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1 se remission or the occurrence of an adverse drug reaction.
2 ing a rare, potentially fatal, T-cell-driven drug reaction.
3 ory or poor risk assessment of recurrence of drug reaction.
4 o the pathophysiology of this severe adverse drug reaction.
5 f hepatocytes, consistent with a cholestatic drug reaction.
6 ils of 10 and 3 reports of suspected adverse drug reactions.
7 e from the eruptions usually associated with drug reactions.
8 g metabolism and have been linked to adverse drug reactions.
9 istance to pathogens and the risk of adverse drug reactions.
10 ne interindividual susceptibility to adverse drug reactions.
11 acotherapy whereas others experience adverse drug reactions.
12 that may underlie susceptibility to adverse drug reactions.
13 metabolites may be involved in idiosyncratic drug reactions.
14 nalysis linking chemical features to adverse drug reactions.
15 bited by variable drug responses and adverse drug reactions.
16 ding compounds is essential to avoid adverse drug reactions.
17 acokinetics, treatment efficacy, and adverse drug reactions.
18 a common target of inflammation and adverse drug reactions.
19 nd reduce the number and severity of adverse drug reactions.
20 and hospital nurses in reporting of adverse drug reactions.
21 distinguish from cytomegalovirus disease or drug reactions.
22 involved in other serious cutaneous adverse drug reactions.
23 annot account for most idiosyncratic adverse drug reactions.
24 histologic changes commonly associated with drug reactions.
25 information on the risks of serious adverse drug reactions.
26 levels, CD4+ lymphocyte counts, and adverse drug reactions.
27 ased screening assays for testing individual drug reactions.
28 ose existing drugs and identify rare adverse drug reactions.
29 r both predictable ADRs and hypersensitivity drug reactions.
30 ns most commonly involved in serious adverse drug reactions.
31 r serious drug-drug interactions and adverse drug reactions.
32 ce system was put in place to detect adverse drug reactions.
33 considering the increased tremor and adverse drug reactions.
34 erapy without increasing the risk of adverse drug reactions.
35 variates that influenced the rate of adverse drug reactions.
36 nor, and potentially iatrogenic; and adverse drug reactions.
37 t specific HLA alleles influence the risk of drug reactions.
38 rine disrupting chemicals (EDCs) and adverse drug reactions.
39 tudies advanced the understanding of adverse drug reactions.
40 or additional drug therapy (31%) and adverse drug reactions (18%) being the most common problems iden
44 % for ST-Cefaz) and highest rates of adverse drug reactions (5.2% vs 4.6% for Hx-Cefaz and 4.7% for S
48 Two spontaneously reported serious adverse drug reactions (ADRs) and 32 spontaneously reported nons
49 es identifying HLA associations with adverse drug reactions (ADRs) and one for the examination of inf
55 the study was to investigate whether adverse drug reactions (ADRs) during immunotherapy with a grass
57 be more likely to have unrecognized adverse drug reactions (ADRs) than established drugs, but no rec
58 neous reports do not reliably detect adverse drug reactions (ADRs) that occur widely separated in tim
59 t carbamazepine 1 is associated with adverse drug reactions (ADRs), including hepatotoxicity; oxidati
60 of 14% of patients experienced minor adverse drug reactions (ADRs), of which 2 cases demonstrated fla
63 thiopurine therapy because of severe adverse drug reactions (ADRs); leukopenia is one of the most ser
64 fy key terms, such as adverse event, adverse drug reaction, adverse drug event, medication error, and
65 s DILI cases reported to the Swedish Adverse Drug Reactions Advisory Committee (1970-2004) for any si
66 patient susceptibility to developing adverse drug reactions, although the underlying mechanism is not
67 anism of undesirable drug effects or adverse drug reactions among those compounds, we examined their
68 ge) between the identification of an adverse drug reaction and the subsequent onset of drug-induced i
72 used to assess treatment completion, adverse drug reactions, and factors associated with treatment di
73 uous drugs, polypharmacology-related adverse drug reactions, and multi-drug therapies, especially can
80 Schemes for spontaneous reporting of adverse drug reactions are important to post-marketing safety su
83 ach to trimethoprim-sulfamethoxazole adverse drug reaction assessment and rechallenge to optimize pro
85 e was to determine the prevalence of adverse drug reactions associated with off-label use and evaluat
86 ating that doctors should report all adverse drug reactions associated with them to the Committee on
87 ypes can range from life-threatening adverse drugs reactions at one end of the spectrum to equally se
88 te adenovirus infections or systemic adverse drug reactions, but levels in patients with KD were not
91 s that increase the risk of life-threatening drug reactions can be clinically silent before drug expo
92 ed thrombocytopenia, a prothrombotic adverse drug reaction caused by immunoglobulin G directed agains
93 rmal necrolysis are severe adverse cutaneous drug reactions characterized by widespread skin and muco
94 Baseline and nonsteroidal anti-inflammatory drug reaction clinical data were correlated with cell ch
95 d evidence of a systemic or life-threatening drug reaction, developed a systemic drug eruption, or ha
96 and the number of harmful and severe adverse drug reactions did not differ for medications used for F
98 had 48 trimethoprim-sulfamethoxazole adverse drug reactions documented either at baseline or during t
100 ence for a genetic predisposition to adverse drug reactions, focusing on gene variants producing alte
102 dications that are associated with lichenoid drug reactions; four patients were postmenopausal; and a
103 graphics, costs, outcomes (including adverse drug reactions, functional status, ventilator time in ho
106 ommon medicines involved in hypersensitivity drug reactions (HDRs) to NSAIDs, no patient series studi
107 telets, leading to the prothrombotic adverse drug reaction heparin-induced thrombocytopenia (HIT).
