ライフサイエンスコーパス: PBC

1 PBC is unrecognized in 13% of those cases.

2 PBC may be another risk factor, perhaps by causing chron

3 PBC recurred in 22% of patients after 5 years and 36% af

4 PBC recurrence reduces odds of graft and patient surviva

5 PBC should be used as a control arm in future trials of

6 n the NRS (-23%, 95% CI -45 to -1; p=0.037), PBC-40 itch domain, (-14%, -26 to -1; p=0.034), and 5-D

7 e-wide association study that included 1,122 PBC cases and 4,036 controls of Han Chinese descent, wit

8 r results show genome-wide association of 14 PBC risk loci including previously identified 6p21 (HLA-

9 iver-infiltrating T cells from PSC (n = 20), PBC (n = 10), and ALD (n = 10) patients, alongside genom

10 nts, 70 completed the trial (95%; 44 PSC, 24 PBC, 2 SSC).

11 Efficacy data were derived from the phase 3 PBC OCA International Study of Efficacy trial, and the n

12 scale (NRS), primary biliary cholangitis-40 (PBC-40) itch domain score and 5-D itch scale, changes in

13 point, bezafibrate led in 45% (41% PSC, 55% PBC) and placebo in 11% to >=50% reduction of severe or

14 uent replication in a separate cohort of 907 PBC cases and 2,127 controls.

15 In Lombardia there were 2,970 PBC cases with a female:male ratio of 2.3:1.

16 tant, Th17 skewing was prominent in advanced PBC patients with intensive secretion of IL-23p19 by inf

17 re the survival and cancer incidence in AIH, PBC, and PSC in the same population.

18 nosorbent assay in 165 serum samples of AIH, PBC, and controls.

19 lignancy on population-based cohorts of AIH, PBC, and PSC in Canterbury, New Zealand.

20 DNA samples from over 500 patients with AIH, PBC, and controls.

21 al Outcomes Study Short Form-36 (SF-36), and PBC-40 questionnaires.

22 netic and immunopathogenic basis for AIH and PBC at the MIF locus.

23 ession was elevated in patients with AIH and PBC versus healthy controls.

24 e in number of transplants for HBV, HCV, and PBC.

25 an clinical trials in patients with NASH and PBC.

26 itor cell activation differs between PSC and PBC and is characterized by a divergent fate commitment

27 In PSC and PBC, disease-associated clonotypes were detected among p

28 to severe pruritus in patients with PSC and PBC.

29 t links different pathogenic features of BA, PBC, and PSC.

30 (PBC) and investigated associations between PBC incidence and sociodemographic factors and spatial c

31 estigate the genetic variants shared between PBC and BMD.

32 he experimental sequence of NPBC followed by PBC at subsequent relapse or the standard reverse treatm

33 in patients with pancreaticobiliary cancers (PBCs).

34 teracts with the phosphate binding cassette (PBC) and base binding region (BBR) of EPAC1, similar to

35 contribution of the peptide-binding cavity (PBC) to C. albicans adhesion and assessed the adhesive p

36 tDNA) copy number in peripheral blood cells (PBC) has been associated with the risk of developing sev

37 n of the most straight periodic bond chains (PBCs) in metatorbernite structure.

38 oH loss, a finding we termed "minimal change PBC." Ten patients were identified prospectively as havi

39 ormal controls, livers with "minimal change" PBC, CHC, and RSLH showed 9.2 +/- 6.0, 0.44 +/- 0.37 (P

40 Purpose Platinum-based chemotherapy (PBC) for patients with progressing ovarian cancer (OC) i

41 seases, such as primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC), are frequ

42 m patients with primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC).

43 gitis (PSC) and primary biliary cholangitis (PBC) are human primary cholangiopathies characterized by

44 Primary biliary cholangitis (PBC) frequently recurs after liver transplantation.

45 Primary biliary cholangitis (PBC) has been regarded as female-predominant without evi

46 Primary biliary cholangitis (PBC) in younger patients has been suggested to require l

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

48 Primary biliary cholangitis (PBC) is a chronic, progressive autoimmune liver disease

49 Primary biliary cholangitis (PBC) is a disease of small bile ducts, which can lead to

50 Primary biliary cholangitis (PBC) is a rare autoimmune liver disease and the first li

51 Primary biliary cholangitis (PBC) is an autoimmune cholestatic liver disease linked t

52 Primary biliary cholangitis (PBC) is an autoimmune liver disease characterized by the

53 Primary biliary cholangitis (PBC) is an autoimmune liver disease with a strong heredi

54 tant feature of primary biliary cholangitis (PBC) pathogenesis and other cholestatic liver diseases.

