ライフサイエンスコーパス: NASH

1 NASH FibroSure risk scores suggesting the development an

2 NASH had higher conjugated to unconjugated chenodeoxycho

3 NASH is a potential outcome of nonalcoholic fatty liver

4 NASH is a progressive disease that can lead to cirrhosis

5 NASH is strongly associated with obesity and the metabol

6 NASH markers remained decreased in M+G49 mice after PH,

7 NASH may be reversible, but it can also result in cirrho

8 NASH resolution occurred in 28% (derivation group) and 2

9 NASH was ameliorated in the M+G49 group, manifested by r

10 NASH was present in 54.5% RYGB and 51.5% SG patients (P

11 A total of 51 NAFL patients, 30 NASH patients, 31 nonalcoholic fatty liver disease patie

12 Of 86 patients (24 controls, 25 NAFL, and 37 NASH; mean age 51.8 years and body mass index 31.9 kg/m(

13 e (38, 8%) patients had NAFL and 33 (61, 7%) NASH.

14 MLK3-deficient mice fed a NASH-inducing diet had reduced concentrations of total p

15 WD induced a NASH phenotype in OLETFs characterized by hepatic fibros

16 loss in NAFLD, where 80% of subjects achieve NASH resolution at 1-year follow-up.

17 Yet, the link between plasma CatD to adult NASH was not examined.

18 Efforts to ameliorate NASH in lipodystrophies with pharmacologic agents have m

19 rbated nonalcoholic fatty liver disease- and NASH-related phenotypes in mice, including glucose metab

20 mice from developing OXPHOS dysfunction and NASH caused by a HFD.

21 16 to 2030 to forecast obesity estimates and NASH-related LT waitlist additions.

22 eater increase in INR in the whole group and NASH patients than SG.

23 WL for HCC in both the HCV and NASH populations increased in both the PI and DAA eras (

24 plasma BA profile in biopsy-proven NAFL and NASH and compared to controls and (2) related the plasma

25 dietary and genetic mouse models of NAFL and NASH and translated the results to humans by correlating

26 cated a decrease of Oscillospira in NAFL and NASH groups and increases of Ruminococcus, Blautia, and

27 from peripheral blood and livers of NAFL and NASH patients.

28 between patients and CTRLs but not NAFL and NASH.

29 tality and overall mortality among NAFLD and NASH were 0.77 per 1,000 (range, 0.33-1.77) and 11.77 pe

30 these processes impact the risk for NASH and NASH cirrhosis.

31 S as a novel therapeutic target for NASH and NASH-driven HCC.

32 emporal trend behind the rise in obesity and NASH-related additions to the LT waitlist in the United

33 ed a time lag between obesity prevalence and NASH-related waitlist additions.

34 iological mechanisms relating sarcopenia and NASH may include insulin resistance (IR) and increased i

35 x inter-relationships between sarcopenia and NASH.

36 iver biopsies of patients with steatosis and NASH compared to controls.

37 ive in patients with prediabetes or T2DM and NASH.

38 Based on these data, annual NASH-related waitlist additions are anticipated to incre

39 mately 20% of NAFLD cases were classified as NASH, increasing to 27% by 2030, a reflection of both di

40 e effectiveness of MSDC-0602 for attenuating NASH in a rodent model and suggest that targeting hepati

41 highlight a distinct pathophysiology between NASH in children and adults.

42 nite NASH compared to not NASH or borderline NASH in multivariable analysis (odds ratio = 1.20, 95% c

43 ic steatohepatitis-hepatocellular carcinoma (NASH-HCC) murine model and compared results for both sex

44 secondary BAs (both P < 0.05) characterized NASH.

45 to our previous observations with childhood NASH, we observed increased levels of plasma CatD in pat

46 enterohepatic disorders such as cholestasis, NASH, and inflammatory bowel disease.

47 acrovesicular steatosis observed in clinical NASH and/or rodent NASH-models.

48 n between moderate alcohol use and decreased NASH and fibrosis; however, heavy episodic drinking may

49 le, mean age 47.7 years), 58.0% had definite NASH, 55.5% had mild/no fibrosis (stage 0-1), and 44.4%

50 tor 1 had a strong association with definite NASH compared to not NASH or borderline NASH in multivar

51 , individuals with hepatic steatosis develop NASH.

52 showed that only WT fed FF (WT-FF) developed NASH and fibrosis.

