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Abstract

Bronchiectasis is a chronic, complex, and heterogeneous respiratory disease characterized by irreversible bronchial dilation, persistent airway inflammation, and recurrent infections. Traditionally viewed from a lung-centered perspective, its pathophysiology has been explained by the “vicious cycle” hypothesis, later refined into the more dynamic concept of the “vicious vortex.” However, emerging evidence highlights the pivotal role of comorbidities in influencing disease progression, symptom burden, and prognosis. This review explores the evolving understanding of bronchiectasis by integrating comorbidities into current pathophysiological frameworks. We illustrate how coexisting conditions interact with components of the vicious vortex, amplifying airway inflammation, impairing host defenses, and disrupting clearance mechanisms. We summarize evidence on the prevalence, clinical impact, and prognostic significance of key comorbidities and discuss their implications for patient management. Finally, we emphasize the importance of an integrated, multidisciplinary approach and the emerging role of the treatable traits framework, which focuses on identifying clinically relevant, biologically measurable, and modifiable traits—regardless of whether they are etiological or nonetiological. In this sense, we propose a conceptual “Copernican Revolution” in bronchiectasis care: recognizing comorbidities not as secondary features, but as potential drivers of disease trajectory. By adopting this pragmatic strategy, clinicians can optimize quality of life, achieve patient-centered care, and improve outcomes in this condition.

Plain language summary

Looking beyond the lungs: how other health problems shape bronchiectasis

Bronchiectasis is a chronic lung condition characterized by persistent cough, mucus accumulation, and recurrent chest infections. Historically considered a disease confined to the lungs, emerging research highlights the significant role of comorbidities in influencing its development, progression, and severity.

In this review, we examine how conditions such as asthma, chronic obstructive pulmonary disease (COPD), upper airway disorders, gastroesophageal reflux disease (GERD), and inflammatory bowel disease (IBD) not only coexist with bronchiectasis but may also exacerbate its clinical course. Other important comorbidities—including cardiovascular disease, osteoporosis, malnutrition, periodontal disease, anxiety, diabetes and depression—are associated with increased exacerbation frequency, more frequent hospitalizations, and reduced quality of life. We also explore the role of immune system dysfunction, particularly primary immunodeficiencies, as potential underlying causes of bronchiectasis that warrant targeted diagnostic evaluation. Clinical tools such as the Bronchiectasis Aetiology Comorbidity Index (BACI) can assist clinicians in assessing the burden and prognostic impact of comorbidities. This review advocates for a paradigm shift: moving beyond a lung-centric model toward a holistic approach that recognizes bronchiectasis as a multisystem condition. This perspective emphasizes the early identification of comorbidities, implementation of practical screening strategies, and collaboration with specialists such as dieticians, psychologists, and immunologists. Addressing comorbid conditions alongside the management of bronchiectasis may alleviate symptoms, reduce infection rates, and improve overall well-being. We propose that this integrated, patient-centered approach will lead to more effective and individualized care for individuals living with bronchiectasis.

Keywords

bronchiectasis comorbidities precision medicine treatable traits

Introduction

Bronchiectasis is a chronic pulmonary disease characterized by irreversible bronchial dilation, persistent airway inflammation, and recurrent infections, leading to progressive lung damage.¹ Clinically, it manifests with chronic cough, daily sputum production, and recurrent exacerbations, significantly impacting patients’ quality of life.¹

Once considered rare, bronchiectasis is now increasingly diagnosed, largely due to the widespread use of high-resolution computed tomography (HRCT) and greater awareness among both respiratory and nonrespiratory physicians, leading to prevalence estimates reaching 566 cases per 100,000 population in the United Kingdom.^2,3 In terms of prognosis, a Belgian prospective cohort study reported a 5-year mortality rate of 20.4% among patients with bronchiectasis, underscoring the disease’s significant clinical impact.⁴ Beyond morbidity and mortality, bronchiectasis also poses a considerable economic burden, with annual healthcare costs per adult patient largely driven by exacerbations and hospitalizations.^5,6

Traditionally, bronchiectasis has been viewed through the lens of the vicious cycle, a self-perpetuating process of impaired mucociliary clearance, chronic airway infection, inflammation, and structural lung damage.⁷ This lung-centric perspective has long dominated the field. However, bronchiectasis is a prototypical example of a complex and heterogeneous chronic respiratory disease. Complexity lies in the way of multiple processes—symptoms, coexisting conditions, lung function decline, and distinct radiological patterns—interact over time in a nonlinear fashion. Heterogeneity reflects the fact that these elements vary between patients and can change within the same patient over the course of their illness.⁸ Bronchiectasis is also characterized by multiple underlying etiologies.⁹ It frequently coexists with other respiratory conditions such as chronic obstructive pulmonary disease (COPD), asthma, and chronic rhinosinusitis (CRS), which may share overlapping pathogenic mechanisms, particularly regarding local airway inflammation.^10,11 Additionally, systemic diseases—including immunodeficiencies, primary ciliary dyskinesia, connective tissue diseases, gastroesophageal reflux disease (GERD), and inflammatory bowel disease (IBD)—have been recognized as important etiological contributors. Beyond respiratory manifestations, bronchiectasis often coexists with a wide range of nonetiological comorbidities that significantly influence its disease trajectory. These include cardiovascular disease, osteoporosis, malnutrition, periodontal disease, diabetes, and psychological conditions.^9,12–14

With advancements in precision medicine and the introduction of the treatable traits framework, growing attention is now focused on the role of comorbidities in modulating disease progression, health-related quality of life, and survival in bronchiectasis.¹⁵ As demonstrated in COPD, the prognostic impact of comorbidities can even exceed that of the underlying pulmonary disease itself, profoundly shaping clinical outcomes and mortality risk.^16,17 However, unlike in COPD, the systematic identification and targeted management of comorbidities in bronchiectasis remains fragmented and often underestimated. Patients increasingly emphasize the need for personalized and flexible management strategies given the heterogeneity and complexity of bronchiectasis.¹⁸ In this context, and considering the paucity of disease-specific therapies, comorbidities emerge as a pragmatic and actionable target to improve patient outcomes.

Cystic fibrosis (CF) and primary ciliary dyskinesia (PCD) are well-recognized etiological conditions leading to bronchiectasis. However, given their distinct pathophysiological mechanisms and genetic implications, they fall outside the scope of this review, which will focus on adult non-CF and non-PCD bronchiectasis.

This review aims to outline the clinical relevance of the most frequent comorbidities in bronchiectasis, highlighting their influence on symptom burden, disease progression, and outcomes. Our goal is to encourage a more integrated, patient-centered approach that places comorbidities at the forefront of prognostic and therapeutic considerations.