109 nto the molecular mechanisms of this adverse drug reaction in adult patients with germ cell testicula
116 ated to calculate incidence rates of adverse drug reactions in the community from spontaneous reports
118 orter genes previously implicated in adverse drug reactions including simvastatin-induced myopathy an
122 idermal necrolysis (TEN) is a severe adverse drug reaction involving extensive keratinocyte death in
123 nintended 'off-targets' that predict adverse drug reactions is daunting by empirical methods alone.
124 nintended 'off-targets' that predict adverse drug reactions, is a daunting task by experimental appro
125 ed cardiotoxicity (ACT) is a serious adverse drug reaction limiting anthracycline use and causing sub
126 enal transplant recipients, reported adverse drug reactions may limit use and increase reliance on co
127 anation for HLA-linked idiosyncratic adverse drug reactions, namely that drugs can alter the repertoi
129 is/granulocytopenia (CIAG), a severe adverse drug reaction occurring in up to 1% of treated individua
130 induced thrombocytopenia (HIT) is an adverse drug reaction occurring in up to 5% of patients exposed
131 is a relatively common prothrombotic adverse drug reaction of unusual pathogenesis that features plat
132 By integrating data sources about adverse drug reactions of drugs with an established cheminformat
134 nduced taste disturbance is a common adverse drug reaction often triggered by drug secretion into sal
137 uisition cost, and costs of treating adverse drug reactions probably or possibly related to study dru
142 ons during hypothermia and increased adverse drug reaction risk complicates concurrent pharmacotherap
143 s with the strongest associations to adverse drug reaction risk in the intensive care unit are presen
144 more frequently with off-label use, adverse drug reaction risk increases with each additional off-la
147 e identified clinically significant systemic drug reactions (SDR) and evaluated risk factors in patie
148 cent advances in pharmacogenetics of adverse drug reactions show promise, the small size of the popul
149 literature documenting the risk for adverse drug reactions specific to bleeding and/or clotting with
151 n of the role that genetics plays in adverse drug reactions that are either predictable extensions of
152 ve of pharmacovigilance is to detect adverse drug reactions that are unknown or novel in terms of the
153 reactions are common clinical acute adverse drug reactions that can exacerbate a patient's condition
154 ole of the adaptive immune system in adverse drug reactions that target the liver has not been define
155 th Organization's classification for adverse drug reactions, the association between bortezomib use a
160 lly lethal, immunologically mediated adverse drug reaction to unfractionated heparin or, less commonl
161 cholesterol levels that could cause adverse drug reactions to cholesterol-lowering drugs such as sta
166 The incidence and severity of other adverse drug reactions were comparable between the 2 groups.
170 tions was 3.2% in the intravenous group, and drug reactions were rare in both groups (intravenous: 0.
175 occus aureus sinusitis, and multiple adverse drug reactions whose T cells were unable to produce IFN-
176 enetic variants associated with this adverse drug reaction will further our mechanistic understanding
177 es virus (HHV) reactivation is well known in drug reaction with eosinophilia and systemic symptom (DR
178 vens-Johnson Syndrome (SJS), and 11 cases of Drug Reaction with Eosinophilia and Systemic Symptoms (D
179 uses (HHVs) contribute to the development of drug reaction with eosinophilia and systemic symptoms (D
180 added significantly to our understanding of drug reaction with eosinophilia and systemic symptoms (D
182 ersensitivity syndrome (DIHS), also known as drug reaction with eosinophilia and systemic symptoms (D
183 is a major mechanism in the pathogenesis of drug reaction with eosinophilia and systemic symptoms (D
185 ar to the more severe eczema vaccinatum, and drug reaction with eosinophilia and systemic symptoms sy
186 DRs, such as drug hypersensitivity syndrome, drug reaction with eosinophilia and systemic symptoms sy
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