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Copyright ©2012 Baishideng Publishing Group Co.
World J Gastroenterol. Nov 7, 2012; 18(41): 5839-5847
Published online Nov 7, 2012. doi: 10.3748/wjg.v18.i41.5839
Table 1 Summary of trials design and results
Ref.Study designInterventionPopulationOutcome measurementsResultsComments
Capanni et al[70]Open-labelOral administration of n-3 PUFA, 1-g capsule/d for 12 mo56 patients with NAFLD (42 subjects receiving therapy; 14 controls)AST, ALT, GGT, TG, FG, n-6/n-3, liver echo texture by US and liver perfusion by DPI↓AST (P = 0.003) and ALT (P = 0.002), ↓ GGT (P = 0.03), ↓ TG (P = 0.02) and FG (P = 0.02) in comparison with controls. Circulating arachidonate and n6:n3 ratio was reduced (P = 0.0002, and P = 0.0001 respectively) in treated patients. Improvement of liver echo texture (P = 0.0001), and increase of DPI (P = 0.001)Limits of this study are the absence of blinding and randomization, and the use for comparison of a self-selected small group consisting of those patients who had been declined entry to the treatment arm
Spadaro et al[72]Randomized; open-labelAHA diet + 2 g/d n-3 PUFA (group DP) vs AHA diet (group D) for 6 mo40 patients with NAFLD (group DP, n = 20; group D, n = 20)Liver fat assessed by abdominal US, ALT, AST, TNF-α serum levels, and HOMAIn DP group: ↓ ALT (P < 0.01), TG (P < 0.01), serum TNF-α (P < 0.05) and HOMA (IR) (P < 0.05). Complete fatty liver regression in 33.4% of patients, and an overall reduction in 50%; In the D group: no significant modification of laboratory tests; no patient achieved complete regression of fatty liver, whereas some amount of reduction occurred in 27.7% of patientsLimits of the study are lack of placebo, and the non blinding of participants and investigators
Zhu et al[74]RandomizedAHA diet + 2 g/d n-3 PUFA from seal oil (Group A) vs AHA diet + 2g of placebo (group B) for 6 mo144 patients with NAFLD and hyperlipidemia (group A = 72; group B = 72)Liver fat assessed by symptom scores, ALT and serum lipid levels after 8, 12, 16, and 24 wk; fatty liver assessed by US at weeks 12 and 24 after treatmentGroup A vs group B showed ↓ of total symptoms score, ALT, TG, LDL (P < 0.05); complete fatty liver regression in 19.7% vs 7.35% (P = 0.004); In both groups there was a tendency in improvement in AST, GGT, TCHO and HDL levels (P < 0.05)
Tanaka et al[77]Open labelEPA 2.7 g/d for 12 mo23 patients with biopsy proven NAFLDALT, FFA, plasma soluble TNF receptor 1 and 2 levels, and serum ferritin and thioredoxin levels, body weight, blood glucose, insulin, and adiponectin concentrations; fatty liver infiltration assessed by histology↓ ALT, AST, TG, TCHO, HOMA-IR, plasma thioredoxin; change in histological grade: steatosis: 2.4 (SD 0.5) vs 1.7 (SD 0.5); fibrosis: 1.7 (SD 1.1) vs 0.7 (SD 0.5); lobular inflammation: 2.1 (SD 0.7) vs 1.1 (SD 0.7); ballooning: 1.6 (SD 0.5) vs 0.9 (SD 0.4); NAS: 6.1 (SD 1.3) vs 3.7 (SD 1.4); Hepatic steatosis grade on the US changed from 2.1 ± 0.9 at baseline to 1.6 ± 1.1 after treatment (P = 0.004)Limits of the study are the absence of a control group and small sample size
Sofi et al[75]RandomizedDietary recommendation + 6.5 mL/d of olive oil enriched with n-3 PUFA (0.83 g n-3 PUFA, of which 0.47 g EPA and 0.24 g DHA) for 12 mo vs dietary recommendation alone11 patients with NAFLD assessed by US (intervention group, n = 6; control group, n = 5)Liver fat content assessed by B-mode US and DPI; liver enzymes, TG and adiponectin levelsIntervention group vs controls showed a ↓ of AST (P = 0.02), ALT (P = 0.03), GGT (P = 0.03), TG (P = 0.04) levels; ↑ of HDL (P = 0.03), adiponectin (P = 0.04). There was a significant (P = 0.02) improvement of DPI in the intervention group, while no change was observed in the control group. Improvement of liver steatosis on US in the intervention group (% of patients at T0 and T12): absent (from 0% to 16.7%); mild (from 16.7% to 50%); moderate (from 33% to 0%); severe (from 50% to 33%)
Nobili et al[78]RandomizedDHA (250 and 500 mg/d) vs placebo for 6 mo60 children with biopsy-proven NAFLD randomly assigned to receive DHA 250 mg/d (n = 20), DHA 500 mg/d (n = 20) or placebo (n = 20)Primary: change in liver fat content as detected by US; secondary: changes in ISI, ALT, TG and BMIDHA 250 mg vs placebo: odds of more severe vs less severe steatosis (OR = 0.01, robust 95% CI: 0.002 to 0.11, P < 0.001); ↑ of ISI (P < 0.01), ↓TG (P < 0.05); ALT and SDS of BMI; DHA 500 mg vs placebo: (OR = 0.04, 0.002 to 0.46; P = 0.01); ↑ of ISI (P < 0.01), ↓TG (P < 0.05); ALT and SDS of BMI; DHA 250 mg vs DHA 200 mg: NS
Vega et al[79]Open label9 g/d of fish oil for 8 wk22 patients with previous elevated liver fat on MRS (17 patients completed the trial)Liver fat content assessed by B-mode US and DPI; liver enzymes, TG and adiponectin levels↓ of plasma triglyceride level by 46% (P < 0.03), VLDL + IDL by 21% (P < 0.03), ApoB by 15% (P < 0.03). Liver fat content 7.9% pre-treatment; 8.0% after PUFA (NS)Causes of liver disease other than NAFLD were not excluded and alcohol intake was not reported. It is unclear whether study participants received any other interventions such as diet or lifestyle advice