Methods

We conducted a comprehensive literature search using the PubMed electronic database, focusing on English-language articles published up to March 2025. A combination of Medical Subject Headings (MeSH) and non-MeSH keywords was used, including “Bronchiectasis” [MeSH], “Comorbidity” [MeSH], “Immune System Diseases” [MeSH], and “Treatable Traits” (non-MeSH term). Relevant studies were reviewed in detail to provide a balanced and comprehensive discussion of the topic.

Rethinking pathophysiology of bronchiectasis: Integrating comorbidities into the framework

For decades, bronchiectasis has been viewed as a lung-centered disease, driven by chronic infection, inflammation, and progressive structural damage. The vicious cycle hypothesis, originally proposed by Cole, described bronchiectasis as a self-perpetuating loop of airway inflammation, infection, mucus stasis, and lung damage.⁷ More recently, this concept has evolved into the vicious vortex, emphasizing the interdependence of pathological components and introducing the role of systemic factors in sustaining disease progression.¹⁹ Exacerbations serve as accelerators, further destabilizing this system.²⁰

Comorbidities may interact with the vicious vortex at multiple levels (Figure 1): (i) Respiratory and nonrespiratory inflammatory diseases (e.g., asthma, COPD, IBD, autoimmune disorders) amplify airway inflammation and perpetuate tissue damage; (ii) Immunodeficiencies and malnutrition impair host defences, increasing susceptibility to infection; (iii) GERD and other chronic airway diseases compromise mucociliary clearance, promoting mucus accumulation, lung inflammation, and pathogen colonization; (iv) Anxiety, depression, cognitive impairment, and cardiovascular and metabolic diseases reduce resilience to exacerbations, worsen symptoms and functional status, and impair treatment adherence; (v) sinonasal and periodontal disease promote systemic inflammation and add to upper airway translocation of pathogens to the lower airways.

Figure 1.

Conceptual model illustrating the interaction between comorbidities and the vicious vortex in bronchiectasis. This schematic highlights how comorbidities can interact with the core components of bronchiectasis pathophysiology—airway infection, inflammation, impaired mucociliary clearance, and structural lung damage. Coexisting conditions may amplify inflammatory responses, impair host defenses, and influence microbial dynamics, thereby accelerating disease progression.

A new framework—the “adapted island model”—further refines our understanding of bronchiectasis pathophysiology.²¹ This model views the lung as a dynamic ecosystem (“island”), shaped by microbial immigration from internal and external sources and elimination (host defences, mucociliary clearance, antibiotics). Disruptions in this balance can result from exogenous factors (e.g., new infections, air pollution) or endogenous factors (e.g., poor control of GERD, IBD, malnutrition, immunodeficiency). These disruptions may lead to dysbiosis (altered microbial composition favoring pathogenic dominance) and/or shifts in the inflammatory milieu, promoting airway inflammation even in the absence of significant changes in microbial composition.²⁰

While bronchiectasis can arise from diverse etiologies, systematic evaluation of both causes and comorbidities remains essential and is recommended, as these subsequently require specific treatments.^22,23 For etiological evaluation, a task force of experts proposed an algorithm to guide etiological diagnosis.²⁴ This approach categorizes potential causes as “Definitive,” “Possible,” or “of exclusion,” to identify factors directly causing bronchiectasis.

However, many patients remain without an identifiable cause, and in these cases, management should rely on recognizing other clinical features that may influence disease expression and prognosis. Over the years, respiratory medicine has progressively shifted from purely descriptive frameworks toward biologically and clinically meaningful classifications, laying the foundation for the treatable traits model, first introduced by Agustí et al.⁸ This approach moves beyond rigid diagnostic categories and focuses instead on identifying clinically relevant, biologically measurable, and modifiable traits—including both etiological factors and comorbidities—that can be specifically targeted in each patient. From a clinical perspective, the treatable traits approach is not simply a classification tool but rather a pragmatic strategy for personalized care, aiming to optimize quality of life and improve prognosis in patients with bronchiectasis.

Importance and clinical impact of comorbidities

The first study to highlight bronchiectasis as a systemic inflammatory disease was conducted by Gale and colleagues, who demonstrated its broader inflammatory consequences, including an increased risk of osteoporosis and cardiovascular conditions such as hypertension and dyslipidemia.²⁵ Comorbidities play a key role in the clinical course of bronchiectasis, negatively impacting quality of life, lung function, and the risk of severe exacerbations. According to McDonnell et al., the presence of concomitant diseases such as COPD, heart failure, diabetes mellitus, and autoimmune disorders significantly increases mortality in bronchiectasis patients.¹³ Furthermore, other studies have shown that patients with a high comorbidity burden are more prone to severe exacerbations, often requiring hospitalization, with a direct impact on long-term survival.^26,27

In this context,—a prognostic tool—the BACI score (Bronchiectasis Aetiology Comorbidity Index) was developed to quantify the impact of comorbidities on patient prognosis. Higher BACI scores are significantly associated with increased 5-year mortality.¹³ Subsequent research showed that patients with a BACI score ⩾6 had lower FEV1 and a higher incidence of respiratory failure, exacerbations, and hospitalizations, making it a valuable tool for identifying individuals at risk of early clinical deterioration and poor long-term outcomes.²⁷ Compared to other prognostic scores, such as the Bronchiectasis Severity Index (BSI) and the FACED score, the BACI score stands out for its focus on comorbidities. While the BSI integrates clinical, microbiological, and radiological parameters to assess overall disease severity, and the FACED score uses a simple set of parameters to predict survival, the BACI score allows for a more specific risk stratification related to associated pathological conditions, making it particularly useful in patients with a high comorbidity burden (Table 1). However, since its inception, literature has revealed new comorbidities that impact the vicious vortex.

Table 1.

Comparison of scoring systems in bronchiectasis—Bronchiectasis Severity Index (BSI), FACED, and Bronchiectasis Aetiology Comorbidity Index (BACI)—highlighting their components and primary purposes.

Scoring system	Components	Purpose
Bronchiectasis Severity Index (BSI)	• Age • Body Mass Index (BMI) • FEV₁ % predicted • Hospitalizations in the past year • Exacerbations in the past year • Chronic Pseudomonas aeruginosa infection • Chronic colonization by other pathogens • Dyspnea (mMRC score) • Radiological severity	Predicts mortality, hospital admissions, exacerbations, and quality of life deterioration.
FACED Score	• FEV₁ % predicted • Age • Chronic Pseudomonas aeruginosa infection • Radiological extent of disease • Dyspnea (mMRC score)	Primarily predicts 5-year mortality.
Bronchiectasis Aetiology Comorbidity Index (BACI)	• Metastatic malignancy • Hematological malignancy • COPD • Cognitive impairment • IBD • Chronic liver disease • Iron deficiency anemia • Diabetes • Asthma • Pulmonary hypertension • Peripheral vascular disease • Ischemic heart disease	Assesses the impact of comorbidities on mortality and morbidity in bronchiectasis patients.

