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1 BL) antibiotics are the most common cause of drug hypersensitivity.
2 al reactivations, autoimmunity, and multiple drug hypersensitivity.
3 res for TP53 loss, retaining their intrinsic drug hypersensitivity.
4 regulation influences susceptibility towards drug hypersensitivity.
5 nce angiogenesis deficits and antiangiogenic drug hypersensitivity.
6 ds might also improve the ability to predict drug hypersensitivity.
7 tiple NSAID-Hs are poor predictors of actual drug hypersensitivity.
8 y the pathologic role of HLA in delayed-type drug hypersensitivity.
9 irect functional role in the pathogenesis of drug hypersensitivity.
10 olerated, although two individuals developed drug hypersensitivity.
11 ng that G269V leads to a unique mechanism of drug hypersensitivity.
12 c mRNAs and displayed a synergistic level of drug hypersensitivity.
13 ation test (DPT) was used to define positive drug hypersensitivity.
14 t have potential for diagnostic purposes in (drug) hypersensitivity.
15 previously been considered in the context of drug hypersensitivities.
16 polymorphisms have previously been linked to drug hypersensitivities.
17      This substitution created broad, severe drug hypersensitivity, although drug binding, ATP hydrol
18 DX11 helicase activity prevents chemotherapy drug hypersensitivity and accumulation of DNA damage.
19 lure, rapid death by cancer, cellular cancer-drug hypersensitivity and severe replication instability
20 8%) and with placebo in 21 patients (16.9%); drug hypersensitivity and skin reactions occurred in the
21 ic requirements for IgE-dependent allergies, drug hypersensitivities, and subsets of autoimmune urtic
22 tailed molecular mechanism of HLA-associated drug hypersensitivity, and has clinical correlations for
23                            Multiple forms of drug hypersensitivity are strongly linked to expression
24 93 cells induces the same toxic phenotype of drug hypersensitivity as PrPDeltaCR.
25 cularly anaphylaxis, including food allergy, drug hypersensitivity, atopic dermatitis (AD), allergic
26 inhibitor often inducing severe delayed-type drug hypersensitivity, can trigger innate immune activat
27 pes, diagnosis, prognosis, and prediction of drug hypersensitivity development, as well on the identi
28        There is still a lack of knowledge on drug hypersensitivity (DH) epidemiology, clinical spectr
29 trongest and best-documented risk factor for drug hypersensitivity (DH) is the history of a previous
30                                   Therefore, drug hypersensitivity diagnosis relies on both in vitro
31 ng drug hypersensitivity: in vitro tools for drug hypersensitivity diagnosis, recently identified bio
32                                           In drug hypersensitivity, drug provocation testing (DPT), a
33 he patient, cutaneous reactions unrelated to drug hypersensitivity, drug-infection interactions, or d
34 lleles are the major genetic determinants of drug hypersensitivity; however, the underlying molecular
35  or C-terminal truncation of CALR eliminated drug hypersensitivity in CALR-mutated cells.
36            However, data on the frequency of drug hypersensitivity in mastocytosis and vice versa are
37           This is the first demonstration of drug hypersensitivity in primary cells of mesenchymal or
38 s recent advances in these 3 areas regarding drug hypersensitivity: in vitro tools for drug hypersens
39                                              Drug hypersensitivity includes allergic (AR) and nonalle
40 re and presents the expert experience of the Drug Hypersensitivity Interest Group of the European Aca
41                                              Drug hypersensitivity involves the activation of T cells
42        Before initiating antibiotic therapy, drug hypersensitivity is an important consideration, and
43                                              Drug hypersensitivity is known to rely on a drug-specifi
44                                     Although drug hypersensitivity is often suspected in patients wit
45                                  In summary, drug hypersensitivity is the end result of a drug intera
46 Collateral sensitivity (CS), a phenomenon of drug hypersensitivity, is defined as the ability of cert
47                                              Drug hypersensitivity may deprive patients of drug thera
48 eactions have tendencies to develop multiple drug hypersensitivities (MDH).