55 Primary biliary cholangitis (PBC) primarily targets cholangiocytes and is characteriz

56 ionship between primary biliary cholangitis (PBC), a chronic cholestatic autoimmune liver disease, an

57 cal evidence of primary biliary cholangitis (PBC), are largely unknown.

58 pathogenesis of Primary Biliary Cholangitis (PBC), we have analyzed the role of Gal-3 in the murine m

59 term outcome in primary biliary cholangitis (PBC).

60 (PSC, SSC) and primary biliary cholangitis (PBC).

61 n comparison to primary biliary cholangitis (PBC).

62 associated with primary biliary cholangitis (PBC).

63 iseases such as primary biliary cholangitis (PBC, previously referred to as primary biliary cirrhosis

64 y atresia [BA], primary biliary cholangitis [PBC], and primary sclerosing cholangitis [PSC]), we buil

65 of patients with primary biliary cirrhosis (PBC) and are present before the onset of clinical diseas

66 the incidence of primary biliary cirrhosis (PBC) and investigated associations between PBC incidence

67 Primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are infreq

68 stasis, including primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC), results f

69 in patients with primary biliary cirrhosis (PBC) being positive or negative for anti-M2 antibodies r

70 hort patients and primary biliary cirrhosis (PBC) control patients were genotyped for the CD14 -260C>

71 Primary biliary cirrhosis (PBC) has a complex clinical phenotype, with debate about

72 Primary biliary cirrhosis (PBC) is a classical autoimmune liver disease for which e

73 Primary biliary cirrhosis (PBC) is a progressive autoimmune liver disease with a lo

74 Primary biliary cirrhosis (PBC) is an autoimmune disease characterized by clinical

75 AIMS: Studies of primary biliary cirrhosis (PBC) phenotypes largely have been performed using small

76 BA homeostasis in primary biliary cirrhosis (PBC) remains unknown.

77 e models of human primary biliary cirrhosis (PBC) suggest that activated T cells, particularly CD8 T

78 Primary biliary cirrhosis (PBC) was first described in the 1950s as a clinical synd

79 Primary biliary cirrhosis (PBC), a chronic autoimmune liver disease, has been assoc

80 ls from explanted primary biliary cirrhosis (PBC), and control liver using a total of 24 individual s

81 onferring risk to primary biliary cirrhosis (PBC), inflammatory bowel disease (IBD) and celiac diseas

82 ic liver diseases primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), and alcoholi

83 logic hallmark of primary biliary cirrhosis (PBC), the antimitochondrial response to the E2 component

84 ndications except primary biliary cirrhosis (PBC).

85 patitis (AIH) and primary biliary cirrhosis (PBC).

86 iopathogenesis of primary biliary cirrhosis (PBC).

87 f these cases had primary biliary cirrhosis (PBC).

88 susceptibility to primary biliary cirrhosis (PBC).

89 y resembles human primary biliary cirrhosis (PBC).

90 in patients with primary biliary cirrhosis (PBC).

91 nt for diagnosing primary biliary cirrhosis (PBC).

92 similar to human primary biliary cirrhosis (PBC).

93 received SLK for primary biliary cirrhosis (PBC, n=76), primary sclerosing cholangitis (n=81), hepat

94 ving first LT for primary biliary cirrhosis (PBC; n=3052), primary sclerosing cholangitis (PSC; n=385

95 with primary biliary cholangitis/cirrhosis (PBC), hepatic levels of miR-210 and KLF4 were highly ele

96 dance in cirrhotic relative to non-cirrhotic PBC patients.

97 ic PBC, seven female patients with cirrhotic PBC, and 11 healthy female controls were recruited by ph

98 al changes to patients with biopsy confirmed PBC.

