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Background:
Systematic Review

The Association Between Asthma and Endometriosis: A Systematic Review and Metanalysis

by
Maria E. Ramos-Nino
1,*,
Abraham Agaya Obadiah
1,
Ifesinachi Ogochukwu Ozugha
1 and
Prakash V. A. K. Ramdass
2
1
Department of Microbiology, Immunology, and Pharmacology, St. George’s University School of Medicine, St. George P.O. Box 7, Grenada
2
Department of Public Health and Preventive Medicine, St. George’s University School of Medicine, St. George P.O. Box 7, Grenada
*
Author to whom correspondence should be addressed.
J. Respir. 2025, 5(2), 6; https://doi.org/10.3390/jor5020006
Submission received: 30 December 2024 / Revised: 8 February 2025 / Accepted: 31 March 2025 / Published: 7 April 2025
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Abstract

:
Observational studies suggest a comorbid link between asthma and endometriosis, but the evidence remains limited and inconsistent. This study presents a meta-analysis examining this association. A comprehensive search of literature databases was conducted through August 2024. Prevalence rates and odds ratios (ORs) were calculated to assess the relationship between asthma and endometriosis. For the prevalence analysis, sixteen studies, including 54,856 endometriosis cases and 300,613 controls, were included. The analysis yielded a prevalence of asthma in endometriosis patients of 14.9% (95% CI [10.3, 19.6], p < 0.001), with high heterogeneity (I2 = 99.9%). In the control group, asthma prevalence was 9.1% (95% CI [6.5, 11.6], p < 0.001, I2 = 99.9%). For the odds ratio (OR) analysis, twelve studies, including 295,845 endometriosis cases and 28,030,081 controls, were included. The meta-analysis demonstrated a significant association between asthma and endometriosis with an OR of 1.59 (95% CI [1.22, 2.07], p = 0.0007, I2 = 100%). Subgroup analyses stratified by study region and study type were also conducted. This meta-analysis suggests a significant association between asthma and endometriosis, indicating that common factors underlying these chronic inflammatory diseases may contribute to this comorbidity. The findings support the biological plausibility of this association.

