ライフサイエンスコーパス: cholangitis

1 ations in patients with secondary sclerosing cholangitis.

2 cially in patients with secondary sclerosing cholangitis.

3 ulosis with features of secondary sclerosing cholangitis.

4 robials were those with secondary sclerosing cholangitis.

5 till rarer is its presentation as sclerosing cholangitis.

6 rally considered reflective of an autoimmune cholangitis.

7 the treatment of pruritus in primary biliary cholangitis.

8 udies as risk factors for primary sclerosing cholangitis.

9 lymphocytes similar to human primary biliary cholangitis.

10 e of Gal-3 in the murine model of autoimmune cholangitis.

11 y tree, is down-regulated in primary biliary cholangitis.

12 rahepatic cholestasis and primary sclerosing cholangitis.

13 rs may be therapeutic for primary sclerosing cholangitis.

14 ry tissues from mice and patients with AP or cholangitis.

15 0-year-old female admitted with severe acute cholangitis.

16 uch as alcoholic liver disease or sclerosing cholangitis.

17 d abrogates progression of murine sclerosing cholangitis.

18 ary biliary cirrhosis and primary sclerosing cholangitis.

19 ary biliary cirrhosis and primary sclerosing cholangitis.

20 d promoted the induction of T-cell-dependent cholangitis.

21 ties, primary (PSC) and secondary sclerosing cholangitis.

22 nsidered as potential therapy for sclerosing cholangitis.

23 OT-II/dnTGFbetaRII/Rag1(-/-) mice developed cholangitis.

24 chronic pancreatitis, and primary sclerosing cholangitis.

25 ckout (Mdr2(-/-) ) mouse model of sclerosing cholangitis.

26 9, and 88% had underlying primary sclerosing cholangitis.

27 ned from 348 consecutive patients with acute cholangitis.

28 vely) and subjected to a model of sclerosing cholangitis.

29 iver fibrosis in early-stage primary biliary cholangitis.

30 olangiopathies, including primary sclerosing cholangitis.

31 here were 7 patients with primary sclerosing cholangitis.

32 severe disorders, such as primary sclerosing cholangitis.

33 ad to complications such as pancreatitis and cholangitis.

34 ibiotic therapy increases mortality of acute cholangitis.

35 iver enzymes associated with primary biliary cholangitis.

36 iary cirrhosis (16%), and primary sclerosing cholangitis (13%) with an odds ratio of 2.3, 2.1, and 1.

37 ing ERCP, 90 (5%) of 1920 patients had acute cholangitis, 14 (<1%) had acute cholecystitis, and five

38 Patients died from tumor progression (55%), cholangitis (18%), pneumonia (7%), hemobilia (7%), esoph

39 nest indications for listing were refractory cholangitis (31%), synthetic failure (25%), and variceal

40 drome(3), subacute biliary injury and immune cholangitis.(4).

41 umerical rating scale (NRS), primary biliary cholangitis-40 (PBC-40) itch domain score and 5-D itch s

42 hepatobiliary (including primary sclerosing cholangitis) (5.5% vs. 0.1%), pancreatic (1.7% vs. 0%) a

43 n addition, there were episodes of ascending cholangitis 6-12 months prior to the current admission t

44 (28%), deep incisional infections (8%), and cholangitis (6%).

45 intraoperative hemobilia (4.58% vs. 10.93%), cholangitis (6.54% vs. 14.06%), postoperative complicati

46 4%) and 114 patients with primary sclerosing cholangitis (62.3%).

47 rimarily indications for ERC were sclerosing cholangitis (75%) and malignant stenosis (9.5%).

48 le duct injury in mouse models of sclerosing cholangitis, a disease so far lacking effective pharmaco

49 Importance: Acute cholangitis (AC), particularly severe AC, has historical

50 , and lower likelihood of primary sclerosing cholangitis (adjusted odds ratio 0.38; 95% CI 0.26-0.55)

51 ne hepatitis (AIH) and autoimmune sclerosing cholangitis (AISC) either through inability of Tregs to

52 rimary biliary cirrhosis, primary sclerosing cholangitis, alcoholic liver disease, and chronic hepati

53 tained from patients with primary sclerosing cholangitis, alcoholic liver disease, or nonalcoholic st

54 XR, is effective in treating primary biliary cholangitis, an autoimmune liver disease.

55 ially suspected to have concurrent gallstone cholangitis and a newly diagnosed hepatocellular carcino

56 medical history included recurrent gallstone cholangitis and a previous cholecystectomy.