99 Patients with confirmed PBCs had a mean of 118.4 +/- 36.8 CTCs/7.5 mL portal vei

100 The parent pentabenzo[a,d,g,j,m]coronene (PBC) compound is shown to exhibit a shifted and rotated

101 cells and/or drugs, indicating that coupling PBCs with MALDI-MSI has the potential to develop rapid,

102 Finally, cultured PBC cholangiocytes showed decreased AE2 activity, togeth

103 Paper-based cultures (PBCs) are an emerging 3D culture platform in which cells

104 tients with AMAs and normal ALP will develop PBC after 5 years.

105 ng MIF and MIF receptor profiles distinguish PBC from the more inflammatory phenotype of AIH and may

106 cimens from 10 patients with confirmed early PBC, 10 with early stage chronic hepatitis C (CHC), and

107 oved by the Food and Drug Administration for PBC treatment, has demonstrated positive effects on bioc

108 l, remained stable for AC, and decreased for PBC, PSC, HCV, CC, and HBV.

109 Our data indicate for PBC a sex ratio significantly lower than previously cite

110 alidate six previously unknown risk loci for PBC (Pcombined<5 x 10(-8)) and used pathway analysis to

111 may show the earliest changes suspicious for PBC, namely, loss of the canals of Hering (CoH).

112 veness of OCA as a second-line treatment for PBC in combination with ursodeoxycholic acid (UDCA) in a

113 the efficacy of ursodiol as a treatment for PBC were published, although it has been clear that urso

114 nd, placebo controlled, cross-over trial for PBC patients with pruritus.

115 Proteomic analysis of BECs from PBC liver compared to normal liver are significantly dif

116 ated from circulating mononuclear cells from PBC patients and healthy controls.

117 Whereas no patients died from PBC, the 5-year survival rate was 75%, as compared to 90

118 IL-23p19, IL-17, and IL-23R using liver from PBC (n = 51) and non-PBC (n = 80) control liver disease

119 ipheral blood mononuclear cells (PBMCs) from PBC patients (n = 33) and age-/sex-matched healthy contr

120 DR1101 is associated with protection from PBC, and its sequence includes an aspartic acid at beta5

121 Als3 features in the absence of a functional PBC.

122 ulticenter, international cohort (the Global PBC Study Group).

123 l to understand the immunopathology of human PBC.

124 In PBC, DR represents a relevant histologic prognostic mark

125 In PBC, DR was strongly correlated with clinical prognostic

126 e shown muscle bioenergetic abnormalities in PBC, including increased muscle acidosis with exercise l

127 27(+)) were found to have lower abundance in PBC than in control.

128 characterized progenitor cell activation in PBC versus PSC.

129 RNA - for the decreased expression of AE2 in PBC.

130 The symptom burden in PBC, which is unrelated to disease severity or ursodeoxy

131 ife and impaired health status was common in PBC patients (35% and 46%, respectively) and more common

132 round the damaged interlobular bile ducts in PBC.

133 we addressed the hypothesis that fatigue in PBC is driven by muscle bioenergetic abnormality related

134 ffectiveness for the treatment of fatigue in PBC.

135 by K19 immunostaining is an early feature in PBC.

136 to PBC, whereas lower frequency was found in PBC, compared to both AIH and healthy controls.

137 D27(-)) subsets were significantly higher in PBC patients with cirrhosis (indicative of late-stage di

138 ing enhanced expression of IL21 and IL21R in PBC livers (particularly in the hepatic portal tracks) s

139 ion of IL-12/Th1-mediated immunopathology in PBC.

140 ne-related loci not previously implicated in PBC and confirmed associations at 19 of 22 established r

141 ier, and had a higher proliferation index in PBC compared with PSC.

142 monocytes and naive B cells were observed in PBC compared to control.

143 rdiovascular disease was significant only in PBC and alcoholic liver disease, owing to high mortality

144 ve been proposed as potential pruritogens in PBC.

145 , a novel class of drug to treat pruritus in PBC.

146 gest a sustained rigorous B-cell response in PBC, likely activated and perpetuated by cognate autoant

147 However, its role in PBC has not been addressed.

148 Strikingly, in PBC, although there were no significant differences in B

149 analysis of the peripheral immune system in PBC at single-cell resolution.

150 In Denmark there were 722 cases of incident PBC, female:male ratio was 4.2:1, and the annual inciden

151 years from North East England with incident PBC diagnosed during 1987-2003.

