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 tional age are at higher risk for developing hyperbilirubinemia.

6 diatrics for the detection and management of hyperbilirubinemia.

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

8 Another right lobe donor had prolonged hyperbilirubinemia.

9 an population, particularly individuals with hyperbilirubinemia.

10 course was remarkable for resolving neonatal hyperbilirubinemia.

11 cal therapy of life-threatening unconjugated hyperbilirubinemia.

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

13 ntage of infants with clinically significant hyperbilirubinemia.

14 hepatic reserve predicts the development of hyperbilirubinemia.

15 potential therapies for treating pathologic hyperbilirubinemia.

16 he neurologic sequelae observed after severe hyperbilirubinemia.

17 er blood analysis showed severe unconjugated hyperbilirubinemia.

18 ntrol developmental repression of UGT1A1 and hyperbilirubinemia.

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

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

21 gastrointestinal symptoms, and asymptomatic hyperbilirubinemia.

22 arunavir, respectively, primarily because of hyperbilirubinemia.

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

24 e stress when neonatal mice encounter severe hyperbilirubinemia.

25 id not distinguish GVHD from other causes of hyperbilirubinemia.

26 and OATP1B3 deficiencies explains Rotor-type hyperbilirubinemia.

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

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

29 fying infants at risk for subsequent, severe hyperbilirubinemia.

30 borns at risk for developing severe neonatal hyperbilirubinemia.

31 ntify infants at risk for subsequent, severe hyperbilirubinemia.

32 lergic reaction, elevated transaminases, and hyperbilirubinemia.

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

34 4 patients; edema, 3 patients; diarrhea and hyperbilirubinemia, 1 patient).

35 18%) levels; hypoalbuminemia (10% and 19%); hyperbilirubinemia (10% and 22%); and alopecia (18%).

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

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

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

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

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

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

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

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

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

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

46 Hyperbilirubinemia after creation of transjugular intrah

47 Severe hyperbilirubinemia after TIPS creation heralds a high ri

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

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

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

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

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

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

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

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

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

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

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

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

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

61 Hyperbilirubinemia and hypoalbuminemia occurred and surv

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

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

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

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

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

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

68 Conjugated hyperbilirubinemia and unconjugated hypercholanemia and

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

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

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

72 >200 U/L, (2) severe ALI (coagulopathy with hyperbilirubinemia), and (3) death, all within 18 months

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

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

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

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

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

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

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

80 toxicities included transaminase elevations, hyperbilirubinemia, and infections.

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

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

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

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

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

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

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

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

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

90 New treatments for hyperbilirubinemia are being evaluated.

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

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

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

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

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

96 19 adults who developed severe hyperbilirubinemia (bilirubin level > 171.0 micromol/L)

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

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

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

100 Hyperbilirubinemia can be reduced by activation of pregn

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

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

103 Hyperbilirubinemia, caused by the accumulation of unconj

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

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

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

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

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

109 Sequelae of severe neonatal hyperbilirubinemia constitute a substantial disease burd

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

111 Hepatic insufficiency (hyperbilirubinemia, decreased serum fibrinogen, elevated

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

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

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

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

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

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

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

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

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

121 Within the hyperbilirubinemia group, those with positive direct ant

122 (0.2 SD) decrease in adjusted scores in the hyperbilirubinemia group.

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

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

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

126 Consistently, patients with hyperbilirubinemia had significantly lower erythrocyte a

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

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

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

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

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

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

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

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

135 Excessive hyperbilirubinemia in human neonates can cause permanent

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

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

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

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

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

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

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

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

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

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

146 Predictors of hyperbilirubinemia included nonalcoholic causes of liver

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

148 1 to eliminate bilirubin that contributes to hyperbilirubinemia-induced neurotoxicity in the developm

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

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

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

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

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

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

155 Hyperbilirubinemia is the subject of ongoing study, whic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 25,409 infants in the Late Impact of Getting Hyperbilirubinemia or Phototherapy (LIGHT) birth cohort.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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