Page 49 - Škrgat, Sabina, ed. 2023. Severe Asthma Forum - Monitoring and Treatable Traits in Severe Asthma. Koper: University of Primorska Press. Severe Asthma Forum, 2
P. 49
other in alternative overlap syndrome. Indirect effects in a bidirectional in- 49
Asthma, with its mechanical effect, has a di- teraction are reflected in prolonged effects
rect impact on OSA, leading to a reduction in of systemic corticosteroids, chronic diseases osa in patients with severe asthma-alternative overlap syndrome
lung volume by reducing the diameter of the of the upper respiratory tract, use of tobac-
airway, as well as by affecting the structure co and increased body weight in asthmatics,
and function of the smooth muscles of the which leads to worsening of OSA symptoms4.
airway. All of this leads to greater collapse
of the upper airway and worsens snoring and GERD and cardiovascular comorbidities in
apnea symptoms in patients with OSA4. OSA patients with O SA affect the poor course of
bronchial asthma. (Figure 1)
also directly affects asthma through nerve re-
flexes, intermittent hypoxia, increases in- Clinical significance of alternative
flammation, increases the production of lep- overlap syndrome
tin and vascular endothelial growth factor as
well as sleep fragmentation4. Intermittent hy- It remains unclear whether OSA in asthmat-
ics is only a comorbidity or a specific new phe-
poxia leads to systemic oxidative stress and notype of asthma. On the one hand, allergic
the development of systemic inflammation, asthma is accompanied by a T2 inflammato-
where an increase in tumor necrosis factor al- ry response and excessive production of in-
pha (TNF-ά), interleukin-6( IL-6) and C re- terleukin 5 and interleukin 13, which lead to
active protein was observed in patients with eosinophilia and hyperreactivity of airway
OPSTRUCTIVE
SLEEP
APNEA
Figure 1. Obstructive sleep apnea and asthma: pathophysiologic links
AHI greater than 1524. Also, intermittent hy- smooth muscles and mucus hypersecretion,
which are complicated by obesity and OSA.
poxia can lead to stimulation of receptors of In contrast, obese patients who developed
the carotid body and initiate reflex bronchoc- non-allergic asthma with late onset develop
onstriction and participate in the occurrence mechanical changes that lead to lung func-
of nocturnal symptoms associated with asth- tion disorders and favor the onset of obstruc-
ma25. Leptin, a hormonal protein produced tive apnea5. In these patients, the adipose tis-
by adipose tissue, has a proinflammatory ef-
fect and stimulates the release of IL-6 and sue secretes several cytokines and adipokines
TNF-ά from adipocytes25. that have direct effects on the airway epitheli-
Asthma, with its mechanical effect, has a di- teraction are reflected in prolonged effects
rect impact on OSA, leading to a reduction in of systemic corticosteroids, chronic diseases osa in patients with severe asthma-alternative overlap syndrome
lung volume by reducing the diameter of the of the upper respiratory tract, use of tobac-
airway, as well as by affecting the structure co and increased body weight in asthmatics,
and function of the smooth muscles of the which leads to worsening of OSA symptoms4.
airway. All of this leads to greater collapse
of the upper airway and worsens snoring and GERD and cardiovascular comorbidities in
apnea symptoms in patients with OSA4. OSA patients with O SA affect the poor course of
bronchial asthma. (Figure 1)
also directly affects asthma through nerve re-
flexes, intermittent hypoxia, increases in- Clinical significance of alternative
flammation, increases the production of lep- overlap syndrome
tin and vascular endothelial growth factor as
well as sleep fragmentation4. Intermittent hy- It remains unclear whether OSA in asthmat-
ics is only a comorbidity or a specific new phe-
poxia leads to systemic oxidative stress and notype of asthma. On the one hand, allergic
the development of systemic inflammation, asthma is accompanied by a T2 inflammato-
where an increase in tumor necrosis factor al- ry response and excessive production of in-
pha (TNF-ά), interleukin-6( IL-6) and C re- terleukin 5 and interleukin 13, which lead to
active protein was observed in patients with eosinophilia and hyperreactivity of airway
OPSTRUCTIVE
SLEEP
APNEA
Figure 1. Obstructive sleep apnea and asthma: pathophysiologic links
AHI greater than 1524. Also, intermittent hy- smooth muscles and mucus hypersecretion,
which are complicated by obesity and OSA.
poxia can lead to stimulation of receptors of In contrast, obese patients who developed
the carotid body and initiate reflex bronchoc- non-allergic asthma with late onset develop
onstriction and participate in the occurrence mechanical changes that lead to lung func-
of nocturnal symptoms associated with asth- tion disorders and favor the onset of obstruc-
ma25. Leptin, a hormonal protein produced tive apnea5. In these patients, the adipose tis-
by adipose tissue, has a proinflammatory ef-
fect and stimulates the release of IL-6 and sue secretes several cytokines and adipokines
TNF-ά from adipocytes25. that have direct effects on the airway epitheli-
