ライフサイエンスコーパス: hyperbilirubinemia

1 equent non-DLTs included diarrhea, rash, and hyperbilirubinemia.

2 n mentation associated with pancytopenia and hyperbilirubinemia.

3 eding, deep wound infection, reoperation, or hyperbilirubinemia.

4 alloporphyrins for the treatment of neonatal hyperbilirubinemia.

5 potential therapies for treating pathologic hyperbilirubinemia.

6 tional age are at higher risk for developing hyperbilirubinemia.

7 ntrol developmental repression of UGT1A1 and hyperbilirubinemia.

8 diatrics for the detection and management of hyperbilirubinemia.

9 in the management and follow-up of neonatal hyperbilirubinemia.

10 Another right lobe donor had prolonged hyperbilirubinemia.

11 an population, particularly individuals with hyperbilirubinemia.

12 cal therapy of life-threatening unconjugated hyperbilirubinemia.

13 stop codon, absence of enzyme activity, and hyperbilirubinemia.

14 hepatic reserve predicts the development of hyperbilirubinemia.

15 sis, lactic acidosis, haemolytic anaemia and hyperbilirubinemia.

16 ested with aminotransferase elevation and/or hyperbilirubinemia.

17 fects were observed, except for asymptomatic hyperbilirubinemia.

18 half exhibiting grade III or higher indirect hyperbilirubinemia.

19 mes (OR 1.81, 1.19-2.76) more likely to have hyperbilirubinemia.

20 acute appendicitis 41 subjects (37.27%) had hyperbilirubinemia.

21 y diagnosis and timely treatment of neonatal hyperbilirubinemia.

22 atal conditions, bronchiolitis, and neonatal hyperbilirubinemia.

23 e a significantly increased risk of neonatal hyperbilirubinemia.

24 ginase allergy, pancreatitis, thrombosis, or hyperbilirubinemia.

25 aminotransferase (ALT) increase and grade 4 hyperbilirubinemia.

26 their potential in the treatment of neonatal hyperbilirubinemia.

27 course was remarkable for resolving neonatal hyperbilirubinemia.

28 ntage of infants with clinically significant hyperbilirubinemia.

29 he neurologic sequelae observed after severe hyperbilirubinemia.

30 er blood analysis showed severe unconjugated hyperbilirubinemia.

31 icemia, biliary atresia, and other causes of hyperbilirubinemia.

32 stem, and cerebellum, and is associated with hyperbilirubinemia.

33 gastrointestinal symptoms, and asymptomatic hyperbilirubinemia.

34 arunavir, respectively, primarily because of hyperbilirubinemia.

35 (UGT) 1A1--to prevent the onset of neonatal hyperbilirubinemia.

36 e stress when neonatal mice encounter severe hyperbilirubinemia.

37 id not distinguish GVHD from other causes of hyperbilirubinemia.

38 and OATP1B3 deficiencies explains Rotor-type hyperbilirubinemia.

39 and loss of expression of UGT1A1, leading to hyperbilirubinemia.

40 nt in the adult bone marrow, but also causes hyperbilirubinemia.

41 fying infants at risk for subsequent, severe hyperbilirubinemia.

42 borns at risk for developing severe neonatal hyperbilirubinemia.

43 ntify infants at risk for subsequent, severe hyperbilirubinemia.

44 lergic reaction, elevated transaminases, and hyperbilirubinemia.

45 Three adverse events [hypoxia (2) and hyperbilirubinemia (1)] were determined to be severe in

46 4 patients; edema, 3 patients; diarrhea and hyperbilirubinemia, 1 patient).

47 18%) levels; hypoalbuminemia (10% and 19%); hyperbilirubinemia (10% and 22%); and alopecia (18%).

48 3 or 4 treatment-related adverse events were hyperbilirubinemia (10%), thrombocytopenia (7%), and IDH

49 imilar numbers of patients with grade 3 or 4 hyperbilirubinemia (12% and 17%), constipation and abdom

50 nib-related adverse events included indirect hyperbilirubinemia (12%) and IDH-inhibitor-associated di

51 er 188 group than the placebo group included hyperbilirubinemia (12.7% vs 5.2%); those more common in

52 Fourteen of the children with hyperbilirubinemia (17 percent) had "questionable" or ab

53 y a week (P =.002), and risk of grade 3 or 4 hyperbilirubinemia (18% v 5%; P =.02).