57 is difficult to distinguish from sclerosing cholangitis and biliary/pancreatic malignancies (CA).

58 ed in human patients with primary sclerosing cholangitis and hepatobiliary cholangiopathies.

59 trong comorbidity between primary sclerosing cholangitis and inflammatory bowel disease is likely the

60 sporidial infections associated with chronic cholangitis and liver disease.

61 sporidial infections associated with chronic cholangitis and liver disease.

62 re a target of therapies for primary biliary cholangitis and nonalcoholic steatohepatitis.

63 ide a rationale to target Gal3 in autoimmune cholangitis and potentially other cholestatic diseases.

64 iated diseases, including primary sclerosing cholangitis and primary biliary cirrhosis, but not with

65 liver diseases, particularly primary biliary cholangitis and primary sclerosing cholangitis (PSC), ev

66 ew on the pathophysiology of primary biliary cholangitis and PSC in the hope that these new drugs can

67 ohn's disease, psoriasis, primary sclerosing cholangitis and ulcerative colitis to investigate pleiot

68 protein loosing enteropathy, and sclerosing cholangitis and was diagnosed with lymphedema cholestasi

69 uration, if they also had primary sclerosing cholangitis) and no history of advanced CRN (high-grade

70 insic compression from pancreatic cysts, and cholangitis), and 3 with bile leak syndromes.

71 iary tree with low rates of leak, stricture, cholangitis, and bile gastritis.

72 ith autoimmune hepatitis, primary sclerosing cholangitis, and primary biliary cirrhosis as a group ha

73 mune hepatitis, recurrent primary sclerosing cholangitis, and recurrent primary biliary cirrhosis in

74 IgG4-associated cholangitis, primary biliary cholangitis, and secondary cholangitides, because the th

75 hogenesis and progression of primary biliary cholangitis are further clarified, specific targeted the

76 bacterial pathogens that caused preoperative cholangitis as well as SSI after PD.

77 toimmune hepatitis and autoimmune sclerosing cholangitis ASC).

78 ing cholangitis (PSC), autoimmune sclerosing cholangitis (ASC), and autoimmune hepatitis (AIH) are no

79 ly distinguish patients with IgG4-associated cholangitis/autoimmune pancreatitis (n = 34) from those

80 ate of complications including pancreatitis, cholangitis, bleeding, and perforation between the two g

81 ivation in the earliest phases of autoimmune cholangitis but subsequently leads to downregulation of

82 does not alter the initiation of autoimmune cholangitis, but does contribute to the exacerbation of

83 rosis in a mouse model of primary sclerosing cholangitis by miR-200b down-regulation.

84 Differentiation of primary sclerosing cholangitis can be challenging because other chronic cho

85 role in biliary atresia, primary sclerosing cholangitis, cellular rejection, and primary biliary cir

86 Biliary drainage can cause cholangitis/cholecystitis, pancreatitis, hemorrhage, por

87 mary sclerosing cholangitis, primary biliary cholangitis, chronic infection with hepatitis B or C vir

88 In patients with primary biliary cholangitis/cirrhosis (PBC), hepatic levels of miR-210 a

89 CCAs and 20 nonmalignant primary sclerosing cholangitis controls), and the methylation status of the

90 validated (34 CCAs and 34 primary sclerosing cholangitis controls).

91 Postoperative serum HMGB1 and cholangitis could predict high recurrence and unfavorabl

92 Up to 70% of patients with primary biliary cholangitis develop pruritus (itch) during the course of

93 Likewise, cholangitis developed in mice expressing ovalbumin simul

94 everity using the Tokyo Guidelines for acute cholangitis diagnosis.

95 Three (13.6%) patients developed cholangitis due to occlusion of unrecognized secondary b

96 knockout (KO) mice, which develop sclerosing cholangitis due to regurgitation of BA from leaky ducts.

97 981 cholangitis episodes from 810 patients were analysed ret

98 nal pain (seven [5%]), pyrexia (seven [5%]), cholangitis (five [3%]), and pleural effusion (five [3%]

99 dihydrocollidine (DDC; a model of sclerosing cholangitis) for 4 weeks.