53 SPIO MR imaging can be used to differentiate NASH from simple steatosis.

54 perating characteristic curve to distinguish NASH from simple steatosis was 0.87 (95% confidence inte

55 es inflammation and fibrosis in experimental NASH.

56 -deficient (MCD) diet to induce experimental NASH and underwent MR imaging with MPO-Gd.

57 6 for NASH vs simple steatosis; P < .001 for NASH vs healthy control subjects).

58 ubjects, 72.2 sec(-1) +/- 22.0; P = .006 for NASH vs simple steatosis; P < .001 for NASH vs healthy c

59 ed results from animal studies (mean CNR for NASH vs control patients, 2.61 [95% CI: 1.48, 3.74] vs 1

60 The relevance of our findings for NASH pathogenesis was highlighted by the normalization o

61 oject a marked increase in demand for LT for NASH given population obesity trends.

62 inistration recently endorsed end points for NASH therapy.

63 development and regression is promising for NASH diagnosis.

64 improve renal outcomes in SLK recipients for NASH.

65 ation of these processes impact the risk for NASH and NASH cirrhosis.

66 ies RANTES as a novel therapeutic target for NASH and NASH-driven HCC.

67 y it as a potential new molecular target for NASH therapy.

68 However, an optimum therapy for NASH is yet to be established, mandating more in-depth i

69 All surviving patients transplanted for NASH at the authors' institution had transient elastogra

70 waitlist or receiving liver transplants for NASH or ALD are increasing, despite different relative b

71 be an effective but expensive treatment for NASH.

72 ease in percentage of patients with CLF from NASH), and hepatocellular carcinoma (HCC) (decreases in

73 ular MR imaging of liver biopsy samples from NASH and control patients confirmed results from animal

74 nd markers that differentiate steatosis from NASH in each subtype.

75 nited States and make projections for future NASH burden on the LT waitlist.

76 The odds of having NASH were significantly higher in those with prediabetes

77 stically significant association of a higher NASH FibroSure hepatic fibrosis score in women (Spearman

78 However, NASH encompasses the spectrum of wound-healing responses

79 veloped steatohepatitis reminiscent of human NASH with ballooning hepatocytes and significant liver f

80 podystrophy-associated hypertriglyceridemia, NASH and diabetes.

81 ctivity score >/=5 may be useful to identify NASH resolution in patients under lifestyle intervention

82 ur objectives in this study were to identify NASH-associated ligands for TLR9, establish the cellular

83 To evaluate if NASH FibroSure, a noninvasive test for nonalcoholic stea

84 ging agent, holds special promise in imaging NASH and other metabolic syndromes, to monitor disease p

85 In NASH, lower levels of Oscillospira were associated with

86 R9, but how the TLR9 pathway is activated in NASH is not clear.

87 aim was to evaluate the effects of ANDRO in NASH and its influence on inflammasome activation in thi

88 Conversely, CNR remained at baseline in NASH mice imaged with gadopentetate dimeglumine and in M

89 among CD4(+) T cells of peripheral blood in NASH, and to a lesser degree in NAFL.

90 Conversely, WL for DC in NASH increased by 41% in the PI era (P < 0.001) and 81%

91 eases of Ruminococcus, Blautia, and Dorea in NASH patients compared to CTRLs.

92 mmune modulatory hepato-protective effect in NASH model.

93 ith advancing disease stage (e.g., higher in NASH than nonalcoholic fatty liver, positive correlation

94 ted primary BAs were significantly higher in NASH versus NAFL (P = 0.047) and versus controls (P < 0.

95 results indicate a function for IBTKalpha in NASH that links autophagy with activation of the UPR.

96 ity rates and in the anticipated increase in NASH-related waitlist additions (P < 0.01).

97 des abundance was significantly increased in NASH and F>/=2 patients, whereas Prevotella abundance wa

98 ocytes and macrophage-driven inflammation in NASH are uncharted.

99 d as a potential therapeutic intervention in NASH patients.

100 trocyte elevated gene-1(AEG-1)/metadherin in NASH using a transgenic mouse with hepatocyte-specific o

101 At 12 months in NASH group, SG induced significant improvement in aspart

102 cells and IL-17 expression were observed in NASH mice and patients, respectively.

103 he NLRP3 inflammasome, a relevant pathway in NASH.

104 key metabolic and inflammatory phenotypes in NASH.