54 Common low-grade toxicities included hyperbilirubinemia (25%) and increased AST (36%).

55 % vs 2.0%; OR, 1.42; 95% CI, 1.07-1.90), and hyperbilirubinemia (3.6% vs 2.5%; OR, 1.47; 95% CI, 1.13

56 headaches (50%), fever (45%), chills (45%), hyperbilirubinemia (34%), lymphopenia (34%), infusion-re

57 n study, 94% of patients had a rash, 56% had hyperbilirubinemia, 61% had diarrhea, and 84% had nausea

58 Other toxicities included grade 3/4 hyperbilirubinemia (7%) and elevated hepatic transaminas

59 Grade 3 or greater hyperbilirubinemia (70%) was the only dose-dependent tox

60 ion resulted in a lower incidence of newborn hyperbilirubinemia (8.8% vs. 29.4%, P = 0.03) and newbor

61 greater toxicities developed, most commonly hyperbilirubinemia (8/75, 11%) and thrombocytopenia (2/7

62 le for 132 of 140 children with a history of hyperbilirubinemia (94 percent) and 372 of 419 controls

63 ealth of the liver, and for the diagnosis of hyperbilirubinemia (a condition that afflicts approximat

64 Hyperbilirubinemia after creation of transjugular intrah

65 Severe hyperbilirubinemia after TIPS creation heralds a high ri

66 compared with 213 adults who did not develop hyperbilirubinemia after TIPS creation.

67 nvasive, quick method to screen for neonatal hyperbilirubinemia, although refinement and validation o

68 romol per liter) in 130 of the newborns with hyperbilirubinemia and 30 mg per deciliter (513 micromol

69 isorders associated with severe unconjugated hyperbilirubinemia and a life-long risk of kernicterus.

70 enetic basis for interpatient variability in hyperbilirubinemia and aminotransferase level elevations

71 in ATP11C are characterized by a conjugated hyperbilirubinemia and an unconjugated hypercholanemia.

72 tion is the result of a common cause of both hyperbilirubinemia and asthma (confounding).

73 l phenotype has been linked to both neonatal hyperbilirubinemia and asthma in several studies.

74 e UGT1A1*28 variant has been associated with hyperbilirubinemia and atazanavir discontinuation.

75 There seems to be no link between hyperbilirubinemia and autism spectrum disorders.

76 s have resulted in the reemergence of severe hyperbilirubinemia and bilirubin encephalopathy, clinica

77 ); these mice spontaneously develop neonatal hyperbilirubinemia and BIND.

78 ression of intestinal UGT1A1, which leads to hyperbilirubinemia and BIND; suppression of this gene ap

79 l phototherapy for the treatment of neonatal hyperbilirubinemia and did not result in any study withd

80 Hepatotoxic effects, including hyperbilirubinemia and elevated alanine aminotransferase

81 Hyperbilirubinemia and hypoalbuminemia occurred and surv

82 duct ligation (CBDL), at which time they had hyperbilirubinemia and hypoalbuminemia.

83 c disorder associated with mild unconjugated hyperbilirubinemia and no clinical illness.

84 atients, i.e., those patients without severe hyperbilirubinemia and renal failure, and retransplantat

85 the sulfadimethoxine model and human newborn hyperbilirubinemia and resulted in increased plasma bili

86 The combined defect leads to severe hyperbilirubinemia and shows how seemingly benign geneti

87 asparaginase-related toxicities were lengthy hyperbilirubinemia and transaminitis, occasionally resul

88 Conjugated hyperbilirubinemia and unconjugated hypercholanemia and

89 tion of Exacerbated Liver Insufficiency with Hyperbilirubinemia and/or Encephalopathy and/or Renal Fa

90 tion of Exacerbated Liver Insufficiency with Hyperbilirubinemia and/or Encephalopathy and/or Renal Fa

91 tion of Exacerbated Liver Insufficiency with Hyperbilirubinemia and/or Encephalopathy and/or Renal Fa

92 >200 U/L, (2) severe ALI (coagulopathy with hyperbilirubinemia), and (3) death, all within 18 months

93 w recommendations on immunizations, neonatal hyperbilirubinemia, and animal-induced injuries.

