ライフサイエンスコーパス: cholestasis

1 iary proliferation and liver fibrosis during cholestasis.

2 te in the promotion of liver fibrosis during cholestasis.

3 ansplant surgical approaches to intrahepatic cholestasis.

4 e contribution of TRPC5 in a murine model of cholestasis.

5 ormly, result in improvement of pruritus and cholestasis.

6 le in subepithelial fibrosis observed during cholestasis.

7 in nonraft (low cholesterol) microdomains in cholestasis.

8 activity decline in 17alpha-ethinylestradiol cholestasis.

9 that inhibit the LKB1/AMPK pathway result in cholestasis.

10 hospholipid "toxic" bile causing progressive cholestasis.

11 ut promoting biliary cell paucity and lethal cholestasis.

12 lated by proliferating cholangiocytes during cholestasis.

13 ans, which is characterized by a canalicular cholestasis.

14 normalities of liver tests, including severe cholestasis.

15 (Mdr2KO) mice as a model of chronic hepatic cholestasis.

16 accelerated liver fibrosis was attributed to cholestasis.

17 thereby regulating hepatocarcinogenesis and cholestasis.

18 is, particularly as a consequence of chronic cholestasis.

19 p2) from the canalicular membrane leading to cholestasis.

20 e, acceleration of hepatocarcinogenesis, and cholestasis.

21 tional regulation of SHP in estrogen-induced cholestasis.

22 much smaller than that shown in EE2-induced cholestasis.

23 de production, hepatic steatosis and biliary cholestasis.

24 tial for neutrophil-mediated liver injury in cholestasis.

25 t soluble vitamin malabsorption with minimal cholestasis.

26 ches for patients suffering from pruritus in cholestasis.

27 hepatic bile ducts that presents as neonatal cholestasis.

28 ruritus and discuss pruritogen candidates in cholestasis.

29 nockout (Mdr2KO) mice, a recognized model of cholestasis.

30 ld be discussed in MVID patients with severe cholestasis.

31 itate liver injury under conditions favoring cholestasis.

32 te formation, and hemorrhage than those with cholestasis.

33 and its downstream effectors in E17G-induced cholestasis.

34 aping of bile acid pool in a rodent model of cholestasis.

35 the role of the SP/NK1R axis during chronic cholestasis.

36 to treat bile acid-related diseases such as cholestasis.

37 genes in normal liver and during obstructive cholestasis.

38 ung disease, intraventricular hemorrhage, or cholestasis.

39 iver of p38alpha-deficient mice upon chronic cholestasis.

40 r IL-17A in neutrophilic inflammation during cholestasis.

41 and female sex were associated with chronic cholestasis.

42 espond to Charcot-Gombault necrosis in human cholestasis.

43 ow cholangiocytes contribute to this form of cholestasis.

44 lic hepatitis (AH), often are accompanied by cholestasis.

45 d hepatic fibrosis in the Mdr2(-/-) model of cholestasis.

46 ine the biological relevance of SIRT1 during cholestasis.

47 d generally did not correlate with degree of cholestasis.

48 ression is increased during human and murine cholestasis.

49 n Fut2(-/-)(high) mice were not explained by cholestasis.

50 ndrome (ALGS), 16 with familial intrahepatic cholestasis-1 (FIC1), 18 with bile salt export pump (BSE

51 onic hepatitis (14%), acute (9%) and chronic cholestasis (10%), and cholestatic hepatitis (29%).

52 Patients with chronic cholestasis (17%) had a reduced 5-y survival rate compar

53 t to portal veins developed mild to moderate cholestasis 2-6 weeks after IRE.

54 for transient abnormal LFTs was drug-induced cholestasis (34.1%), whereas fatty liver was the most fr

55 rate compared with patients without chronic cholestasis (38% and 62%, respectively).

56 During PN, liver histology weighted with cholestasis (38% of patients on PN versus 0% of patients

57 icacy of nontransplant surgery for pediatric cholestasis, 58 clinically diagnosed children, including

58 modulating BSEP activity in estrogen-induced cholestasis, a novel finding that might help us to bette

59 During cholestasis, accumulation of conjugated bile acids may o

60 Cholestasis activates bile acid receptor farnesoid X rec

61 tified, with 76% demonstrating resolution of cholestasis after FO therapy.

