ライフサイエンスコーパス: liver disease

1 abolic syndrome, such as non-alcoholic fatty liver disease.

2 f cancer or predisposing factors for chronic liver disease.

3 a survival benefit in patients with advanced liver disease.

4 nance imaging (MRI) in patients with chronic liver disease.

5 tic adults aged 18 to 79 years without known liver disease.

6 cohol consumption, and genetic risk of fatty liver disease.

7 the development of cardiomyopathy in severe liver disease.

8 as LTx-recipients or patients with end-stage liver disease.

9 ium-term survival of patients with end-stage liver disease.

10 trition is a major risk factor for end-stage liver disease.

11 important measure of the severity of chronic liver disease.

12 cohol use or any other identifiable cause of liver disease.

13 epatitis B virus (HBV) is a leading cause of liver disease.

14 duce the risk for NAFLD and related advanced liver disease.

15 Z genotype among persons without preexisting liver disease.

16 the increasing morbidity and mortality from liver disease.

17 lmark of human pediatric non-alcoholic fatty liver disease.

18 r CCI in patients with fatty and cryptogenic liver disease.

19 serious AEs can occur in those with advanced liver disease.

20 medications used in treatment of cholestatic liver disease.

21 ibody production associated with cholestatic liver disease.

22 and translational findings in the context of liver disease.

23 pulation with increasing prevalence of fatty liver disease.

24 isk factor for cirrhosis in individuals with liver disease.

25 with NAFLD and control participants without liver disease.

26 (NAFLD) is the most common pediatric chronic liver disease.

27 agnostic accuracy in patients with end-stage liver disease.

28 ld increase in the risk of developing severe liver disease.

29 by the risk of missing patients with severe liver disease.

30 sis and management of gestational alloimmune liver disease.

31 d with the development of nonalcoholic fatty liver disease.

32 ) was recently found to protect from chronic liver disease.

33 c steatosis assessment in nonalcoholic fatty liver disease.

34 is C (HCV) coinfected patients with advanced liver disease.

35 the economic burden associated with chronic liver disease.

36 ly examined patients with nonalcoholic fatty liver disease.

37 risk for developing advanced alcohol-related liver disease.

38 oagulation (AC) are understudied in advanced liver disease.

39 antioxidant therapy with vitamin E prevented liver disease.

40 iously been implicated in nonalcoholic fatty liver disease.

41 ubstantially increase the risk of developing liver disease.

42 to assess fibrosis in patients with chronic liver disease.

43 0% to improve features of nonalcoholic fatty liver diseases.

44 siRNAs) have revolutionized the treatment of liver diseases.

45 ntribute to development of acute and chronic liver diseases.

46 d function are also largely impacted by many liver diseases.

47 y used mainly in studies of lung, heart, and liver diseases.

48 Comorbidities included chronic liver disease, 12.8% (n=59), cancer, 11.7% (n=54), chron

49 t-time recipients with a model for end-stage liver disease 15-34, without primary biliary cirrhosis,

50 ing rates of obesity and non-alcoholic fatty liver disease(2-4).

51 r alcohol abuse; 2.37 (95% CI 1.53-3.68) for liver disease; 2.04 (95% CI 1.30-3.20) for kidney diseas

52 ] vs 12 [4.0%]; p=0.04), and moderate-severe liver disease (4 [3.3%] vs 1 [0.3%]; p=0.01).

53 hepatitis C (13.4%), and non-alcoholic fatty liver disease (5.7%).

54 H and disease activity by nonalcoholic fatty liver disease activity score (NAS) using the three imagi

55 282 significantly reduced nonalcoholic fatty liver disease activity score (NAS; -1.9; 95% confidence

56 a 2-point improvement in nonalcoholic fatty liver disease activity score without worsening of fibros

57 ant effect on fibrosis or nonalcoholic fatty liver disease activity score, and liver-related outcomes

58 Liver diseases affecting the mother and infant dyad may

59 Among HIV-infected, model of end-stage liver disease (aHR, 1.04; P < 0.001), body mass index <2

60 Alcoholic liver disease (ALD) accounts for 15%-30% of transplants

61 Alcohol-related liver disease (ALD) accounts for the majority of cirrhos

62 Alcohol-associated liver disease (ALD) is a common chronic liver disease wo

63 morbidity and mortality from alcohol-related liver disease (ALD) is increasing in the United States.