1. Introduction

Asthma is a chronic inflammatory disease of the airways, characterized by airway hyper-responsiveness and variable airflow obstruction [1]. Globally, the number of prevalent cases of asthma rose from 226.9 million in 1990 to 262.4 million in 2019, highlighting its increasing public health burden [2]. In the United States, nearly 25 million people (7.7% of the population) had asthma in 2021 [3]. Asthma’s development is influenced by interactions between genetic and environmental factors, particularly during early life. The interplay between innate and adaptive immune responses is significant, particularly the Th1/Th2 cytokine balance [4].
(1)
Host Factors:
  • Genetics: A complex inheritance pattern influences asthma expression, IgE production, and response to therapies [5].
  • Sex: Epidemiological studies have also shown gender differences in asthma risk [6,7,8,9]. While asthma prevalence is higher in male children compared to females, this trend reverses around the ages of 15 to 19, after which asthma becomes more common among women [2]. Additionally, after puberty, women are observed to have a higher incidence and greater severity of asthma compared to men [10,11,12]. Furthermore, premenopausal women often experience a decline in pulmonary function along with increased asthma exacerbations and hospitalizations during the premenstrual and menstrual phases. Studies suggest that the use of oral contraceptives and hormone replacement therapy can improve pulmonary function and reduce the frequency of asthma exacerbations, providing potential therapeutic benefits during these phases [13].
(2)
Environmental Factors [4]
  • Allergens: Exposure to specific allergens (e.g., house dust mites) contributes significantly to asthma’s onset and persistence.
  • Respiratory Infections: Viral infections in early life, such as RSV, are associated with asthma development, although certain infections may also offer protective effects.
(3)
Other Factors [4,14]: Environmental tobacco smoke, air pollution, diet, and obesity also play roles in asthma development, but their exact contributions are still under investigation.
Endometriosis, an estrogen-dependent chronic inflammatory disorder, affects about 196 million women worldwide, particularly those of reproductive age [15]. Epidemiological studies estimate the prevalence of endometriosis to be between 2% and 15% among women of reproductive age [16,17,18], with variation across different populations [19]. For instance, prevalence is significantly higher, around 20–30%, in women experiencing infertility [20]. Since endometriosis is typically diagnosed through laparoscopy, an invasive procedure, the prevalence of asymptomatic cases remains unknown but is estimated to be 2–20% [21]. Endometriosis is characterized by the ectopic growth of endometrial-like tissue outside the uterus [18]. Symptoms are diverse and may include nausea, vomiting, heavy menstrual bleeding, dyschezia, dysuria, inflammation, dysmenorrhea, non-menstrual pelvic pain, and infertility [19,22,23]. The exact cause of endometriosis remains unclear, but several theories have been proposed to explain its development, as follows: (1) retrograde menstruation leading to the adhesion of endometrial cells on peritoneal surfaces, triggering inflammation [24,25]; (2) immunological disturbances such as impaired apoptosis, which allow ectopic endometrial implants [26,27,28]; (3) immune system abnormalities, including altered T and B lymphocyte function [29], high T and B lymphocyte count [30], elevated serum autoantibodies [31], and the reduced activity of natural killer (NK) cells [31,32]; (4) genetic factors [33]; and (5) the hormone 17β-Estradiol (E2), which plays a crucial role in the growth and persistence of endometriotic lesions and the associated inflammation and pain [34]. Notably, women with endometriosis tend to have higher levels of estrogen or a greater lifetime exposure to estrogen [35] and (6) environmental factors. Endocrine disruptors like dioxins and polychlorinated biphenyls seem to have the most significant impact among the proposed risk factors. Emerging evidence also suggests potential links between endometriosis and factors such as night shift work, sun exposure, and red meat consumption. However, for other lifestyle-related risk factors, including tobacco use, alcohol, coffee, soy, and physical activity, the data are insufficient to draw firm conclusions. Overall, the epidemiological evidence does not establish a strong scientific connection between environmental factors and endometriosis [36].
A growing body of observational studies has examined the comorbid association between asthma and endometriosis, but the evidence has been inconsistent. Some studies report a higher prevalence of asthma among women with endometriosis [37,38], while others have found no significant association [39]. Figure 1 illustrates several potential common underlying mechanisms that may link endometriosis and asthma, supporting a possible association between the two conditions. These mechanisms include genetic factors (shared loci), inflammatory processes (common cytokines involved), immunological abnormalities (imbalances in immune cell numbers and function), and hormonal influences (particularly estrogen). In this context, we present a metanalysis assessing the potential association between asthma and endometriosis. Clinicians should recognize the link between asthma and endometriosis to enhance patient care. Both involve immune dysregulation, inflammation, and hormonal influences, suggesting shared mechanisms that could guide treatment. Identifying this connection may enable earlier diagnosis, personalized therapies, and holistic management to improve outcomes and reduce healthcare burdens. Moreover, recognizing this association can drive research and refine clinical guidelines for standardized, multidisciplinary care.

2. Materials and Methods

This systematic review and meta-analysis were completed according to the PRISMA guidelines [41], and the protocol was pre-registered and published in PROSPERO (596126).

2.1. Data Sources and Search Strategy

A comprehensive search on Medline, Google Scholar, and Embase was conducted using the keywords “asthma” AND “endometriosis”. Search dates were from inception to 31 August 2024. The search was not limited by language.

2.2. Study Selection and Eligibility

Citation files from each database were imported into Zotero 6.0.36, where duplicates were removed. Two reviewers (M.E.R. and P.R.) independently screened the titles and abstracts for eligibility. Full texts of articles that met the inclusion criteria were then reviewed for final inclusion. Any disagreements regarding study eligibility were resolved through discussion with a third author. The selection criteria for the meta-analysis included (1) all study designs, (2) data sufficient to calculate odds ratios for the association between endometriosis and asthma, and (3) confirmed diagnosis of endometriosis. Exclusion criteria were (1) studies based on cell or animal models; (2) reviews, comments, abstracts, or case reports; and (3) studies without matched control groups.

