ライフサイエンスコーパス: hepatic dysfunction

1 diovascular dysfunction and does not include hepatic dysfunction.

2 -renal dysfunction and no additional risk of hepatic dysfunction.

3 hat usually presents in early childhood with hepatic dysfunction.

4 multiorgan injury, including intestinal and hepatic dysfunction.

5 rmacokinetics of vorinostat in patients with hepatic dysfunction.

6 not associated with respiratory symptoms or hepatic dysfunction.

7 iary sludge and gallstones, which exacerbate hepatic dysfunction.

8 omplicated by underlying liver cirrhosis and hepatic dysfunction.

9 t and did not develop the bimodal pattern of hepatic dysfunction.

10 frequently not recommended for patients with hepatic dysfunction.

11 effective but costly treatment for end-stage hepatic dysfunction.

12 ith hereditary apoAI amyloidosis who develop hepatic dysfunction.

13 ing renal insufficiency and 13 patients with hepatic dysfunction.

14 Granular cell tumor is a rare cause of hepatic dysfunction.

15 their role in mediating pancreatitis-induced hepatic dysfunction.

16 not feasible because of thrombocytopenia and hepatic dysfunction.

17 and explaining the mechanism of IL-2-induced hepatic dysfunction.

18 s limited by associated toxicities including hepatic dysfunction.

19 increased toxicity occurred in patients with hepatic dysfunction.

20 l implications for the management of various hepatic dysfunctions.

21 flammation, fever, and multiorgan, including hepatic, dysfunction.

22 even patients receiving intravenous PGE1 for hepatic dysfunction (0.11-1.30 microg/kg/hr) had a pulmo

23 59 years; females, n = 24); 42 patients had hepatic dysfunction (16 mild, 15 moderate, and 11 severe

24 regated albumin ((99m)TcMAA), or measures of hepatic dysfunction, 5-year survival associated with OLT

25 During liver failure and hepatic dysfunction, a marked reduction of bile acid syn

26 the hypothesis that this form of preexisting hepatic dysfunction alters the kinetics of circulating T

27 Septic hepatic dysfunction, an important determinant of outcome

28 n (>60%) is frequently associated with early hepatic dysfunction and an increased incidence of primar

29 the drug in patients with varying degrees of hepatic dysfunction and definitively establish the role

30 diabetes, dwarfism, renal Fanconi syndrome, hepatic dysfunction and hypercholestrolemia.

31 MSCs ameliorated hepatic dysfunction and improved liver regeneration afte

32 A strong clinical association exists between hepatic dysfunction and increased morbidity and mortalit

33 believed to be a critical factor leading to hepatic dysfunction and may be important in the pathogen

34 interleukin-6 is an important determinant of hepatic dysfunction and mortality in sepsis.

35 hether loss of interleukin-6 activity caused hepatic dysfunction and mortality, we induced sepsis in

36 nt diets deplete humans of choline and cause hepatic dysfunction and steatosis.

37 Patients with renal or hepatic dysfunction and those who received enteral nutri

38 lence of steroid exposure, and prevalence of hepatic dysfunction, and all were immunoglobulin G posit

39 Smaller patient size, renal dysfunction, hepatic dysfunction, and biventricular assist device use

40 hypertension, infections, renal dysfunction, hepatic dysfunction, and malignancies) were consistent w

41 was shown to include carpal tunnel syndrome, hepatic dysfunction, and possibly angioedema.

42 toprotein, hepatitis serologies, severity of hepatic dysfunction, and presence of cirrhosis were eval

43 ejection treatment and presented with fever, hepatic dysfunction, and progressive leukopenia.

44 h Evaluation II score, severity of renal and hepatic dysfunction, and red cell transfusions were all

45 or vasopressors; neurologic, respiratory, or hepatic dysfunction; and acute noninfectious condition)

46 Central nervous system, pulmonary, and hepatic dysfunctions are intimately involved in the mort

47 plasma PGE1 concentrations in patients with hepatic dysfunction being treated with PGE1 and in a swi

48 armacokinetic parameters among the normal or hepatic dysfunction categories.

49 ly vorinostat dose was escalated within each hepatic dysfunction category.

50 HCV-seropositive patients due to concerns of hepatic dysfunction caused by immunosuppression.

51 as designed to evaluate whether pre-existing hepatic dysfunction (cirrhosis) leads to increased morbi

52 months of pioglitazone therapy, significant hepatic dysfunction developed.