62 , tacrolimus use, and biochemical markers of cholestasis after liver transplantation are associated w

63 hosis because of PNALD who had resolution of cholestasis after treatment with FO from 2004 to 2012.

64 Interestingly, estrogen-induced cholestasis also led to increased recruitment of estroge

65 EE2 at a low dose (that does not cause cholestasis) also increased SHP (by approximately 50%) a

66 treated with FO, 86% achieved resolution of cholestasis and 14% failed therapy.

67 cause of renal dysfunction in patients with cholestasis and advanced liver disease, but the underlyi

68 in the transmembrane domain associated with cholestasis and anemia in mice was expressed at WT level

69 n of TRPC5 contributes to the development of cholestasis and associated dyslipidemia.

70 A measures in ALGS correlate with markers of cholestasis and bone fracture history.

71 d be reserved for situations of intercurrent cholestasis and cholangitis, not for cholestasis in end-

72 that loss of VDR restricts the adaptation to cholestasis and diminishes bile duct integrity in the se

73 A liver biopsy demonstrated centrilobular cholestasis and focal rosetting of hepatocytes, consiste

74 linical data were obtained from infants with cholestasis and from children without liver disease (con

75 cl3(-/-)Mdr2(-/-) mice developed more severe cholestasis and had increased markers of liver injury an

76 ver axis) and by episodes of sepsis to cause cholestasis and IFALD.

77 d CN might be the result of toxic effects of cholestasis and in part be responsible for the impairmen

78 ritical illness does not necessarily reflect cholestasis and instead may be an adaptive response that

79 e (Mdr2(-/-)), a mouse model of inflammatory cholestasis and liver fibrosis.

80 Markers of cholestasis and liver injury, alkaline phosphatase (ALP)

81 nt between more benign and potentially fatal cholestasis and makes these patients more acutely sensit

82 ls from two unrelated families with neonatal cholestasis and mutations in NR1H4, which encodes the fa

83 as a therapeutic target for the treatment of cholestasis and nonalcoholic steatohepatitis.

84 e of NHERF-1 in the inflammatory response in cholestasis and other forms of liver injury should lead

85 Bile ducts from rats with cholestasis and patients with cholangiopathic disorders

86 Cholestasis and performance significantly improved when

87 es such as progressive familial intrahepatic cholestasis and primary sclerosing cholangitis.

88 , most children now experience resolution of cholestasis and rarely progress to end-stage liver disea

89 actor 19 (FGF19) are associated with chronic cholestasis and survival in adult CIF patients, and to d

90 CIT and FGF19 predict chronic cholestasis and survival in this cohort of adult CIF pat

91 iations of plasma CIT and FGF19 with chronic cholestasis and survival were estimated by logistic and

92 w that MYO5B deficiency may lead to isolated cholestasis and that MYO5B should be considered as an ad

93 between patients who achieved resolution of cholestasis and those who failed therapy.

94 iltrates and ductular proliferation, lobular cholestasis, and acute liver cell necrosis, together wit

95 ve variable risks of progressive ductopenia, cholestasis, and biliary fibrosis.

96 hyperplasia, steatohepatitis, hemosiderosis, cholestasis, and cirrhosis with hepatic steatosis.

97 tial lung disease, and jaundice, and grade 4 cholestasis, and died on treatment on day 40; the death

98 s for interleukin-13 in fibrosis, steatosis, cholestasis, and ductular reaction.

99 lier onset of jaundice (<9 months), neonatal cholestasis, and higher ALT levels.

100 D responded to FO therapy with resolution of cholestasis, and liver transplantation was rarely requir

101 ontent, can lower the risk of IFALD, reverse cholestasis, and reduce complications, although the sign

102 This eventually leads to cholestasis, and this causes bile salt (BS)-mediated tox

103 The liver has a great capacity to adapt to cholestasis, and this may contribute to a variable sympt

104 re," "DILI," "hepatitis," "hepatotoxicity," "cholestasis," and "aminotransferase," cross-referenced w

105 Arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome is caused by deficiencies in

106 Arthrogryposis-renal dysfunction-cholestasis (ARC) syndrome-associated mutations in VPS33

107 , outcomes for cirrhosis after resolution of cholestasis are unknown and patients continue to be cons

108 sion of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflamma

109 4 age-appropriate subjects with intrahepatic cholestasis as diseased controls and seven normal contro

110 Here we report a rare case of KD with cholestasis as principal symptom.

111 tatic disease, in two experimental models of cholestasis, as well as in human and murine liver cells

112 Adaptation to cholestasis, ascertained by expression of genes involved

113 th features of benign recurrent intrahepatic cholestasis associated with a heterozygous mutation in t

114 -activated receptor (PPAR) agonist, relieves cholestasis-associated itch by alleviating hepatobiliary

115 nts still exhibited mild gradually improving cholestasis at the end of follow-up).