“Etiological” comorbidities

Respiratory comorbidities

Among comorbidities, respiratory diseases are among the most frequently identified and clinically relevant in patients with bronchiectasis.

The coexistence of bronchiectasis with asthma and COPD is particularly common and carries significant clinical implications. According to the two most recent analyses from the EMBARC registry, 31% of bronchiectasis patients have a diagnosis of asthma, while 25% have COPD.^28,29 These conditions, along with CRS, may present with either a neutrophilic or eosinophilic inflammatory profile, potentially amplifying airway inflammation and exacerbation risk by fueling key components of the vicious vortex.^30–32 Patients with multiple coexisting airway diseases report significantly worse quality of life compared to those with bronchiectasis alone, reflected in lower Bronchiectasis Health Questionnaire scores, increased dyspnea, fatigue, and sleep disturbances.^10,33,34

Asthma and allergic bronchopulmonary aspergillosis

The prevalence of asthma in bronchiectasis varies geographically. Western cohorts report prevalences around 30%, much higher than Chinese and Korean registries.^35–39 While radiological severity may not differ significantly, the presence of asthma is consistently associated with more intense symptoms and greater use of inhaled therapies in bronchiectasis.³³ Asthma also increases the risk of acute exacerbations: patients with both conditions experience nearly double the exacerbation rate and a shorter time to first flare-up.³⁴ In severe phenotypes, such as corticosteroid-dependent asthma, bronchiectasis has been associated with significantly increased mortality.⁴⁰

In the differential diagnosis of type 2 inflammation-associated bronchiectasis, Allergic Bronchopulmonary Aspergillosis (ABPA) should always be considered, particularly in patients with characteristic radiological findings and peripheral eosinophilia. Assessment should include total IgE levels and sensitization to Aspergillus spp., as ABPA represents a distinct, common, and treatable condition. Its prevalence as an underlying cause of bronchiectasis ranges from 1.3% to 8.9% across registries, highlighting its clinical relevance.^41–43

Chronic obstructive pulmonary disease

The prevalence of COPD as a comorbidity in bronchiectasis varies more widely than asthma. It approaches 40% in Central and Eastern Europe, Korea, and Australia, whereas lower rates are reported in the Chinese cohort.^35–39 In COPD, the presence of bronchiectasis is associated with greater bacterial colonization, more frequent and prolonged exacerbations, severe functional impairment and more importantly, is an independent prognostic factor for mortality.^4,44

Chronic rhinosinusitis

CRS is also a frequent comorbidity, although its prevalence in bronchiectasis is less consistently reported across registries. A systematic review estimated a pooled prevalence of 62% in patients with bronchiectasis, with high variability among studies due to diagnostic heterogeneity.⁴⁵ CRS contributes to a more symptomatic phenotype, worsening both upper and lower airway symptoms, and significantly impairing physical, mental, and social well-being.⁴⁶ The coexistence of CRS is linked to a higher treatment burden, increased healthcare utilization, faster disease progression, and more frequent hospitalizations.⁴⁷ While a direct increase in mortality has not been demonstrated, CRS appears to contribute to poorer quality of life and greater exacerbation frequency in patients with bronchiectasis.

Clinicians should actively screen for respiratory comorbidities using appropriate tools, including functional tests, laboratory markers of type 2 inflammation, imaging and otorhinolaryngological evaluation when indicated, as early recognition and targeted management can significantly improve outcomes in patients with bronchiectasis.

Nonrespiratory etiological comorbidities

Immunodeficiencies in bronchiectasis

Compared to respiratory comorbidities, immunodeficiency is less frequently reported as a cause or comorbidity of bronchiectasis across international registries. In the US Bronchiectasis Research Registry, it was documented in 5% of patients as a comorbidity, while in Europe, it was identified as an underlying cause in 4.1% of cases (with higher rates in Northern and Western regions). Lower prevalence was observed in China, Australia, and Korea, where immunodeficiency was not among the top five reported causes.^35–39 Notably, these registries do not always distinguish between primary and secondary immunodeficiencies in their reports.

Primary immunodeficiencies

Primary immunodeficiencies, also known as inborn errors of immunity, lead to impaired host defense mechanisms, resulting in increased susceptibility to infections, autoimmunity, allergy, and malignancy.⁴⁸ While severe combined immunodeficiencies are associated with recurrent respiratory infections in early childhood, predominantly antibody deficiencies are the most commonly associated with bronchiectasis in adults.^48,49 Immunoglobulins play a fundamental role in pulmonary surface defense. Different immunoglobulins have specific roles and locations. Secretory IgA and IgM predominate in upper and lower airways. Secretory IgA prevent bacterial adhesion and neutralize toxins avoiding an excessive inflammatory response; IgM, through complement activation, enhance pathogen opsonization. IgG predominate in the alveolar space (originating from systemic circulation) offering protection against bacterial and viral infections.⁵⁰

Common variable immunodeficiency (CVID) is the primary antibody deficiency most strongly associated with bronchiectasis.⁴⁹ Registry data indicate that up to 58% of CVID patients develop airway disease, including bronchiectasis.⁵¹ Notably, this prevalence is higher than in patients with X-linked agammaglobulinemia (XLA), despite CVID being characterized by relatively higher IgG levels. This observation supports the hypothesis that nonhumoral mechanisms, including T-cell dysfunction, may play a role in bronchiectasis development in CVID.⁵² XLA, in contrast, is characterized by a profound absence of all immunoglobulins and B cells, leading to early-onset recurrent infections and progressive pulmonary damage. Interestingly, a randomized controlled trial in patients with CVID and XLA with chronic infection-related lung disease—over 80% of whom had bronchiectasis at baseline—found that long-term low-dose azithromycin significantly reduced the annual rate of respiratory exacerbations.⁵³

Selective IgA deficiency (SIgAD) is the most common primary immunodeficiency, with an estimated prevalence of approximately 1 in 600 to 1 in 1000 in Caucasian populations, and significantly lower rates in East Asian countries such as Japan (1 in ~18,000).^54,55 While many affected individuals remain asymptomatic, some develop recurrent sinopulmonary infections, which can lead to bronchiectasis. A subset of these patients may require immunoglobulin replacement therapy, especially if they also have an associated IgG subclass deficiency.^54–57

Selective IgG subclass deficiencies, despite normal total IgG, IgA, and IgM levels, can impar immune defense and predispose individuals to recurrent respiratory infections and bronchiectasis.^58,59 Each IgG subclass plays a distinct role in host immunity. IgG1 and IgG3 are essential for defense against protein antigens, including bacterial toxins, with IgG3 having strong complement-activating properties. IgG2 is particularly crucial for recognizing polysaccharide antigens, offering protection against encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae. IgG4, while having a limited role in antimicrobial defense, may influence immune regulation.⁴⁸