152 oss-sectional study using the United Kingdom-PBC, patient cohort.

153 ss spectrometry imaging with PBCs (MALDI-MSI-PBC) as a drug screening platform.

154 ed that prolonging PFI with single-agent non-PBC (NPBC) may offer a strategy to improve overall outco

155 IL-23R using liver from PBC (n = 51) and non-PBC (n = 80) control liver disease patients.

156 Thirteen female patients with noncirrhotic PBC, seven female patients with cirrhotic PBC, and 11 he

157 In conclusion, our study identified a novel PBC susceptibility variant that has been shown to be str

158 8/CTLA4/ICOS, CD58, ARID3A and IL16 as novel PBC risk loci.

159 (2mM) which did not change the amplitude of PBC significantly decreased peak afferent firing from 79

160 -E2), the major mitochondrial autoantigen of PBC and xenobiotic cross reactive chemicals.

161 pe of the major mitochondrial autoantigen of PBC, 2-octynoic acid (2-OA) coupled to BSA (2OA-BSA) and

162 We focused on the incident cases of PBC, including gender and outcome, among 9.7 million inh

163 (IgM) and using sera from a large cohort of PBC patients and controls (n = 516), we examined in deta

164 The lifetime cost of PBC treatment would increase from $63,000 to $902,000 (1

165 cal model to simulate the lifetime course of PBC patients treated with OCA+UDCA versus UDCA alone.

166 re critical components in the development of PBC.

167 enetic factors at play in the development of PBC.

168 tal-based field-effect transistor devices of PBC exhibited efficient charge transport behavior, givin

169 = 216), or with nonestablished diagnosis of PBC (n = 229).

170 feature may support a clinical diagnosis of PBC even in the absence of characteristic, granulomatous

171 The diagnosis of PBC was established with International Classification of

172 cal practice does not lead to a diagnosis of PBC.

173 of AMA-positive patients without evidence of PBC was 16.1 per 100,000.

174 IL-12/Th1 and IL-23/Th17 in the evolution of PBC.

175 gnostic or suggestive histologic features of PBC, but with near complete CoH loss; six had available

176 ient mice, capturing several key features of PBC, including liver-specific inflammation focused on po

177 and immunologically, reflect key features of PBC, providing a useful generic model to understand the

178 f Efficacy trial, and the natural history of PBC was informed by published clinical studies.

179 e findings confirm that overall incidence of PBC did not rise over time, but sociodemographic variati

180 The age/sex-adjusted annual incidence of PBC was 16.7 per million.

181 Loss of PBC function resulted in an adhesion phenotype that was

182 clusion, we developed a novel mouse model of PBC that may help to elucidate the detailed mechanism of

183 F-beta receptor II (dnTGF-betaRII) (model of PBC) and wild-type mice at 12 wk of age were treated wit

184 dvantage of our well-defined murine model of PBC, in which mice are immunized with 2-octynoic acid co

185 Fifth, several mouse models of PBC highlight the importance of loss of tolerance to PDC

186 rove existing long-term prognostic models of PBC using data from the UK-PBC Research Cohort.

187 The reported high familial occurrence of PBC could imply screening with AMA of FDR with at least

188 stantially improve the long-term outcomes of PBC patients, but at its current annual price of $69,350

189 ave been used to clarify the pathogenesis of PBC and are generally considered reflective of an autoim

190 The pathogenesis of PBC is thought to be orchestrated by Th1 and/or Th17.

191 patient cohort to obtain a better picture of PBC phenotypes.

192 Conclusion: The prevalence of PBC among the Medicare beneficiaries has increased.

193 verall survival, incidence and prevalence of PBC in two well defined population-based studies over a

194 The prognosis of PBC patients can be accurately evaluated using the UK-PB

195 acid (UDCA), which slows the progression of PBC, particularly in stage I and II of the disease.

196 e of cirrhosis, the 5-year incidence rate of PBC was 16%.

197 s could identify patients with recurrence of PBC (based on histologic analysis).