64 C virus (HCV) infection, and alcohol-related liver disease (ALD) listed for LT during 2004-2017.

65 comparison was performed using the alcoholic liver disease (ALD) transcriptomic public dataset.

66 a severe manifestation of alcohol-associated liver disease (ALD) with high mortality.

67 as an exercise mimetic in settings of fatty liver disease, an important finding given the compliance

68 As controls, 9 individuals without liver disease and 13 patients with mild primary biliary

69 rosis in mouse models of non-alcoholic fatty liver disease and advanced fibrosis, as well as to detec

70 of magnetic-resonance imaging for diagnosing liver disease and assessing liver health before liver tr

71 Chronic HBV infection is a major cause of liver disease and cancer worldwide.

72 erations correlated with model for end-stage liver disease and Child-Pugh scores and organ failure an

73 ansplantation were recurrence of the primary liver disease and cholangitis in 15 (33.3%) cases each.

74 -matched nontransplant patients with chronic liver disease and COVID-19 (n = 375), incidence of acute

75 increasing prevalence of nonalcoholic fatty liver disease and its aggressive form, nonalcoholic stea

76 ependent risk increase for incident advanced liver disease and malignancies.

77 mics and dysbiosis play an important role in liver disease and may represent targetable pathways to t

78 s of alanine transaminase (ALT) and clinical liver disease and mortality in 111,612 individuals from

79 disease (CVD) may increase the risk of fatty liver disease and other metabolic disorders.

80 ctive in HCV-HIV patients with decompensated liver disease and post-LT, with post-LT survival rates c

81 ore the relationship between the severity of liver disease and the degree of myocardial involvement.

82 liary cholangitis (PBC) is a rare autoimmune liver disease and the first line available treatment is

83 apies that aim to reverse nonalcoholic fatty liver disease and type-2 diabetes.

84 ion of the risk score with plasma markers of liver disease and with cirrhosis and HCC in 110,761 indi

85 er mechanistic studies in the progression of liver diseases and in the discovery of drugs for the tre

86 r iron excess is observed in several chronic liver diseases and is associated with the development of

87 idate to liver transplantation for alcoholic liver diseases and severe acute alcoholic hepatitis.

88 without HCC, 2,588 alcohol misusers with no liver disease, and 899 healthy controls.

89 ient demographics, clinical risk factors for liver disease, and access to specialty liver care.

90 creasing prevalence of obesity, nonalcoholic liver disease, and alcohol overuse worldwide.

91 iseases such as diabetes, nonalcoholic fatty liver disease, and anorexia-cachexia syndrome.

92 iovascular disease, diabetes mellitus, fatty liver disease, and cancer.

93 flicted deaths from suicide, alcohol-related liver disease, and drug overdose among young adults has

94 tients with advanced HCC, Child-Pugh class A liver disease, and ECOG PS 0-1.

95 s, liver transplant providers, patients with liver disease, and liver transplant recipients.

96 itis (PBC), a chronic cholestatic autoimmune liver disease, and the peripheral immune system remains

97 across the full range and nonalcoholic fatty liver disease are associated with cardiometabolic risk f

98 nic hepatitis B (CHB) and nonalcoholic fatty liver disease are increasingly observed together in clin

99 The pathogenetic mechanisms underlying the liver disease are not completely understood.

100 Liver disease as a result of chronic hepatitis C virus (

101 with individuals without obesity and without liver disease, as well as animal models with steatosis a

102 d to estimate hazard ratios (HRs) for severe liver disease at 5, 10, and a maximum follow-up time of

103 covariance, adjusted for model for end-stage liver disease at time of hospital admission, serum level

104 end-stage liver disease/model for end-stage liver disease at transplant for infants (29 versus 30; P

105 exercise program in patients with cirrhotic liver disease awaiting LT.

106 ed at older ages than individuals with other liver diseases, but the effect of age on liver transplan

107 hy that progresses to fibrosis and end-stage liver disease by 2 years of age.