116 P < .001), and biochemical markers of severe cholestasis (bilirubin >=100 mumol or alkaline phosphata

117 intermittent (benign recurrent intrahepatic cholestasis; BRIC) to progressive familial intrahepatic

118 e phosphatase (AP) is not only a signpost of cholestasis but also a surrogate marker of the severity

119 MRP3, MRP4 was also observed in ANIT-induced cholestasis but were attenuated or normalized by YCHT.

120 r disease, progressive familial intrahepatic cholestasis, but cause and effect is less clear, with ma

121 can cause progressive familial intrahepatic cholestasis, but known genes cannot account for all fami

122 Phytosterols are elevated in neonatal cholestasis, but the relation remains controversial.

123 ndings indicate that adult lampreys tolerate cholestasis by altering hepatic bile salt composition, w

124 Drugs induce cholestasis by diverse and still poorly understood mecha

125 0.05); we interpreted this result to be mild cholestasis caused by the catheter.

126 e to myosin 5B (MYO5B) mutations may develop cholestasis characterized by a progressive familial intr

127 al protein glycosylation that result in mild cholestasis, chronic elevation of aminotransferases, ele

128 psin deficiency (A1AT), chronic intrahepatic cholestasis (CIC), and Alagille syndrome (ALGS).

129 riety of complications, including steatosis, cholestasis, cirrhosis, and liver failure.

130 displayed greater numbers of HCC and severe cholestasis compared with NEMO(Deltahepa) animals.

131 Cholestasis comprises aetiologically heterogeneous condi

132 ere analyzed to determine whether markers of cholestasis could identify patients with recurrence of P

133 isruption of Cxcr2 shortened the duration of cholestasis, decreased the incidence of bile duct obstru

134 erwent liver transplantation for progressive cholestasis despite treatment with corticosteroids and u

135 Patients whose cholestasis does not resolve with FO may progress to end

136 er hepatic impairment of expected in chronic cholestasis downregulation of CYP7A1 and upregulation of

137 While drug-induced cholestasis due to the inhibition of the bile salt expor

138 Here we show that maternal cholestasis (due to Abcb11 deficiency) produces neonatal

139 rations parallel the portal inflammation and cholestasis during PN, thereby reinforcing their contrib

140 he differential diagnosis of severe neonatal cholestasis even in the absence of more typical features

141 rum markers associated with liver damage and cholestasis, extensive bile duct proliferation, and incr

142 tifactorial and related to growth, degree of cholestasis, fracture vulnerability, and contribution of

143 In experimental cholestasis, FXR agonism improved ileal barrier function

144 additional progressive familial intrahepatic cholestasis gene.

145 Elucidating genetic causes of cholestasis has proved to be important in understanding

146 liary ductules, which progressively leads to cholestasis, hepatic fibrosis, cirrhosis, and eventually

147 unable to improve BSEP protein expression in cholestasis; however, its transport activity, assessed b

148 Intrahepatic cholestasis (IHC) was observed in 4.9% of InO recipients

149 o the mechanisms of 17alpha-ethinylestradiol cholestasis improvement, we studied the biliary output o

150 sting with acute granulomatous hepatitis and cholestasis in a 48-year-old female with psoriatic arthr

151 DAM17 activity, resulting in amelioration of cholestasis in a murine model of bile duct ligation (BDL

152 that inflammation might be the cause for the cholestasis in Cic-L(-/-) mice.

153 current cholestasis and cholangitis, not for cholestasis in end-stage disease.

154 alpha-naphthylisothiocyanate (ANIT)-induced cholestasis in male Wistar rats.

155 We also induced cholestasis in mouse livers via common bile duct ligatio

156 Our results suggest that cholestasis in MVID patients results from (1) impairment

157 affect hepatic biliary function and lead to cholestasis in MVID patients.