198 d risk factors associated with recurrence of PBC and its effects on patient and graft survival in a m

199 with time-dependent covariate, recurrence of PBC significantly associated with graft loss (HR, 2.01;

200 PBC is increased irrespective of the risk of PBC development.

201 Risk of PBC increased in areas with higher levels of socioeconom

202 whereas use of cyclosporine reduced risk of PBC recurrence (HR, 0.62; 95% CI, 0.46-0.82; P = .001).

203 = .008) were associated with higher risk of PBC recurrence, whereas use of cyclosporine reduced risk

204 The study of PBC in the 2000s has been buoyed by two basic science ad

205 al human cholangiocytes, and transfection of PBC cholangiocytes with anti-miR-506 was able to improve

206 DCA formulations applied in the treatment of PBC.

207 ations could lead to better understanding of PBC pathogenesis and progression, and also to the discov

208 s have greatly advanced our understanding of PBC.

209 nt trends in mortality and healthcare use of PBC patients in the Medicare program.

210 an be used for molecular characterization of PBCs and share features of metastatic tissue.

211 to study the pathogenesis and progression of PBCs, as well as a diagnostic or prognostic tool to stra

212 Structural analysis of purified loss-of-PBC-function mutant proteins showed that the mutations d

213 the opposing effects of these HLA alleles on PBC susceptibility, we compared the features of epitopes

214 4(+) helper T subsets and their cytokines on PBC using our previous established murine model of 2-OA-

215 measured using quantitative real-time PCR on PBC DNA samples from participants in the UK-based Breakt

216 Compared with older adults, early-onset PBC in younger patients requiring LT had higher percenta

217 = 5) and from patients with PSC (n = 20) or PBC (n = 20).

218 luated on a numerical rating scale and other PBC symptoms in an electronic diary completed twice dail

219 at E2A-PBX1 self-associates through the PBX1 PBC-B domain of the chimeric protein to form higher-orde

220 Strategies are needed to prevent PBC recurrence or reduce its negative effects.

221 10 on visual analog scale [VAS]) due to PSC, PBC, or SSC were recruited for this double-blind, random

222 ezafibrate on pruritus in patients with PSC, PBC, and SSC.

223 static, resectable, or borderline-resectable PBCs had a mean of 83.2 CTCs/7.5 mL portal vein blood (m

224 taRII mice expressed features of early-stage PBC along with enhanced Sct/SR axis activation and Sct s

225 ared to patients with diagnostic early-stage PBC biopsies, showed identical treatment responses to ur

226 Human early-stage PBC patients had an increase in hepatobiliary Sct and SR

227 s of SR antagonist treatment for early-stage PBC.

228 iliary and hepatic damage during early-stage PBC.

229 In both early and late-stage PBC, the predominant Ig isotype to SAc is IgM, with tite

230 to rPDC-E2 in early-stage versus late-stage PBC.

231 eloped that are widely used to risk stratify PBC patients and guide their management.

232 udy, we evaluated 18 patients with suspected PBCs.

233 isease risk does not vary spatially and that PBC cases occur independently.

234 We conclude that PBC induces characteristic changes in liver expression o

235 sion MITO-8 supports the recommendation that PBC not be delayed in favor of an NPBC in patients with

236 The PBC group demonstrated significantly reduced cerebral St

237 The PBC mutant phenotype was evaluated in assays using monol

238 Hospital reduced 66.1% the PBC treatment costs using manufactured UDCA.

239 dated symptom assessment tools including the PBC-40 was also undertaken and is reported here.

240 omplexes that contain one member each of the PBC and MEIS/PREP subclasses.

241 rate the essential and principal role of the PBC in Als3 adhesion.

242 Expression of the PBC protein PBX1 in the SVZ has been reported, but its f

243 Hospital reduced the PBC treatment costs using the manufactured UDCA by the u

244 analyses are needed to demonstrate that the PBC model can be effectively applied in clinical setting

245 Model outcomes were validated using the PBC Global Study.

246 ults, and symptom impact (assessed using the PBC-40 and other related measures).

247 sure was fatigue severity assessed using the PBC-40 fatigue domain at 3 months.

248 the average overlap of 0.77% seen within the PBC (P = 0.024) and ALD groups (0.40%, P < 0.0001).