100 Primary biliary cholangitis (formerly called primary biliary cirrhosis)

101 Bile samples from patients with IgG4-related cholangitis had significant increases in levels of Th2 c

102 Patients with primary sclerosing cholangitis have a poor prognosis; progression to liver

103 Many patients with primary biliary cholangitis have an inadequate response to first-line th

104 Up to 40% of patients with primary biliary cholangitis have an incomplete response to first-line tr

105 munological abnormalities in primary biliary cholangitis have been studied but their effectiveness va

106 mary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infection, autoimmun

107 adiologic signs of bile duct obstruction and cholangitis, her blood analysis showed severe unconjugat

108 addition of immunoglobulin (Ig)G4-associated cholangitis (IAC), also called IgG4-related sclerosing c

109 Liver histology of sclerosing cholangitis improved, and extent of fibrosis decreased c

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

111 In unselected patients treated for acute cholangitis in a large tertiary refferential center, use

112 y to migrate to the liver, where they caused cholangitis in a strictly antigen-dependent manner.

113 d provide the first link between colitis and cholangitis in an antigen-dependent mouse model.

114 ter (ASBT), blocks progression of sclerosing cholangitis in mdr2(-/-) mice.

115 break in tolerance that leads to autoimmune cholangitis in NOD.Abd3 congenic mice.

116 nitiated after the development of autoimmune cholangitis in previously immunized mice, also resulted

117 f Gal-3 significantly exacerbates autoimmune cholangitis in these mice.

118 luences on the natural history of autoimmune cholangitis in this model.

119 collidine (DDC) feeding to induce sclerosing cholangitis in wild-type (WT) and knockout (MGL(-/-) ) m

120 but not in biliary diseases (obstruction or cholangitis) in which DR was contained within the portal

121 arisen from studies of secondary sclerosing cholangitis, in which a similar clinical profile is asso

122 Symptoms of primary sclerosing cholangitis include fatigue, jaundice, pruritus, or stea

123 Postoperative serum HMGB1 and reflux cholangitis indicated recurrence and unfavorable prognos

124 angitis, whereas male mice were resistant to cholangitis induction.

125 th ulcerative colitis and primary sclerosing cholangitis, inflammatory diseases with a high cancer ri

126 , we propose to stratify patients with acute cholangitis into a high and low risk group.

127 lps physicians to assign patients with acute cholangitis into different management groups.

128 rs promising to stratify patients with acute cholangitis into different management groups.

129 rimary biliary cirrhosis, primary sclerosing cholangitis, intrahepatic cholestasis of pregnancy, or h

130 s (IAC), also called IgG4-related sclerosing cholangitis (IRSC), to the spectrum of chronic cholangio

131 Primary sclerosing cholangitis is a chronic cholestatic liver disease.

132 Primary sclerosing cholangitis is a chronic immune-mediated liver disease.

133 IgG4-related cholangitis is a chronic inflammatory biliary disease th

134 Primary sclerosing cholangitis is a chronic, progressive cholangiopathy tha

135 Acute cholangitis is a life-threatening bacterial infection of

136 Primary biliary cholangitis is an autoimmune liver disease that predomin

137 a strengthen the notion that immune-mediated cholangitis is caused by T cells primed in the GALT and

138 Treatment of pruritus in primary biliary cholangitis is challenging and novel therapies are neede

139 r T cells function in the natural history of cholangitis is essential and illustrates that precision

140 The etiopathogenesis of primary sclerosing cholangitis is unknown.

141 function tests but bilirubin <4 mg/dL and no cholangitis) is a matter of debate.

142 ard first-line treatment for primary biliary cholangitis, is largely ineffective for pruritus.

143 n in vitro and in vivo in primary sclerosing cholangitis liver specimens.

144 concomitant diagnosis of primary sclerosing cholangitis, longstanding colitis (>10 years), male sex,

145 ator of inflammatory signaling in autoimmune cholangitis, mediating the activation of NLRP3 inflammas

146 Primary sclerosing cholangitis mice and patients have increased MCs.

147 A BDL-induced acute cholangitis model was characterized by increased relativ

148 Mdr2(-/-)) knockout (KO) mice, a sclerosing cholangitis model.

149 26% vs 82%), despite a higher rate of severe cholangitis (n = 131 [67%] vs n = 29 [25%]).

150 (n = 34) from those with primary sclerosing cholangitis (n = 17) and CA (n = 17).