Screening for IgG subclass deficiencies is particularly useful in cases of selective IgA deficiency and specific antibody deficiency.⁵⁷ While many individuals with low IgA are asymptomatic, the presence of concurrent IgG subclass deficiencies can increase the risk and severity of recurrent infections and help identify a subset needing closer monitoring or intervention. Furthermore, a patient with recurrent infections and normal total IgG but a marked deficiency in a specific IgG subclass—such as IgG2, which is critical for polysaccharide antigen responses—may warrant further investigation into their ability to mount an adequate immune response to these antigens. Notably, in patients with CVID, low serum IgA levels (<0.07 g/L) have been identified as an independent risk factor for increased prevalence of bronchiectasis.⁵⁰

Secondary immunodeficiencies

Secondary immunodeficiencies are less commonly reported compared to primary immunodeficiencies but may help in understanding the immune mechanisms in bronchiectasis. These conditions arise from various conditions that impair various components of innate and adaptive immunity, including hematologic malignancies, HIV infection, solid organ transplantations, and immunosuppressive medications.⁶⁰

Immunodeficiencies identification and potential treatment

Clinical guidelines suggest that patients who experience difficult-to-treat or recurrent infections, present with deep abscesses or unusual pathogens such as Aspergillus, or display structural lung damage (i.e., bronchiectasis) should undergo immunological assessment. Unfortunately, there is no universally accepted definition of what constitutes “recurrent infections” that warrant investigation.^48,61,62

Evidence is also evolving regarding the correct immunological evaluation for bronchiectasis patients. Not all immunodeficiencies require immunoglobulin replacement therapy. Mandatory indications for treatment include CVID, XLA, and secondary hypogammaglobulinemia in patients with severe or recurrent infections.^48,61,62 In contrast, the role of immunoglobulin supplementation in specific antibody deficiency, selective IgA deficiency, and IgG subclass deficiency remains less defined. International guidelines suggest that immunoglobulin replacement may be considered when IgG levels fall below 4–5 g/L in the presence of recurrent infections.^48,61 In selective IgA deficiency, which does not have a specific replacement therapy, evaluation of coexisting IgG subclass deficiencies (particularly IgG2 and IgG3) may help guide decisions on prophylaxis or immunoglobulin use.^48,61

Recent initiatives have introduced the concept of “treatable immunodeficiency” in bronchiectasis, advocating for a broader immunological workup beyond the standard recommendations outlined in the European Respiratory Society bronchiectasis guidelines.^23,63 In a recent multicenter study, this expanded approach—which includes IgE and IgG subclass testing as well as lymphocyte subset analysis—increased the detection rate of treatable immunodeficiencies from 3% to 16%.⁶³ It is noteworthy that assessment of immunological responses to polysaccharide and protein antigens was performed as part of second-line testing. A stepwise diagnostic strategy, with each test addressing a specific clinical suspicion—from common humoral defects to more complex cellular or functional disorders—is summarized in Supplemental Table 1.

Based on these recommendations, patients with primary or secondary immunodeficiencies may be considered for immunoglobulin replacement therapy if they have a history of three or more exacerbations per year, a systemic infection requiring treatment in the past year, hospitalization due to bacterial infection, or significantly reduced quality of life due to recurrent infections.⁶³

Even this expanded approach has limitations. Its primary focus on antibody deficiencies may overlook defects in other immune pathways—such as complement disorders—that can also contribute to the development and severity of bronchiectasis.^64–66 For instance, mannose-binding lectin (MBL) deficiency may be overlooked by conventional screening strategies, despite being associated with increased susceptibility to infection and recurrent exacerbations.⁶⁴ However, for most of these conditions, specific treatments targeting the underlying defect are currently lacking. Therefore, the clinical utility of routine screening for MBL and complement deficiencies remains uncertain and requires further investigation in the context of bronchiectasis.

Gastrointestinal diseases, bronchiectasis, and the “gut–lung axis”

The interaction between the respiratory and gastrointestinal systems begins early in development, as these structures share common embryological origin from the primitive foregut. The discovery of the gut–lung axis reinforces this association, highlighting shared immunological pathways, microbial interactions, and systemic inflammatory responses that link gastrointestinal and respiratory health.^67,68

Several gastrointestinal disorders have been associated with bronchiectasis or considered potential etiological factors, with IBD and gastroesophageal reflux disease (GERD) being the most frequently implicated.⁹

Inflammatory bowel disease and bronchiectasis

IBD, encompassing Crohn’s disease and ulcerative colitis, has been recognized as a potential etiology of bronchiectasis. It serves as an intriguing disease model within the vicious vortex, where inflammation acts as a common driver in both gastrointestinal and pulmonary manifestations. However, data on bronchiectasis in IBD remain limited and heterogeneous, necessitating further research to clarify its prevalence, mechanisms, and clinical implications.

Bronchiectasis is a recognized but uncommon pulmonary extra-intestinal manifestation of IBD, while IBD itself is an infrequent etiology of bronchiectasis, with a reported prevalence of <1% across international registries.^35–39 However, prevalence estimates vary widely across studies—some reporting low rates, while others describe bronchiectasis as the most common form of airway involvement in IBD, found in 9.5% of IBD patients undergoing HRCT.^69,70

Clinically, bronchiectasis in IBD may have distinctive features. Individuals with IBD and incident bronchiectasis have higher rates of all-cause mortality, emergency department visits, and hospitalizations compared to those without bronchiectasis, with IBD itself representing an independent predictor of mortality in this population.^71,72 In ulcerative colitis, new or worsening respiratory symptoms short after colectomy may indicate a shift in inflammatory activity from the bowel to the lungs.^69,73 A strong response to corticosteroids (oral or inhaled) is another hallmark, with improvements in symptoms, lung function, and radiological findings.^69,73,74 These observations support the emerging concept of a gut–lung interactome, in which dysregulation of the intestinal immune environment may influence pulmonary inflammation and vice versa. Disruption of gut inflammatory homeostasis—through IBD activity, surgery, or antibiotic exposure—may affect the lung ecosystem via immune or microbial cross-talk, potentially contributing to a change in disease activity or phenotype in bronchiectasis.^67,75,76

Current treatment strategies are largely based on studies conducted up to the early 2010s, in which corticosteroids were the most frequently used therapy and demonstrated efficacy for both gastrointestinal and respiratory manifestations. The effects of other medications—such as immunosuppressants (e.g., azathioprine, methotrexate) and newer biologic agents targeting TNF-α, IL-12/IL-23, and JAK pathways—on bronchiectasis-related outcomes remain largely unexplored and warrant further investigation.