2.3. Data Extraction

Two independent reviewers (M.E.R. and P.R.) extracted key information from the eligible studies, including the first author, study design, location, and the diagnostic criteria for both endometriosis and asthma.
Studies with data presented in distinctive subgroups (study location) were included separately in the analysis. Any disagreement was resolved by discussion between the two reviewers.

2.4. Quality Assessment

The quality of the included studies was assessed using the Newcastle–Ottawa Scale by two independent reviewers (M.E.R. and P.R.). The scale evaluated selection, comparability, and outcome, with scores ranging from 0 to 9. Studies were classified as high quality (≥7 points), medium quality (4–6 points), or low quality (<4 points) (Supplementary Materials).

2.5. Statistical Analysis

Data analysis was conducted using OpenMeta [Analyst] software for prevalence and Review Manager 5.4.1 (The Cochrane Collaboration, 2014; The Nordic Cochrane Centre, Copenhagen, Denmark) for odds ratios. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the risk of asthma in patients with endometriosis. Heterogeneity among the studies was evaluated using the Cochrane Q test and the I2 index. A value of I2 > 50% indicated significant heterogeneity, and a random effects model was applied. Statistical significance was set at p < 0.05. A sensitivity analysis was performed by sequentially omitting each study to assess its impact on the overall effect. Publication bias was examined using funnel plots generated in Revman 5.4.1 and Egger’s test in MedCalc® Statistical Software version 22.023.

3. Results

3.1. Study Characteristics

As depicted in Figure 2, 92 titles and abstracts were screened for relevance, and 32 were selected for full-text review. After further evaluation, 16 studies met the inclusion criteria for the systematic review, of which 12 were included in the odd ratios (OR) calculations and 16 in the prevalence calculations.
The characteristics of the 12 studies [35,39,42,43,44,45,46,47,48,49,50,51], with 295,845 endometriosis patients and 28,030,081 controls included in the meta-analysis (Table 1), and with 4 more studies added to the prevalence analysis [19,37,38,52].

Quality Assessment and Publication Bias

Table 1 presents the risk of bias for individual studies, as assessed using the Newcastle–Ottawa Scale. Eight studies were of high quality (≥7 points), three were of moderate quality (4–6 points), and one was of poor quality (<4 points).

3.2. Asthma in Endometriosis Patients

Figure 3 presents the forest plot of the pooled prevalence of asthma in endometriosis patients as 14.9% (95% CI [10.3,19.6], I2 = 99.9%, p < 0.001). The prevalence of individual studies ranged from 1.3% [42] to 29.7% [52]. Figure 4 presents the forest plot of the pooled prevalence of asthma in endometriosis-free patients as 9.1% (95% CI [6.5,11.6], I2 = 99.9%, p < 0.001). The prevalence of individual studies ranged from 1.3% [42] to 24.7% [51].
Figure 5 presents the forest plot of the pooled odds ratio of asthma in endometriosis patients. The pooled odds ratio was 1.59 (95% CI [1.22,2.07], I2 = 100%, p = 0.0007). The odds ratio of individual studies ranged from 0.41 [39] to 3.40 [49].
Visual inspection of the funnel plots is shown in Figure 6. No publication bias for the studies was observed.
Subgroup analysis based on:
(a)
The region of the study (Figure 7):
  • America (OR: 2.24 [1.59, 3.16], I2 = 100%, p < 0.00001);
  • Europe (OR: 1.27 [0.88, 1.84], I2 = 6%, p = 0.34);
  • Asia (OR: 1.46 [1.10, 1.95], I2 = 90%, p = 0.009).
(b)
Study design (Figure 8):
  • Cross-sectional studies (OR: 1.39 [0.96, 2.02], I2 = 90%, p = 0.09);
  • Cohort studies (OR: 2.12 [1.24, 3.64], I2 = 98%, p = 0.006);
  • Case–control studies (OR: 1.22 [1.15, 1.30], I2 = 0%, p < 0.00001).
These findings suggest that some of the heterogeneity observed among the studies can be attributed to differences in region and study design.
A subgroup analysis based on asthma diagnostic criteria revealed no significant differences between studies that relied on self-reported asthma diagnoses and those that used medical records.

