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Journal articleSory DR, Heyraud ACM, Jones JR, et al., 2026,
SiO2-CaOCME/Poly(Tetrahydrofuran)/Poly(Caprolactone) 3D-Printed Scaffolds Drive Human-Bone Marrow Stromal Cell Osteogenic Differentiation.
, Adv Healthc MaterThis article addresses the unmet clinical need of scaffolds for bone regeneration that can combine osteogenic properties, such as the promotion of bone marrow stem cell differentiation into osteoblasts, with the ability to withstand cyclic loading. In our previous study, we demonstrated that discs of SiO2-CaOCME/poly(tetrahydrofuran)/poly(caprolactone) hybrids or their dissolution products can drive terminal osteogenic differentiation of human bone marrow stromal cells (h-BMSCs) in vitro. The current study shows that the 3D-printed hybrid scaffolds with physiologically relevant 3D architecture further promote h-BMSC osteogenesis. The 3D-printed scaffolds support spatially organized cell behavior in an environment mirroring conditions relevant to off-the-shelf implant applications. Primary cellular functions, including viability, adhesion, and proliferation, were maintained across 3D scaffold surfaces and within inter-strut regions. osteogenic commitment was evidenced by the upregulation of lineage-specific transcripts, hydroxyapatite deposition, and the organized assembly of extracellular matrix (ECM) proteins. Our results demonstrate that 3D-printed scaffolds drive osteogenesis by modulating cell metabolism, inducing osteogenic morphological transitions, and promoting the expression of osteocalcin and collagen type I alpha 1 chain, alongside hydroxyapatite matrix mineralization. Collectively, our findings highlight the SiO2-CaOCME/poly(tetrahydrofuran)/poly(caprolactone) scaffold's strong osteogenic properties-driven by composition, surface architecture, and ion release - and its promise for clinical bone regeneration.
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Journal articleKlimek L, Mullol J, Hummel T, et al., 2026,
The Unmet Need of Olfactory Testing in Inflammatory Disorders of the Upper Airways-An EAACI Position Paper.
, AllergyThe sense of smell, with its extensive evolutionary history, is highly prone to disorders that can have a profound impact on daily life. Anosmia affects approximately 5% of the population, with an additional 15% exhibiting reduced olfactory function. The prevalence of olfactory dysfunction (OD) varies by population and age group, and standardized testing reveals a broad range of impacts. OD includes various causes, most commonly aging, inflammation of the olfactory epithelium, upper respiratory tract infections (URTI), traumatic brain injury, and neurological conditions. The recent COVID-19 pandemic has highlighted the association between viral infections and olfactory dysfunction, with severe hyposmia/anosmia being an early marker of infection. Despite its importance, the assessment of olfactory function remains inconsistent across clinical practices. Psychophysical smell tests, while vital for diagnosis and patient management, are underutilized, especially outside of specialized centers. Standardized testing methods are crucial for objective diagnosis, but significant challenges, including test variability, lack of comparability, and healthcare reimbursement issues, persist. The European Academy of Allergy and Immunology (EAACI) advocates for improvements in the quality and standardization of chemosensory assessments. Future efforts must prioritize education, incentives for better testing, and the integration of digital tools to expand access to olfactory testing and diagnosis in remote or quarantine situations. However, office-based testing remains irreplaceable, even with advancements in telemedicine.
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Journal articleStewart I, John A, Bin L, et al., 2026,
Residual lung abnormality following COVID-19 hospitalisation is characterised by biomarkers of epithelial injury
, EBioMedicine, Vol: 124, ISSN: 2352-3964Some survivors of acute COVID-19 infection have long-term symptoms that could suggest ongoing lung impairment. Searches performed in MEDLINE and Embase for SARS-COV-2 studies with radiological lung follow-up estimated that 50% of participants had inflammatory patterns and 29% had fibrotic patterns at a median of 3 months post infection. Analysis of the UK nationwide Post-hospitalisation COVID-19 Study at 5-months follow-up suggested that up to 11% of people discharged from hospital following COVID-19 infection were at-risk of radiological residual lung abnormalities, such as ground glass opacity and reticulation. In people with pulmonary fibrosis, these radiological patterns are often consistent with persistent epithelial lung injury. Biomarker studies have identified associations with COVID-19 severity, however there are few studies that explore the relationship between biomarkers of epithelial injury and parenchymal lung abnormalities post-hospitalisation.