94 anges in the areas of immunization, neonatal hyperbilirubinemia, and animal-induced injury.

95 s had dose-limiting but reversible asthenia, hyperbilirubinemia, and azotemia or acidosis; however, i

96 atively high incidences of myelosuppression, hyperbilirubinemia, and elevated hepatic transaminases,

97 inal pain, acute hepatomegaly, coagulopathy, hyperbilirubinemia, and fulminant hepatic failure.

98 DLTs were hepatic transaminitis, hyperbilirubinemia, and hand foot syndrome (HFS) on the

99 with a lower rate of development of ascites, hyperbilirubinemia, and hepatocellular carcinoma.

100 mia, progressive hepatomegaly, liver injury, hyperbilirubinemia, and increased ductular reaction unde

101 toxicities included transaminase elevations, hyperbilirubinemia, and infections.

102 Both patients presented with jaundice, hyperbilirubinemia, and mild-to-moderate elevations in s

103 olus, 70-mg/m(2) infusion) with tumor lysis, hyperbilirubinemia, and mucositis.

104 e-limiting toxicities including neutropenia, hyperbilirubinemia, and nausea or vomiting.

105 tcomes, including respiratory complications, hyperbilirubinemia, and NICU admission, were increased i

106 th injury, need for intensive neonatal care, hyperbilirubinemia, and preeclampsia.

107 Onset at an early age, acute presentation, hyperbilirubinemia, and presence of HLA DRB1*03 characte

108 aundice resulting from isolated unconjugated hyperbilirubinemia, and rash or photosensitivity were mo

109 ts were myelosuppression, transient indirect hyperbilirubinemia, and rashes.

110 r transplantation is performed before marked hyperbilirubinemia, and when possible, using a living-do

111 , some developed ascites, generalized edema, hyperbilirubinemia, and/or coagulopathy that prompted un

112 New treatments for hyperbilirubinemia are being evaluated.

113 hat may alleviate or worsen the condition of hyperbilirubinemia are discussed.

114 for detecting and preventing severe neonatal hyperbilirubinemia are reviewed, as well as anticipated

115 t study, establishment of a possible role of hyperbilirubinemia as a marker of gangrenous/perforated

116 mbocytopenia (n = 1; 2.5%), and proteinuria, hyperbilirubinemia, back pain, hyperkalemia, and anorexi

117 is recommended that monitoring for neonatal hyperbilirubinemia be more thorough to prevent the conse

118 e that were fed breast milk developed severe hyperbilirubinemia because of suppression of UGT1A1 in t

119 19 adults who developed severe hyperbilirubinemia (bilirubin level > 171.0 micromol/L)

120 ntensification, 50% had increased ALT and 3% hyperbilirubinemia (both grade 3/4 and correlated with a

121 eased among patients with HLA mismatching or hyperbilirubinemia but not among those with other risk f

122 NIM811 also blunted hyperbilirubinemia by 54%, increased serum albumin by 51

123 espread or prophylactic use in neonates with hyperbilirubinemia can be recommended.

124 Hyperbilirubinemia can be reduced by activation of pregn

125 n as kernicterus Although a large portion of hyperbilirubinemia cases in newborns are associated with

126 isorder characterized by severe unconjugated hyperbilirubinemia caused by a deficiency of uridine dip

127 Hyperbilirubinemia, caused by the accumulation of unconj

128 emonstrate that the onset of severe neonatal hyperbilirubinemia, characterized by seizures, leads to

129 the 2 groups in terms of the development of hyperbilirubinemia, cirrhosis, or virologic and immunolo

130 nant hepatic failure with subsequent extreme hyperbilirubinemia, coagulopathy, and pericardial tampon

131 ariable constellation of findings, including hyperbilirubinemia, coagulopathy, encephalopathy, and as

132 ower cardiac index, anemia, hypoalbuminemia, hyperbilirubinemia, cognitive impairment, and depression

133 of unacceptable toxicity defined as grade 3 hyperbilirubinemia (Common Terminology Cancer Adverse Ev

134 Sequelae of severe neonatal hyperbilirubinemia constitute a substantial disease burd

135 cessive disorder characterized by conjugated hyperbilirubinemia, coproporphyrinuria, and near-absent

