Page 96 - Škrgat, Sabina, ed. 2022. Severe Asthma - Basic and Clinical Views. Koper: University of Primorska Press. Severe Asthma Forum, 1
P. 96
of smell, and also similar upper and lower re- nasal polyposis and multiple (two or more) re-
spiratory symptoms after intake of alcohol11,12. actions after a single NSAID or reactions after
severe asthma forum 1: severe asthma - basic and clinical views Symptoms usually appear 1-5 years before two different NSAIDs in the last 5 years the
asthma develops14. diagnosis could be based on history alone11,12.
However, in some cases, further diagnostic
Epidemiology tests are necessary to avoid underdiagnosing
The prevalence of AERD is estimated is re- or over diagnosing the disease.
ported to be: 7% in patients with asthma,
15% in patients with severe asthma, 24% in As the disease is not IgE mediated skin
patients with life-threatening asthma, 10% tests or measurements of specific IgE are not
in patients with nasal polyposis, and 9% in applicable. Several other approaches have
patients with unspecific chronic rhinosinusi- been proposed and researched (like sulfido-
tis5,15,16. Reported prevalence is likely to be un- leukotrienes release assay, 15-HETE test, ba-
derestimated due to low awareness of the dis- sophil activation test) but are not used in clin-
ease. ical practice25-25. Therefore, unfortunately,
there is currently no other clinically applicable
Symptoms of AERD usually appears in in vitro test available to confirm the diagnosis.
patients with adult onset asthma between the This means that the only testing available is
age of 20-40 years17,18. AERD in children is drug provocation testing, which is time-con-
rare. The ratio of male to female patients is suming, complicated, and potentially danger-
1:217. AERD was previously not associated ous, and should therefore only be carried out
with atopy or any other respiratory allergy, in experienced centers by experienced physi-
although some newer studies report a higher cian and trained nurse. Emergency treatment
prevalence of atopy in these patients19,20. Non equipment should be at hand. Indications for
steroidal anti-inflammatory drugs that most performing drug provocation test with aspi-
common cause respiratory reactions are: aspi- rin in suspected AERD are confirmation of
rin (80%), ibuprofen (41%), naproxen (4%)13. AERD in patients with unreliable history and
assessment of provocation dose before oral
Pathophysiology desensitization procedure12,26. Absolute con-
NSAIDs inhibit cyclooxygenase 1, increas- traindication for drug provocation tests are
ing leukotriene production and decreasing the the history of severe anaphylactic reaction
production of anti-inflammatory prostaglan- after any NSAID, unstable asthma, FEV1 ≤
dins. Patients with AERD have higher levels 70%, recent respiratory infection, pregnan-
of leukotrienes due to inflammation mediat- cy, severe underlying disease such as cardio-
ed by neutrophils, monocytes, and basophils, vascular, renal or liver disease12,26. There are
eosinophils, and mast cells. Increased leukot- different routes of aspirin administration for
riene production with NSAID ingestion leads provocation tests: inhaled intranasal, oral and
to bronchoconstriction, eosinophilic inflam- intravenous. Most commonly used are nasal
mation, increased mucus production in the and oral provocation tests27. Both have their
bronchi. Also in nasal polyps tissue, there are advantages and disadvantages. Nasal inhala-
elevated concentrations of leukotrienes21,22. tion of lysine-aspirin is safer and less time con-
suming in comparison to standard oral prov-
Diagnostics ocation tests. The nasal provocation test has
Due to distinctive symptoms, the diagnosis a lower sensitivity (80-87%) compared to the
could be often based on reliable history. In oral test, which has a sensitivity of 89-90%.
patients with adult-onset asthma, recurrent However, the specificity of both tests is high
(93-100%)12,26 .28-32 Inhalation challenge with
spiratory symptoms after intake of alcohol11,12. actions after a single NSAID or reactions after
severe asthma forum 1: severe asthma - basic and clinical views Symptoms usually appear 1-5 years before two different NSAIDs in the last 5 years the
asthma develops14. diagnosis could be based on history alone11,12.
However, in some cases, further diagnostic
Epidemiology tests are necessary to avoid underdiagnosing
The prevalence of AERD is estimated is re- or over diagnosing the disease.
ported to be: 7% in patients with asthma,
15% in patients with severe asthma, 24% in As the disease is not IgE mediated skin
patients with life-threatening asthma, 10% tests or measurements of specific IgE are not
in patients with nasal polyposis, and 9% in applicable. Several other approaches have
patients with unspecific chronic rhinosinusi- been proposed and researched (like sulfido-
tis5,15,16. Reported prevalence is likely to be un- leukotrienes release assay, 15-HETE test, ba-
derestimated due to low awareness of the dis- sophil activation test) but are not used in clin-
ease. ical practice25-25. Therefore, unfortunately,
there is currently no other clinically applicable
Symptoms of AERD usually appears in in vitro test available to confirm the diagnosis.
patients with adult onset asthma between the This means that the only testing available is
age of 20-40 years17,18. AERD in children is drug provocation testing, which is time-con-
rare. The ratio of male to female patients is suming, complicated, and potentially danger-
1:217. AERD was previously not associated ous, and should therefore only be carried out
with atopy or any other respiratory allergy, in experienced centers by experienced physi-
although some newer studies report a higher cian and trained nurse. Emergency treatment
prevalence of atopy in these patients19,20. Non equipment should be at hand. Indications for
steroidal anti-inflammatory drugs that most performing drug provocation test with aspi-
common cause respiratory reactions are: aspi- rin in suspected AERD are confirmation of
rin (80%), ibuprofen (41%), naproxen (4%)13. AERD in patients with unreliable history and
assessment of provocation dose before oral
Pathophysiology desensitization procedure12,26. Absolute con-
NSAIDs inhibit cyclooxygenase 1, increas- traindication for drug provocation tests are
ing leukotriene production and decreasing the the history of severe anaphylactic reaction
production of anti-inflammatory prostaglan- after any NSAID, unstable asthma, FEV1 ≤
dins. Patients with AERD have higher levels 70%, recent respiratory infection, pregnan-
of leukotrienes due to inflammation mediat- cy, severe underlying disease such as cardio-
ed by neutrophils, monocytes, and basophils, vascular, renal or liver disease12,26. There are
eosinophils, and mast cells. Increased leukot- different routes of aspirin administration for
riene production with NSAID ingestion leads provocation tests: inhaled intranasal, oral and
to bronchoconstriction, eosinophilic inflam- intravenous. Most commonly used are nasal
mation, increased mucus production in the and oral provocation tests27. Both have their
bronchi. Also in nasal polyps tissue, there are advantages and disadvantages. Nasal inhala-
elevated concentrations of leukotrienes21,22. tion of lysine-aspirin is safer and less time con-
suming in comparison to standard oral prov-
Diagnostics ocation tests. The nasal provocation test has
Due to distinctive symptoms, the diagnosis a lower sensitivity (80-87%) compared to the
could be often based on reliable history. In oral test, which has a sensitivity of 89-90%.
patients with adult-onset asthma, recurrent However, the specificity of both tests is high
(93-100%)12,26 .28-32 Inhalation challenge with