4. Discussion

This systematic review and meta-analysis, where endometriosis was evaluated as an exposure and as an outcome, provides compelling evidence that patients with endometriosis have an increased risk of developing asthma or vice versa. The prevalence of asthma in patients with endometriosis was 14.9%, compared to 9.1% in those without endometriosis. This 9.1% prevalence aligns with the generally reported asthma prevalence of 8–10% [53,54] and is similar to the 7.7% estimate provided by the CDC in 2018 [3]. Studies by Ferrero et al. [39] and Caserta et al. [42], both from the European region (Italy), and the online study by Nowakowska et al. [51] did not demonstrate this association. These studies were hospital-based/online and may not represent the total population, but genetics and environmental influence factors may also be involved and require population-based studies in this region.
The pathophysiology underlying the association between asthma and endometriosis remains unclear. Several potential mechanisms have been suggested, as both conditions share common biological factors:
(1)
Genetics: A genome-wide association (GWA) study conducted by Adewuyi et al. on individuals of European descent has identified a significant genetic overlap between endometriosis and asthma. Utilizing SNP-level assessments through SECA and LDSC methods, the study suggests shared genetic predispositions among patients. This finding is further supported by independent gene-based analyses, which highlight genetic connections at the gene level between the two disorders. These results align with some earlier studies indicating co-occurrence, despite conflicting evidence from previous observational research. A meta-analysis of GWAS data from the IEC endometriosis and UK Biobank asthma studies identified 14 genomic loci that reached genome-wide significance for both conditions, with five being potentially novel. Notably, three loci—MLLT10, SMAD3, and MFHAS1—were replicated in an independent asthma GWAS and confirmed through additional analyses. The MFHAS1 gene is expressed in several tissues, including the lungs and endometrium, and is associated with systemic lupus erythematosus [55], while MLLT10, a transcription factor, is expressed in various tissues, including reproductive organs and the lungs [56,57]. These genes are among the most plausible candidates for the association between endometriosis and asthma. However, Mendelian Randomization (MR) analyses did not provide evidence of a causal relationship between the two disorders, suggesting that the observed association may not be causal [15].
(2)
Inflammation: Inflammation plays a critical role in both asthma and endometriosis. Key cytokines, such as transforming growth factor-beta (TGF-beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), interleukin-6 (IL-6), and vascular endothelial growth factor (VEGF), contribute to airway remodeling in asthma [58,59,60,61,62] as well as the proliferation of endometriotic cells [63,64,65,66]. Additionally, elevated TGF-beta activity in the peritoneal fluid of women with endometriosis correlates with disease severity, while TGF-beta produced by Th2 cells is increased in the airways of asthma patients [67]. Chronic inflammation, a hallmark of asthma, is believed to exert systemic effects that may extend beyond the respiratory system, potentially impacting reproductive organs [68,69,70,71].
(3)
Hormones (Estrogen): A study by Peng et al. [35] found that estrogen use was higher among asthmatic patients and was associated with a lower risk of endometriosis. This suggests that estrogen may play a dual role in influencing both conditions. Supportive of these findings GWAS studies identified informative biological pathways, including the sex hormone-related pathology shared by these disorders [15]. Furthermore, previous observational studies support the role of sex hormones in the development of both endometriosis and asthma [72,73]. High estrogen levels and frequent exposure to the hormone increase the risks for both disorders [50,74,75,76,77]. Early menarche and frequent menstrual cycles, driven by estrogen, are established risk factors for endometriosis [75], while female sex hormones are believed to influence pulmonary inflammation and smooth muscle function, which can lead to asthma [13,78].
(4)
Immunological Factors: The immune system’s failure to eliminate ectopic endometrial cells is a key factor in endometriosis. Endometriotic cells may resist immune surveillance, or there may be deficits in the immune response [18,79]. Immune cells, particularly neutrophils and peritoneal macrophages, are involved in inducing inflammation in endometriosis [26,80,81], while NK cells and macrophages exhibit reduced ability to clear endometrial cells from the peritoneal cavity [26]. Both IL-6 and TGF-b are known to suppress NK cell activity [82,83].
In addition, T cells play a crucial role in endometriosis development. The imbalance between T helper (Th) cell subsets leads to abnormal cytokine secretion and inflammation [84]. Elevated concentrations of cytokines are typical of Th2 lymphocytes, but the predominance of Th1 lymphocytes, along with an increased proportion of T regulatory (Treg) cells, has been observed in the peritoneal fluid of endometriosis patients, with a higher CD4/CD8 ratio and increased Th17 correlating with disease severity [80,85]. Endometriosis is also frequently associated with autoimmunity, further implicating the humoral immune response in its pathogenesis [80,86,87]. Similarly, asthma is influenced by various T-cell subsets. Th2 cells promote eosinophil recruitment, while Th1 cells and Th17 contribute to more severe, steroid-resistant asthma characterized by neutrophil infiltration [88]. The reduced or altered function of T regulatory cell populations provides a possible explanation for the inappropriate immune response to allergens observed in patients with asthma [88]. The involvement of the immune system in endometriosis and asthma, along with their heterogeneity, suggests common elements in the observed association. However, the absence of detailed data on the specific phenotypes of asthma and endometriosis limits the interpretation of these findings.
There are notable limitations in this meta-analysis. Firstly, the studies included exhibit high heterogeneity. Sensitivity analysis, which excluded one study at a time, identified that large studies by Imbroane et al. [49] and Alqaisi et al. [44] in the American region, significantly contributed to the observed heterogeneity (the exclusion of both studies reduced the I2 to 85% with OR = 1.38 (1.10, 1.78) p = 0.005). However, this alone does not explain the variation. Additionally, many studies lacked detailed reporting on the specific phenotype of asthma and endometriosis, and some relied on self-reported asthma diagnoses, which may have introduced bias or errors.

