ライフサイエンスコーパス: drug hypersensitivity

1 ds might also improve the ability to predict drug hypersensitivity.

2 tiple NSAID-Hs are poor predictors of actual drug hypersensitivity.

3 y the pathologic role of HLA in delayed-type drug hypersensitivity.

4 irect functional role in the pathogenesis of drug hypersensitivity.

5 olerated, although two individuals developed drug hypersensitivity.

6 ng that G269V leads to a unique mechanism of drug hypersensitivity.

7 c mRNAs and displayed a synergistic level of drug hypersensitivity.

8 polymorphisms have previously been linked to drug hypersensitivities.

9 This substitution created broad, severe drug hypersensitivity, although drug binding, ATP hydrol

10 tailed molecular mechanism of HLA-associated drug hypersensitivity, and has clinical correlations for

11 93 cells induces the same toxic phenotype of drug hypersensitivity as PrPDeltaCR.

12 cularly anaphylaxis, including food allergy, drug hypersensitivity, atopic dermatitis (AD), allergic

13 inhibitor often inducing severe delayed-type drug hypersensitivity, can trigger innate immune activat

14 There is still a lack of knowledge on drug hypersensitivity (DH) epidemiology, clinical spectr

15 trongest and best-documented risk factor for drug hypersensitivity (DH) is the history of a previous

16 lleles are the major genetic determinants of drug hypersensitivity; however, the underlying molecular

17 However, data on the frequency of drug hypersensitivity in mastocytosis and vice versa are

18 This is the first demonstration of drug hypersensitivity in primary cells of mesenchymal or

19 Drug hypersensitivity includes allergic (AR) and nonalle

20 re and presents the expert experience of the Drug Hypersensitivity Interest Group of the European Aca

21 Drug hypersensitivity involves the activation of T cells

22 Before initiating antibiotic therapy, drug hypersensitivity is an important consideration, and

23 Drug hypersensitivity is known to rely on a drug-specifi

24 In summary, drug hypersensitivity is the end result of a drug intera

25 Collateral sensitivity (CS), a phenomenon of drug hypersensitivity, is defined as the ability of cert

26 Drug hypersensitivity may deprive patients of drug thera

27 eactions have tendencies to develop multiple drug hypersensitivities (MDH).

28 ts that induce TolC opening also reverse the drug hypersensitivity phenotype of the AcrB beta-hairpin

29 tion mutant to engage with TolC leads to the drug hypersensitivity phenotype, which is reversed by co

30 m a low-copy-number plasmid confers a severe drug hypersensitivity phenotype.

31 Two validated tools were used: the Drug Hypersensitivity Quality-of-Life Questionnaire (DrH

32 Results: Two cases are reported of drug hypersensitivity reaction that were treated with cy

33 tember 1996 and July 2015 for a suspicion of drug hypersensitivity reaction to BLs, with negative ST

34 Drug hypersensitivity reactions (DHRs) are a matter of g

35 ns resembling allergy occur, they are called drug hypersensitivity reactions (DHRs) before showing th

36 Drug hypersensitivity reactions (DHRs) represent growing

37 Immediate drug hypersensitivity reactions (IDHR) to moxifloxacin c

38 Immune-mediated drug hypersensitivity reactions (IDHRs) represent a sign

39 Drug hypersensitivity reactions are an important clinica

40 al evidence that some exanthematous allergic drug hypersensitivity reactions are mediated by drug-spe

41 Mechanisms for DIL modeled after drug hypersensitivity reactions are unsupported experime

42 10% of patients with severe immune-mediated drug hypersensitivity reactions have tendencies to devel

43 ions are among the most commonly encountered drug hypersensitivity reactions in clinical practice.

44 p performed a literature search on immediate drug hypersensitivity reactions in clonal MC disorders u

45 dies have identified strong linkages between drug hypersensitivity reactions to several drugs and spe

46 t mechanisms proposed in the pathogenesis of drug hypersensitivity reactions, including the hapten hy

47 For certain HLA allele-associated drug hypersensitivity reactions, the parent drug has bee

48 In some HLA-associated drug hypersensitivity reactions, the presence of a risk

49 re the most frequent medicaments involved in drug hypersensitivity reactions, with NSAID-induced urti

50 d clinical setting will help to avoid severe drug hypersensitivity reactions.

51 f paramount importance for the evaluation of drug hypersensitivity reactions.

52 tization has been well documented in delayed drug hypersensitivity reactions.

53 in reducing ADRs, especially those caused by drug hypersensitivity reactions.

54 Incidences of vomiting and drug-hypersensitivity reactions were significantly highe

55 port the advances and use of the pioneering "Drug hypersensitivity" subsection of ICD-11 and implemen

56 that can significantly inhibit CTL-mediated drug hypersensitivity, such as that seen in patients wit

57 mmunologically mediated type B ADRs, such as drug hypersensitivity syndrome, drug reaction with eosin

58 kidney, lungs, and/or heart) in the case of drug hypersensitivity syndrome.

59 in the immunopathogenesis of T-cell mediated drug hypersensitivity syndromes.

60 Drug hypersensitivity was confirmed by histopathologic t

61 WRN-deficient diploid fibroblasts, in which drug hypersensitivity was entirely due to reduced cell p

62 The diagnosis of drug hypersensitivity was obtained by skin tests in 72.9

63 s (NSAIDs) are the most frequent triggers of drug hypersensitivity with NSAIDs-induced urticaria/angi