158 ments in liver biochemistries and markers of cholestasis in patients with PSC.

159 In conclusion, chronic cholestasis in PSC induces adaptive changes in expressio

160 estrogen receptor alpha) that lead to acute cholestasis in rat liver with retrieval of the canalicul

161 ligation (BDL) is a frequently used model of cholestasis in rodents.

162 inal Study of Genetic Causes of Intrahepatic Cholestasis in the Childhood Liver Disease Research Netw

163 r genes relevant to the adaptive response to cholestasis in tissues from non-cirrhotic (n = 24) and c

164 AC inhibitor parthenolide during obstructive cholestasis in vivo promote genomic reprogramming, leadi

165 features of severe, persistent NR1H4-related cholestasis include neonatal onset with rapid progressio

166 Cholestasis, including primary biliary cirrhosis (PBC) a

167 is, conjugation, and transport, resulting in cholestasis, increased cholangiocyte proliferation, and

168 together, our data indicate that EE2-induced cholestasis increases SHP and represses CYP2D6 expressio

169 ere measured in liver tissues from rats with cholestasis (induced by administration of alpha-napthyli

170 le in regulating the biliary contribution to cholestasis-induced hepatic fibrosis.

171 Cholestasis induces adaptive mechanisms protecting the l

172 le canaliculi system, which was disrupted by cholestasis-inducing drugs such as troglitazone.

173 bited a 50% decrease in mean life-span after cholestasis induction.

174 s include growth retardation, aminoaciduria, cholestasis, iron overload, lactic acidosis and early de

175 Cholestasis is a clinical disorder defined as an impairm

176 Cholestasis is a common complication in liver diseases t

177 Neonatal cholestasis is a potentially life-threatening condition

178 Cholestasis is characterized by impairment of excretion

179 Early FO initiation once biochemical cholestasis is detected in parenteral nutrition-dependen

180 r, the role of mitochondrial shape change in cholestasis is not defined.

181 its role in the pathogenesis of drug-induced cholestasis is poorly understood.

182 cholestatic injuries, however Ghr's role in cholestasis is poorly understood.

183 lished ciliopathy phenotype, severe neonatal cholestasis is rarely recognized as such.

184 d granulomatous hepatitis leading to chronic cholestasis is reported along with a review of the hepat

185 Our study demonstrates that intrahepatic cholestasis leading to hepatocyte exposure to bile acids

186 If left untreated, cholestasis leads to liver fibrosis and cirrhosis, which

187 le duct ligation (BDL) experimental model of cholestasis leads to rapid and significant changes in th

188 clinical features, including severe neonatal cholestasis (lethal in one and necessitating liver trans

189 to adolescent development of an intrahepatic cholestasis-like condition with attendant hypercholester

190 rized by a progressive familial intrahepatic cholestasis-like phenotype with normal serum gamma-gluta

191 ients with progressive familial intrahepatic cholestasis-like phenotype with normal serum gamma-gluta

192 We also demonstrate that during cholestasis, macrophages contribute to promoting intesti

193 hat the intestinal microbiome contributes to cholestasis-mediated cell death and inflammation through

194 In a mouse model of intrahepatic cholestasis, metformin treatment induced FXR phosphoryla

195 Liver histology showed canalicular cholestasis, mild-to-moderate fibrosis, and ultrastructu

196 ent to treat enterohepatic disorders such as cholestasis, NASH, and inflammatory bowel disease.

197 Cholestasis occurred before (n = 5) or after (n = 3) ITx

198 Estrogen-induced cholestasis occurs in subjects receiving estrogen for co

199 drome is a genetic disorder characterized by cholestasis, ocular abnormalities, characteristic facial

200 Intrahepatic cholestasis of pregnancy (ICP) affects 1/140 UK pregnanc

201 pregnancy outcome in women with intrahepatic cholestasis of pregnancy (ICP) and treatment with ursode

202 Intrahepatic cholestasis of pregnancy (ICP) can predispose offspring

203 Intrahepatic cholestasis of pregnancy (ICP) causes increased transfer

204 Intrahepatic cholestasis of pregnancy (ICP) is a liver disease of pre

205 Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific d

206 Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific l

207 Intrahepatic cholestasis of pregnancy (ICP) is associated with advers

208 Intrahepatic cholestasis of pregnancy (ICP) is the most common liver

209 Intrahepatic cholestasis of pregnancy (ICP) is the most prevalent dis

210 Intrahepatic cholestasis of pregnancy (ICP) is the most prevalent pre

211 the skin is an early symptom of intrahepatic cholestasis of pregnancy (ICP) or due to benign pruritus

212 Women with intrahepatic cholestasis of pregnancy (ICP), a disorder characterised

213 endogenous serum bile acids in intrahepatic cholestasis of pregnancy (ICP).

