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Comorbidities

Various comorbidities are often associated with asthma.1 These can influence the clinical expression of asthma, alter asthma responses to therapy and ultimately reduce a patient’s QoL.2 Of these, some of the most frequently reported are chronic rhinitis (allergic and nonallergic), chronic sinusitis and rhinosinusitis, gastro-oesophageal reflux disease (GORD), obstructive sleep apnoea, hormonal disorders, depression and anxiety disorders.1 It is not yet known how many of these comorbidities interact with asthma, particularly in cases of severe asthma. Further research is needed on the relationships between these conditions and asthma.1

COMORBIDITIES ASSOCIATED WITH ASTHMA

The most frequently reported asthma comorbid conditions include:1
  • Chronic rhinitis (allergic and nonallergic)
  • Chronic sinusitis and rhinosinusitis
  • GORD
  • Obstructive sleep apnoea
  • Hormonal disorders
  • Depression and anxiety disorders
These conditions may:1
  • Share a common pathophysiological mechanism with asthma
  • Influence asthma control, phenotype, and response to treatment
  • Be more prevalent in asthmatic patients but without obvious influence of the disease
Asthmacomorbidities may share a common pathophysiological mechanism with asthma1
ASTHMA AND ALLERGIC
RHINITIS FREQUENTLY
CO-EXIST IN THE SAME
INDIVIDUAL1

Research indicates that 20–50% of people with allergic rhinitis have asthma and more than 80% of people with asthma have rhinitis.1

While a clear mechanism of interaction between asthma and rhinitis remains unclear, there is evidence that:

  • Asthma and rhinitis may manifest from a shared inflammatory process. Studies have demonstrated common immunological processes between asthma and rhinitis, involving the action of mast cells, eosinophils and Th2 cytokines3–5
  • Airway epithelial cells are key to the pathogenesis of both asthma and allergic rhinitis, acting as the airway and lung’s first-line of defence from inflammatory stimuli and antigens6
  • The impaired filtering function of the nose caused by allergic rhinitis can lead sufferers to breathe through their mouth. This can result in increased exposure of the lower airways to allergens and other asthma triggers1
CHRONIC RHINOSINUSITIS
CAN CAUSE ASTHMA TO BE
MORE SEVERE AND DIFFICULT
TO CONTROL2

Almost 100% of individuals with severe asthma have been reported to have radiological sinus abnormalities. Chronic rhinosinusitis can cause asthma to be both more severe and difficult to control.2

Chronic rhinosinusitis with nasal polyps is one important phenotype associated with severe asthma comorbidity. The mechanism is disputed, however, there is evidence to suggest that nasal polyps are associated with increased production of cytokines, prolonged survival of eosinophils and increased expression of IL-5.2

THE RISK OF GORD
INCREASES IN ASTHMATIC
PATIENTS1

Around 50–80% of asthmatics reported suffering from GORD symptoms.1

There are two main mechanisms associating GORD with asthma:

  • The ‘reflux’ theory suggests that gastro-oesophageal reflux causes an aspirate which stimulates the pharynx or larynx, causing acute injury to the lung and other pulmonary symptoms such as a bronchial cough reflex7
  • The ‘reflex’ theory suggests distal oesophageal reflux stimulates the vagal nerve leading to bronchoconstriction7

In addition, evidence suggests that asthma may also worsen GORD symptoms. An increased pressure gradient between an asthma sufferers’ abdomen and thorax can lead to the lower oesophageal sphincter to herniate into the thorax. This reduces the sphincter’s barrier function leading to increased reflux.7

The causal relationship between GORD and asthma may not necessarily be direct. Asthma and GORD are both considered to be comorbidities of obesity meaning planning effective treatment is not always straightforward.1,8

OBESITY HAS BEEN LINKED
WITH SPECIFIC PHENOTYPES
OF ASTHMA11

The prevalence of obesity continues to increase worldwide and is associated with an increased incidence of asthma and poor asthma control.1,9

The direction of causality is unclear; however studies have suggested that:

  • Obesity is associated with increased proinflammatory adipokines in the circulation, which may contribute to asthma by inducing airway hyper-responsiveness10
  • Obesity can result in epithelial cells transitioning to mesenchymal cells leading to persistent inflammation. This inflammation in the airway and associated remodelling of the airway can lead to symptoms of asthma11

However, immunological pathways are not the only potential cause for obesity acting as a comorbidity of asthma. Reducing physical activity to attempt to limit asthmatic symptoms may, over time, promote weight gain.12

Obesity has also been linked with specific phenotypes of asthma including a reduced response to asthma medications.1,11

OTHER COMORBIDITIES

There are many other comorbidities associated with asthma and for some, the level of influence remains undetermined.

Associations are not always clear and are regularly multifactorial. Determining underlying causality of comorbidities is complex, often with immunological, genetic and environmental impacts. Future research will continue to provide us with further insights into these interactions, allowing treatment strategies to improve.

BURDEN OF
ASTHMA

Learn about the prevalence and
healthcare burden of asthma.

Explore facts & figures

DEFINING
ASTHMA CONTROL

Discover how asthma control goes
beyond exacerbation reduction.

Get more information

PATHOPHYSIOLOGY
OF TYPE 2 ASTHMA

Learn about the key drivers of
Type 2 inflammation.

Explore key drivers

ABPA, allergic bronchopulmonary aspergillosis; COPD, chronic obstructive pulmonary disease; GORD, gastro-oesophageal reflux disease; IL, interleukin; OSA, obstructive sleep apnoea; QoL, quality of life; Th2, T helper cell type 2.

References:
  1. Boulet L and Boulay M. Asthma-related comorbidities. Expert Rev Respir Med. 2011;5(3):377–393.
  2. Boulet L. Influence of comorbid conditions on asthma. Eur Respir J. 2009;33(4):897–906.
  3. Giavina-Bianchi P, et al. United airway disease: current perspectives. J Asthma Allergy. 2016;9:93–100.
  4. Kim H, Bouchard J and Renzi P. The link between allergic rhinitis and asthma: A role for antileukotrienes? Can Respir J. 2008;15(2):91–98.
  5. Togias A. Rhinitis and asthma: Evidence for respiratory system integration. Allergy Clin Immunol. 2003;111(6):1171–1183.
  6. Wang Y, et al. Role of epithelial cells in development of asthma and allergic rhinitis. Resp Med. 2008;102:949–955.
  7. Havemann B, Henderson C and El-Serag H. The association between gastro-oesophageal reflux disease and asthma: a systematic review. Gut. 2007;56:1654–1664.
  8. El-Serag H. The Association Between Obesity and GERD: A review of the Epidemiological Evidence. Dig Dis Sci. 2008;53(9):2307–2312.
  9. Juel C, et al. Asthma and obesity: does weight loss improve asthma control? A systematic review. J Asthma Allergy. 2012;5:21–26.
  10. Cazzola M, et al. Comorbidities of asthma: current knowledge and future research needs. Curr Opin Pulm Med. 2013;19(1):36–41.
  11. Mohanan S, et al. Obesity and asthma: Pathophysiology and implications for diagnosis and management in primary care. Exp Biol Med. 2014;239:1531–1540.
  12. Khalid F and Holguin F. A review of obesity and asthma across the life span. J Asthma. 2018.