Page 105 - Škrgat, Sabina, ed. 2022. Severe Asthma - Basic and Clinical Views. Koper: University of Primorska Press. Severe Asthma Forum, 1
P. 105
T2-low Asthma 5.2
Žarko Vrbica1,2
Abstract 1 University of Dubrovnik,
T2-low asthma represents between 30-40% of severe asthma patients. It is less well defined Dubrovnik, Croatia
compared to the allergic and eosinophilic asthma (T2-high asthma). There are no specific bi-
omarkers for T2-low asthma but is often connected with the smoking, air pollution and obesi- 2 Dubrovnik general Hospital,
ty. Most of the patients have late onset asthma with more symptoms that are induced by exer- Dubrovnik, Croatia
cise and cold exposure with frequent infective exacerbations and bronchiectasis. The responce
to inhaled steroid treatment is poor, so the available therapeutic options and the targeted ther-
apies effective in both T2-high and T2-low asthma like new anti-TSLP monoclonal antibody
tezepelumab are discussed. Ongoing trials with sophisticated transcriptomic and proteomic
characterisations of different T2-low asthma patients should provide us tools to better charac-
terise these patients and choose the precise therapeutic approaches.
Keywords: T2-low asthma, neutrophylic asthma, paucigranulocytic asthma
Introduction airway inflammation will be a mixture of
both pathways with either T2 or the non-T2
Non-eosinophilic (T2-low) severe asthma is being dominant, and possibly reflecting a
somewhat an „orphan“ entity in the severe therapeutic target for greater disease control2.
asthma spectrum1. Severe asthma is a heter-
ogeneous disease involving diverse pathobio- Clinical Characteristics
logical mechanisms (endotypes) with differ-
ent clinical presentations (phenotypes). While T2-low asthma represents between 30-40%
the allergic asthma and non-allergic eosino- of severe asthma patients. Persistently non-eo-
philic asthma (T2-high asthma) are better sinophilic asthma prevalence has been report-
defined and their pathobiology is better de- ed up to 47% but most patients (>90%) con-
scribed with increasing number of specific sidered to have neutrophilic bronchitis may
treatment options, non-eosinophillic (T2-low have a re‐emergence of sputum eosinophils
asthma) is less defined, different mechanisms when their steroid doses are tapered for long
are involved in its pathobiology. The path- enough3.
ways are likely different in individual pa-
tients, vary over time and circumstances, and T2-low asthma is more frequent in the
are more complex than a simple division into late-onset asthma patients, obese females and
arbitrary groups: T (Type) 2 and non-T2 in- high symptomatic patients and has a poor re-
flammation. More likely, the end product of sponce to inhaled steroid treatment. Neutro-
philic inflammation is frequently associated
https://doi.org/10.26 493/978 -961-293 -157-5.105 -113
Žarko Vrbica1,2
Abstract 1 University of Dubrovnik,
T2-low asthma represents between 30-40% of severe asthma patients. It is less well defined Dubrovnik, Croatia
compared to the allergic and eosinophilic asthma (T2-high asthma). There are no specific bi-
omarkers for T2-low asthma but is often connected with the smoking, air pollution and obesi- 2 Dubrovnik general Hospital,
ty. Most of the patients have late onset asthma with more symptoms that are induced by exer- Dubrovnik, Croatia
cise and cold exposure with frequent infective exacerbations and bronchiectasis. The responce
to inhaled steroid treatment is poor, so the available therapeutic options and the targeted ther-
apies effective in both T2-high and T2-low asthma like new anti-TSLP monoclonal antibody
tezepelumab are discussed. Ongoing trials with sophisticated transcriptomic and proteomic
characterisations of different T2-low asthma patients should provide us tools to better charac-
terise these patients and choose the precise therapeutic approaches.
Keywords: T2-low asthma, neutrophylic asthma, paucigranulocytic asthma
Introduction airway inflammation will be a mixture of
both pathways with either T2 or the non-T2
Non-eosinophilic (T2-low) severe asthma is being dominant, and possibly reflecting a
somewhat an „orphan“ entity in the severe therapeutic target for greater disease control2.
asthma spectrum1. Severe asthma is a heter-
ogeneous disease involving diverse pathobio- Clinical Characteristics
logical mechanisms (endotypes) with differ-
ent clinical presentations (phenotypes). While T2-low asthma represents between 30-40%
the allergic asthma and non-allergic eosino- of severe asthma patients. Persistently non-eo-
philic asthma (T2-high asthma) are better sinophilic asthma prevalence has been report-
defined and their pathobiology is better de- ed up to 47% but most patients (>90%) con-
scribed with increasing number of specific sidered to have neutrophilic bronchitis may
treatment options, non-eosinophillic (T2-low have a re‐emergence of sputum eosinophils
asthma) is less defined, different mechanisms when their steroid doses are tapered for long
are involved in its pathobiology. The path- enough3.
ways are likely different in individual pa-
tients, vary over time and circumstances, and T2-low asthma is more frequent in the
are more complex than a simple division into late-onset asthma patients, obese females and
arbitrary groups: T (Type) 2 and non-T2 in- high symptomatic patients and has a poor re-
flammation. More likely, the end product of sponce to inhaled steroid treatment. Neutro-
philic inflammation is frequently associated
https://doi.org/10.26 493/978 -961-293 -157-5.105 -113
