Page 93 - Škrgat, Sabina, ed. 2022. Severe Asthma - Basic and Clinical Views. Koper: University of Primorska Press. Severe Asthma Forum, 1
P. 93
hma and Aspirin Exacerbated Respiratory 5.1
Disease
Peter Kopač1,2 and Mihaela Zidarn1,2
Abstract 1 University Hospital
Aspirin exacerbated respiratory disease (AERD) is a disease characterized by the triad of asth- of Respiratory and Allergic
ma, chronic rhinosinusitis with nasal polyposis, and respiratory reaction to cyclooxygenase 1 Diseases, Golnik, Slovenia
inhibitors. The prevalence of AERD is estimated is reported to be: 7% in patients with asthma,
15% in patients with severe asthma, 24% in patients with life-threatening asthma, 10% in pa- 2 Faculty of Medicine,
tients with nasal polyposis, and 9% in patients with unspecific chronic rhinosinusitis. University of Ljubljana,
Aspirin and other nonsteroidal antiinflamatory drugs (NSAID) can cause hypersensitivity by Ljubljana, Slovenia
different immunological mechanisms that can be classified into 5 categories: NSAID exacer-
bated cutaneous disease, NSAID induced urticaria or angioedema, single NSAID anaphylax-
is, aspirin-exacerbated respiratory disease, single NSAID induced delayed reaction. The clin-
ical picture, pattern of cross-reactivity, disease course, and course of desensitization may also
be quite different. It is important to diagnose which disease phenotype is involved. This can be
determined in most cases by history.
Due to distinctive symptoms, the diagnosis of AERD could often be based on reliable history.
In patients with adult-onset asthma, recurrent nasal polyposis and multiple (two or more) reac-
tions after a single NSAID or reactions after two different NSAIDs in the last 5 years the diag-
nosis could be based on history alone. However, in some cases, further diagnostic tests are neces-
sary to avoid underdiagnosing or over-diagnosing the disease. Cross reactivity between NSAIDs
in AERD is not associated with similarity of chemical structure, as it is in IgE mediated hyper-
sensitivity, but it is associated with the strength of COX-1 inhibitions therefore the patient with
AERD must avoid all the other drugs which are strong COX-1 inhibitors. Aspirin desensitiza-
tion in AERD could be performed for two purposes: aspirin tolerance in cardiovascular indi-
cation or symptoms improvement in severe cases of chronic rhinosinusitis with nasal polyposis.
Keywords: aspirin, asthma, drug hypersensitivity, nonsteroidal antiinflamatory drugs
Introduction 19221. Since then this condition has been giv-
en many different names from “Morbus
Aspirin exacerbated respiratory disease Widal”, “Samter’s triad”, “ASA induced asth-
(AERD) is a disease characterized by the tri- ma with nasal polyposis” and “NSAID-Exac-
ad of asthma, chronic rhinosinusitis with na- erbated Respiratory Disease - NERD”. Var-
sal polyposis, and respiratory reaction to ious specialists, including pulmonologists,
cyclooxygenase 1 inhibitors. It was first de- otorhinolaryngologists, and allergists, treat
scribed in the literature as a case report by patients with this condition.
French professors Widal and colleges in
https://doi.org/10.26 493/978 -961-293 -157-5.93 -103
Disease
Peter Kopač1,2 and Mihaela Zidarn1,2
Abstract 1 University Hospital
Aspirin exacerbated respiratory disease (AERD) is a disease characterized by the triad of asth- of Respiratory and Allergic
ma, chronic rhinosinusitis with nasal polyposis, and respiratory reaction to cyclooxygenase 1 Diseases, Golnik, Slovenia
inhibitors. The prevalence of AERD is estimated is reported to be: 7% in patients with asthma,
15% in patients with severe asthma, 24% in patients with life-threatening asthma, 10% in pa- 2 Faculty of Medicine,
tients with nasal polyposis, and 9% in patients with unspecific chronic rhinosinusitis. University of Ljubljana,
Aspirin and other nonsteroidal antiinflamatory drugs (NSAID) can cause hypersensitivity by Ljubljana, Slovenia
different immunological mechanisms that can be classified into 5 categories: NSAID exacer-
bated cutaneous disease, NSAID induced urticaria or angioedema, single NSAID anaphylax-
is, aspirin-exacerbated respiratory disease, single NSAID induced delayed reaction. The clin-
ical picture, pattern of cross-reactivity, disease course, and course of desensitization may also
be quite different. It is important to diagnose which disease phenotype is involved. This can be
determined in most cases by history.
Due to distinctive symptoms, the diagnosis of AERD could often be based on reliable history.
In patients with adult-onset asthma, recurrent nasal polyposis and multiple (two or more) reac-
tions after a single NSAID or reactions after two different NSAIDs in the last 5 years the diag-
nosis could be based on history alone. However, in some cases, further diagnostic tests are neces-
sary to avoid underdiagnosing or over-diagnosing the disease. Cross reactivity between NSAIDs
in AERD is not associated with similarity of chemical structure, as it is in IgE mediated hyper-
sensitivity, but it is associated with the strength of COX-1 inhibitions therefore the patient with
AERD must avoid all the other drugs which are strong COX-1 inhibitors. Aspirin desensitiza-
tion in AERD could be performed for two purposes: aspirin tolerance in cardiovascular indi-
cation or symptoms improvement in severe cases of chronic rhinosinusitis with nasal polyposis.
Keywords: aspirin, asthma, drug hypersensitivity, nonsteroidal antiinflamatory drugs
Introduction 19221. Since then this condition has been giv-
en many different names from “Morbus
Aspirin exacerbated respiratory disease Widal”, “Samter’s triad”, “ASA induced asth-
(AERD) is a disease characterized by the tri- ma with nasal polyposis” and “NSAID-Exac-
ad of asthma, chronic rhinosinusitis with na- erbated Respiratory Disease - NERD”. Var-
sal polyposis, and respiratory reaction to ious specialists, including pulmonologists,
cyclooxygenase 1 inhibitors. It was first de- otorhinolaryngologists, and allergists, treat
scribed in the literature as a case report by patients with this condition.
French professors Widal and colleges in
https://doi.org/10.26 493/978 -961-293 -157-5.93 -103