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Journal articleKong E, Cucco A, Custovic A, et al., 2026,
Machine learning in allergy research: A bibliometric review
, IMMUNOLOGY LETTERS, Vol: 277, ISSN: 0165-2478 -
Journal articleMaher T, Jenkins G, Saini G, et al., 2026,
A Prospective Study of Fibrosis in the Lung Endpoints (PROFILE): characteristics of an incident cohort of patients with idiopathic pulmonary fibrosis
, BMJ Open Respiratory Research, ISSN: 2052-4439Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrotic lung disease. The PROFILE study was a prospective, observational cohort study designed to better define the natural history of IPF, understand disease biology and identify biomarkers to support disease management and enhance clinical trial design.Methods: Individuals with an incident diagnosis of IPF were recruited between 2010 and 2017 across two co-ordinating centres in the UK. Demographics, clinical measurements and blood samples were obtained at baseline, and 1, 3, 6, 12, 24, 36 months. Disease progression events were defined as death or relative FVC decline>10% at 12 months. Survival estimates were modelled using cox proportional hazards; longitudinal lung function decline was estimated using mixed effect models, specified with restricted cubic splines, a random intercept for participant and random effect for study visit. All models were adjusted for baseline age, sex and continuous baseline percent predicted forced vital capacity (ppFVC).Results: A total of 632 participants were recruited, 77.1% were male and mean age at enrolment was 70.4 years (SD 8.4). Mean baseline ppFVC was 79.5% (SD 19.2), mean percent predicted DLCO (ppDLCO) was 45.7% (SD 15.1). A total of 304 (48.1%) participants met disease progression criteria at 1 year. Median survival was 3.7 years (95%CI 3.3; 4.0). More severe baseline physiology, 12-month relative lung function decline ≥10%, older age, and short telomeres were independent risk factors for mortality. Twelve-month estimated change in ppFVC was -5.28% (95%CI -6.34; -4.22) with an average FVC decline of 186.9ml (95%CI -225.4.0; -148.5), 12-month estimated change in ppDLCO was -3.35% (95%CI -4.30; -2.40).Conclusion: The PROFILE cohort confirms that untreated, IPF is inexorable progressive and inevitably fatal with a poor median survival from diagnosis.
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Journal articleWilson-Morkeh H, Seluk L, Bosch P, et al., 2026,
Targeting Immunologic Pathways in Eosinophilic Granulomatosis With Polyangiitis: Translating Emerging Evidence Into Clinical Practice.
, AllergyEosinophilic granulomatosis with polyangiitis (EGPA) is a rare and potentially life-threatening systemic, inflammatory disease with multi-organ manifestations, variable presentation and complex pathology. Multiple interconnected immunological pathways are implicated in EGPA pathology, including a type-2 immune response driving predominantly eosinophilic inflammation, B-cell mediated autoimmunity, neutrophil activation, and the generation of pathogenic anti-neutrophil cytoplasmic antibodies, all of which can contribute to tissue/organ damage. High-dose glucocorticoids are the mainstay treatment for EGPA, but over the past two decades the development of biologic treatments targeting interleukin (IL)-5, eosinophils and B-cells has revitalized the treatment landscape. Mepolizumab, a humanized monoclonal antibody that specifically targets IL-5, and benralizumab, which targets the IL-5 receptor (IL-5Rα), are both approved for the treatment of patients with non-severe relapsing or refractory EGPA. In Phase III trials, these biologics have demonstrated favorable safety profiles and efficacy, with treatment leading to remission induction, remission maintenance, and oral glucocorticoid sparing benefits. However, as understanding of the full complexity of EGPA pathogenesis improves, new treatment targets are emerging. Consequently, understanding key pathogenic mechanisms at the patient level, enabling a more tailored treatment approach, is an important goal for future research.