108 on in type 2 diabetes and nonalcoholic fatty liver disease by reestablishing a conventional proinflam

109 he detection of compensated advanced chronic liver disease (cACLD) is very important, the new guideli

110 liver injury (DILI) is a necro-inflammatory liver disease caused by several drugs commonly used in c

111 clerosing cholangitis (PSC) is a cholestatic liver disease characterised by chronic inflammation and

112 Liver fibrosis, a common outcome of chronic liver disease characterized by excessive accumulation of

113 Sixty-eight participants with end-stage liver disease (Child-Turcotte-Pugh score >=7 and Model f

114 ate-wide variability in mortality rates from liver disease (cirrhosis + hepatocellular carcinoma), bu

115 LD, but the majority do not develop advanced liver disease: cirrhosis, hepatic decompensation, or hep

116 ther chronic diseases, patients with chronic liver disease (CLD) have significantly higher inpatient

117 Chronic liver disease (CLD) is usually asymptomatic but earlier

118 wine beverages doubled the risk for advanced liver disease compared to lifetime abstainers.

119 A GRS for fatty liver disease confers up to a 12-fold higher risk of cir

120 es of scoring systems for fatal and nonfatal liver disease, determine which scoring system has the hi

121 al therapies, for example, in the context of liver disease diagnosis.

122 nting for recipient sex, ethnicity, cause of liver disease, donor age, cold ischemia time, and waitin

123 In cholestatic liver diseases, ductular reactive (DR) cells extend into

124 Nonalcoholic fatty liver disease encompasses a spectrum of diseases ranging

125 End-stage liver disease (ESLD) is a major burden on public health,

126 Patients with end-stage liver disease (ESLD) suffer from a high symptom burden a

127 dence rates between HCV groups for end-stage liver disease (ESLD; including hepatocellular carcinoma

128 Despite uniform HCC Model for End-Stage Liver Disease exception across height and sex, shorter p

129 n to awarding additional Model for End-Stage Liver Disease exception points to these patients.

130 alcoholic cirrhosis, and nonalcoholic fatty liver disease, genetic factors that contribute to the HC

131 R) was estimated using the GFR assessment in liver disease (GRAIL) developed among patients with cirr

132 Liver tissues from patients with liver disease had increased expression of genes that def

133 Women with chronic liver disease have lower rates of hepatocellular carcino

134 on Category 83), 2.55 (2.35-2.77); end-stage liver disease (Hierarchical Condition Category 27), 2.53

135 95% CI: 1.72-6.92; P = 0.0005), and chronic liver disease (HR 4.36, 95% CI: 1.29-14.71; P = 0.018) w

136 betes, chronic kidney disease, and end-stage liver disease (HR = 1.2, 95% CI = 1.0-1.4 when 1 comorbi

137 y life environmental exposures contribute to liver disease in adulthood.

138 ring the Sox9 gene dosage on the severity of liver disease in an ALGS mouse model.

139 m the TONIC (Treatment of Nonalcoholic Fatty Liver Disease in Children) trial.

140 entive measures and treatments for end-stage liver disease in elderly patients.

141 dihydrocollidine diet, to induce cholestatic liver disease in germ-free mice and germ-free mice conve

142 9 expression in the liver and outcome of the liver disease in patients with ALGS.

143 The presence of pre-existing liver disease in patients with elevated LFTs on admissio

144 nt, pointing to a target in the treatment of liver disease in telomere-syndrome patients.

145 rdiac dysfunction in patients with end-stage liver disease in the absence of prior heart disease.

146 y bowel disease and cirrhosis, whereas other liver disease, including biliary stone disease (OR, 4.06

147 iver transplantation resulting from advanced liver disease, including bridging fibrosis, cirrhosis, a

148 ve mortality was 33.2% overall and 1.1% with liver disease, including primary liver cancer.

149 ole of these autoimmune responses in various liver diseases, including alcoholic hepatitis, autoimmun

150 uman cells that can be used to model complex liver diseases, including NASH.

151 l microbiome and the changes associated with liver disease into practice.

152 Liver disease is a leading cause of morbidity and mortal

153 Nonalcoholic fatty liver disease is a major risk factor for cardiometabolic

154 Although fibrocystic liver disease is an established ciliopathy phenotype, se

155 Liver disease is an important cause of morbidity and mor

156 The course of the liver disease is highly variable in ALGS.

157 oring the progression of non-alcoholic fatty liver disease is hindered by a lack of suitable non-inva

158 Alcohol-related liver disease is often undetected until irreversible lat

159 Alcohol-related liver disease is one of the most prevalent liver disease

160 Liver disease is prevalent in the United States, and as

161 Chronic liver disease is reaching epidemic proportions with the

162 Nonalcoholic fatty liver disease is the most prevalent liver disease worldw

163 rs protection from specific risk factors for liver disease is unclear.

