hypersensitivity reactions to nonsteroidal anti-inflammatory drugs
TRANSCRIPT
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Hypersensitivity reactions to �Non-Steroidal Anti-Inflammatory Drugs: Single versus multiple reactors
Ana Reis Ferreira, Natacha Santos, Carmen Botelho , Eunice Castro, Josefina R. Cernadas
Serviço de Imunoalergologia, Hospital de São João, EPE, Porto, Portugal
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Background • Non-‐Steroidal Anti-‐Inflammatory Drugs (NSAIDs)
COX-‐2 COX-‐1
Prostaglandins / Thromboxanes
NSAIDs
Non-‐selective COX inhibitors – Acetylsalicylic acid (ASA) – Diclofenac – Ibuprofen Weak COX-‐1 inhibitor – Paracetamol
COX-‐2 preferencial inhibitors – Nimesulide – Meloxicam
COX-‐2 selective inhibitors – Coxibes
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Background
• NSAID hypersensitivity reactions (HSR) prevalence in the general populaGon – 0.6% to 2.5%
• COX-‐1 inhibition responsible for HSR to NSAIDs?
Stevenson et al. Ann Allergy Asthma Immunol. 2001 Sep;87(3):177-‐80.
Single vs
Multiple reactors
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Aim
To characterize clinical data of the patients referred to our
Drug Allergy Unit for NSAID hypersensitivity reactions:
– Demographical data
– Type of reaction
– Suspected drug(s)
• Single versus Multiple reactors
• Tolerance to weak COX – 1 inhibitors
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Methods
• Clinical data from the records of the patients referred in the last 10 years for NSAID hypersensitivity
• Patients grouped according to symptoms:
– Cutaneous symptoms (Urticaria and/or angioedema)
– Aspirin-‐Exacerbated Respiratory Disease (AERD)
– Anaphylaxis
• Fisher’s exact test was used to compare frequencies
(significance level of 5%).
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Results
• 204 patients, 143♀:♂61
• 16-‐81 years-‐old (47.3±13.7)
• 36.8% were atopic
• 29.4% had a previous medical diagnosis of asthma
• Mean age for 1st reaction was 37.4 ± 14.1 years
• Symptoms occurred in the 1st hour after exposure in 45.6%
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Results
Number of implicated NSAIDs
46,6%
23,5%
19,1%
8,3% 2,5%
1 2 3 4 ≥5
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Results
Most implicated drugs:
– Acetilsalicilic acid (ASA) – 63.2% of the patients
– Ibuprofen – 30.9% of the patients
– Paracetamol – 29.9% of the patients
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Results
Cutaneous symptoms (urticaria and/or angioedema)
• 154 patients (75.5%)
• Reaction to 1 NSAID in 42.2% of the patients.
• Most implicated drugs:
– ASA -‐ 63%
– Paracetamol -‐ 35.1%
– Ibuprofen -‐ 33.8%
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Results
Aspirin-‐Exacerbated Respiratory Disease (AERD)
• 18 patients (8.8%) -‐ 4 without previous asthma diagnosis
• Reaction to 1 NSAID in 44.4% of the patients.
• Most implicated drugs
– ASA -‐ 77.8%
– Ibuprofen -‐ 38.9%
– Diclofenac -‐ 27.8%
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Results
Anaphylaxis
• 21 patients (10.3%)
• All these patients referred HR to only 1 NSAID
• 8 to ASA, 6 to diclofenac and the others to different NSAIDs
Eleven patients presented different types of reactions to NSAIDs
and were not included in the previous groups.
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Results Suspected NSAIDs according to symptoms (single vs multiple)
0%
20%
40%
60%
80%
100%
Cutaneous AERD
Single
Multiple
Single
Multiple
Single
Multiple
Single
Multiple
ASA
Paracetamol
Ibuprofeno
Diclofenac
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Results Tolerance to ASA and weak COX-‐1 inhibitors when asked
Cutaneous AERD
2% 0%
54%
93%
24%
75%
ASA
Paracetamol
Nimesulide
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Results
Cutaneous AERD
52,6%
16,7%
p=0.0051
HSR to weak COX-‐1 inhibitors (paracetamol and nimesulide)
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Conclusion
• ASA was the most frequently implicated drug.
• Almost half the patients reported HR to only one NSAID.
• Urticaria and/or angioedema were the most common symptoms, with AERD and anaphylaxis occurring each in approximately 10% of the patients.
• HR to weak COX-‐1 inhibitors was more frequent in patients with cutaneous symptoms.
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Comments
• This may suggest that COX-‐1 inhibition plays a less important role in patients with cutaneous symptoms than in those with AERD.
• Drug challenges with NSAIDs with different COX-‐1 inhibition patterns may provide a more accurate diagnosis of NSAID HRS and confirm this hypotesis.