53 n the source of infection, sex, age, chronic hepatic dysfunction, diabetes, severity of illness, nutr

54 ociated with thrombocytosis (p = 0.05), with hepatic dysfunction (elevated alanine aminotransferase;

55 s in body temperature, signs of modest early hepatic dysfunction (hyperlactemia, hyperammonemia, prol

56 Instead, analyses revealed hepatic dysfunction, hypoalbuminemia, and vascular/oxyge

57 nal features such as dilated cardiomyopathy, hepatic dysfunction, hypothyroidism, male hypogonadism,

58 hyperammonemia is an underlying link between hepatic dysfunction in cirrhosis and skeletal muscle los

59 orms may have potential for evaluating acute hepatic dysfunction in critically ill trauma patients.

60 Hepatic dysfunction in cystic fibrosis (CF) has been att

61 ds of managing the major diseases related to hepatic dysfunction in pregnancy.

62 hs from pulmonary toxic effects and one from hepatic dysfunction in the escalated-therapy group.

63 At this early stage in ethanol-dependent hepatic dysfunction, infiltration of inflammatory cells

64 al circulatory support, hypoalbuminemia, and hepatic dysfunction), intraoperative blood loss, surgica

65 Hepatic dysfunction is a recognized complication after F

66 Hepatic dysfunction is an important but poorly understoo

67 Hepatic dysfunction is an important determinant of the c

68 Inclusion of patients with mild to moderate hepatic dysfunction may be possible when the totality of

69 armacokinetics of erlotinib in patients with hepatic dysfunction or renal dysfunction.

70 75, 100, and 150 mg, starting with 50 mg in hepatic dysfunction patients and 75 mg in renal dysfunct

71 d Chronic Health Evaluation III score, acute hepatic dysfunction, pneumonia and aspiration, sepsis/se

72 cement of the hepatic parenchyma, leading to hepatic dysfunction, portal hypertension, and hepatomega

73 so restores hepatic homeostasis and improves hepatic dysfunction postburn via alterations in the sign

74 eration of the Mini-Mental Status Exam), and hepatic dysfunction (presenting as the syndrome of hepat

75 esection because of tumor size, location, or hepatic dysfunction related to cirrhosis.

76 Patients with varying degrees of hepatic dysfunction require appropriate dose reduction e

77 ), single (RR, 0.77; 95%CI, 0.67, 0.88), had hepatic dysfunction (RR, 0.73; 95%CI, 0.66, 0.89), had n

78 f metabolic abnormalities, and regression of hepatic dysfunction secondary to recurrent steatosis.

79 Before and during the onset of hepatic dysfunction, sera were tested on immunoblottings

80 pteran insecticides might be associated with hepatic dysfunction, serum glucose elevation, inflammati

81 Despite severe hepatic dysfunction, serum TPO levels were initially nor

82 age, 30 years; range, 17-41 years) developed hepatic dysfunction severe enough to require transfer to

83 Patients with hepatic dysfunction should be treated at a reduced dose

84 atients with CM, nonketotic hypoglycemia and hepatic dysfunction, skeletal myopathy, or sudden death

85 Under conditions of ethanol-dependent hepatic dysfunction, steatosis is increased, and this is

86 pecially in populations with MetS-associated hepatic dysfunction that likely impairs alpha-tocopherol

87 ency virus (HIV) patients, and the resulting hepatic dysfunction that occurs is the primary cause of

88 different groups depending on the degree of hepatic dysfunction, the presence of portal-systemic shu

89 Hepatic dysfunction was categorized as mild, moderate, o

90 Hepatic dysfunction was common (33%).

91 To determine the mechanism for IL-2-induced hepatic dysfunction, we hypothesized that IL-2 activatio

92 rinostat doses in mild, moderate, and severe hepatic dysfunction were 300, 200, and 100 mg, respectiv

93 ots stained by sera collected at the time of hepatic dysfunction were more numerous and more intensel

94 The majority of patients have underlying hepatic dysfunction, which complicates patient managemen

95 ion before ECMO, and development of renal or hepatic dysfunction while on ECMO.

96 Fifteen patients with hepatic dysfunction who were mechanically ventilated, ei

97 (n = 3), hepatic infarction (n = 1), and/or hepatic dysfunction with portal hypertension (n = 1).

98 e HE, and there were 3 control groups: acute hepatic dysfunction without severe HE (n = 50), chronic

99 F) is a rare syndrome of severe, rapid-onset hepatic dysfunction-without prior advanced liver disease