105 tion, and mean annual rate of progression in NASH were 40.76% (95% CI: 34.69-47.13) and 0.09 (95% CI:

106 ed risks for fibrotic disease progression in NASH, and plasma lumican FSR correlates with hepatic col

107 oxylesterase 2 (CES2) is markedly reduced in NASH patients, diabetic db/db mice, and high-fat diet (H

108 d oxidative damage in pericentral regions in NASH.

109 this study demonstrates that hepatic scar in NASH is actively remodeled even in advanced fibrosis, a

110 To study antioxidant status in NASH non-invasively, we applied the redox probe hyperpol

111 ession of liver injury to steatohepatitis in NASH produced by high-fat feeding during development but

112 to the regulation of hepatocyte viability in NASH.

113 o, the vascular response by FMD was worse in NASH as compared with NAFL.

114 artial to complete loss of lipid zonation in NASH.

115 esized that a western diet (WD) would induce NASH in the Otsuka Long-Evans Tokushima Fatty (OLETF) ra

116 tion act in concert to mediate AEG-1-induced NASH.

117 In the diet-induced NASH model, an increased CNR was also found compared wit

118 -/-) mice are protected against diet-induced NASH, in an obesity-independent manner.

119 e protected from high-fat diet (HFD)-induced NASH.

120 provided marked protection from HFD-induced NASH in WT mice.

121 led to complete resolution of the WD-induced NASH phenotype, both independently benefitted liver fibr

122 adopentetate dimeglumine and in MPO knockout NASH mice with MPO-Gd, which proves specificity of MPO-G

123 that promotes tissue integrity and limiting NASH progression to fibrosis.

124 and cost-effectiveness of surgery to manage NASH.

125 In mice, NASH development in response to a high-fat diet required

126 olved in the inflammatory response in murine NASH and the extent to which inhibition of the chemotact

127 ated sterile inflammatory response in murine NASH.

128 e no significant differences among the NAFL, NASH, and obese groups.

129 microbiota signatures of NAFL onset and NAFL-NASH progression, respectively.

130 to affect both insulin sensitivity and NAFLD/NASH pathogenesis at multiple levels, and these approach

131 hepatic cholesterol in human non-obese NAFLD/NASH patients.

132 with NASH (n = 48), simple steatosis but no NASH (n = 11), and healthy controls (n = 23), we discove

133 The factors that determine whether or not NASH progresses to cirrhosis are also unclear.

134 sociation with definite NASH compared to not NASH or borderline NASH in multivariable analysis (odds

135 ity was highest in CTRLs, followed by obese, NASH, and NAFL patients; and beta-diversity distinguishe

136 ch can progress to cirrhosis in up to 20% of NASH patients.

137 ecific effects of BAs on specific aspects of NASH.

138 ded to reduce the projected future burden of NASH.

139 This review summarizes key components of NASH pathogenesis and discusses how inherent and acquire

140 ns that interact with ASK1 in the context of NASH, we identified the deubiquitinase tumor necrosis fa

141 thways that contribute to the development of NASH and NAFLD and selection of the most applicable mous

142 The development of NASH in animal models requires intact TLR9, but how the

143 n of MPC2 were protected from development of NASH on this diet.

144 e TLR9 antagonist blocked the development of NASH when given prophylactically and therapeutically.

145 improvement in the histological features of NASH that coincided with alterations in markers of hepat

146 and correlated with histological features of NASH; these observations provide the foundation for futu

147 G-1 overexpression was observed in livers of NASH patients and wild-type (WT) mice that developed ste

148 We review the pathogenic mechanisms of NASH and therapeutic options, as well as strategies that

149 search studies have elucidated mechanisms of NASH pathogenesis, which could lead to therapeutic targe

150 Using a murine model of NASH, we demonstrate that DX5(+)NKp46(+) NK cells are in

151 aKtide was administered to a murine model of NASH: the C57Bl6 mouse fed a "western" diet containing h

152 in both mouse and nonhuman primate models of NASH substantially blocked the onset and progression of

153 In animal models of NASH, particularly the methionine-choline deficient (MCD

154 nificantly increased 44.9% and the number of NASH-related annual waitlist additions increased from 39

155 se from 2000 to 2014 to obtain the number of NASH-related LT waitlist additions.