GERD, hiatal hernia, and dysphagia

GERD and hiatal hernia (HH) have been investigated in the context of bronchiectasis, with studies suggesting they carry significant clinical implications. The prevalence of these conditions in bronchiectasis is noteworthy: McDonnell and colleagues reported HH in 35.8% of patients—substantially higher than the 10%–20% seen in the general population. Similarly, GERD affects 26%–75% of bronchiectasis patients, depending on the diagnostic criteria used.^77,78 A Korean nationwide study also reported a rising prevalence of GERD among bronchiectasis patients over a nine-year period, particularly in individuals over 50 years of age. From a healthcare perspective, GERD was associated with increased resource utilization and costs, including more outpatient visits, emergency room visits, and hospitalizations.⁷⁹

Notably, data from the EMBARC registry indicate that GERD is identified as the primary etiology of bronchiectasis in only 1.6% of cases in Europe.³⁵ This low reported prevalence likely reflects that respiratory physicians rarely see GERD as a direct etiology of bronchiectasis. However, earlier studies found much higher rates because they considered GERD and HH as comorbidities, not causes. This difference shows how their role in bronchiectasis is complex and classification varies across studies. It is important to note that the etiological significance of reflux and aspiration differs markedly between pediatric and adult bronchiectasis. In pediatric cohorts, these are consistently reported as major causes and are routinely screened for.⁸⁰

Upper gastrointestinal disorders are associated with more severe bronchiectasis. The presence of HH correlates with lower FEV1%, greater radiological involvement (including cystic bronchiectasis and a higher number of affected lobes), and elevated BSI and FACED scores. Similarly, patients with GERD tend to exhibit more severe disease manifestations, including greater symptom burden, higher exacerbation frequency, more frequent hospitalizations, chronic infections, more extensive radiological findings, impaired pulmonary function, and reduced quality of life.^77,78

Regarding pathophysiology, HH and GERD may contribute to bronchiectasis progression via pulmonary microaspiration of gastric contents—such as acid, bile, and pepsin—leading to airway inflammation and damage. Additionally, a recent study highlighted the high prevalence of asymptomatic dysphagia and silent aspiration in patients with idiopathic bronchiectasis, suggesting an alternative or complementary mechanism that links upper aerodigestive dysfunction with disease severity.⁸¹ These findings reinforce the concept that bronchiectasis pathogenesis may involve both reflux-mediated lung injury and direct aspiration of oral contents due to impaired swallowing.

Interestingly, azithromycin may provide therapeutic benefit in this context beyond its antimicrobial and immunomodulatory properties. Macrolides have been proposed to attenuate airway inflammation triggered by acid reflux. Moreover, their prokinetic effects may enhance gastric emptying, thereby reducing reflux and the associated risk of aspiration. This dual mechanism may partly explain their observed efficacy in certain bronchiectasis patients, particularly those with coexisting GERD.⁷⁸

Management strategies for GERD and HH in bronchiectasis include lifestyle modifications, pharmacologic therapies (e.g., antacids, proton pump inhibitors), and surgical interventions. However, the effectiveness of these approaches in improving bronchiectasis outcomes remains uncertain and requires further investigation.

Respiratory physicians should remain alert to gastrointestinal symptoms that may suggest underlying IBD or upper gastrointestinal disorders. Symptoms such as chronic diarrhea, abdominal pain, and rectal bleeding should raise suspicion for IBD. Alarm features—including dysphagia, unexplained weight loss, or persistent GERD symptoms (heartburn and/or regurgitation) despite adequate acid suppression—warrant further evaluation with endoscopy. In such cases, timely referral to a gastroenterology specialist is crucial to ensure early diagnosis and appropriate management.^82,83

To support clinical decision-making, Supplemental Table 2 outlines a pragmatic approach to gastrointestinal assessment in bronchiectasis, highlighting key symptoms, red flags, and indications for further investigation and referral. This framework is intended to facilitate early identification of underlying gastrointestinal disorders and promote integrated multidisciplinary care.

Autoimmune and connective tissue diseases

Systemic autoimmune diseases can affect every compartment of the respiratory system—including the airways, alveoli, blood vessels, and pleura—rendering the lungs particularly vulnerable to infections, inflammation, and structural damage.⁸⁴ Among pulmonary manifestations, bronchiectasis is increasingly recognized in association with autoimmune and connective tissue diseases (CTDs), where it may function either as an underlying cause or as a comorbidity. Patients with autoimmune inflammatory drivers, particularly rheumatoid arthritis (RA), experience significantly worse outcomes, roughly doubling mortality risk with seropositive RA carrying the highest hazard ratios.⁸⁵

RA is the most frequently reported autoimmune disease linked to bronchiectasis, with the highest prevalence observed in Europe (2.7% overall), particularly in the United Kingdom (3.8%), compared to lower rates in Asian countries such as China (1.1%) and Korea (1.0%). In the US registry, a broader category of “rheumatologic disease” reaches a prevalence of 8%. Under the umbrella of CTDs, many studies do not specify which conditions are included, but these generally encompass autoimmune, inflammatory, and genetic disorders, with higher prevalence rates in Northern and Western Europe.^35–39

RA appears to have the strongest epidemiological and clinical relevance. The prevalence of bronchiectasis is higher in patients with RA than in the general population. A systematic review and meta-analysis reported pooled prevalence rates of 2.7% for clinically diagnosed bronchiectasis and 25% for radiologically confirmed cases.⁸⁶ While the clinical significance of radiological bronchiectasis remains uncertain—since many patients with CT abnormalities do not present with persistent respiratory symptoms or recurrent infections—the prevalence of clinically diagnosed bronchiectasis in RA is nonetheless noteworthy. Genetic studies suggest a causal link, with RA independently increasing bronchiectasis risk.⁸⁷ RA patients with bronchiectasis typically show higher disease activity, greater autoantibody burden, and worse outcomes.⁸⁸

In terms of temporal relationship, bronchiectasis may precede or follow the onset of joint symptoms, often with a long latency period.⁸⁶ Shared mechanisms likely involve systemic inflammation damaging the bronchial walls or chronic airway infection triggering autoimmunity via persistent antigenic stimulation. In particular, bronchiectasis has been proposed as a source of chronic antigenic stimulation from pulmonary mucus and persistent bacterial infection, contributing to autoimmune activation.⁸⁶ Notably, elevated levels of anticitrullinated protein antibodies have been identified in patients with bronchiectasis.⁸⁹ Furthermore, in a subgroup of RA patients, an inverse correlation was observed between disease activity score and lung function suggesting that worsening RA may parallel respiratory decline.⁹⁰