164 CRT could lead to new therapies for lung and liver diseases linked to AAT deficiency.

165 dren aged younger than 12 years with chronic liver disease, listed for deceased donor livers January

166 We examined relationships of liver disease markers, including patatin-like phospholip

167 ious model consisting of Model for End-Stage Liver Disease (MELD) and LA at admission may predict inp

168 ease severity, using the Model for End-Stage Liver Disease (MELD) in 8387 French patients wait-listed

169 Our primary outcome was Model for End-Stage Liver Disease (MELD) score at waitlist removal for "too

170 .5, 6.9), and the median Model for End-Stage Liver Disease (MELD) score was 11.6 (9.4, 14.0).

171 Model for End-Stage Liver Disease (MELD) score-based liver transplant alloca

172 were younger; had lower Model for End-stage Liver Disease (MELD) scores, AFP levels, and neutrophil-

173 e Mayo Risk Score (MRS), Model for End-Stage Liver Disease (MELD), Model for End-Stage Liver Disease-

174 tivariate analysis, high Model for End-Stage Liver Disease (MELD; odds ratio [OR], 1.10; confidence i

175 he hypothesis that patients with cholestatic liver disease might benefit from UDCA with respect to pe

176 led to decreased median pediatric end-stage liver disease/model for end-stage liver disease at trans

177 er disease-related mortality and hotspots of liver disease mortality.

178 brosis scores were associated with increased liver disease mortality.

179 les were obtained from patients with chronic liver disease (n = 50) undergoing FibroScan (ultrasound

180 lcoholic liver disease was the main cause of liver disease (n = 51; 45%).

181 y, defined as decrease in nonalcoholic fatty liver disease (NAFLD) Activity Score >=2 points without

182 Nonalcoholic fatty liver disease (NAFLD) affects a quarter of the adult pop

183 metabolism is common in non-alcoholic fatty liver disease (NAFLD) and appears to also be associated

184 ted with human and rodent nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC)

185 nce), and the presence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (

186 The prevalence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (

187 aptured under the acronym nonalcoholic fatty liver disease (NAFLD) and provide suggestions on termino

188 contribution of ChREBP to nonalcoholic fatty liver disease (NAFLD) development in a mouse model for h

189 Nonalcoholic fatty liver disease (NAFLD) encompasses a range of conditions,

190 ns (n = 122,419), and the nonalcoholic fatty liver disease (NAFLD) fibrosis scores (NFS, n = 13,160).

191 dietary risk factors for nonalcoholic fatty liver disease (NAFLD) from population-based studies, par

192 o monitor key features of nonalcoholic fatty liver disease (NAFLD) in children that relate to improve

193 ndrial adaptation during non-alcoholic fatty liver disease (NAFLD) include remodeling of ketogenic fl

194 Non-alcoholic fatty liver disease (NAFLD) is a frequent condition in obese p

195 Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chronic live

196 Nonalcoholic fatty liver disease (NAFLD) is a leading etiology for chronic

197 ith HIV (PLWH), of which non-alcoholic fatty liver disease (NAFLD) is an increasingly recognised caus

198 HIV-uninfected patients, nonalcoholic fatty liver disease (NAFLD) is associated with incident metabo

199 Nonalcoholic fatty liver disease (NAFLD) is associated with obesity but als

200 Nonalcoholic fatty liver disease (NAFLD) is considered the next major healt

201 Non-alcoholic fatty liver disease (NAFLD) is highly prevalent and causes ser

202 The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide.

203 ss in the development of non-alcoholic fatty liver disease (NAFLD) is largely unexplored.