156 ASK1 hyperactivation in the pathogenesis of NASH and identify it as a potential new molecular target

157 stigation into the molecular pathogenesis of NASH to identify novel regulatory molecules and develop

158 epts that are central to the pathogenesis of NASH.

159 43; P < 0.01) were independent predictors of NASH resolution.

160 The prevalence of NASH was higher in those with type 2 diabetes (43.2%) co

161 ance of lipid peroxidation in progression of NASH beyond simple steatosis.

162 targets that may prevent the progression of NASH to fibrosis.

163 ule regulating initiation and progression of NASH.

164 ercentage points]) and 51% had resolution of NASH (treatment difference, 32 percentage points [CI, 13

165 The primary outcome was resolution of NASH without fibrosis worsening, using protocol-defined

166 The reversal of NASH with no evidence of progression to advanced fibrosi

167 re linked to the pathogenesis and therapy of NASH.

168 y elevated expression in the liver tissue of NASH patients.

169 st-line recommendations for the treatment of NASH.

170 tiveness of the pharmacological treatment of NASH.

171 like peptide-1/glucagon receptor agonist, on NASH and hepatic regeneration.

172 d into two groups by the presence of NAFL or NASH.

173 dergoing liver biopsy for suspected NAFLD or NASH, or during liver or bariatric surgeries.

174 le and noninvasive scoring system to predict NASH resolution without fibrosis worsening after 1 year

175 15) to 100.9 million (2030), while prevalent NASH cases will increase 63% from 16.52 million to 27.00

176 ) cells play an important role in preventing NASH progression to fibrosis by regulating M1/M2 polariz

177 rmed in 68 of 69 patients with biopsy-proved NASH (37 boys and 31 girls; mean age, 12.6 years +/- 2.4

178 ) with prediabetes or T2DM and biopsy-proven NASH were recruited from the general population and outp

179 Recently, NASH has increased as an indication for LT in this age g

180 recurrent NAFLD, whereas 41.2% had recurrent NASH.

181 Mvarphi and NK cells contributes to regulate NASH progression to fibrosis.

182 ld decrease hypertriglyceridemia and reverse NASH and diabetes in a mouse model (fatless AZIP/F-1 mic

183 CRMP treatment also reversed NASH as reflected by reductions in plasma aspartate amin

184 osis observed in clinical NASH and/or rodent NASH-models.

185 cholesterol for 24 weeks developed a severe NASH with fibrosis phenotype.

186 ate between simple steatosis and more severe NASH, based on a set of short-chain TAGs and FFAs.

187 Alb/AEG-1 mice developed spontaneous NASH whereas AEG-1(DeltaHEP) mice were protected from hi

188 NASH develop non-alchoholic steatohepatitis (NASH), histologically defined by lobular and portal infl

189 sterol causes non-alcoholic steatohepatitis (NASH) and fibrosis.

190 o progress to non-alcoholic steatohepatitis (NASH) and NAFLD-related fibrosis or cirrhosis in these p

191 atosis but no non-alcoholic steatohepatitis (NASH) lesions were found.

192 ent models of non-alcoholic steatohepatitis (NASH) that resemble the human condition are limited.

193 ease (NAFLD), non-alcoholic steatohepatitis (NASH), hereditary dyslipidaemia, or cryptogenic cirrhosi

194 imal model of non-alcoholic steatohepatitis (NASH).

195 udes fatty liver (NAFL) and steatohepatitis (NASH), which can progress to cirrhosis in up to 20% of N

196 Nonalcoholic steatohepatitis (NASH) affects 2%-3% of the US population and is expected

197 Nonalcoholic steatohepatitis (NASH) affects 3%-5% of the U.S. population, having sever

198 progression of nonalcoholic steatohepatitis (NASH) and a promising target for treatment of the condit

199 patients with nonalcoholic steatohepatitis (NASH) and fibrosis are at the greatest risk of progressi

200 asive test for nonalcoholic steatohepatitis (NASH) and hepatic fibrosis, can be used for patients wit

201 lic defects of nonalcoholic steatohepatitis (NASH) and prediabetes or type 2 diabetes mellitus (T2DM)

202 and resulting nonalcoholic steatohepatitis (NASH) are highly prevalent in the United States, where t

203 developmental nonalcoholic steatohepatitis (NASH) by feeding a high polyunsaturated fat liquid diet

204 e apoptosis in nonalcoholic steatohepatitis (NASH) can lead to fibrosis and cirrhosis, which permanen

205 Nonalcoholic steatohepatitis (NASH) cirrhosis is the fastest growing indication for li

206 nrolled in the Nonalcoholic Steatohepatitis (NASH) Clinical Research Network.