151 5), choledocholithiasis (n = 3), idiopathic cholangitis (n = 2), and deceased donor or live donor li

152 Adverse events were cholangitis (n=4), liver abscess (n=2), cholecystitis (n

153 ry cirrhosis (PBC, n=76), primary sclerosing cholangitis (n=81), hepatitis C virus (HCV) (n=945), alc

154 , disease was a) Sclerosing pancreatitis and cholangitis, n = 21; b) Sclerosing cholangitis, n = 9; c

155 titis and cholangitis, n = 21; b) Sclerosing cholangitis, n = 9; c) Sclerosing pancreatitis, n = 4; d

156 She developed cholangitis, necessitating an emergent endoscopic retrog

157 r situations of intercurrent cholestasis and cholangitis, not for cholestasis in end-stage disease.

158 l-related serious adverse events, most often cholangitis, occurred in 27.3% of patients.

159 developing organ/space SSI were preoperative cholangitis (odds ratio, 10.07; 95% confidence interval,

160 Patients with cholangitis or pancreatitis were excluded.

161 llidine (DDC) feeding (a model of sclerosing cholangitis) or bile duct ligation (BDL).

162 rimary biliary cirrhosis, primary sclerosing cholangitis, or alcoholic cirrhosis (group I), NASH, and

163 thiasis, cholecystitis, choledocholithiasis, cholangitis, or biliary pancreatitis), mortality, and co

164 r, anastomosis-related complications (leaks, cholangitis, or strictures) were fewer in the duodenal t

165 3), as well as absence of primary sclerosing cholangitis (P = .011).

166 ac disease (P = 0.22) and primary sclerosing cholangitis (P = 0.078) were not associated with PDAC.

167 r samples from control or primary sclerosing cholangitis patients were evaluated for MC markers by qu

168 ive in only about 50%-60% of primary biliary cholangitis patients, with no effective therapy in PSC.

169 ction, particularly among primary sclerosing cholangitis patients.

170 atic liver diseases, such as primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PS

171 in livers from patients with primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PS

172 rosing cholangitis (PSC) and primary biliary cholangitis (PBC) are human primary cholangiopathies cha

173 Primary biliary cholangitis (PBC) frequently recurs after liver transpla

174 Primary biliary cholangitis (PBC) has been regarded as female-predominan

175 Primary biliary cholangitis (PBC) in younger patients has been suggested

176 Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease

177 Primary biliary cholangitis (PBC) is a chronic, progressive autoimmune l

178 Primary biliary cholangitis (PBC) is a disease of small bile ducts, whic

179 Primary biliary cholangitis (PBC) is a rare autoimmune liver disease and

180 Primary biliary cholangitis (PBC) is an autoimmune cholestatic liver dis

181 Primary biliary cholangitis (PBC) is an autoimmune liver disease charact

182 Primary biliary cholangitis (PBC) is an autoimmune liver disease with a

183 n is an important feature of primary biliary cholangitis (PBC) pathogenesis and other cholestatic liv

184 Primary biliary cholangitis (PBC) primarily targets cholangiocytes and i

185 The relationship between primary biliary cholangitis (PBC), a chronic cholestatic autoimmune live

186 but no clinical evidence of primary biliary cholangitis (PBC), are largely unknown.

187 tical to the pathogenesis of Primary Biliary Cholangitis (PBC), we have analyzed the role of Gal-3 in

188 redicts long-term outcome in primary biliary cholangitis (PBC).

189 rved in PSC in comparison to primary biliary cholangitis (PBC).

190 ade has been associated with primary biliary cholangitis (PBC).

191 g cholangitis (PSC, SSC) and primary biliary cholangitis (PBC).

192 tatic liver diseases such as primary biliary cholangitis (PBC, previously referred to as primary bili

193 thies (biliary atresia [BA], primary biliary cholangitis [PBC], and primary sclerosing cholangitis [P

194 de dysplasia, strictures, primary sclerosing cholangitis, post-inflammatory polyps, family history of

195 HR, 1.35; P < 0.001), and primary sclerosing cholangitis pre-LT (compared with hepatitis C virus, P <

196 differential diagnosis with IgG4-associated cholangitis, primary biliary cholangitis, and secondary

197 issues from patients with primary sclerosing cholangitis, primary biliary cholangitis, chronic infect

198 amples from patients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or

199 After adjusting for the variables acute cholangitis prior to ERC and incomplete biliary drainage

200 The prevalence of primary sclerosing cholangitis (PSC) among patients with inflammatory bowel

201 during the progression of primary sclerosing cholangitis (PSC) and is characterized by accumulation o

202 Primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC)

203 Patients with primary sclerosing cholangitis (PSC) are at an increased risk for cholangio

204 liary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are infrequent autoimmune cholestatic

205 ring systems specific for primary sclerosing cholangitis (PSC) are not validated.