136 Hepatic insufficiency (hyperbilirubinemia, decreased serum fibrinogen, elevated

137 Unconjugated hyperbilirubinemia develops in up to 25% of patients rec

138 mbocytopenia, anemia, persistent bacteremia, hyperbilirubinemia, diarrhea, vomiting, nausea, elevated

139 These results suggest that hyperbilirubinemia during critical illness does not nece

140 , continuous veno-venous hemofiltration, and hyperbilirubinemia during extracorporeal membrane oxygen

141 The latest practice guidelines on hyperbilirubinemia emphasize close follow-up of all newb

142 these mice have cholestasis with conjugated hyperbilirubinemia, failure to excrete technetium-labele

143 cause liver damage, such as phenylketonuria, hyperbilirubinemias, familial hypercholesterolemia, prim

144 lines for common problems, including asthma, hyperbilirubinemia, febrile seizures, gastroenteritis, a

145 transplantation there was frequent temporary hyperbilirubinemia (five of eight recipients; bilirubin

146 h strong trends in hypoalbuminemia grade and hyperbilirubinemia grade emerged across the CRBN rs16727

147 Within the hyperbilirubinemia group, those with positive direct ant

148 (0.2 SD) decrease in adjusted scores in the hyperbilirubinemia group.

149 and 28 (relative risk [RR] 2.4, P = .0002), hyperbilirubinemia > or =6 mg/dL during the first 20 day

150 a similar model with low marrow cellularity, hyperbilirubinemia > or =6 mg/dL, and elevated serum cre

151 By 90 days, 95% of patients with hyperbilirubinemia had died or had undergone liver trans

152 riptome analysis revealed that patients with hyperbilirubinemia had enhanced expression of hepatic UP

153 Consistently, patients with hyperbilirubinemia had significantly lower erythrocyte a

154 or decades, phenobarbital (PB) treatment for hyperbilirubinemia has been known to increase expression

155 found that diet-induced obese mice with mild hyperbilirubinemia have reduced WAT size and an increase

156 for the clinical features, risk factors for hyperbilirubinemia, health related quality of life [Shor

157 ifest as elevated serum transaminase levels, hyperbilirubinemia, hypoalbuminemia, and prolongation of

158 death and neonatal complications, including hyperbilirubinemia, hypoglycemia, hyperinsulinemia, and

159 ed anemia, leukopenia, pancytopenia, nausea, hyperbilirubinemia, hypophosphatemia, and anorexia.

160 limiting toxicity observed included grade 3 hyperbilirubinemia in 1 of 6 patients on DL1, and grade

161 tributable toxicity was asymptomatic grade 3 hyperbilirubinemia in 1 recipient of vitamin A at day +3

162 shed with US from other causes of conjugated hyperbilirubinemia in 98% of infants if multiple US feat

163 toring for newborn jaundice and treatment of hyperbilirubinemia in an effort to prevent kernicterus a

164 3 ALT elevation and one patient had grade 3 hyperbilirubinemia in cycle 1.

165 It was Mixed Type of Hyperbilirubinemia in gangrenous/perforated appendicitis

166 corepressor 1 (NCoR1) completely diminishes hyperbilirubinemia in hUGT1 neonates because of intestin

167 Excessive hyperbilirubinemia in human neonates can cause permanent

168 Severe unconjugated hyperbilirubinemia in humans that suffer from Crigler-Na

169 Our aim was to determine whether isolated hyperbilirubinemia in liver transplant recipients was du

170 liver and present with isolated unconjugated hyperbilirubinemia in liver transplant recipients.

171 ted with the UGT1A1*28 allele contributes to hyperbilirubinemia in mice.

172 Debate exists on how to screen for hyperbilirubinemia in neonates and new strategies are em

173 xt, the continued study of the management of hyperbilirubinemia in preventing kernicterus is examined

174 nventional phototherapy for the treatment of hyperbilirubinemia in term and late-preterm neonates in

175 ic, five patients with isolated unconjugated hyperbilirubinemia in the absence of hemolysis, recurren

176 clude that complete, long-term correction of hyperbilirubinemia in the Gunn rat model of Crigler-Najj

177 Here we explore this hyperbilirubinemia in two independent Atp11c mutant mous

178 Predictors of hyperbilirubinemia included nonalcoholic causes of liver

179 and activation of PXR led to protection from hyperbilirubinemia induced by bilirubin infusion or hemo

180 1 to eliminate bilirubin that contributes to hyperbilirubinemia-induced neurotoxicity in the developm

181 ocus and the Ugt1a1 gene in liver to promote hyperbilirubinemia-induced seizures and central nervous

182 on receptor, Toll-like receptor 2 (TLR2), to hyperbilirubinemia-induced signaling.