207 Nonalcoholic steatohepatitis (NASH) has become a major cause of cirrhosis and liver-re

208 biopsy-proven nonalcoholic steatohepatitis (NASH) in a hospital cohort of individuals undergoing gas

209 in adults with nonalcoholic steatohepatitis (NASH) in a multi-center study, using central histology a

210 NAFLD and nonalcoholic steatohepatitis (NASH) in AYAs often go unrecognized and, if untreated, c

211 Nonalcoholic steatohepatitis (NASH) is a necro-inflammatory response that ensues when

212 Nonalcoholic steatohepatitis (NASH) is an inflammatory lipotoxic disorder, but how inf

213 Because nonalcoholic steatohepatitis (NASH) is associated with impaired liver regeneration, we

214 Therapy for nonalcoholic steatohepatitis (NASH) is limited.

215 Nonalcoholic steatohepatitis (NASH) is the most common liver disease in industrialized

216 Nonalcoholic steatohepatitis (NASH) is the most prevalent cause of chronic liver disea

217 PO activity in nonalcoholic steatohepatitis (NASH) mouse models and human liver biopsy samples.

218 se (NAFLD) and nonalcoholic steatohepatitis (NASH) patients.

219 ced liver fat, nonalcoholic steatohepatitis (NASH) remission, and also reduction of fibrosis.

220 thod to assess nonalcoholic steatohepatitis (NASH) resolution after therapeutic interventions.

221 isease (NAFLD)/nonalcoholic steatohepatitis (NASH) was found in CHIP(-/-)-mice over the first 8-9-mon

222 rus (HBV), and nonalcoholic steatohepatitis (NASH) were identified.

223 early signs of nonalcoholic steatohepatitis (NASH) when challenged with a lipogenic, high-fat, high-s

224 ggressive form nonalcoholic steatohepatitis (NASH) will require novel therapeutic approaches to preve

225 increasing in nonalcoholic steatohepatitis (NASH) with good post-transplant outcomes.

226 r to NAFLD and nonalcoholic steatohepatitis (NASH) without changes to body weight or fat pad weights.

227 patients with nonalcoholic steatohepatitis (NASH), 27 patients with NAFLD, 15 healthy obese individu

228 Nonalcoholic steatohepatitis (NASH), a clinically aggressive variant of nonalcoholic f

229 cy in treating nonalcoholic steatohepatitis (NASH), but their widespread use is constrained by dose-l

230 ver [NAFL]) to nonalcoholic steatohepatitis (NASH), cirrhosis, and cancer.

231 to progressive nonalcoholic steatohepatitis (NASH), fibrosis, and ultimately hepatocellular carcinoma

232 liver (NAFL), nonalcoholic steatohepatitis (NASH), or obesity and 54 healthy controls (CTRLs), match

233 pathologies is nonalcoholic steatohepatitis (NASH), which is associated with induction of the unfolde

234 D will develop nonalcoholic steatohepatitis (NASH), which is associated with progression to cirrhosis

235 ey features of nonalcoholic steatohepatitis (NASH)-driven hepatocellular carcinoma (HCC), including s

236 n resulting in nonalcoholic steatohepatitis (NASH).

237 steatosis and nonalcoholic steatohepatitis (NASH).

238 olescents with nonalcoholic steatohepatitis (NASH).

239 sk factors for nonalcoholic steatohepatitis (NASH).

240 urine model of nonalcoholic steatohepatitis (NASH).

241 patients with nonalcoholic steatohepatitis (NASH).

242 s of NAFLD and nonalcoholic steatohepatitis (NASH).

243 ver (NAFL) and nonalcoholic steatohepatitis (NASH).

244 progresses to nonalcoholic steatohepatitis (NASH).

245 fatty liver or nonalcoholic steatohepatitis (NASH).

246 diabetes, and nonalcoholic steatohepatitis (NASH).

247 y in patients with NAFLD or steatohepatitis (NASH) may impair liver function.

