Genetic and ethnic risk factors associated with drug hypersensitivity

Kim, Seung Hyun; Ye, Young-Min; Palikhe, Nami Shrestha; Kim, Jeongeun; Park, Hae‐Sim

doi:10.1097/aci.0b013e32833b1eb3

Cited by 54 publications

(32 citation statements)

References 110 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some studies have shown a possible specific genetic profile in patients with both chronic urticaria and NSAID hypersensitivity [25,26,27]; it would be interesting to establish whether otherwise normal multiple NSAID reactors also show the same profile. Recently, a new classification of NSAID hypersensitivity reactions has been suggested [1], and subsequent amendments have been proposed [28].…”

Section: Discussionmentioning

confidence: 99%

Multiple Nonsteroidal Anti-Inflammatory Drug-Induced Cutaneous Disease: What Differentiates Patients with and without Underlying Chronic Spontaneous Urticaria?

Asero¹

2013

Int Arch Allergy Immunol

View full text Add to dashboard Cite

Background: Multiple nonsteroidal anti-inflammatory drug (NSAID) cutaneous reactors may be otherwise normal or have underlying chronic spontaneous urticaria (CSU). This study compared these two phenotypes of NSAID-hypersensitive subjects. Methods: A total of 97 multiple NSAID reactors underwent oral challenges with paracetamol, etoricoxib and tramadol. Atopic status was investigated in all patients, and autoreactivity was ascertained in some cases as well. Otherwise normal multiple NSAID reactors were reevaluated after 1-5 years in order to detect their proneness to CSU. Results: At the first visit, 41 patients had CSU and 56 had multiple NSAID intolerance without any underlying cutaneous disease. Altogether, 22, 10 and 6% of patients did not tolerate paracetamol, etoricoxib and tramadol, respectively, on oral challenge. Intolerance to these alternative drugs showed a strong association (p < 0.01 with all combinations). The two subgroups of patients did not show any difference in terms of mean age, gender distribution, prevalence of atopic diseases, prevalence of single offending NSAIDs and prevalence of intolerance to paracetamol, etoricoxib or tramadol on oral challenge. In all, 20% of multiple NSAID reactors without CSU at presentation developed CSU between 6 months and 5 years after the initial clinical evaluation. Conclusions: Multiple NSAID cutaneous reactors with or without CSU seem identical from a clinical point of view, and some of the latter group show a propensity to acquire the former phenotype over time. A subset of patients apparently identical to the general population of multiple NSAID reactors also react to drugs exerting little or no cyclooxygenase-1 enzyme inhibition and might represent a distinct phenotype of NSAID-hypersensitive patients possibly characterized by a different underlying pathogenesis.

show abstract

Section: Discussionmentioning

confidence: 99%

Multiple Nonsteroidal Anti-Inflammatory Drug-Induced Cutaneous Disease: What Differentiates Patients with and without Underlying Chronic Spontaneous Urticaria?

Asero¹

2013

Int Arch Allergy Immunol

View full text Add to dashboard Cite

show abstract

“…A recent update on genetic and ethnic associations with drug hypersensitivity to different drugs has been reviewed in detail elsewhere [130].…”

Section: Genetics Of Drug Allergymentioning

confidence: 99%

Epidemiology and risk factors for drug allergy

Thong

Tan

2011

Brit J Clinical Pharma

298

218

View full text Add to dashboard Cite

The aim of this review was to describe the current evidence-based knowledge of the epidemiology, prevalence, incidence, risk factors and genetic associations of drug allergy. Articles published between 1966 and 2010 were identified in MEDLINE using the key words adult, adverse drug reaction reporting systems, age factors, anaphylactoid, anaphylaxis, anaesthetics, antibiotics, child, drug allergy, drug eruptions, ethnic groups, hypersensitivity, neuromuscular depolarizing agents, neuromuscular nondepolarizing agents, sex factors, StevensJohnson syndrome and toxic epidermal necrolysis. Additional studies were identified from article reference lists. Relevant, peer-reviewed original research articles, case series and reviews were considered for review. Current epidemiological studies on adverse drug reactions (ADRs) have used different definitions for ADR-related terminology, often do not differentiate immunologically and non-immunologically mediated drug hypersensitivity, study different study populations (different ethnicities, inpatients or outpatients, adults or children), utilize different methodologies (spontaneous vs. non-spontaneous reporting, cohort vs. case-control studies), different methods of assessing drug imputability and different methods of data analyses. Potentially life-threatening severe cutaneous adverse reactions (SCAR) are associated with a high risk of morbidity and mortality. HLA associations for SCAR associated with allopurinol, carbamazepine and abacavir have been reported with the potential for clinical use in screening prior to prescription. Identification of risk factors for drug allergy and appropriate genetic screening of at-risk ethnic groups may improve the outcomes of drug-specific SCAR. Research and collaboration are necessary for the generation of clinically-relevant, translational pharmacoepidemiological and pharmacogenomic knowledge, and success of health outcomes research and policies on drug allergies.

show abstract

“…NSAIDs can also be associated with nonallergic hypersensitivity related to disequilibrium in the arachidonic acid degradation pathways, even though the exact reasons by which this happens have not been well clarified [4]. This adverse event may be related to a prostaglandin E2 deficit, to an excess of cysteinyl leukotrienes and to some genetic polymorphisms [5]. Nonallergic hypersensitivity reactions may express themselves in the same way as allergic reactions, so that, clinically, it is not possible to distinguish between them.…”

Section: Introductionmentioning

confidence: 99%

How Can We Better Classify NSAID Hypersensitivity Reactions? – Validation from a Large Database

Caimmi

Bousquet

et al. 2012

Int Arch Allergy Immunol

View full text Add to dashboard Cite

Background: Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) is one of the most common drug hypersensitivities. Several clinical subtypes have been distinguished depending on symptomatology (respiratory, cutaneous, anaphylaxis), timing (immediate, delayed), underlying chronic disease (asthma, chronic urticaria) or putative mechanism of the reaction (allergic, nonallergic mediated). The aim of the present study was to better classify the many hypersensitivity reactions to NSAIDs. Methods: In the present retrospective study, duringan 11-year study period, we collected data from all patients with a proven NSAID hypersensitivity. Reactions were classified according to clinical patterns, chronology, underlying diseases and the results of oral provocation tests into 5 and 7 groups in line with two published classifications, respectively. Results: Forty-nine and 88 out of 307 reactions (in 122 patients) could not be classified on the basis of the two previously published classifications. We created a new classification which could include all patient reactions. Conclusions: Our new classification is more suitable for clinical expression of NSAID hypersensitivity. It allows clinicians to identify patients at a high risk, based on the clinical history and clinical manifestations. Moreover, it is helpful for a better understanding and teaching of these reactions.

show abstract

Genetic and ethnic risk factors associated with drug hypersensitivity

Cited by 54 publications

References 110 publications

Multiple Nonsteroidal Anti-Inflammatory Drug-Induced Cutaneous Disease: What Differentiates Patients with and without Underlying Chronic Spontaneous Urticaria?

Multiple Nonsteroidal Anti-Inflammatory Drug-Induced Cutaneous Disease: What Differentiates Patients with and without Underlying Chronic Spontaneous Urticaria?

Epidemiology and risk factors for drug allergy

How Can We Better Classify NSAID Hypersensitivity Reactions? – Validation from a Large Database

Contact Info

Product

Resources

About