49 re increased alanine aminotransferase (n=1), drug hypersensitivity (n=1), nephritis (n=1), and panic
50 rred in four (8%) of 48 patients, which were drug hypersensitivity (n=1), panic attack (n=1), pyrexia
51  a suspected non-steroidal anti-inflammatory drug hypersensitivity (NSAIDH), challenge tests with the
52 tic conditions needed for the elicitation of drug hypersensitivity or tolerogenic pathways.
53 ts that induce TolC opening also reverse the drug hypersensitivity phenotype of the AcrB beta-hairpin
54 tion mutant to engage with TolC leads to the drug hypersensitivity phenotype, which is reversed by co
55 m a low-copy-number plasmid confers a severe drug hypersensitivity phenotype.
56           Two validated tools were used: the Drug Hypersensitivity Quality-of-Life Questionnaire (DrH
57 ome (MDH) is used to describe persons with a drug hypersensitivity reaction (DHR) to at least two che
58           Results: Two cases are reported of drug hypersensitivity reaction that were treated with cy
59 tember 1996 and July 2015 for a suspicion of drug hypersensitivity reaction to BLs, with negative ST
60 e), between 1997 and 2017 for a suspicion of drug hypersensitivity reaction to NSAIDs.
61 SJS/TEN), which are the most severe types of drug hypersensitivity reaction with a mortality rate up
62 toms (DRESS) is a rare but potentially fatal drug hypersensitivity reaction.
63 ESS) syndrome is a rare, severe delayed-type drug hypersensitivity reaction.
64                                              Drug hypersensitivity reactions (DHR) are based on disti
65                                              Drug hypersensitivity reactions (DHR) are heterogeneous
66         Virus infections and T-cell-mediated drug hypersensitivity reactions (DHR) can influence each
67 ities, the prevalence and characteristics of drug hypersensitivity reactions (DHR) in pediatric patie
68 nrolled 104 CMD patients with a suspicion of drug hypersensitivity reactions (DHR) or without known t
69                                              Drug hypersensitivity reactions (DHRs) are a matter of g
70                                              Drug hypersensitivity reactions (DHRs) are associated wi
71                                              Drug hypersensitivity reactions (DHRs) are common, and t
72     The immunological mechanisms involved in drug hypersensitivity reactions (DHRs) are complex, and
73                                              Drug hypersensitivity reactions (DHRs) are nowadays the
74 ns resembling allergy occur, they are called drug hypersensitivity reactions (DHRs) before showing th
75                 Despite their low frequency, drug hypersensitivity reactions (DHRs) can be serious an
76                       A correct diagnosis of drug hypersensitivity reactions (DHRs) is very important
77                                              Drug hypersensitivity reactions (DHRs) represent growing
78                                              Drug hypersensitivity reactions (DHRs) to platinum-based
79 ated adverse reactions-collectively known as drug hypersensitivity reactions (DHRs).
80                                    Immediate drug hypersensitivity reactions (IDHR) to moxifloxacin c
81        They can be classified into immediate-drug hypersensitivity reactions (IDHRs) and delayed-DHRs
82                                    Immediate drug hypersensitivity reactions (IDHRs) are a burden for
83                         Diagnosing immediate drug hypersensitivity reactions (IDHRs) can pose a signi
84                                    Immediate drug hypersensitivity reactions (IDHRs) pose significant
85                              Immune-mediated drug hypersensitivity reactions (IDHRs) represent a sign
86                                    Immediate drug hypersensitivity reactions (IDHRs) to clavulanic ac
87 upation as a putative mechanism of immediate drug hypersensitivity reactions (IDHRs), we also specula
88 s been widely used to evaluate non-immediate drug hypersensitivity reactions (NIDHRs).