206 el data on the effects of primary sclerosing cholangitis (PSC) in patients with inflammatory bowel di

207 Primary sclerosing cholangitis (PSC) is a cholestatic liver disease charact

208 Primary sclerosing cholangitis (PSC) is a chronic cholestatic disease that

209 Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disorde

210 Primary sclerosing cholangitis (PSC) is a chronic inflammatory cholangiopat

211 Primary sclerosing cholangitis (PSC) is a chronic inflammatory liver diseas

212 Primary sclerosing cholangitis (PSC) is a chronic, fibroinflammatory cholan

213 Primary sclerosing cholangitis (PSC) is a chronic, idiopathic, fibroinflamm

214 Primary sclerosing cholangitis (PSC) is a heterogeneous and progressive fib

215 Primary sclerosing cholangitis (PSC) is a rare progressive disorder leading

216 Primary sclerosing cholangitis (PSC) is a rare, but serious, cholestatic di

217 Because primary sclerosing cholangitis (PSC) is a risk factor for CCA, serum metabo

218 Primary sclerosing cholangitis (PSC) is an idiopathic, progressive cholangi

219 Primary sclerosing cholangitis (PSC) is an incurable cholangiopathy of unkn

220 BACKGROUND & AIMS: Primary sclerosing cholangitis (PSC) is an orphan hepatobiliary disorder as

221 Patients with primary sclerosing cholangitis (PSC) may be at higher risk of malignancy af

222 redict colectomy, whereas primary sclerosing cholangitis (PSC) may be protective.

223 ary tract cancer (BTC) in primary sclerosing cholangitis (PSC) may exceed 20%, and BTC is currently t

224 Pathogenesis of primary sclerosing cholangitis (PSC) may involve impaired bile acid (BA) ho

225 ormation in patients with primary sclerosing cholangitis (PSC) or after liver transplantation (LTx) r

226 ally in cholangiocytes of primary sclerosing cholangitis (PSC) patients and in mice subjected to DDC

227 Primary sclerosing cholangitis (PSC) patients pose a particularly difficult

228 Primary sclerosing cholangitis (PSC) patients suffer from comorbidities una

229 The pathogenesis of primary sclerosing cholangitis (PSC) remains poorly understood.

230 Primary sclerosing cholangitis (PSC) represents a major unmet medical need.

231 cells from patients with primary sclerosing cholangitis (PSC) show a prominent IL-17 response upon s

232 cells from patients with primary sclerosing cholangitis (PSC) show a prominent interleukin (IL)-17 r

233 The pathogenesis of primary sclerosing cholangitis (PSC), a progressive biliary tract disease w

234 ding 28 with PBC, 13 with primary sclerosing cholangitis (PSC), and 18 healthy controls.

235 biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), and alcoholic liver disease (ALD).

236 or death in patients with primary sclerosing cholangitis (PSC), and to develop and validate a contemp

237 ary cholangitis (PBC) and primary sclerosing cholangitis (PSC), are frequently associated with damage

238 veral conditions, such as primary sclerosing cholangitis (PSC), are risk factors.

239 from patients with AP or primary sclerosing cholangitis (PSC), as well as from mice.

240 ural history of pediatric primary sclerosing cholangitis (PSC), autoimmune sclerosing cholangitis (AS

241 In primary sclerosing cholangitis (PSC), bile fluid is frequently colonized wi

242 y biliary cholangitis and primary sclerosing cholangitis (PSC), evolve over time with anatomically an

243 nstrated in patients with primary sclerosing cholangitis (PSC), must be accompanied by functional cha

244 The influence of sex on primary sclerosing cholangitis (PSC), pre and post-liver transplantation (L

245 liary cirrhosis (PBC) and primary sclerosing cholangitis (PSC), results from an impairment or disrupt

246 In primary sclerosing cholangitis (PSC), the focus of this review, the cholang

247 scence has been linked to primary sclerosing cholangitis (PSC).

248 giopathies, in particular primary sclerosing cholangitis (PSC).

249 no information exists in primary sclerosing cholangitis (PSC).

250 matory diseases including primary sclerosing cholangitis (PSC).

251 n animal models and human primary sclerosing cholangitis (PSC).

252 activity and prognosis in primary sclerosing cholangitis (PSC).

253 ncreased in patients with primary sclerosing cholangitis (PSC).

