ライフサイエンスコーパス: gastrointestinal toxicity

1 estinal membrane integrity and contribute to gastrointestinal toxicity.

2 or bladder dose or in acute genitourinary or gastrointestinal toxicity.

3 xtensively researched, and radiation-induced gastrointestinal toxicity.

4 s respectively 72% and 25% for mucositis and gastrointestinal toxicity.

5 or bladder dose or in acute genitourinary or gastrointestinal toxicity.

6 setting because of platelet dysfunction and gastrointestinal toxicity.

7 omise, but special attention must be paid to gastrointestinal toxicity.

8 trations of SN-38, which are associated with gastrointestinal toxicity.

9 tory and clinically, toward reducing NSAIDs' gastrointestinal toxicity.

10 COX inhibition, they also cause significant gastrointestinal toxicity.

11 ducing nonsteroidal anti-inflammatory drugs' gastrointestinal toxicity.

12 article reviews mechanisms of NSAID-induced gastrointestinal toxicity.

13 rescription dose) is associated with serious gastrointestinal toxicity.

14 ANSAIDs) increases the risk of serious upper gastrointestinal toxicity.

15 associated with an increased risk of serious gastrointestinal toxicity.

16 s without the same concerns over significant gastrointestinal toxicity.

17 phrotoxicity (25%), neurotoxicity (23%), and gastrointestinal toxicity (21%).

18 nts had grade 3 or greater treatment-related gastrointestinal toxicity (22.0% during chemoradiotherap

19 ted to substantially increased incidences of gastrointestinal toxicity (58% of sucralfate patients v

20 urotoxicity (16%), nephrotoxicity (13%), and gastrointestinal toxicity (9%).

21 ations of c.1679T>G and c.1236G>A/HapB3 with gastrointestinal toxicity (adjusted RR 5.72, 95% CI 1.40

22 a side effect, they have been known to cause gastrointestinal toxicity, although the molecular mechan

23 are antiinflammatory and analgesic but lack gastrointestinal toxicity, an undesirable side effect at

24 percent of patients experienced grade 3 to 4 gastrointestinal toxicity and 62% experienced grade 2 to

25 I, 1.11-19.2]) polymorphisms were related to gastrointestinal toxicity and infection, respectively.

26 distinct advantages with regard to both low gastrointestinal toxicity and restored therapeutic activ

27 The effects of combination therapy on the gastrointestinal toxicity and therapeutic activity of fr

28 d with foretinib were fatigue, hypertension, gastrointestinal toxicities, and nonfatal pulmonary embo

29 cities occurred in 7.6% and 0% (p = 0.4) and gastrointestinal toxicities, and, in 15.2% and 5% (p = 0

30 ive ACs was 240 mg/m2, and myelosuppression, gastrointestinal toxicity, and fatigue were the DLTs.

31 e major side effects observed with CPT-11 is gastrointestinal toxicity, and we supposed that this mig

32 Acute genitourinary and gastrointestinal toxicity as defined by the Radiation Th

33 equency of late radiation grades 3, 4, and 5 gastrointestinal toxicity ascribed to the LTAD-RT arm (2

34 The agents lacked the bone marrow and gastrointestinal toxicities associated with antiprolifer

35 etes without the concern for hypoglycemia or gastrointestinal toxicities associated with some other m

36 aling drugs) in preventing the serious upper gastrointestinal toxicity associated with another exposu

37 eces may serve as a noninvasive biomarker of gastrointestinal toxicity associated with perturbed Notc

38 tive for Cox-2 over Cox-1) seem to have less gastrointestinal toxicity associated with their use; how

39 ring pelvic radiotherapy resulted in reduced gastrointestinal toxicity both acutely and at 1 y compar

40 rtezomib-related toxicities: hematologic and gastrointestinal toxicities by Common Terminology Criter

41 subset of tumors, but may avoid the limiting gastrointestinal toxicity caused by pharmacological inhi