89 hich is of major importance in prevention of drug hypersensitivity reactions and drug-induced pruritu
90               Delayed-type, T cell-mediated, drug hypersensitivity reactions are a serious unwanted m
91                                              Drug hypersensitivity reactions are an important clinica
92                                 Delayed-type drug hypersensitivity reactions are major causes of morb
93 al evidence that some exanthematous allergic drug hypersensitivity reactions are mediated by drug-spe
94             Mechanisms for DIL modeled after drug hypersensitivity reactions are unsupported experime
95 mation about the diagnosis and management of drug hypersensitivity reactions due to current and candi
96  10% of patients with severe immune-mediated drug hypersensitivity reactions have tendencies to devel
97 ions are among the most commonly encountered drug hypersensitivity reactions in clinical practice.
98 p performed a literature search on immediate drug hypersensitivity reactions in clonal MC disorders u
99 establish a better differential diagnosis of drug hypersensitivity reactions in the course of the dis
100 ons (cADRs) are potentially life-threatening drug hypersensitivity reactions involving the skin and i
101 cutaneous findings, some being the result of drug hypersensitivity reactions such as maculopapular dr
102 the diagnosis and clinical management of the drug hypersensitivity reactions that can potentially occ
103 dies have identified strong linkages between drug hypersensitivity reactions to several drugs and spe
104 asophil activation test in the evaluation of Drug Hypersensitivity Reactions" from the European Acade
105 t mechanisms proposed in the pathogenesis of drug hypersensitivity reactions, including the hapten hy
106            For certain HLA allele-associated drug hypersensitivity reactions, the parent drug has bee
107                       In some HLA-associated drug hypersensitivity reactions, the presence of a risk
108 re the most frequent medicaments involved in drug hypersensitivity reactions, with NSAID-induced urti
109 matitis, allergic rhinitis, food allergy and drug hypersensitivity reactions.
110 h as drug-induced pruritus to prevent severe drug hypersensitivity reactions.
111  the allergological work-up in this field of drug hypersensitivity reactions.
112  data emerged on the pathogenesis of delayed drug hypersensitivity reactions.
113 in reducing ADRs, especially those caused by drug hypersensitivity reactions.
114 d clinical setting will help to avoid severe drug hypersensitivity reactions.
115 f paramount importance for the evaluation of drug hypersensitivity reactions.
116 tization has been well documented in delayed drug hypersensitivity reactions.
117 n and inflammation, are the main triggers of drug hypersensitivity reactions.
118 r unique mechanistic insights into immediate drug hypersensitivity reactions.
119                   Incidences of vomiting and drug-hypersensitivity reactions were significantly highe
120 port the advances and use of the pioneering "Drug hypersensitivity" subsection of ICD-11 and implemen
121                                              Drug hypersensitivity such as severe cutaneous adverse r
122  that can significantly inhibit CTL-mediated drug hypersensitivity, such as that seen in patients wit
123                                     Multiple drug hypersensitivity syndrome (MDH) is used to describe
124                                     Multiple drug hypersensitivity syndrome almost exclusively appear
125 mmunologically mediated type B ADRs, such as drug hypersensitivity syndrome, drug reaction with eosin
126  kidney, lungs, and/or heart) in the case of drug hypersensitivity syndrome.
127 in the immunopathogenesis of T-cell mediated drug hypersensitivity syndromes.
128 n key paradigm shifts in knowledge regarding drug hypersensitivity, there are still many open and una
129 st consumed medicines worldwide and the main drug hypersensitivity triggers.
130                                              Drug hypersensitivity was confirmed by histopathologic t
131  WRN-deficient diploid fibroblasts, in which drug hypersensitivity was entirely due to reduced cell p
132                             The diagnosis of drug hypersensitivity was obtained by skin tests in 72.9
133 s (NSAIDs) are the most frequent triggers of drug hypersensitivity with NSAIDs-induced urticaria/angi

 
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