183 ing the causes and physiopathology of severe hyperbilirubinemia, investigating molecular mechanisms u

184 can progress to end-stage liver disease and hyperbilirubinemia is a hallmark of cholestasis.

185 However, hyperbilirubinemia is a well-recognized adverse effect o

186 raft injury; specifically, marked, transient hyperbilirubinemia is associated with the subsequent dev

187 Jaundice resulting from unconjugated hyperbilirubinemia is easily treated with exposure to bl

188 However, in hUGT1/Pxr(-/-) mice, hyperbilirubinemia is greatly reduced due to induction o

189 Hyperbilirubinemia is the subject of ongoing study, whic

190 atal hUGT1 mice that display severe neonatal hyperbilirubinemia leads to induction of intestinal UGT1

191 Pre-LT hyperbilirubinemia levels and creatinine >100 umol/L wer

192 omegaly (summary LR, 6.5; 95% CI, 3.9-11.0), hyperbilirubinemia (LR, 7.3; 95% CI, 5.5-9.6), or thromb

193 y Drainage, Functional Drained Liver Volume, Hyperbilirubinemia, Malignant Biliary Obstruction, Objec

194 vity, this drug has not been associated with hyperbilirubinemia, most likely because of the higher K(

195 ally, respondents suggested that "persistent hyperbilirubinemia" must be defined by a time-and-value

196 Grade 3 and 4 toxicities included hyperbilirubinemia (n = 10), thrombocytopenia (n = 6), o

197 ss with NICU admission, neonatal jaundice or hyperbilirubinemia, neonatal hypoglycemia, and neonatal

198 investigate the correlation between neonatal hyperbilirubinemia (NHB) and hypoglycemia (NH) in Chines

199 were examined in a preclinical model for the hyperbilirubinemia observed with some HIV PIs, and both

200 Grade 3 or 4 hyperbilirubinemia occurred in 13% of patients at any ti

201 Grade 3 or 4 hyperbilirubinemia occurred in 17% of patients.

202 aths occurred on study; reversible grade 3/4 hyperbilirubinemia occurred in 2 patients.

203 emoglobin decrease and a single case of mild hyperbilirubinemia occurred in the tafenoquine group.

204 38409 were associated with increased risk of hyperbilirubinemia (odds ratio [OR], 2.18 [95% CI, 1.89-

205 mia (odds ratio, 5.8; 95% CI, 2.2-15.1), and hyperbilirubinemia (odds ratio, 9.1; 95% CI, 2.6-31.8) w

206 Fifty-one patients (26%) developed hyperbilirubinemia of 68.4 microM (4 mg/dL) or greater,

207 logy Criteria for Adverse Events (version 4) hyperbilirubinemia of grade 3 or higher and elevated liv

208 ls more susceptible to developing high-grade hyperbilirubinemia on ATV/r.

209 ed hepatic transaminases (two patients), and hyperbilirubinemia (one patient).

210 RRV-infected Ig-alpha(-/-) mice did not have hyperbilirubinemia or bile duct obstruction.

211 Kernicterus generally occurs in untreated hyperbilirubinemia or cases where treatment is delayed.

212 Conventional phototherapy does not prevent hyperbilirubinemia or eliminate the need for exchange tr

213 Neonatal hyperbilirubinemia or jaundice is associated with kernic

214 rsus-host HLA mismatching, and in those with hyperbilirubinemia or multiple sites affected by chronic

215 25,409 infants in the Late Impact of Getting Hyperbilirubinemia or Phototherapy (LIGHT) birth cohort.

216 CU admission (OR = 1.12; 95% CI, 1.07-1.17), hyperbilirubinemia (OR = 1.09; 95% CI, 1.04-1.14), respi

217 cs, ART regimens, or laboratory profiles and hyperbilirubinemia (p > 0.05).

218 ucuronosyltransferase polymorphism predicted hyperbilirubinemia (P = .017, P < .001, and P < .001) an

219 which was also independently associated with hyperbilirubinemia (P = .026).