249 This method discriminated regions of the PBCs with and without cells and/or drugs, indicating tha

250 ng peripheral blood CD4+ T cells compared to PBC patients and healthy controls, indicating increased

251 peripheral blood CD4(+) T cells compared to PBC patients and healthy controls, indicating increased

252 +/- standard error of the mean) compared to PBC samples (1.13 +/- 0.17, P < 0.0001) and ALD samples

253 Compared to PBC, 5-year outcomes were worse for NASH, HCV, and HCC f

254 ession -794 CATT7 allele in AIH, compared to PBC, whereas lower frequency was found in PBC, compared

255 tory IFN-gamma production that contribute to PBC pathology.

256 which has the closest serologic features to PBC is a mouse with a T-cell-restricted expression of th

257 Intriguingly, two PBC susceptibility loci identified through genome-wide a

258 gnostic models of PBC using data from the UK-PBC Research Cohort.

259 nts can be accurately evaluated using the UK-PBC risk scores.

260 literature of AIH type 2 with an unexpected PBC-specific AMA positivity in a young child.

261 ll subsets in 59 subjects, including 28 with PBC, 13 with primary sclerosing cholangitis (PSC), and 1

262 ery 8 weeks through week 20), in adults with PBC and an inadequate response to ursodeoxycholic acid t

263 t chronic liver inflammation associated with PBC can impact brain function.

264 er liver transplantation are associated with PBC recurrence.

265 = 0.044) were significantly associated with PBC.

266 es and subsets significantly associated with PBC.

267 de significant BMD SNPs for association with PBC using two European GWAS data sets (n = 8392), with r

268 ly charges and payments per beneficiary with PBC increased from $3,065 and $777 (2005) to $5,773 and

269 ly charges and payments per beneficiary with PBC increased from $59,765 and $19,406 (2007), to $98,94

270 Compared with PBC, 5-year graft and patient survival were (a) similar

271 e progenitor cell niche in PSC compared with PBC.

272 ith PBC (n = 275), previously diagnosed with PBC (n = 216), or with nonestablished diagnosis of PBC (

273 e categorized as either newly diagnosed with PBC (n = 275), previously diagnosed with PBC (n = 216),

274 Compared to those newly diagnosed with PBC, the patients were slightly younger, had lower AMA t

275 d crossover study in patients diagnosed with PBC.

276 Younger age at the time of diagnosis with PBC or at liver transplantation, tacrolimus use, and bio

277 cal data from 785 patients (89% female) with PBC who underwent liver transplantation (mean age, 54 +/

278 57 participants aged 18 years or older with PBC and moderate to severe fatigue were randomized to re

279 In liver tissues from patients with PBC and dnTGF-betaRII mice, a model of autoimmune cholan

280 uld be able to determine which patients with PBC are likely to progress despite treatment with ursodi

281 ion medicine may be needed for patients with PBC at various stages of their disease process.

282 tes, resource use for Medicare patients with PBC continues to rise.

283 echnique, to determine whether patients with PBC exhibit reduced cerebral oxygen saturation (StO(2) )

284 ics and outcome of LT in young patients with PBC in comparison with older adults.

285 r levels of CD74 were found in patients with PBC versus AIH and controls.

286 c acid (UDCA) therapy in early patients with PBC was associated with increased cerebral tHb concentra

287 Using NIRS, patients with PBC were found to have hypoxia, increased cerebral hemog

288 A total of 2084 patients with PBC were included in the analysis with 158 young patient

289 database was analyzed for all patients with PBC who underwent LT between 2000 and 2012.

290 ty for osteoporosis therapy in patients with PBC, although adherence is higher with the monthly regim

291 evated in cholestatic mice and patients with PBC, promoting BA-induced liver injury in part by target

292 Among patients with PBC, response to UDCA, treatment and symptoms are relate

293 estigative therapeutic tool in patients with PBC.

294 rebrovascular dysregulation in patients with PBC.

295 nd treatment cost reduction in patients with PBC.

296 d from 90% among patients who presented with PBC when they were older than age 70, to less than 50% f

297 2-year study in 42 postmenopausal women with PBC and osteoporosis.

298 on/ionization-mass spectrometry imaging with PBCs (MALDI-MSI-PBC) as a drug screening platform.

299 portal vein blood samples from patients with PBCs, but less than 25% of peripheral blood samples.

300 e mortality of AMA-positive patients without PBC is increased irrespective of the risk of PBC develop