5. Conclusions

This review provides compelling evidence of an association between asthma and endometriosis. However, the strength of this association is influenced by factors such as study region, study type, and potentially other characteristics not accounted for in this meta-analysis. By pooling estimates of the prevalence and risk of asthma in women with endometriosis, this meta-analysis offers a more comprehensive understanding of the connection between these two chronic inflammatory conditions. The common ground between asthma and endometriosis lies in their shared genetic predispositions, inflammatory pathways, hormonal influences, and immune system dysregulation. This overlap suggests that these two chronic inflammatory diseases may have interrelated pathophysiological mechanisms, warranting further research into their association and potential common therapeutic strategies. Prospective or longitudinal cohort studies are essential for establishing cause-and-effect relationships and for accurately classifying endometriosis and asthma subtypes. Investigating the correlation between endometriosis severity or location and asthma severity could provide more clinically actionable insights. Furthermore, standardizing diagnostic criteria across future studies is crucial to minimizing methodological heterogeneity and improving comparability.
Early screening for endometriosis in women with asthma could reduce diagnostic delays, while personalized treatment strategies may improve symptom management. Hormonal fluctuations in endometriosis could also impact asthma control, requiring tailored therapeutic adjustments.

Supplementary Materials

The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/jor5020006/s1, Table S1: Newcastle–Ottawa Scale Quality Assessment.