214 s independently associated with intrahepatic cholestasis of pregnancy (relative risk [RR], 10.64; 95%

215 irth is increased in women with intrahepatic cholestasis of pregnancy and singleton pregnancies when

216 criteria were studies defining intrahepatic cholestasis of pregnancy based upon pruritus and elevate

217 regate data meta-analysis (5557 intrahepatic cholestasis of pregnancy cases and 165 136 controls), an

218 occurred in 45 (0.83%) of 4936 intrahepatic cholestasis of pregnancy cases and 519 (0.32%) of 163 94

219 .13%; 95% CI 0.02-0.38) of 2310 intrahepatic cholestasis of pregnancy cases in women with serum total

220 ols), and 27 provided IPD (5269 intrahepatic cholestasis of pregnancy cases).

221 Because most women with intrahepatic cholestasis of pregnancy have bile acids below this conc

222 he adverse perinatal effects of intrahepatic cholestasis of pregnancy in women with increased serum b

223 Intrahepatic cholestasis of pregnancy is associated with adverse peri

224 rinatal outcomes for women with intrahepatic cholestasis of pregnancy when serum bile acid concentrat

225 te fatty liver of pregnancy and intrahepatic cholestasis of pregnancy, and their impact on the fetus,

226 Intrahepatic cholestasis of pregnancy, characterised by maternal prur

227 primary sclerosing cholangitis, intrahepatic cholestasis of pregnancy, or hereditary pediatric choles

228 We recruited women with intrahepatic cholestasis of pregnancy, who were aged 18 years or olde

229 id-associated cholelithiasis or intrahepatic cholestasis of pregnancy.

230 erinatal outcomes in women with intrahepatic cholestasis of pregnancy.

231 erinatal outcomes in women with intrahepatic cholestasis of pregnancy.

232 absent in cholangiocytes from patients with cholestasis of sepsis and from those with severe AH.

233 investigated the effects of estrogen-induced cholestasis on CYP2D6 expression.

234 further investigated the effect of maternal cholestasis on the metabolism of adult offspring in the

235 replace the native CBD, with no evidence of cholestasis or occlusion of the lumen.

236 rum bilirubin, and no evidence of hepatitis, cholestasis, or haemolysis.

237 -1.2 +/- 4.6, 12 months after resolution of cholestasis (P < 0.001).

238 esterol was 3.9-fold higher in patients with cholestasis (P < 0.05 for both).

239 cadian disruption activates CAR by promoting cholestasis, peripheral clock disruption, and sympatheti

240 r has been described in progressive familial cholestasis (PFIC), and we found that similar to individ

241 ; BRIC) to progressive familial intrahepatic cholestasis (PFIC).

242 se akin to progressive familial intrahepatic cholestasis (PFIC).

243 as not been reported in patients with such a cholestasis phenotype in the absence of intestinal disea

244 imilar with respect to age, BMD, severity of cholestasis, previous fractures, and bone markers.

245 .001) weaning off PN and was correlated with cholestasis (r = 0.428), portal inflammation (r = 0.511)

246 al inflammation (r = 0.549-0.510, P < 0.05), cholestasis (r = 0.501-0.491, P = 0.048-0.053), and seru

247 argeting of MCL1 in a mouse model of chronic cholestasis reduces DR-cell and B-cell populations and h

248 se at therapy initiation than patients whose cholestasis resolved, as evidenced by lower median (IQR)

249 7.3, 21.4 wk); P = 0.02] than patients whose cholestasis resolved.

250 D may be stable rather than progressive once cholestasis resolves with FO therapy.

251 Chronic cholestasis results from bile secretory defects or impai

252 iral hepatitis, and sickle cell intrahepatic cholestasis (SCIC).

