopsy was taken and repeated 12 months later. NAFLD severity was evaluated using the NAFLD Activity Score (NAS) and Kleiner Fibrosis score. RYGB and SG patients were comparable at baseline. Mean (standard deviation, SD) NAS was 3.3 (0.9) in RYGB and 3.1 (1.4) in SG (p = 0.560) with similar degrees of steatosis, inflammation, and ballooning. Two RYGB patients, and six SG patients, had NASH (p = 0.439). Twelve months after surgery, NAS was significantly and comparably (p = 0.241) reduced in both RYGB (−3.00 (95% CI −3.79–−2.21), p <0.001) and SG (−2.25 (95% CI −2.92–−1.59), p < 0.001) patients. RYGB patients had significantly more reduced (p = 0.007) liver steatosis (−0.91 (95% CI −1.47–−1.2) than SG patients (−0.33 (95% CI −0.54–−0.13) and greater improvement in the plasma lipid profile. Fibrosis declined non-significantly. NASH was resolved in seven of eight patients without a worsening of their fibrosis. RYGB and SG have similar beneficial effects on NAS and NASH without the worsening of fibrosis. RYGB is associated with a more pronounced reduction in liver steatosis.

OriginalsprogEngelsk
Artikelnummer3783
TidsskriftJournal of Clinical Medicine
Vol/bind10
Udgave nummer17
Antal sider12
ISSN2077-0383
DOI
StatusUdgivet - 2021

Bibliografisk note

Funding Information:
Julie Steen Pedersen, Marte Opseth Rygg and Flemming Bendtsen were supported by a Challenge Grant ?MicroBLiver? (grant number NNF15OC0016692) from the Novo Nordisk Foundation. Julie Steen Pedersen receives grants from Michaelsen Foundation (grant number 10-100012) and Aase and Ejnar Danielsen Foundation (grant number 19-10-0284). Nicolai J Wever Albrechtsen weas supported by the Novo Nordisk Foundation (NNF) Tandem Program (31526), NNF Project support in Endocrinology and Metabolism?Nordic Region (34250), and NNF Excellence Emerging Investigator Grant?Endocrinology and Metabolism (NNF19OC0055001). The authors wish to thank the MicroBLiver Consortium.

Funding Information:
Funding: Julie Steen Pedersen, Marte Opseth Rygg and Flemming Bendtsen were supported by a Challenge Grant “MicroBLiver” (grant number NNF15OC0016692) from the Novo Nordisk Foundation. Julie Steen Pedersen receives grants from Michaelsen Foundation (grant number 10-100012) and Aase and Ejnar Danielsen Foundation (grant number 19-10-0284). Nicolai J Wever Albrechtsen weas supported by the Novo Nordisk Foundation (NNF) Tandem Program (31526), NNF Project support in Endocrinology and Metabolism—Nordic Region (34250), and NNF Excellence Emerging Investigator Grant—Endocrinology and Metabolism (NNF19OC0055001).

Funding Information:
Conflicts of Interest: Julie Steen Pedersen, Marte Opseth Rygg, Nicolai J. Wever Albrechtsen and Flemming Bendtsen have received grants from Novo Nordisk. Sten Madsbad consults for and receives grants from Novo Nordisk. Lise Lotte Gluud consults for and receives grants from Novo Nordisk, Gilead and Alexion.

Publisher Copyright:
© 2021 by the authors. Li-censee MDPI, Basel, Switzerland.

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