204 Nonalcoholic fatty liver disease (NAFLD) is now the most common liver condi

205 Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease,

206 Nonalcoholic fatty liver disease (NAFLD) is the most common pediatric chron

207 t least 4 hours using the nonalcoholic fatty liver disease (NAFLD) liver fat score and NAFLD fibrosis

208 In non-alcoholic fatty liver disease (NAFLD) patients and obese mice, occupancy

209 Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning worldwide

210 is a progressive form of Non-alcoholic fatty liver disease (NAFLD), a chronic liver disease with a si

211 with reduced severity of nonalcoholic fatty liver disease (NAFLD), based on histologic analysis, com

212 In nonalcoholic fatty liver disease (NAFLD), fibrosis is the most important fa

213 pment of type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), or cardiovascular disease.

214 abnormalities including non-alcoholic fatty liver disease (NAFLD).

215 sis during the pathogenesis of non-alcoholic liver disease (NAFLD).

216 uch information to assess nonalcoholic fatty liver disease (NAFLD).

217 n of advanced fibrosis in nonalcoholic fatty liver disease (NAFLD).

218 GI-58) mutations manifest nonalcoholic fatty liver disease (NAFLD).

219 or beta-cryptoxanthin in non-alcoholic fatty liver disease (NAFLD).

220 es in the development of non-alcoholic fatty liver disease (NAFLD).

221 ainst the development of non-alcoholic fatty liver disease (NAFLD).

222 er of diseases, including nonalcoholic fatty liver disease (NAFLD).

223 pularity in management of nonalcoholic fatty liver disease (NAFLD).

224 manifests in the liver as nonalcoholic fatty liver disease (NAFLD).

225 bolism and development of nonalcoholic fatty liver disease (NAFLD).

226 and promotes spontaneous non-alcoholic fatty liver disease (NAFLD).

227 atitis (n=19) or other chronic non-alcoholic liver diseases (NALD) (n=27).

228 orce cannot meet the demand of patients with liver disease nationwide, particularly in less densely p

229 he pathogenesis of renal fibrosis, alcoholic liver disease, non-alcoholic steatohepatitis, pulmonary

230 as high levels of ALP in blood can indicate liver disease or bone disorders.

231 nhibition by drugs can cause severe, chronic liver disease or drug-induced liver injury.

232 ) or after adjusting for Model for End-stage Liver Disease or Sequential Organ Failure Assessment.

233 ne-deficient diet causing nonalcoholic fatty liver disease or to Lieber DeCarli diet causing ethanol-

234 stroke, end-stage renal diseases, end-stage liver diseases, or death.

235 a modest increase in risk of incident severe liver disease outcomes (adjusted HR 1.20, 95% CI 1.12-1.

236 Studies were included that reported severe liver disease outcomes (defined as liver cirrhosis, comp

237 risk factors and their potential to predict liver disease outcomes in the general population at risk

238 SERPINA1) and key pathways involved in fatty liver disease pathobiology.

239 ow microbes and their products contribute to liver disease pathogenesis, putative microbial biomarker

240 Remarkably, in non-alcoholic fatty liver disease patients, hepatic expression of JMJD3, ATG

241 The current pediatric end-stage liver disease (PELD) score underestimates pediatric wait

242 =4.9, 95% CI: [4.8,5.1]), moderate or severe liver disease (PR=2.2 [2.0,2.4]), and chronic pulmonary

243 sitive and HIV-negative admissions were mild liver disease (PR=4.9, 95% CI: [4.8,5.1]), moderate or s

244 een participants died, 10 with decompensated liver disease pre-LT and three post-LT.

245 iabetic CHCpatients and might have a role in liver disease progression.

246 of progressive intestinal failure-associated liver disease, progressive loss of central vein access,

247 IT results, and PROs (Short Form-36, Chronic Liver Disease Questionnaire-NASH, EuroQol-5D, and Work P

248 ntify factors associated with variability in liver disease-related mortality and hotspots of liver di

249 strate significant intrastate differences in liver disease-related mortality, with more than 60% of t

250 or diabetes or with conditions such as fatty liver disease remains fragmented and is not linked to co

251 Biliary atresia (BA) is a severe pediatric liver disease resulting in necroinflammatory obliteratio

252 Controls had advanced liver disease, right ventricular (RV) systolic pressure

253 A pediatric end -stage liver disease score >=40, postoperative hospital stays,

254 cotte-Pugh score >=7 and Model for End-Stage Liver Disease score 6-29) were enrolled, 26 had hepatoce

255 nts transplanted, median model for end-stage liver disease score at LT was 7 ((interquartile range [I

256 to three groups based on Model for End-Stage Liver Disease score at transplant: lower-score (regions

257 cated by a higher median Model for End-Stage Liver Disease score, and associated with increased 90-da

258 ts, the weighting of the model for end-stage liver disease score, and the increased prevalence of non

259 ariate analysis adjusting for comorbidities, liver disease severity, and other factors including gast

260 ndently of classical risk factors, including liver disease severity.

