Page 94 - Škrgat, Sabina, ed. 2022. Severe Asthma - Basic and Clinical Views. Koper: University of Primorska Press. Severe Asthma Forum, 1
P. 94
It is important to diagnose if the patient for several days. It is important to distinguish
has an AERD, as NSAIDs are widely used these symptoms from anaphylaxis. In NECD
severe asthma forum 1: severe asthma - basic and clinical views as analgesic, antipyretic and cardio-protec- there are only cutaneous symptoms present,
tive drugs. NSAID asthma exacerbations in without systemic involvement. The intensi-
these patients may occur unexpectedly and ty and the threshold dose for the reaction are
may be severe2. Also, aspirin-associated asth- changing through time and the course of the
ma is a specific phenotype of eosinophilic disease. The severity of the symptoms is also
asthma and with a different treatment deci- dose-dependent. Usually, NSAIDs are well
sion. Asthma control can be improved by ad- tolerated when chronic spontaneous urticaria
ditional treatment with antileukotrienes and, is in remission. Sometimes there are addition-
in selected cases, by desensitization to aspirin. al co-factors, such as viral disease, psychical
Therefore, it is important to define the tolera- or physical stress present, which aggravate the
bility of NSAIDs in all patients with asthma disease, and patients better tolerate NSAID
and nasal polyposis. without these co-factors. Therefore it is some-
times difficult to confirm the diagnosis with
NSAID Hypersensitivity a drug provocation test, as results are not al-
ways replicable. Skin tests have no diagnos-
Prevalence of hypersensitivity to NSAID tic value in NECD. NSAID exacerbated cu-
is reported to be 1.6%3. Aspirin and other taneous disease is unpleasant, but it is not life
NSAIDs can cause hypersensitivity by differ- threatening. Patients with NECD usually well
ent immunological mechanisms. Therefore, tolerate selective COX-2 inhibitors and also
the clinical picture, cross-reactivity, disease the lower dose of aspirin (eg 100 mg as in an-
course, and course of desensitization may also tithrombotic treatment). However, desensiti-
be quite different. It is important to diagnose zation to aspirin is rarely successful in NECD
which disease phenotype is involved. This can patients and patients should avoid all COX-1
be determined in most cases by history. inhibitors in therapeutic dose5,6.
NSAID hypersensitivity can be classified NSAID induced urticaria or angioede-
into 5 categories: NSAID exacerbated cuta- ma (NIUA) occurs in patients without the
neous disease (NECD), NSAID induced urti- underlying cutaneous disease, but similar to
caria or angioedema (NIUA), single NSAID NECD patients develop isolated skin symp-
anaphylaxis, aspirin-exacerbated respiratory toms up to 24 hours after ingestion of at least
disease (AERD), single NSAID induced de- two chemical unrelated NSAIDs. Again,
layed reaction (SNIDR)4-7. Mixed pattern, there is no systemic involvement, in contrast
called “blended reactions” represent the sec- to IgE mediated anaphylaxis. Sometimes
ond most frequent entity in NSAID hyper- NIUA occurs in patients several years before
sensitivity simultaneously involving skin and they develop chronic spontaneous urticarial,
airways8 Immunological and clinical charac- but this is not always the case. Cross reactivity
teristics of various types of NSAID hypersen- is associated with the strength of COX-1 inhi-
sitivity are summarized in Table 1. bitions and not with the chemical structure of
NSAID. Also these patients tolerate well selec-
NSAID exacerbated cutaneous disease tive COX-2 inhibitors. In contrast to NECD
(NECD) occurs in patients who are suffer- patients, desensitization with aspirin is rare-
ing from chronic spontaneous urticaria. Ap- ly successful in NIUA patients. When desen-
proximately 12-30% of patients with chron- sitized to aspirin, patients do tolerate also oth-
ic urticaria have worsening of their disease er NSAIDs5,6.