Author Contributions

M.E.R.-N., conceptualization, methodology, investigation, formal analysis, writing, project administrator. A.A.O. and I.O.O., review P.V.A.K.R., data curation, review, and editing. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

All data are provided in the review.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. Endometriosis and asthma—one a gynecological disorder [40] and the other a respiratory condition (https://ginasthma.org accessed on 1 October 2024)—share several underlying biological mechanisms that suggest common ground in their pathophysiology.
Figure 1. Endometriosis and asthma—one a gynecological disorder [40] and the other a respiratory condition (https://ginasthma.org accessed on 1 October 2024)—share several underlying biological mechanisms that suggest common ground in their pathophysiology.
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Figure 2. Flow diagram of the included studies.
Figure 2. Flow diagram of the included studies.
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Figure 3. The pooled prevalence of asthma in patients with endometriosis. Square boxes represent the estimates from individual studies, horizontal lines indicate their 95% confidence intervals (CIs), and the diamond-shaped figure represents the 95% CI for the overall pooled estimates. Sinaii N (2002) [37], Ferrero S (2005) [39], Metalliotakis H (2012) [50], Smorgick N (2013) [38], Caserta D (2016) [42], Peng Yi-Hao (2017) [35], Al-Jefout M (2017) [43], Matalliotakis M (2017) [52], Alqaisi S (2018) [44], Shafir A.L. (2021) [45], Yoshii E (2021) [46], Joud A (2022) [47], Nowakoska A (2022) [51], Pan (2024) [48], Imbroane M.R. (2024) [49], Cialuj T.A. (2024) [19].
Figure 3. The pooled prevalence of asthma in patients with endometriosis. Square boxes represent the estimates from individual studies, horizontal lines indicate their 95% confidence intervals (CIs), and the diamond-shaped figure represents the 95% CI for the overall pooled estimates. Sinaii N (2002) [37], Ferrero S (2005) [39], Metalliotakis H (2012) [50], Smorgick N (2013) [38], Caserta D (2016) [42], Peng Yi-Hao (2017) [35], Al-Jefout M (2017) [43], Matalliotakis M (2017) [52], Alqaisi S (2018) [44], Shafir A.L. (2021) [45], Yoshii E (2021) [46], Joud A (2022) [47], Nowakoska A (2022) [51], Pan (2024) [48], Imbroane M.R. (2024) [49], Cialuj T.A. (2024) [19].
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Figure 4. The pooled prevalence of asthma in patients without endometriosis. The square boxes represent individual study estimates, the horizontal lines indicate the 95% confidence intervals (CIs), and the diamond-shaped figure represents the 95% CI for the overall pooled estimates. Ferrero S (2005) [39], Matalliotakis H (2012) [50], Caserta D (2016) [42], Peng Y-H (2017) [35], Al-Jefout M (2017) [43], Alqaisi S (2018) [44], Shafir A.L. (2021) [45], Yoshii E (2021) [46], Joud A (2022) [47], Nowakowska A (2022) [51], Pan G (2024) [48], Imbroane M.R. (2024) [49].
Figure 4. The pooled prevalence of asthma in patients without endometriosis. The square boxes represent individual study estimates, the horizontal lines indicate the 95% confidence intervals (CIs), and the diamond-shaped figure represents the 95% CI for the overall pooled estimates. Ferrero S (2005) [39], Matalliotakis H (2012) [50], Caserta D (2016) [42], Peng Y-H (2017) [35], Al-Jefout M (2017) [43], Alqaisi S (2018) [44], Shafir A.L. (2021) [45], Yoshii E (2021) [46], Joud A (2022) [47], Nowakowska A (2022) [51], Pan G (2024) [48], Imbroane M.R. (2024) [49].
