Posters
Arab, JP, Baeza, N, Diaz, LA, Idalsoaga, FJ, Arraez, DM, Ventura-Cots, M, Zhang, W, Ahn, J, Simonetto, DA, Mehta, T, Stefanescu, H, Horhat, A, Bumbu, A, Dunn, W, Attar, BM, Agrawal, R, Cabezas, J, Parker, R, Sans, MP, Pastor, GS, Sarin, SK, Maiwall, R, Jalal, PK, Abdulsada, S, De La Tijera, MH, Kulkarni, AV, Salazar, PG, Skladany, L, Bystrianska, N, Gonzalez, VEP, Clemente, A, Rincon, D, Haider, T, Cairo, F, Cohelo, MD, Romero, G, Pollarsky, F, Restrepo, JC, Rendon, LGT, Yaquich, P, Mendizabal, M, Garrido, ML, Marciano, S, Bessone, FO, Marcelo, JS, Piombino, D, Dirchwolf, M, Arancibia, JP, Altamirano, J, Kim, W, Araujo, RC, Duarte-Rojo, A, Blasco, VMV, Rautou, PE, Zamarripa, F, Aldo, T, Lucey, MR, Mathurin, P, Garcia-Tsao, G, Gonzalez, JA, Verna, BC, Brown, RS, Roblero, JP, Abraldes, JG, Arrese, M, Shah, V, Kamath, PS, Singal, AK, Bataller, R
Abstract
Background: Retrospective cross‐sectional studies link sarcopenia and myosteatosis with non‐alcoholic fatty liver disease (NAFLD) stages. In the present prospective study, we aimed at clarifying the dynamic relationship between sarcopenia, myosteatosis and NAFLD severity. Methods: A cohort of 48 obese patients were stratified according to NAFLD severity, evaluated with transient elastography (TE) derived steatosis and stiffness measurements. Skeletal muscle mass index (SMI) and fat index (SMFI; a surrogate of myosteatosis) were evaluated in whole muscle at the third lumbar vertebrae (L3) using the gold standard computed tomography (CT) scan. After baseline assessment (M0), patients were assigned to a dietary regimen supplemented with inulin or maltodextrin (16g/day) and muscles and liver were re‐evaluated after 3 months (M3). Results: All patients had NAFLD evaluated by TE. Sarcopenia was uncommon in those patients (4/48, 8.3%). SMFI was higher in patients with high liver stiffness (compatible with liver fibrosis) than in the others (640.6±114.3 cm2/HU vs 507.9±103.0 cm2/HU, p<0.001) (Fig. 1a). In multivariate analysis, SMFI, but not SMI, was robustly associated with fibrosis even when adjusted for multiple confounders (all p<0.05). After dietary regimen (n=35), there was no liver stiffness improvement when patients were stratified according to weight loss, treatment group allocation, liver steatosis decrease or muscle mass increase. Interestingly, only patients that decreased SMFI (regardless of intervention) had decreased liver stiffness (M0 = 6.36 kPa ± 2.15 vs M3= 5.55 kPa ± 1.97, ‐12.7 %, p=0.04) (Fig. 1b). Conclusion: High SMFI (indicative of myosteatosis), but not sarcopenia, is strongly and independently associated with high liver stiffness in obese NAFLD patients. A significant decrease in liver stiffness is observed only in patients with reduced myosteatosis, following a 3‐month intervention. The potential role of myosteatosis as an independent contributor to liver disease progression and perhaps as a novel therapeutic target in NAFLD should be investigated.