Page 95 - Škrgat, Sabina, ed. 2022. Severe Asthma - Basic and Clinical Views. Koper: University of Primorska Press. Severe Asthma Forum, 1
P. 95
le 1. Immunological and clinical characteristics of various types of NSAID hypersensitivity.
Terminology Aspirin-exacerbat- NSAID exacerbat- NSAID induced Single NSAID Single NSAID
ed respiratory dis- ed cutaneous dis- urticaria or anaphylaxis induced delayed
Pathophysiology angioedema IgE mediated reaction (SNIDR)
Underlying disease ease (AERD) ease (NECD) (NIUA) T-cell mediated
none
Cross reactivity COX-1 inhibition COX-1 inhibition Unknown, probably selective none
Timing Asthma, nasal COX-1 inhibition immediate selective
polyposis (up to 1h) delayed
NSAID Cross Chronic urticaria none
reactive Anaphylaxis Various delayed
NSAID Cross NSAID Cross reactions
reactive reactive
Contraindicated
30-180 min 1-6 h up to 24h in most cases 95
Symptoms Bronchial obstruc- Urticaria Urticaria
tion, nasal conges- and/or angioedema and/or angioedema
tion and/or rhin-
orrhea, wheezing,
coughing, dyspnea
Desensitization Successful Rarely successful Rarely successful Successful
hypersensitivity described above. The mech- drug reaction, Steven Johnson syndrome, tox- asthma and aspirin exacerbated respiratory disease
anism is IgE mediated immediate allergy. ic epidermal necrolysis, drug induced nephri-
Therefore classical symptoms of anaphylaxis, tis, pneumonitis, etc. The pathomechanism
with pruritus, flush, hives, angioedema, and include specific T cell stimulation. Diagnostic
systemic involvement with bronchospasm, tests are specific and different for each clin-
hypotension, and gastrointestinal symptoms ical manifestation. Desensitization to aspirin
occur immediate, or within 1 hour after ex- is contraindicated in case of a severe delayed
posure to NSAID. The severity of the disease reaction5,6.
is usually not dose dependent. Patients usual-
ly react to other NSAIDs with similar chem- Clinical Characteristics of AERD
ical structures (and not with similar strength
of COX-1 inhibition). Skin tests and also ba- The symptoms of AERD do not develop im-
sophil activation tests may be useful in di- mediately after taking NSAIDs, but some-
agnosing this disease. Drug provocation test what later, on average 30-180 min after ad-
can confirm the diagnosis of allergy to cul- ministration9. This can sometimes make it
prit drug, but it is contraindicated in case of difficult to identify the culprit of the reaction.
a very severe reaction. Drug provocation test The reaction starts with upper respiratory
is useful to confirm tolerance of alternative tract symptoms like nasal congestion and/or
NSAID. Desensitization to culprit NSAID rhinorrhea, followed by lower airway symp-
is possible, but usually not recommended as toms like wheezing, coughing, and shortness
there are many alternatives on the market5,6. of breath. In patients with not, well controlled
asthma symptoms usually occur much quick-
Single NSAID induced delayed reaction er with more severe bronchospasm which may
is rare. It occurs in patients with no underly- even lead to a fatal outcome10-12. The onset
ing skin or respiratory disease. The onset of and severity are dose-related, lowest dose pro-
the disease is delayed, usually more than 1 voking a reaction for individual patients vary
day up to weeks after exposure to the NSAID. between 100-300 mg ASA11-13.
It has various clinical manifestations and var-
ious organ involvement such as maculopap- Patients also frequently have chron-
ular exanthema, drug reaction with eosino- ic symptoms such as recurrent nasal polyp-
philia and systemic symptoms (DRESS), fixed osis with the need for frequent surgery, loss
Terminology Aspirin-exacerbat- NSAID exacerbat- NSAID induced Single NSAID Single NSAID
ed respiratory dis- ed cutaneous dis- urticaria or anaphylaxis induced delayed
Pathophysiology angioedema IgE mediated reaction (SNIDR)
Underlying disease ease (AERD) ease (NECD) (NIUA) T-cell mediated
none
Cross reactivity COX-1 inhibition COX-1 inhibition Unknown, probably selective none
Timing Asthma, nasal COX-1 inhibition immediate selective
polyposis (up to 1h) delayed
NSAID Cross Chronic urticaria none
reactive Anaphylaxis Various delayed
NSAID Cross NSAID Cross reactions
reactive reactive
Contraindicated
30-180 min 1-6 h up to 24h in most cases 95
Symptoms Bronchial obstruc- Urticaria Urticaria
tion, nasal conges- and/or angioedema and/or angioedema
tion and/or rhin-
orrhea, wheezing,
coughing, dyspnea
Desensitization Successful Rarely successful Rarely successful Successful
hypersensitivity described above. The mech- drug reaction, Steven Johnson syndrome, tox- asthma and aspirin exacerbated respiratory disease
anism is IgE mediated immediate allergy. ic epidermal necrolysis, drug induced nephri-
Therefore classical symptoms of anaphylaxis, tis, pneumonitis, etc. The pathomechanism
with pruritus, flush, hives, angioedema, and include specific T cell stimulation. Diagnostic
systemic involvement with bronchospasm, tests are specific and different for each clin-
hypotension, and gastrointestinal symptoms ical manifestation. Desensitization to aspirin
occur immediate, or within 1 hour after ex- is contraindicated in case of a severe delayed
posure to NSAID. The severity of the disease reaction5,6.
is usually not dose dependent. Patients usual-
ly react to other NSAIDs with similar chem- Clinical Characteristics of AERD
ical structures (and not with similar strength
of COX-1 inhibition). Skin tests and also ba- The symptoms of AERD do not develop im-
sophil activation tests may be useful in di- mediately after taking NSAIDs, but some-
agnosing this disease. Drug provocation test what later, on average 30-180 min after ad-
can confirm the diagnosis of allergy to cul- ministration9. This can sometimes make it
prit drug, but it is contraindicated in case of difficult to identify the culprit of the reaction.
a very severe reaction. Drug provocation test The reaction starts with upper respiratory
is useful to confirm tolerance of alternative tract symptoms like nasal congestion and/or
NSAID. Desensitization to culprit NSAID rhinorrhea, followed by lower airway symp-
is possible, but usually not recommended as toms like wheezing, coughing, and shortness
there are many alternatives on the market5,6. of breath. In patients with not, well controlled
asthma symptoms usually occur much quick-
Single NSAID induced delayed reaction er with more severe bronchospasm which may
is rare. It occurs in patients with no underly- even lead to a fatal outcome10-12. The onset
ing skin or respiratory disease. The onset of and severity are dose-related, lowest dose pro-
the disease is delayed, usually more than 1 voking a reaction for individual patients vary
day up to weeks after exposure to the NSAID. between 100-300 mg ASA11-13.
It has various clinical manifestations and var-
ious organ involvement such as maculopap- Patients also frequently have chron-
ular exanthema, drug reaction with eosino- ic symptoms such as recurrent nasal polyp-
philia and systemic symptoms (DRESS), fixed osis with the need for frequent surgery, loss