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Figure 5. Pooled odds ratios of asthma in endometriosis patients. Square boxes represent individual studies, horizontal lines represent 95% confidence intervals (CIs), and diamond-shaped figures 95% CIs of pooled estimates. Ferrero S (2005) [39], Matalliotakis H (2012) [50], Caserta D (2016) [42], Al-Jefout M (2017) [43], Peng Y-H (2017) [35], Alqaisi S (2018) [44], Yoshii E (2021) [46], Shafir A.L. (2021) [45], Nowakowska A (2022) [51], Joud A (2022) [47], Imbroane M.R. (2024) [49], Pan G (2024) [48].
Figure 5. Pooled odds ratios of asthma in endometriosis patients. Square boxes represent individual studies, horizontal lines represent 95% confidence intervals (CIs), and diamond-shaped figures 95% CIs of pooled estimates. Ferrero S (2005) [39], Matalliotakis H (2012) [50], Caserta D (2016) [42], Al-Jefout M (2017) [43], Peng Y-H (2017) [35], Alqaisi S (2018) [44], Yoshii E (2021) [46], Shafir A.L. (2021) [45], Nowakowska A (2022) [51], Joud A (2022) [47], Imbroane M.R. (2024) [49], Pan G (2024) [48].
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Figure 6. Funnel plot for publication bias on selected studies. The circles indicate each study and the dotted line the overall effect.
Figure 6. Funnel plot for publication bias on selected studies. The circles indicate each study and the dotted line the overall effect.
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Figure 7. Pooled odds ratios of asthma in endometriosis patients, categorized by region. Square boxes represent estimates from individual studies, horizontal lines indicate their 95% confidence intervals (CIs), and the diamond-shaped figure represents the 95% CI for the overall pooled estimate. Matalliotakis H (2012) [50], Alqaisi S (2018) [44], Shafir AL (2021) [45], Imbroane MR (2024) [49], Pan G (2024) [48], Ferrero S (2005) [39], Caserta D (2016) [42], Joud A (2022) [47], Peng Y-H (2017) [35], Al-Jefout M (2017) [43], and Yoshii E (2021) [46].
Figure 7. Pooled odds ratios of asthma in endometriosis patients, categorized by region. Square boxes represent estimates from individual studies, horizontal lines indicate their 95% confidence intervals (CIs), and the diamond-shaped figure represents the 95% CI for the overall pooled estimate. Matalliotakis H (2012) [50], Alqaisi S (2018) [44], Shafir AL (2021) [45], Imbroane MR (2024) [49], Pan G (2024) [48], Ferrero S (2005) [39], Caserta D (2016) [42], Joud A (2022) [47], Peng Y-H (2017) [35], Al-Jefout M (2017) [43], and Yoshii E (2021) [46].
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Figure 8. Pooled odds ratios of asthma in endometriosis patients by study type. Square boxes represent individual studies; horizontal lines represent 95% confidence intervals (CIs); and diamond-shaped figures 95% CIs of pooled estimates. Ferrero, S. [39], AL-Jefout, M. [43], Alqaisi, S. [44], Shafir, A.L. [45], Nowakowska, A. [51], Pan, G. [48], Matalliotakis, H. [50], Peng, Yin-Hao [35], Joud, A. [47], Imbroane, M.R. [49], Caserta, D. [42], Yoshii, E. [46].
Figure 8. Pooled odds ratios of asthma in endometriosis patients by study type. Square boxes represent individual studies; horizontal lines represent 95% confidence intervals (CIs); and diamond-shaped figures 95% CIs of pooled estimates. Ferrero, S. [39], AL-Jefout, M. [43], Alqaisi, S. [44], Shafir, A.L. [45], Nowakowska, A. [51], Pan, G. [48], Matalliotakis, H. [50], Peng, Yin-Hao [35], Joud, A. [47], Imbroane, M.R. [49], Caserta, D. [42], Yoshii, E. [46].
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Table 1. Information on the studies included.
Table 1. Information on the studies included.