In Sjögren’s syndrome, HRCT studies report bronchiectasis prevalence rates of up to 46%, while the prevalence of clinically significant disease was approximately 8% in the largest available study.^88,91 Affected patients were older and exhibited distinct autoantibody profiles, including a lower frequency of anti-Ro/SSA antibodies, a higher frequency of antismooth muscle antibodies, and, interestingly, lower total immunoglobulin levels.⁸⁸ Although the exact mechanisms linking Sjögren’s syndrome and bronchiectasis are not fully understood, one proposed pathway involves autoimmune inflammation of the exocrine glands within the respiratory tract. This leads to dryness of the nasal passages and airways, resulting in thick, tenacious secretions that cannot be effectively cleared from the small airways—ultimately contributing to mucus plugging and airway damage.⁸⁴ Another hypothesized mechanism involves autoimmune damage to the smooth muscle of the airways mediated by antismooth muscle antibodies, which could impair bronchomotor tone and mucociliary clearance, facilitating airway dilation and structural damage.⁹¹

Bronchiectasis is less commonly reported in systemic lupus erythematosus and systemic sclerosis, in which restrictive lung disease and pulmonary hypertension are more prominent pulmonary manifestations.⁸⁴

The treatment of bronchiectasis in patients with systemic autoimmune diseases generally follows standard management protocols, focusing on airway clearance and the treatment of exacerbations. However, the use of biologic disease-modifying anti-rheumatic drugs (DMARDs) in these patients should be approached with caution, as they may increase the risk of lower respiratory tract infections. Respiratory physicians should consider autoimmune diseases in the differential diagnosis of bronchiectasis, particularly in nonsmoking women, middle-aged adults, or patients with multisystem features such as joint pain, sicca symptoms, skin rashes, or Raynaud’s phenomenon. As recommended by the European Respiratory Society, autoimmune screening is part of the standard aetiological work-up for adults with bronchiectasis of unknown cause.^23,24

“Nonetiological” comorbidities

Cardiovascular diseases and diabetes

Cardiovascular diseases (CVD) are common and clinically impactful comorbidities in bronchiectasis. Large-scale population studies have shown a higher prevalence of coronary artery disease and stroke in bronchiectasis patients compared to the general population.⁹² Their presence is associated with worsened respiratory symptoms that further impair physical function and reduce quality of life.⁹² Additionally, CVD independently predicts exacerbations and contributes to a more rapid decline in pulmonary function.⁹³ A recent meta-analysis further confirmed that bronchiectasis is associated with a 42% increased risk of coronary heart disease and a 71% increased risk of stroke.⁹⁴

Beyond prevalence data, an emerging body of evidence highlights a temporal association between bronchiectasis exacerbations and cardiovascular events. In a study by Navaratnam and colleagues, lower respiratory tract infections were shown to significantly increase the risk of myocardial infarction and stroke within a three-month window following the infection.⁹⁵ This finding was echoed by Méndez et al. in a retrospective analysis of 250 bronchiectasis patients, where nearly 30% experienced a cardiovascular event during a median follow-up of 35 months, with most events occurring after an exacerbation.⁹⁶ In a Korean study, two retrospective cohorts of bronchiectasis patients with first-time atherosclerotic cardiovascular or cerebrovascular events were analyzed. More than 13.5% had experienced a severe exacerbation requiring emergency care or hospitalization in the year prior to the cardiovascular event. Those with prior exacerbations had significantly higher 90-day and 1-year cardiovascular and cerebrovascular mortality compared to those without exacerbations.⁹⁷

Moreover, chronic hyperglycemia promotes persistent systemic inflammation and increases susceptibility to respiratory infections, thereby accelerating lung function decline.⁹⁸ In a recent retrospective Chinese cohort study, bronchiectasis patients with diabetes exhibited poorer nutritional status, more severe respiratory symptoms, a higher risk of acute exacerbations, and greater disease severity as measured by the BSI score, compared to nondiabetic patients.⁹⁹

Taken together, these findings suggest a bidirectional relationship between bronchiectasis and metabolic or cardiovascular diseases. Systemic inflammation and infection-related physiological stress may trigger acute cardiovascular events, while cardiovascular comorbidities in turn exacerbate the burden of bronchiectasis. These insights underscore the importance of comprehensive cardiovascular and metabolic assessment in selected patients with bronchiectasis.

Periodontal disease

Periodontal disease is an emerging, yet overlooked, comorbidity in bronchiectasis that can negatively impact quality of life. In COPD, a systematic review found a potential association between poor periodontal health and increased exacerbation frequency, though with moderate to low certainty.¹⁰⁰ Symptoms such as gingival bleeding and oral pain impair masticatory function and overall well-being. The oral cavity is increasingly recognized as a potential reservoir for pathogens due to its anatomical continuity with the airways. Multiple mechanisms may explain how oral pathogens contribute to pulmonary infection, including aspiration of oropharyngeal secretions, spread from contiguous upper airway sites, or even hematogenous dissemination from distant foci.^101,102 Dental plaque, in particular, may serve as a persistent niche for pathogenic bacteria. Inhaled corticosteroids, widely used in airway diseases, may exacerbate this risk by altering local immunity and oral microbiota. Preliminary data suggest that patients with both bronchiectasis and periodontitis show heightened systemic inflammation compared to those without bronchiectasis.¹⁰³

Malnutrition and vitamin deficiency

Malnutrition is an important and often underestimated factor in bronchiectasis. It can impair airway epithelial barrier function, reduce cellular immunity and antibody production, and increase susceptibility to infections.^104,105 King et al. in their study demonstrated that, even in patients with a seemingly normal BMI, deficits in body composition, muscle strength, and nutritional status were more common in patients with bronchiectasis, especially the younger and the PCD subgroup.¹⁰⁶ Low-protein intake, sarcopenia, and vitamin D deficiency are particularly concerning, as they promote systemic inflammation and contribute to functional decline.^106,107

Zinc, a key micronutrient involved in immune modulation and epithelial repair, may also play a role in bronchiectasis. A cross-sectional study by Javad-Moosavi et al. compared serum zinc concentrations between 34 bronchiectasis patients and 29 healthy controls. The results showed significantly lower zinc levels in bronchiectasis patients compared to controls, particularly among women. Despite its limitations of sample size and design, it suggests a potential link between zinc deficiency and bronchiectasis.¹⁰⁸

Vitamin D is a key regulator of calcium and phosphate homeostasis, enhancing intestinal calcium absorption and supporting bone health. It also plays a role in immune function, as its receptors are expressed on a wide range of immune cells—including monocytes, T cells, B cells, and dendritic cells. The role of vitamin D in respiratory diseases has been extensively studied. Deficiency (defined as <30 ng/mL) is common in conditions such as COPD, asthma, and respiratory infections, and is often associated with increased disease severity. However, evidence from high-quality randomized controlled trials and meta-analyses regarding the benefits of vitamin D supplementation in chronic respiratory diseases remains inconsistent. While some studies suggest a protective effect against acute respiratory infections—particularly in individuals with severe deficiency (<10 ng/mL)—others have not demonstrated strong evidence to support routine supplementation.^109–111