and occurrence of generalized hives and/or
angioedema within 1-6 hours after applica- Single NSAID anaphylaxis is dif-
tion of NSAID. Skin symptoms may persist ferent from both phenotypes of NSAID
has an AERD, as NSAIDs are widely used these symptoms from anaphylaxis. In NECD
severe asthma forum 1: severe asthma - basic and clinical views as analgesic, antipyretic and cardio-protec- there are only cutaneous symptoms present,
tive drugs. NSAID asthma exacerbations in without systemic involvement. The intensi-
these patients may occur unexpectedly and ty and the threshold dose for the reaction are
may be severe2. Also, aspirin-associated asth- changing through time and the course of the
ma is a specific phenotype of eosinophilic disease. The severity of the symptoms is also
asthma and with a different treatment deci- dose-dependent. Usually, NSAIDs are well
sion. Asthma control can be improved by ad- tolerated when chronic spontaneous urticaria
ditional treatment with antileukotrienes and, is in remission. Sometimes there are addition-
in selected cases, by desensitization to aspirin. al co-factors, such as viral disease, psychical
Therefore, it is important to define the tolera- or physical stress present, which aggravate the
bility of NSAIDs in all patients with asthma disease, and patients better tolerate NSAID
and nasal polyposis. without these co-factors. Therefore it is some-
times difficult to confirm the diagnosis with
NSAID Hypersensitivity a drug provocation test, as results are not al-
ways replicable. Skin tests have no diagnos-
Prevalence of hypersensitivity to NSAID tic value in NECD. NSAID exacerbated cu-
is reported to be 1.6%3. Aspirin and other taneous disease is unpleasant, but it is not life
NSAIDs can cause hypersensitivity by differ- threatening. Patients with NECD usually well
ent immunological mechanisms. Therefore, tolerate selective COX-2 inhibitors and also
the clinical picture, cross-reactivity, disease the lower dose of aspirin (eg 100 mg as in an-
course, and course of desensitization may also tithrombotic treatment). However, desensiti-
be quite different. It is important to diagnose zation to aspirin is rarely successful in NECD
which disease phenotype is involved. This can patients and patients should avoid all COX-1
be determined in most cases by history. inhibitors in therapeutic dose5,6.
NSAID hypersensitivity can be classified NSAID induced urticaria or angioede-
into 5 categories: NSAID exacerbated cuta- ma (NIUA) occurs in patients without the
neous disease (NECD), NSAID induced urti- underlying cutaneous disease, but similar to
caria or angioedema (NIUA), single NSAID NECD patients develop isolated skin symp-
anaphylaxis, aspirin-exacerbated respiratory toms up to 24 hours after ingestion of at least
disease (AERD), single NSAID induced de- two chemical unrelated NSAIDs. Again,
layed reaction (SNIDR)4-7. Mixed pattern, there is no systemic involvement, in contrast
called “blended reactions” represent the sec- to IgE mediated anaphylaxis. Sometimes
ond most frequent entity in NSAID hyper- NIUA occurs in patients several years before
sensitivity simultaneously involving skin and they develop chronic spontaneous urticarial,
airways8 Immunological and clinical charac- but this is not always the case. Cross reactivity
teristics of various types of NSAID hypersen- is associated with the strength of COX-1 inhi-
sitivity are summarized in Table 1. bitions and not with the chemical structure of
NSAID. Also these patients tolerate well selec-
NSAID exacerbated cutaneous disease tive COX-2 inhibitors. In contrast to NECD
(NECD) occurs in patients who are suffer- patients, desensitization with aspirin is rare-
ing from chronic spontaneous urticaria. Ap- ly successful in NIUA patients. When desen-
proximately 12-30% of patients with chron- sitized to aspirin, patients do tolerate also oth-
ic urticaria have worsening of their disease er NSAIDs5,6.
and occurrence of generalized hives and/or
angioedema within 1-6 hours after applica- Single NSAID anaphylaxis is dif-
tion of NSAID. Skin symptoms may persist ferent from both phenotypes of NSAID
