Page 132 - Škrgat, Sabina, ed. 2022. Severe Asthma - Basic and Clinical Views. Koper: University of Primorska Press. Severe Asthma Forum, 1
P. 132
immunoglobulin E (IgE), eosinophils in It is very difficult to distinguish whether
blood and (induced) sputum, alsofraction- chronic airflow limitation is due to asthma or
severe asthma forum 1: severe asthma - basic and clinical views al exhaled nitric oxide (FeNO). It is impor- a CD, especially in smokers and the older pop-
tant to find fungi in sputum if they are pres- ulation. Prevalence of FAO is higher in more
ent and to distinguish if it is just sensitisation severe degrees of asthma, in severe or diffi-
(SAFS - severe asthma fungal sensitisation), cult-to-treat asthma there are 55% to 60% of
or colonisation and/or invasion (like ABA – patients with FAO; of them fulfiling the crite-
allergic bronchopulmonary aspergillosis). ria for COPD (42).When we compare asthma
Imaging like radiography or computed to- patients with asthma with and without FAO,
mography (CT scan) will disclose bronchiec- those with FAO are more likely to be male and
tasis, eosinophilic infiltrates, also eosinophil- to have a longer asthma duration43. Mannino
ic granulomatosis with polyangiitis (EGPA),
as well as signs of bronchiolitis or mucoid im- et al. found that up to 30% of subjects with
pactions. In some cases, it will be necessary airflow obstruction have a history of asthma
to perform bronchoscopy for a differential rather than COPD, but reversibility was not
diagnosis or to remove thick and sticky eosin- assessed in this epidemiologic survey, which
ophilic secretion in the airways. could make this number even higher44.
Second Dilemma: How Should Third Dilemma: How to Make the Right
we Distinguish Asthma From COPD Personalized Choice of Biologicals?
in Middle-aged Smoking Patients?
As phenotype may or may not be associated
The answer to this question at the beginning with underlying disease mechanisms, clini-
lies in detailed anamnesis, which no single cal phenotypes alone are not precise enough
diagnostic test could replace. A connection to guide targeted immune-modulator thera-
of symptoms to certain triggers, like aller- py without a “biologic” marker to reveal un-
gen exposure worsening respiratory symp- derlying biologic heterogeneity45.This means
toms, or coexistence of respiratory symptoms that the mandatory choice of biologicals is bi-
with comorbidities like eosinophilic lung in- omarkers, total and specific immunoglobulin
filtrate, rhinosinusitis with or without nasal E (IgE), eosinophils in blood and (induced)
polyps, urticaria, atopic dermatitis, psoria- sputum, as well as fractional exhaled nitric
sis, fungi sensitisation, etc., should be asso- oxide (FeNO). When we take everything into
ciated to asthma. Also, an allergy should al- account, clinical and laboratory aspects, to-
ways be looked for, or an aspirin sensitivity, gether with functional tests and imaging, we
as well as multiple episodes of respiratory can make a responsible choice.
symptoms during childhood and family his-
tory of allergies, whether in predecessors or Still, there are a few problems to be re-
descendants. solved. We need to develop biomarkers, which
could lead us to a more precise choice of
Another important factor, after medi- which biological therapy to start with, which
cal history data, is lung function variabili- will have a better predictive value for respon-
ty. The situation is not so clear when there is siveness to biologics. Also, those biomarkers
fixed airway obstruction (FAO) or persistent should be predictive for effective monitoring,
airflow limitation (PAL). Asthma and COPD or to give a signal when to stop biologics. Not
are syndromes consisting of several endotypes to mention how important it is to find new bi-
and phenotypes, consequently comprising a omarkers for the T2-low asthma phenotype
spectrum of diseases41. (or non-T2 endotype), after which a search for
an effective treatment could become a more
realistic option for such patients.
blood and (induced) sputum, alsofraction- chronic airflow limitation is due to asthma or
severe asthma forum 1: severe asthma - basic and clinical views al exhaled nitric oxide (FeNO). It is impor- a CD, especially in smokers and the older pop-
tant to find fungi in sputum if they are pres- ulation. Prevalence of FAO is higher in more
ent and to distinguish if it is just sensitisation severe degrees of asthma, in severe or diffi-
(SAFS - severe asthma fungal sensitisation), cult-to-treat asthma there are 55% to 60% of
or colonisation and/or invasion (like ABA – patients with FAO; of them fulfiling the crite-
allergic bronchopulmonary aspergillosis). ria for COPD (42).When we compare asthma
Imaging like radiography or computed to- patients with asthma with and without FAO,
mography (CT scan) will disclose bronchiec- those with FAO are more likely to be male and
tasis, eosinophilic infiltrates, also eosinophil- to have a longer asthma duration43. Mannino
ic granulomatosis with polyangiitis (EGPA),
as well as signs of bronchiolitis or mucoid im- et al. found that up to 30% of subjects with
pactions. In some cases, it will be necessary airflow obstruction have a history of asthma
to perform bronchoscopy for a differential rather than COPD, but reversibility was not
diagnosis or to remove thick and sticky eosin- assessed in this epidemiologic survey, which
ophilic secretion in the airways. could make this number even higher44.
Second Dilemma: How Should Third Dilemma: How to Make the Right
we Distinguish Asthma From COPD Personalized Choice of Biologicals?
in Middle-aged Smoking Patients?
As phenotype may or may not be associated
The answer to this question at the beginning with underlying disease mechanisms, clini-
lies in detailed anamnesis, which no single cal phenotypes alone are not precise enough
diagnostic test could replace. A connection to guide targeted immune-modulator thera-
of symptoms to certain triggers, like aller- py without a “biologic” marker to reveal un-
gen exposure worsening respiratory symp- derlying biologic heterogeneity45.This means
toms, or coexistence of respiratory symptoms that the mandatory choice of biologicals is bi-
with comorbidities like eosinophilic lung in- omarkers, total and specific immunoglobulin
filtrate, rhinosinusitis with or without nasal E (IgE), eosinophils in blood and (induced)
polyps, urticaria, atopic dermatitis, psoria- sputum, as well as fractional exhaled nitric
sis, fungi sensitisation, etc., should be asso- oxide (FeNO). When we take everything into
ciated to asthma. Also, an allergy should al- account, clinical and laboratory aspects, to-
ways be looked for, or an aspirin sensitivity, gether with functional tests and imaging, we
as well as multiple episodes of respiratory can make a responsible choice.
symptoms during childhood and family his-
tory of allergies, whether in predecessors or Still, there are a few problems to be re-
descendants. solved. We need to develop biomarkers, which
could lead us to a more precise choice of
Another important factor, after medi- which biological therapy to start with, which
cal history data, is lung function variabili- will have a better predictive value for respon-
ty. The situation is not so clear when there is siveness to biologics. Also, those biomarkers
fixed airway obstruction (FAO) or persistent should be predictive for effective monitoring,
airflow limitation (PAL). Asthma and COPD or to give a signal when to stop biologics. Not
are syndromes consisting of several endotypes to mention how important it is to find new bi-
and phenotypes, consequently comprising a omarkers for the T2-low asthma phenotype
spectrum of diseases41. (or non-T2 endotype), after which a search for
an effective treatment could become a more
realistic option for such patients.