248 cirrhosis from nonalcoholic steatohepatitis [NASH]), CLF (decreases in percentages of patients with C

249 stitution cohort, these results suggest that NASH FibroSure may be used, especially among female pati

250 The NASH FibroSure test can be used to monitor changes in fi

251 The NASH is the most rapidly growing indication for SLK tran

252 with biopsy-confirmed NAFLD enrolled in the NASH Clinical Research Network.

253 We used the NASH Clinical Research Network system to score the histo

254 ent of eNOS phosphorylation in comparison to NASH (p < 0.01).

255 NAFL does not inevitably lead to NASH because NAFL is a heterogeneous condition.

256 NAFL to NASH progression is marked by an increased frequency of

257 In hepatic tissue, NAFL to NASH progression was marked by an increase in IL-17(+) c

258 wenty percent of cases progress from NAFL to NASH.

259 nd Genomes pathways significantly related to NASH and fibrosis F>/=2 were mostly related to carbohydr

260 ssociated with progression from steatosis to NASH in liver biopsies.

261 sms that combine to define the transition to NASH and progressive disease are complex, and consequent

262 acological therapy currently exists to treat NASH.

263 he promise of bariatric surgery for treating NASH and underscore the need for clinical trials in this

264 0602) would retain its efficacy for treating NASH in a rodent model.

265 ing treatment with MTX, 69 (53.5%) underwent NASH FibroSure testing prior to starting MTX; 19 of thos

266 ith psoriasis treated with MTX who underwent NASH FibroSure testing between January 1, 2007, and Dece

267 Among the 107 patients who underwent NASH FibroSure testing during MTX therapy, the cumulativ

268 mean [SD] age, 83.3 [13.5] years) underwent NASH FibroSure testing during MTX therapy and were eligi

269 0/F1 fibrosis stage at liver biopsy (10 with NASH), and 27 patients had significant F>/=2 fibrosis (2

270 AFLD (353 with simple steatosis and 182 with NASH) and compared them with serum metabolomes of mice.

271 ents had significant F>/=2 fibrosis (25 with NASH).

272 We collected data from 113 adults with NASH participating in a multi-center, randomized, double

273 2 randomized controlled trial of adults with NASH, PDFF estimated by MRI scanners of different field

274 Bacteroides as independently associated with NASH and Ruminococcus with significant fibrosis.

275 enzyme, cathepsin D (CatD), in children with NASH compared to children without NASH.

276 observation that plasma CatD correlated with NASH development and regression is promising for NASH di

277 on its chromosomal location, correlated with NASH grade (r = 0.51, P = 8.11 x 10(-7) ), lobular infla

278 hether plasma CatD in adults correlates with NASH development and regression.

279 As in 82 liver samples from individuals with NASH (n = 48), simple steatosis but no NASH (n = 11), an

280 of the ROCK1 inhibitor fasudil to mice with NASH reduced serum levels of EVs; this reduction was ass

281 phase 2b and phase 3 trials in patients with NASH and early stage fibrosis.

282 novel therapeutic approach for patients with NASH and particularly those requiring PH.

283 ase 2 human clinical trials in patients with NASH and PBC.

284 ss the impact of sarcopenia in patients with NASH and therapeutic options for the management of sarco

285 Patients with NASH are at increased risk for cirrhosis and hepatocellu

286 eased levels of plasma CatD in patients with NASH compared to adults without hepatic inflammation.

287 ated that plasma from mice and patients with NASH contains high levels of mitochondrial DNA (mtDNA) a

288 Approximately one-third of patients with NASH develop non-alchoholic steatohepatitis (NASH), hist

289 markers that could distinguish patients with NASH from patients with simple steatosis for each subtyp

290 whether these can distinguish patients with NASH from patients with simple steatosis.

291 Patients with NASH had a significantly lower DeltaR2* 72 hours after U

292 s that hepatic USPIO uptake in patients with NASH is decreased and that USPIO MR imaging can be used

293 Patients with NASH resolution after receiving elafibranor 120 mg had r

294 Patients with NASH undergoing RYGB are more susceptible to early trans

295 ean +/- standard deviation for patients with NASH, 37.0 sec(-1) +/- 16.1; patients with simple steato

296 e and cost-effective for obese patients with NASH, regardless of fibrosis stage; in overweight patien

297 developed for the treatment of patients with NASH.

298 d a small increase in HCC among persons with NASH).

299 ldren with NASH compared to children without NASH.

300 fibrosis stages compared with those without NASH resolution (mean reduction of 0.65 +/- 0.61 in resp