Page 108 - Škrgat, Sabina, ed. 2022. Severe Asthma - Basic and Clinical Views. Koper: University of Primorska Press. Severe Asthma Forum, 1
P. 108
signaling molecules, including G protein‐cou- cases, investigations of transcriptome and
pled receptors, transmembrane proteins, and proteome in sputum may lead to the better
severe asthma forum 1: severe asthma - basic and clinical views growth transcriptional factors, can be possi- differentiation of T2 high and T2 low asth-
ble mechanisms promoting AHR independ- ma.
ent of airway inflammation.
Non-pharmacological Treatment
Secretion of mast cell mediators could
lead to bronchial obstruction, airway remod- Active or passive smoking can induce neutro-
eling and AHR so the mast cell infiltration in philic inflammation, so the first measure in
ASM can play a role in the pathogenesis of those patients is to promote smoking cessa-
this asthma phenotype. tion.
Some patients may show both Th17 and Low-fat diet should be tried especially in
Th2 mediated inflammation and mixed gran- obese patients. The high-calorie and high-fat
ulocytic inflammation might be a transition meal can increase the neutrophil recruitment
between neutrophilic and eosinophilic phe- in the airways. Because of that, in obese pa-
notypes. tients weight reduction program with weight
loss can lead to significant improvement in
Management of T2-low Asthma asthma control and forced vital capacity, re-
duction in symptom days, rescue‐medication
No specific therapies have shown any clinical use and emergency room visits18.
benefits in patients with asthma that is asso-
ciated with a non‐T2 inflammatory process. Bariatric surgery can be considered in
It remains to be seen if such an endotype tru- morbid obese patients If there is no effect of
ly exists and to identify treatments to target weight reduction programs.
that endotype. There is a high unmet need in
the endotype-driven approach for the T2-low Bronchial thermoplasty (BT) can im-
asthma1. prove asthma control, peak expiratory flow,
quality of life, symptom‐free days and de-
Meanwhile, identifying intense airway crease the rescue medication use, severe ex-
neutrophilia as an indicator of airway infec- acerbations, emergency department visits and
tion and airway hyperresponsiveness as an days missed from work/school. BT should
indicator of smooth muscle dysfunction, and be reserved for uncontrolled asthmatics with
treating them appropriately, and not increas- persistent symptoms, frequent exacerbations
ing glucocorticosteroids in patients who do and severe AHR19. One limitation of bron-
not have obvious T2 inflammation, seem rea- chial thermoplasty is the difficulty of predict-
sonable3. ing clinical responders, so the discussion with
experts about the feasibility and necessity of
First, we should confirm the T2-low na- bronchial thermoplasty is adviced20.
ture of asthma with documented AHR and
the absence of T2 inflammation (normal Mucus clearance procedures: In the pa-
blood or sputum eosinophils, serum IgE or tients with mucus hypersecretion, smoking
FeNO) or high sputum neutrophil. This is im- cessation, physiotherapy in different body
portant because most of such patients (with positions with high-frequency chest wall os-
the exception of mast-cell mediated disease) cillation and eduaction about deep breath-
may not benefit from increasing the dosage of ing with effective coughing can improve mu-
maintenance ICS. cus clearance and alleviate the symptoms. In
addition, intermittent positive end-expirato-
Neutrophilic bronchitis can mask the un- ry pressure (PEEP) can dilate the small air-
derlying eosinophillic component so it is im- way, reduce small airway obstruction, pro-
portant to recheck the cell counts after the mote the sputum drainage and accelerate
blood neutrophilia has resolved. In unresolved
pled receptors, transmembrane proteins, and proteome in sputum may lead to the better
severe asthma forum 1: severe asthma - basic and clinical views growth transcriptional factors, can be possi- differentiation of T2 high and T2 low asth-
ble mechanisms promoting AHR independ- ma.
ent of airway inflammation.
Non-pharmacological Treatment
Secretion of mast cell mediators could
lead to bronchial obstruction, airway remod- Active or passive smoking can induce neutro-
eling and AHR so the mast cell infiltration in philic inflammation, so the first measure in
ASM can play a role in the pathogenesis of those patients is to promote smoking cessa-
this asthma phenotype. tion.
Some patients may show both Th17 and Low-fat diet should be tried especially in
Th2 mediated inflammation and mixed gran- obese patients. The high-calorie and high-fat
ulocytic inflammation might be a transition meal can increase the neutrophil recruitment
between neutrophilic and eosinophilic phe- in the airways. Because of that, in obese pa-
notypes. tients weight reduction program with weight
loss can lead to significant improvement in
Management of T2-low Asthma asthma control and forced vital capacity, re-
duction in symptom days, rescue‐medication
No specific therapies have shown any clinical use and emergency room visits18.
benefits in patients with asthma that is asso-
ciated with a non‐T2 inflammatory process. Bariatric surgery can be considered in
It remains to be seen if such an endotype tru- morbid obese patients If there is no effect of
ly exists and to identify treatments to target weight reduction programs.
that endotype. There is a high unmet need in
the endotype-driven approach for the T2-low Bronchial thermoplasty (BT) can im-
asthma1. prove asthma control, peak expiratory flow,
quality of life, symptom‐free days and de-
Meanwhile, identifying intense airway crease the rescue medication use, severe ex-
neutrophilia as an indicator of airway infec- acerbations, emergency department visits and
tion and airway hyperresponsiveness as an days missed from work/school. BT should
indicator of smooth muscle dysfunction, and be reserved for uncontrolled asthmatics with
treating them appropriately, and not increas- persistent symptoms, frequent exacerbations
ing glucocorticosteroids in patients who do and severe AHR19. One limitation of bron-
not have obvious T2 inflammation, seem rea- chial thermoplasty is the difficulty of predict-
sonable3. ing clinical responders, so the discussion with
experts about the feasibility and necessity of
First, we should confirm the T2-low na- bronchial thermoplasty is adviced20.
ture of asthma with documented AHR and
the absence of T2 inflammation (normal Mucus clearance procedures: In the pa-
blood or sputum eosinophils, serum IgE or tients with mucus hypersecretion, smoking
FeNO) or high sputum neutrophil. This is im- cessation, physiotherapy in different body
portant because most of such patients (with positions with high-frequency chest wall os-
the exception of mast-cell mediated disease) cillation and eduaction about deep breath-
may not benefit from increasing the dosage of ing with effective coughing can improve mu-
maintenance ICS. cus clearance and alleviate the symptoms. In
addition, intermittent positive end-expirato-
Neutrophilic bronchitis can mask the un- ry pressure (PEEP) can dilate the small air-
derlying eosinophillic component so it is im- way, reduce small airway obstruction, pro-
portant to recheck the cell counts after the mote the sputum drainage and accelerate
blood neutrophilia has resolved. In unresolved