261 ty is adjudicated by the Model for End Stage Liver Disease-Sodium (MELD-Na) score.

262 ge Liver Disease (MELD), Model for End-Stage Liver Disease-Sodium MELD-Na, and Child-Turcotte-Pugh (C

263 wever, patients with low Model for End-Stage Liver Disease-Sodium scores still suffer from liver-rela

264 xposure to TBT has been shown to cause fatty liver disease (steatosis), as well as increased adiposit

265 olism may prevent or slow the progression of liver diseases such as NASH.

266 l changes associated with nonalcoholic fatty liver disease, such as decay of bile canaliculi network

267 iocytes are the target of a group of chronic liver diseases termed the "cholangiopathies," in which c

268 Primary biliary cholangitis is an autoimmune liver disease that predominantly affects women.

269 In liver diseases that arise from dysregulated lipid metabo

270 g extrahepatic manifestations of cholestatic liver diseases, the mechanism underlying this phenomenon

271 periodontitis is epidemiologically linked to liver diseases, the question arises weather UDCA holds a

272 nificant dyslipidemia and nonalcoholic fatty liver disease; the diet has an especially strong effect

273 ho were transplanted for other etiologies of liver disease, there was no significant difference in gr

274 g evidence of a gut microbial basis for many liver diseases, therefore, better diagnostic, prognostic

275 cause endoplasmic reticulum (ER) stress and liver disease through a gain-of-function toxic mechanism

276 c diseases, which include nonalcoholic fatty liver diseases, through the gut-liver axis.

277 ts in the progression of non-alcoholic fatty liver disease to non-alcoholic steatohepatitis and fibro

278 n-alcoholic chronic liver failure from fatty liver disease to steatohepatitis are unavailable.

279 d 17 (15.1%) died (13 deaths were related to liver disease, two not).

280 Main exclusions were baseline clinical liver disease, viral hepatitis, ethanol intake >50 g/day

281 red with MR elastography in children without liver disease was 2.1 kPa (similar to that in adults).

282 Alcoholic liver disease was the main cause of liver disease (n = 5

283 ex (FIB-4), developed to predict fibrosis in liver disease, was used to identify patients with corona

284 Patients with advanced liver disease were at risk of treatment failure.

285 re renal (creatine clearance <=30 mL/min) or liver disease were included in this analysis (n=17 423).

286 aged 7-17.9 years without a known history of liver disease were recruited at four sites for a researc

287 is delta virus (HDV) infection causes severe liver disease which often leads to cirrhosis and hepatoc

288 ndings may also apply to non-alcoholic fatty liver disease, which shares similar pathological and met

289 RI identified patients with advanced chronic liver disease who are at increased risk for a first hepa

290 of the American Association for the Study of Liver Diseases who were eligible for treatment with TACE

291 l hepatitis or other known causes of chronic liver disease, who underwent liver biopsy for abnormal l

292 rove case finding for people at high risk of liver disease will allow for effective management to hel

293 holic fatty liver disease (NAFLD), a chronic liver disease with a significant unmet clinical need.

294 se (NAFLD) is a leading etiology for chronic liver disease with an immense public health impact and a

295 These mice spontaneously developed liver disease with hepatic steatosis, inflammation, and

296 ahepatic biliary atresia (BA) is a pediatric liver disease with no approved medical therapy.

297 tty liver disease (NAFLD) is the most common liver disease, with a worldwide prevalence of 25%.

298 ated liver disease (ALD) is a common chronic liver disease worldwide with high morbidity and mortalit

299 ic fatty liver disease is the most prevalent liver disease worldwide, affecting 20%-25% of the adult

300 isease (NAFLD) is a leading cause of chronic liver disease worldwide.

301 d liver disease is one of the most prevalent liver diseases worldwide and is the second most common i