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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
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
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
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
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%).
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%
Results
Number of implicated NSAIDs
46,6%
23,5%
19,1%
8,3% 2,5%
1 2 3 4 ≥5
Results
Most implicated drugs:
– Acetilsalicilic acid (ASA) – 63.2% of the patients
– Ibuprofen – 30.9% of the patients
– Paracetamol – 29.9% of the patients
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%
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%
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.
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
Results Tolerance to ASA and weak COX-‐1 inhibitors when asked
Cutaneous AERD
2% 0%
54%
93%
24%
75%
ASA
Paracetamol
Nimesulide
Results
Cutaneous AERD
52,6%
16,7%
p=0.0051
HSR to weak COX-‐1 inhibitors (paracetamol and nimesulide)
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.
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.
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