Vitamin D deficiency is also associated with increased disease severity. Chalmers et al. observed that deficient patients had a higher prevalence of chronic bacterial colonization, lower FEV₁, more frequent exacerbations, and more rapid lung function decline. Ferri et al. demonstrated a significant inverse correlation between vitamin D levels and both the Bronchiectasis Severity Index (BSI) and radiological severity.^112–114

The study by Oriano et al. added a genetic perspective by examining vitamin D binding protein (DBP) isoforms. The GC1f isoform was associated with greater disease severity, chronic infections, and lower BACI scores, while the GC1s isoform was linked to higher vitamin D levels and a milder phenotype. These findings suggest that genetic variations in DBP may influence disease severity and susceptibility to chronic infections in bronchiectasis, potentially independent of serum vitamin D levels.¹¹⁴

Vitamin D supplementation is primarily recommended for bone health, particularly in older women and individuals with chronic conditions.¹¹⁵ In bronchiectasis, routine supplementation is not currently supported by strong evidence; however, assessing vitamin D status and fracture risk is often appropriate. In many cases, supplementation should be considered, balancing potential skeletal and respiratory health benefits while avoiding excessive dosing.

Osteoporosis

Osteoporosis is an epidemiologically significant yet underexplored comorbidity in patients with bronchiectasis. Reported prevalence varies widely among geographical regions, ranging from 3.9% to over 13%.^35–39 Furthermore, multiple studies indicate that osteoporosis is significantly more common in bronchiectasis than in the general population. A retrospective review by Diehl found that over 85% of bronchiectasis patients had low bone mineral density (BMD), with 27% having osteoporosis and 59% osteopenia.¹¹⁶ A Chinese cohort study reported a 21.2% prevalence of osteoporosis in hospitalized bronchiectasis patients.¹¹⁷ In Korea, 31.5% of male bronchiectasis patients were found to have osteoporosis—much higher than the 17.9% seen in healthy controls.¹¹⁸ In these studies, several risk factors have been identified as contributors to osteoporosis in bronchiectasis, including age ⩾65 years old, female sex, history of inhaled corticosteroid use, low BMI (<18.5 kg/m²), and smoking history. Beyond its high prevalence, osteoporosis in bronchiectasis has been linked to worse clinical outcomes. Bronchiectasis patients with osteoporosis exhibited higher disease severity and comorbidity burden (assessed by the BSI and BACI), and poorer quality of life. Moreover, all-cause mortality was significantly higher in patients with osteoporosis (29% vs 7.1% in those without).¹¹⁷

Interestingly, a study by Huang conducted in Taiwan, identified oxygen desaturation during the 6-minute walk test as a predictive factor for osteoporosis, with 82% of desaturators showing low BMD.¹¹⁹ Additionally, the abovementioned Spanish experience highlights the relationship between nutritional status and bone mineral density, reporting that low fat-free mass and vitamin D deficiency are strongly associated with osteoporosis in bronchiectasis patients.¹²⁰

The link between bronchiectasis and osteoporosis is multifactorial, driven by several interconnected mechanisms. Persistent respiratory infections and inflammation in bronchiectasis lead to elevated levels of pro-inflammatory cytokines, suppressing osteoblast function and promoting bone resorption. Furthermore, reduced physical inactivity due to respiratory symptoms and increased corticosteroid exposure accelerate BMD loss.

Anxiety/depression and cognitive impairment

Multiple studies consistently stress the increasing prevalence of anxiety and depression among individuals living with bronchiectasis. Data from the EMBARC and BE-China registries report a prevalence of approximately 14% for both conditions. However, studies specifically designed to assess psychological symptoms using validated tools often report much higher rates, though these findings vary widely depending on the assessment methods, cut-off values, and study populations.^121,122 This variability reflects the heterogeneous methodology across studies but consistently points to a significant psychological burden in many patients. Some studies suggest that anxiety and depression are associated with greater disease severity, worse symptoms, and increased exacerbation frequency, while others find no clear correlation.^121–123 Importantly, psychological comorbidities have also been linked to poorer adherence to treatment, higher healthcare utilization, and increased costs.^123,124 Factors including female gender, longer disease duration, frequent exacerbations, and adverse social circumstances, have been associated with higher levels of psychological distress in bronchiectasis.^122,125

Interestingly, recent preliminary evidence suggests that cognitive function may have an impact in bronchiectasis. In a small Turkish study, patients with reduced cognitive performance reported greater dyspnea and more severe depressive symptoms compared to those with preserved cognition.¹²⁶

Taken together, this evidence suggests that anxiety, depression, and cognitive impairment worsen symptom perception and self-management, contributing to the vicious vortex in bronchiectasis.

Points for clinical practice

The heterogeneity of bronchiectasis, coupled with the growing recognition that comorbidities are major contributors to symptoms, exacerbation risk, and disease outcomes, calls for a more systematic and holistic approach to clinical management. Respiratory physicians should move beyond a strictly lung-centered model and incorporate comprehensive comorbidity assessment into routine care. This involves evaluating not only airway diseases, such as asthma, COPD, and CRS, but also systemic conditions including IBD, GERD, autoimmune diseases, immunodeficiencies, and modifiable risk factors such as malnutrition, osteoporosis, vitamin D deficiency, and psychological distress. Many of these conditions may remain clinically silent, and underdiagnosis is common (Table 2).

Table 2.

Clinical practice points and research priorities for comorbidities in bronchiectasis.