253 erating ductular epithelial cells, and lower cholestasis serum markers within 2 weeks after DDC treat

254 Interventional treatments for pain or cholestasis should be done by specialists only, and earl

255 eroids can reflect liver pathologies such as cholestasis, steatosis and viral hepatitis.

256 systemic entry and consequent injury during cholestasis, such as from biliary pancreatitis.

257 s to hepatic inflammation during obstructive cholestasis, suggesting that bile acids and IL-17A may i

258 holangitis and was diagnosed with lymphedema cholestasis syndrome (LCS).

259 sorder Arthrogryposis, Renal dysfunction and Cholestasis syndrome caused by VIPAR and VPS33B deficien

260 ts with arthrogryposis renal dysfunction and cholestasis syndrome.

261 This may contribute to the cholestasis that can be observed in conditions such as s

262 Our results demonstrate that cholestasis, the accumulation of bile acids in the liver

263 d histological features with other causes of cholestasis, the diagnosis requires an intraoperative ch

264 Patients suffering from cholestasis, the slowing or stoppage of bile flow, commo

265 er fibrosis in a mouse model of inflammatory cholestasis, therefore suggesting that GH resistance pla

266 n identified here may predispose patients to cholestasis through a delocalization process of BSEP at

267 YP2D6-humanized transgenic (Tg-CYP2D6) mice, cholestasis triggered by administration of 17alpha-ethin

268 Progressive familial intrahepatic cholestasis type 2 (PFIC2) is a result of mutations in A

269 olution in progressive familial intrahepatic cholestasis type 2 patients and how they relate to bile

270 orders and progressive familial intrahepatic cholestasis type 2.

271 ldren with progressive familial intrahepatic cholestasis type 2.

272 tient with progressive familial intrahepatic cholestasis type 3 (PFIC-3).

273 including progressive familial intrahepatic cholestasis type 3 (PFIC3), a rare disease that can be l

274 Progressive familial intrahepatic cholestasis type 3 (PFIC3), an inherited juvenile-onset,

275 enicity of progressive familial intrahepatic cholestasis type 3 and, with further refinement, the pot

276 Progressive familial intrahepatic cholestasis type 3 is caused by biallelic variations of

277 ntified in progressive familial intrahepatic cholestasis type 3 patients.

278 model for progressive familial intrahepatic cholestasis type 3.

279 P8B1 cause progressive familial intrahepatic cholestasis type1 in humans, which is characterized by a

280 of jaundice and liver disorders, against the cholestasis using the alpha-naphthylisothiocyanate (ANIT

281 Resolution of cholestasis was defined as sustained direct bilirubin (D

282 A mouse model of acute cholestasis was induced by common BDL technique, during

283 Localized dyslipidaemia, secondary to cholestasis, was investigated utilizing a selected lipid

284 ids (BAs) may contribute to kidney injury in cholestasis, we established a mouse model for detailed i

285 n studies of liver tissues from infants with cholestasis, we identified a 14-gene expression pattern

286 tecture of the interlobular bile duct during cholestasis, we used 3D confocal imaging, surface recons

287 layed regeneration, hepatocyte necrosis, and cholestasis were observed in P2X4-KO mice.

288 No cases of cholestasis were observed in the S and OS groups.

289 ith ciliary dysgenesis and/or dysfunction or cholestasis were prioritized according to pathogenicity,

290 The detrimental effects of SIRT1 during cholestasis were validated in vivo and in vitro.

291 drug known for years to induce intrahepatic cholestasis, were investigated using the differentiated

292 xamined, including steatosis, apoptosis, and cholestasis, when exposed to nine known hepatotoxins.

293 PKA inhibition prevented E17G-induced cholestasis, whereas exchange protein activated directly

294 p/Taz mutant bile ducts degenerated, causing cholestasis, which stalled the recruitment of phagocytic

295 CV RNA of 12 000 000 IU/mL, and histological cholestasis with pericellular fibrosis.

296 ients with fever, chills, abdominal pain and cholestasis with progressive jaundice, particularly in s

297 ANIT feeding induced significant cholestasis with substantially increased intrahepatic re

298 dL (P < 0.001) 12 months after resolution of cholestasis, with a mean time to resolution of 74 days.

299 difying treatment focuses on amelioration of cholestasis, with weight-dosed oral ursodeoxycholic acid

300 Because cholestasis worsens after ITx, indication of a combined