42 Described herein is a FGSI-mediated gastrointestinal toxicity characterized by cell populati

43 Gastrointestinal toxicity correlated significantly with

44 Unlike upper gastrointestinal toxicity, cyclooxygenase-mediated mecha

45 Unlike upper gastrointestinal toxicity, cyclooxygenase-mediated mecha

46 ding the development of malignancies, severe gastrointestinal toxicities, diabetes, cardiac arrhythmi

47 ted, and common adverse events included mild gastrointestinal toxicities (diarrhea [46%], constipatio

48 ontoured) correlated with grade 3 or greater gastrointestinal toxicity during chemoradiotherapy (45%

49 most common methods to reduce NSAID-induced gastrointestinal toxicity has been to co-prescribe proph

50 limited antileukemic cytotoxicity and severe gastrointestinal toxicity have restricted the clinical a

51 nonsteroidal anti-inflammatory drug-induced gastrointestinal toxicity, identification of groups at h

52 ted preoperative chemotherapy with grade 3-4 gastrointestinal toxicity in 7% (seven of 94) of patient

53 ted in modest efficacy and mild but frequent gastrointestinal toxicity in MF patients.

54 , and high-fiber diets for the prevention of gastrointestinal toxicity in patients undergoing pelvic

55 ay (ED50 = 38.7 mg/kg) with no indication of gastrointestinal toxicity in rats at doses as high as 20

56 The lack of gastrointestinal toxicity is likely due to the low absor

57 Gastrointestinal toxicity is the primary limiting factor

58 Gastrointestinal toxicity (nausea, vomiting, and diarrhe

59 Except for the instance of grade 3 gastrointestinal toxicity, nonhematologic toxicity was r

60 ity of 23.2%, grade 3 or 4 treatment-related gastrointestinal toxicity of 26.4% (including diarrhea,

61 entiate the primary determinants of skin and gastrointestinal toxicity of erlotinib.

62 heory that inhibition of COX-1 underlies the gastrointestinal toxicity of NSAIDs in man.

63 tients, five were taken off study because of gastrointestinal toxicity or intolerance to SC.

64 educed folate carrier polymorphism predicted gastrointestinal toxicity (OR, 10.4 [95% CI, 1.35-80.4])

65 one hemorrhage, anemia, febrile neutropenia, gastrointestinal toxicity, pain, fatigue, neuropathy (on

66 A decreased risk of gastrointestinal toxicity remains the primary justificat

67 Hepatotoxicity and gastrointestinal toxicity represented the major adverse

68 a dramatic decrease in chemotherapy-induced gastrointestinal toxicities, significant potentiation of

69 Multiple gastrointestinal toxicities that often occurred together

70 patients at this dose level experienced late gastrointestinal toxicity that required surgical managem

71 Bortezomib-related toxicities (gastrointestinal toxicity, thrombocytopenia, and paresth

72 Gastrointestinal toxicity was also significantly lower f

73 Gastrointestinal toxicity was most common, with 21 patie

74 Consequently, a marked reduction in gastrointestinal toxicity was observed relative to irino

75 insufficiency, secondary to dehydration from gastrointestinal toxicity, was also seen.

76 Acute urinary and gastrointestinal toxicities were similar to those expect

77 Gastrointestinal toxicities were the most common treatme

78 Grades 3 and 4 hematologic and gastrointestinal toxicity were more frequent in the RT +

79 ytopenia, neurotoxicity, nephrotoxicity, and gastrointestinal toxicity were more severe with cisplati

80 ficant differences in acute genitourinary or gastrointestinal toxicity were observed.

81 etastasis, blood perfusion, oxygenation, and gastrointestinal toxicity were studied.

82 ith AML were grade 1 or 2 constitutional and gastrointestinal toxicities, which were generally manage

83 protected WT mice from DNA damage and acute gastrointestinal toxicity, which resulted in improved ov

84 efficacy, with less hematologic and greater gastrointestinal toxicity with IP.

85 There is evidence of increased gastrointestinal toxicity with the three-drug combinatio

86 Gastrointestinal toxicity with this regimen is most prom