Area	Clinical practice points	Research priorities
Asthma	- Frequent (up to 30%) - Associated with more symptoms, increased exacerbation rates, - Considered both etiological and modifying factor - Always exclude ABPA	- Impact and safety of biologic therapies on outcomes in coexisting asthma - Impact safety of inhaled therapies in coexisting asthma
COPD	- High prevalence (from 25% to 40%) - Associated with worse lung function and increased mortality - Recommend smoking cessation - Enhances bacterial colonization and exacerbation burden	- Effects of dual or triple inhaled therapy on bronchiectasis outcomes - Longitudinal impact of coexisting COPD on clinical and microbiological profiles
Chronic rhinosinusitis	- Affects up to 62% of patients - Worsens symptoms and quality of life - Increases healthcare burden	- Role of upper airway management strategies (biologics, surgery) in bronchiectasis control
Immunodeficiencies	- CVID most common primary immunodeficiency - Up to 58% of CVID patients develop lung damage - Consider broader immunologic testing (IgG subclass, vaccine response, lymphocyte subpopulation)	- Approved and validated definition of treatable immunodeficiencies in bronchiectasis - Define clear indications for immunoglobulin therapy in bronchiectasis
IBD	- Uncommon etiology but may trigger airway inflammation - Bronchiectasis may worsen postcolectomy in ulcerative colitis - Corticosteroids often effective	- Understand pathophysiological links between gut–lung axis and bronchiectasis - Role of biologic therapies on bronchial disease progression
GERD hiatal hernia	- Common (up to 75%) and under-recognized - Associated with worse symptoms and radiological severity - Potential microaspiration mechanism	- Efficacy of antireflux strategies (PPIs, antacids, surgery) on bronchiectasis outcomes - Efficacy of azithromycin in GERD-associated bronchiectasis
Autoimmune diseases	- RA most frequent, especially in Europe - Autoimmune screening is recommended in idiopathic cases - May precede or follow joint symptoms	- Discover pathophysiological link between bronchiectasis and autoimmunity to develop target therapies - Impact of DMARDs on bronchiectasis
Cardiovascular Disease	- Increases dyspnea, exacerbation risk, and mortality - Exacerbations may trigger CV events - Common in elderly with comorbid burden	- Develop targeted and feasible strategies for CV risk assessment and reduction in bronchiectasis - Role of inflammation control on cardiac outcomes
Malnutrition Vitamin D deficiency	- Affects muscle strength, immunity, and outcomes - Vitamin D deficiency highly prevalent and associated with disease severity	- Evaluate benefits of nutritional interventions
Osteoporosis	- High prevalence, especially in older patients - Linked to increased mortality and disease severity - Assess bone health in at-risk patients	- Impact of vitamin D and physical activity - Value of fracture prevention in overall bronchiectasis care
Anxiety depression cognitive impairment	- Prevalence underestimated - Affects quality of life, adherence, and healthcare use	- Develop simple and feasible screening strategies for psychological burden - Mental health interventions and bronchiectasis control
Periodontal disease	- Linked to increased systemic inflammation - Pay attention to oral symptoms	- Role of oral health in bronchiectasis outcomes - Benefit of dental care interventions

A major barrier remains the heterogeneity in tools and strategies used across settings to detect comorbidities. Diagnostic approaches range from symptom questionnaires to lab tests and imaging studies, and many of these are unfamiliar to pulmonologists. There is a pressing need for standardized, pragmatic screening pathways—especially in domains such as nutrition, mental health, or gastrointestinal disease, where respiratory clinicians may have limited confidence. Structured protocols and multidisciplinary collaboration can help close this gap.

Tools like the BACI score can aid in risk stratification and guide targeted interventions. In line with the treatable traits framework, comorbidities should be addressed not only for their systemic consequences but also for their potential to alter the course of bronchiectasis. Coordinated, multidisciplinary care involving pulmonologists, immunologists, gastroenterologists, nutritionists, and mental health specialists can enhance disease control, improve quality of life, and reduce healthcare utilization.

Future directions

Despite the progress made in recognizing the role of comorbidities, many knowledge gaps remain. Long- term prospective studies are needed to clarify to what extent comorbidities play a causal role in bronchiectasis progression or merely coexist as epiphenomena. Evidence is also lacking on how to prioritize and implement screening in real-world settings. For instance, it remains unclear which patients benefit most from extended immunologic workup, when to assess bone health, or how to detect hidden nutritional deficiencies and psychological distress efficiently and systematically. Furthermore, interventional studies are needed to evaluate whether actively treating comorbidities can modify bronchiectasis outcomes. The potential impact of biologic therapies for coexisting asthma or IBD, macrolides in patients with GERD, or nutritional and vitamin D interventions in frail patients remains an open and clinically relevant question.

Beyond an etiological approach, a more integrative perspective is needed, one in which all comorbidities are recognized as disease modifiers that are capable of shaping disease activity, severity and control. Given the current paucity of disease-specific therapies for bronchiectasis, a pragmatic strategy is needed. Since associated conditions frequently define clinical trajectory and therapeutic needs of patients, they represent a concrete and actionable target for intervention.¹⁸

In light of the paucity of disease-specific therapies for bronchiectasis, comorbidities represent a concrete and actionable target for clinical intervention in this context, we propose a conceptual framework—a “Copernican Revolution” in bronchiectasis care—in which comorbidities are placed at the center of the disease model, much like the Sun in a heliocentric system (Figure 2). This paradigm shift emphasizes how comorbidities can drive the dynamic interactions of the vicious vortex components—representing the complex, orbiting factors that influence disease progression. The lung, depicted as Earth, revolves around and is continually shaped by these interconnected forces throughout the disease’s natural history, highlighting the intricate and evolving nature of bronchiectasis.

Figure 2.

Conceptual model illustrating the influence of comorbidities in bronchiectasis. This schematic proposes a speculative paradigm in which comorbidities occupy a central position in the bronchiectasis ecosystem, potentially exerting “gravitational” influence on disease pathophysiology and progression. Inspired by a solar system analogy, the lung is represented as Earth, orbiting around comorbidities and passing through dynamic “orbits” corresponding to key pathophysiological processes: infection, inflammation, impaired mucociliary clearance, and structural damage. These orbits are interactive and variable over time; their alignment may represent periods of clinical instability, such as exacerbations. The model aims to encourage integrative thinking and support a holistic, multidisciplinary approach to care.

Embracing this paradigm may facilitate the development of a more tailored, multidimensional model of care—one that integrates etiological, clinical, and systemic factors to guide more effective and individualized treatment strategies.

Conclusion

Comorbidities are frequent and impactful contributors to the clinical course of bronchiectasis. Their systematic identification and targeted management represent a pragmatic and patient-centered strategy to improve quality of life, reduce exacerbations, and optimize outcomes. Integrating comorbidities into diagnostic and therapeutic frameworks, through structured screening and new perspectives may help reshape the current care model and guide future research directions.

Supplemental Material

sj-docx-1-tar-10.1177_17534666251390086 – Supplemental material for Screening and impact of comorbidities in bronchiectasis: a forward-looking perspective

Supplemental material, sj-docx-1-tar-10.1177_17534666251390086 for Screening and impact of comorbidities in bronchiectasis: a forward-looking perspective by Alessandro De Angelis, Vincenzo Alberto Artuso, Stefano Aliberti and Pieter Goeminne in Therapeutic Advances in Respiratory Disease

Footnotes

Acknowledgements

None.

Declarations

ORCID iD

Alessandro De Angelis

Supplemental material

Supplemental material for this article is available online.

Artificial intelligence policy

The authors did not use any Generative Artificial Intelligence (AI) in creating the text, references, figures, or other content of this manuscript. All authors are fully responsible for ensuring the accuracy, originality, and integrity of the submitted material.

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The authors declare that all images included in this manuscript were prepared by the authors and have not been previously published elsewhere.

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