220 cally assessed for risk of developing severe hyperbilirubinemia prior to hospital discharge.

221 lso discuss the possible mechanisms by which hyperbilirubinemia protects against cardiovascular disea

222 lated with age, alcoholism, hypoalbuminemia, hyperbilirubinemia, renal insufficiency, hyponatremia, a

223 rth, large or small for gestational age, and hyperbilirubinemia requiring phototherapy.

224 unit (NICU) admission, NICU length of stay, hyperbilirubinemia, respiratory distress syndrome, apnea

225 rome type I is characterized by unconjugated hyperbilirubinemia resulting from an autosomal recessive

226 isorder characterized by severe unconjugated hyperbilirubinemia resulting from deficiency of the hepa

227 uppression (RR, 2.37; 95% CI, 1.16 to 4.88), hyperbilirubinemia (RR, 1.06; 95% CI, 1.03 to 1.08 per 1

228 -glutamyl transpeptidase (eight of 44, 18%), hyperbilirubinemia (seven of 44, 16%), elevated alanine

229 enemia, coagulopathy, hepatic transaminitis, hyperbilirubinemia, severe neutropenia, elevated lactate

230 ities included hand-foot syndrome, diarrhea, hyperbilirubinemia, skin rash, myalgia, and arthralgia.

231 Severe neonatal hyperbilirubinemia (SNH) and the onset of bilirubin ence

232 mechanistic basis of bilirubin excretion and hyperbilirubinemia syndromes is largely understood, but

233 bsence of which leads to severe unconjugated hyperbilirubinemia that can cause irreversible neurologi

234 of its rarity, the much more common indirect hyperbilirubinemia that occurs in the newborn period, an

235 characteristics and laboratory profile with hyperbilirubinemia through univariate and multivariate l

236 events that connect developmentally induced hyperbilirubinemia to bilirubin-induced neurological dys

237 consecutive fasting infants with conjugated hyperbilirubinemia underwent detailed US studies perform

238 Diagnosis and treatment of neonatal hyperbilirubinemia uses population and hour-based norms

239 as preventive treatment options for neonatal hyperbilirubinemia using the hUGT1*1 humanized mice and

240 when phototherapy was unavailable, neonatal hyperbilirubinemia was associated with an increased risk

241 No evidence of ascites or prolonged hyperbilirubinemia was encountered in any right- or left

242 allelic polymorphism in the UGT1A1 promoter, hyperbilirubinemia was monitored in humanized UGT1 mice

243 fer significantly between groups except that hyperbilirubinemia was more common in the longer-term st

244 Hyperbilirubinemia was present in over 85% of the patien

245 Hyperbilirubinemia was the RLT and occurred in 60% of pa

246 city, including elevated hepatic enzymes and hyperbilirubinemia, was less common.

247 In two mouse models of pathologic hyperbilirubinemia, we show that genetic deletion of eit

248 iver function tests, incidence of conjugated hyperbilirubinemia, weight, length, mortality, and brain

249 ever, malaise, and fatigue) and asymptomatic hyperbilirubinemia were the chief dose-limiting toxic ef

250 hand-foot syndrome (P <.00001) and grade 3/4 hyperbilirubinemia were the only toxicities more frequen

251 hUGT1/Pxr-null mice did not develop severe hyperbilirubinemia, whereas hUGT1/Car-null mice were sus

252 miting toxicity (DLT) consisting of rash and hyperbilirubinemia, whereas one of six patients develope

253 ients with malignant biliary obstruction and hyperbilirubinemia who underwent de novo PTBD between Ja

254 Eight (24%) cases of hyperbilirubinemia with or without liver enzyme elevatio

255 ischarge risk assessment for severe neonatal hyperbilirubinemia with the goal of minimizing subsequen

256 hUGT1) and the UGT1A1 gene, develop neonatal hyperbilirubinemia, with 8-10% of hUGT1 mice succumbing

257 There was a high prevalence of indirect hyperbilirubinemia, with a significant proportion experi

258 contrast, neonatal hUGT1 mice display severe hyperbilirubinemia, with limited expression of the UGT1A

259 s characterized by intermittent unconjugated hyperbilirubinemia without structural liver damage, affe

260 roups, with the exception of mild reversible hyperbilirubinemia, without serum aminotransferase abnor