254 ry injury is a feature of primary sclerosing cholangitis (PSC).

255 nign disease, tumour, and primary sclerosing cholangitis (PSC).

256 nt of adult patients with primary sclerosing cholangitis (PSC).

257 eference for diagnosis of primary sclerosing cholangitis (PSC).

258 outcomes in patients with primary sclerosing cholangitis (PSC).

259 from patients affected by primary sclerosing cholangitis (PSC).

260 ary cholangitis (PBC) and primary sclerosing cholangitis (PSC).

261 nd liver of patients with primary sclerosing cholangitis (PSC).

262 n 9%-15% of patients with primary sclerosing cholangitis (PSC); it is not clear whether this increase

263 ases such as primary or secondary sclerosing cholangitis (PSC, SSC) and primary biliary cholangitis (

264 cirrhosis (PBC; n=3052), primary sclerosing cholangitis (PSC; n=3854), hepatitis C virus (HCV; n=15,

265 ry cholangitis [PBC], and primary sclerosing cholangitis [PSC]), we built a comprehensive platform of

266 r 12 months in patients with primary biliary cholangitis resulted in decreases from baseline in alkal

267 logy samples from patients with IgG4-related cholangitis revealed increased levels of IL-13 mRNA, com

268 y; down-regulation of AE2 in primary biliary cholangitis sensitizes cholangiocytes to apoptotic insul

269 HCC) (SMR 38.4-18.8), and primary sclerosing cholangitis (SMR 11.0-4.2), and deterioration in alcohol

270 nd dnTGF-betaRII mice, a model of autoimmune cholangitis, the expression of Gal3, NLRP3, and the adap

271 In contrast to previous mouse models of cholangitis, this model displayed a strong sexual dimorp

272 lcoholic steatohepatitis, primary sclerosing cholangitis, total parenteral nutrition-associated liver

273 in biliary lithiasis and primary sclerosing cholangitis, two cholangiopathies regarded as risk facto

274 mmatory bowel disease and primary sclerosing cholangitis underscores the need to further understand t

275 holic acid for patients with primary biliary cholangitis using 3-year interim data from the 5-year op

276 we report a novel mouse model of autoimmune cholangitis via immunization with syngeneic bile duct pr

277 Cirrhosis not related to primary sclerosing cholangitis was associated with both intrahepatic and pe

278 Acute experimental cholangitis was induced by adoptive transfer of OVA-spec

279 sis of hepatobiliary sepsis due to ascending cholangitis was made.

280 Primary sclerosing cholangitis was more strongly associated with perihilar

281 ory bowel disease without primary sclerosing cholangitis was not associated with any CCA subtype.

282 Sclerosing cholangitis was the most important risk factor.

283 ecipients, female sex and primary sclerosing cholangitis were associated with improved survival, wher

284 se and 13 patients with mild primary biliary cholangitis were included in the analysis.

285 ile neutropenia, intestinal perforation, and cholangitis-were reported by one patient each.

286 cific antigen migrate to the liver and cause cholangitis when they recognize the same antigen on chol

287 ual dimorphism: female mice developed marked cholangitis, whereas male mice were resistant to cholang

288 tides, the most common is primary sclerosing cholangitis, which is associated with inflammatory bowel

289 cholic acid in patients with primary biliary cholangitis who are intolerant to or inadequately respon

290 treatment for patients with primary biliary cholangitis who are unresponsive to ursodeoxycholic acid

291 ary biliary cirrhosis and primary sclerosing cholangitis with genes encoding major histocompatibility

292 ancreatic pseudotumour, n = 7; e) Sclerosing cholangitis with hepatic pseudotumour, n = 3; f) Scleros

293 patients with and without primary sclerosing cholangitis with higher levels of sensitivity than UroVy

294 of POISE, 217 patients with primary biliary cholangitis with inadequate response to or intolerance t

295 titis, n = 4; d) Sclerosing pancreatitis and cholangitis with pancreatic pseudotumour, n = 7; e) Scle

296 RPRETATION: In patients with primary biliary cholangitis with pruritus, 14 days of ileal bile acid tr

297 ter (IBAT), in patients with primary biliary cholangitis with pruritus.

298 , small bile duct, granulomatous lymphocytic cholangitis, with typical seroreactivity for antimitocho

299 For patients with community-acquired cholangitis without biliary prosthesis who do not need i

300 Minimizing the occurrence of preoperative cholangitis would decrease the incidence of developing o