YearStudy SourceAgeStudyStudy
Design		RegionAsthma/
Endo
Cases		TotalDiagnosis
Criteria Asthma/Endo		Quality Score *
2002Endometriosis Association (1998)AllSinaii N [37]Cross-sectionalAmerica (USA, Canada)442/
3680		3680Self-reported/LaparoscopyNA
2005San Martino Hospital (2001–2004)~28–40Ferrero S [39]Cross-sectionalEurope (Italy)45/
467		879ATS criteria/Histology8
2012Yale University School of Medicine (1996–2002)~28–41Matalliotakis, H [50]Retrospective CohortAmerica (USA)53/
501		689Medical records and interview/American Society for Reproductive Medicine7
2013University of Michigan Medical Center (2001–2011)≤21Smorgick N [38]Retrospective cohortAmerica (USA)31/
138		138Records/IC-9 617.1 to 617.5 and 617.8–617.9NA
2016Andrea Hospital (2009–2013)19–53Caserta D [42]Case–ControlEurope (Italy)8/
304		622Medical Records/Laparoscopy–Histology5
2017LHID 2000 database (1996–2013)12–50Peng Y-H [35]Retrospective CohortAsia (Taiwan)7337/
1297		36,685ICD-9-CM 493.xx and treatment/CD-9-CM 617.xx9
2017Self-administered questionnaire (2015)15 to 55Al-Jefout M [43]Cross-sectionalAsia (Jordan)42/
45		1772Questionnaire/Laparoscopy or Laparotomy with histology report7
2017Yale University Hospital, University of Crete and Venizeleio General Hospital of Heraklion (1996–2016)13–21Matalliotakis M [52]Retrospective cohortAmerica (USA) and Greece267/
900		900Medical Records/Medical recordsNA
2018Explorys® database (2012–2017)20–40Alqaisi S [44]Cross-sectionalAmerica (USA)437,470/
64,150		327,202Medical records/Medical records6
2021Woman Health Study (2012–2018)7–55Shafir AL [45]Cross-sectionalAmerica (USA)267/
551		1203Questionnaire/Surgical diagnosis8
2021JMDC Claims Database (2011–2018)16–40Yoshii E [46]Case–ControlAsia (Japan)5801/
30,516		151,492ICD-10 codes: J45.0,J45.8,J46/N808
2022Skåne Healthcare Register (1998–2019)15–45Joud A [47]Retrospective CohortEurope (Sweden)6445/
413		206,693ICD-10 codes: J45- j46 (all subcategories) plus health visits/N809
2022Internet-based≥18Nowakoska A [51]Cross-sectionalOpen43/
364		501Questionnaire/Mixed (included 49.6% laparoscopy or laparotomy)2
2024NHANES (1999–2006)≥20Pan G [48]Cross-sectionalAmerica (USA)782/
380		5556Questionnaire: RHQ_D/MCQ6
2024TriNetX: US collaborative network (2023)12 to 50Imbroane MR [49]Retrospective CohortAmerica (USA)1,581,644/
196,857		24,647,797ICD-10 J45/ICD-10 N807
2024Pediatric Surgery10–24Cialuj TA [19]Retrospective CohortAsia (Philippines)5/
50		50Medical records/Medical recordsNA
* Newcastle–Ottawa score to assess risk of publication bias.
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Ramos-Nino, M.E.; Obadiah, A.A.; Ozugha, I.O.; Ramdass, P.V.A.K. The Association Between Asthma and Endometriosis: A Systematic Review and Metanalysis. J. Respir. 2025, 5, 6. https://doi.org/10.3390/jor5020006

AMA Style

Ramos-Nino ME, Obadiah AA, Ozugha IO, Ramdass PVAK. The Association Between Asthma and Endometriosis: A Systematic Review and Metanalysis. Journal of Respiration. 2025; 5(2):6. https://doi.org/10.3390/jor5020006

Chicago/Turabian Style

Ramos-Nino, Maria E., Abraham Agaya Obadiah, Ifesinachi Ogochukwu Ozugha, and Prakash V. A. K. Ramdass. 2025. "The Association Between Asthma and Endometriosis: A Systematic Review and Metanalysis" Journal of Respiration 5, no. 2: 6. https://doi.org/10.3390/jor5020006

APA Style

Ramos-Nino, M. E., Obadiah, A. A., Ozugha, I. O., & Ramdass, P. V. A. K. (2025). The Association Between Asthma and Endometriosis: A Systematic Review and Metanalysis. Journal of Respiration, 5(2), 6. https://doi.org/10.3390/jor5020006

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