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Journal articleBush A, 2026,
Back to the Mucus: Introduction to an <i>AJRCCM</i> Special Section on Airway Mucus
, American Journal of Respiratory and Critical Care Medicine, ISSN: 1073-449X -
Journal articleStölting H, Raftery AL, Walker SA, et al., 2026,
Epidermal growth factor receptor controls sex differences in lung type 2 responses to inhaled allergen.
, Sci Immunol, Vol: 11Hormonal disruptions are associated with poor asthma control in females, yet how these phenomena are linked remains unknown. Here, we investigated distinct allergen-induced immune responses between the sexes during maturation. By 6 weeks of life, female mice exposed to the aeroallergen house dust mite (HDM) from postnatal day 7 exhibited stronger type 2 (T2) immune responses and higher lung interleukin-33 (IL-33) than males. IL-33 administration to HDM-sensitized males was sufficient to augment T2 immunity and up-regulated epidermal growth factor receptor (EGFR) on T helper 2 (TH2) cells. EGFR inhibition abrogated T2 cytokine production in vitro. In vivo, EGFR inhibition reduced T2 immunity in females only, thereby abolishing any sex differences. 17β-estradiol (E2) heightened lung Il33 expression and T2 responses of HDM-sensitized males, akin to levels in females. EGFR's ability to drive sex differences in lung T2 responses downstream of E2 and IL-33 may link hormonal disruptions to poor asthma control.
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Journal articleMolyneaux PL, Mogulkoc N, Gunen H, et al., 2026,
Oral Nalbuphine in Idiopathic Pulmonary Fibrosis-Associated Cough: The CORAL Randomized Clinical Trial.
, JAMAIMPORTANCE: For patients with idiopathic pulmonary fibrosis (IPF), cough impairs quality of life; effective treatments for IPF-associated cough are needed. OBJECTIVE: To determine if nalbuphine extended release (ER), a κ opioid receptor agonist and μ-opioid receptor antagonist, decreases cough compared with placebo in patients with IPF-associated cough. DESIGN, SETTING, AND PARTICIPANTS: In this randomized, double-blind, placebo-controlled phase 2b trial conducted at 52 sites in 10 countries, patients with IPF, chronic cough for at least 8 weeks, and a Cough Severity Numerical Rating Scale (0, no cough; 10, worst possible cough) score of 4 or higher were enrolled from February 2024 to February 2025, with last follow-up in April 2025. Statistical analyses were conducted from May to August 2025. INTERVENTION: Patients were randomized 1:1:1:1 to receive nalbuphine ER at doses of 27 mg, 54 mg, or 108 mg or placebo twice daily for 6 weeks. MAIN OUTCOMES AND MEASURES: The primary outcome was the relative change from baseline in 24-hour cough frequency (coughs/h), measured with a digital cough monitor, for nalbuphine ER compared with placebo at week 6. The key secondary outcome was the relative change from baseline in the patient-reported cough frequency (Evaluating Respiratory Symptoms in IPF cough subscale; scores range from 0-4, lower scores indicate lesser cough frequency) at week 6. RESULTS: Of the 223 patients screened, 165 were randomized (42, 43, 40, and 40 to receive nalbuphine ER 27 mg, 54 mg, and 108 mg, and placebo, respectively) and 160 were included in the primary analysis (median age, 71 [range, 51-85] years; 28.5% female). The baseline mean (SD) cough count was 28.3 (27.4) coughs/h. In the nalbuphine ER 27 mg, 54 mg, and 108 mg twice-daily groups, the mean relative decrease in the cough count and the absolute decrease in coughs/h were 47.9% (from 24.6 to 11.9; P = .008), 53.4% (from 28.0 to 14.9; P < .001), and 60.2%
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Journal articleKhan F, Stewart I, Howard L, et al., 2026,
Comprehensive characterisation of individuals with fibrotic interstitial lung disease: baseline insights from the INJUSTIS study.
, BMJ Open Respir Res, Vol: 13BACKGROUND: Interstitial lung disease (ILD) represents a group of complex parenchymal conditions characterised by varying clinical trajectories. The It's Not JUST Idiopathic Pulmonary Fibrosis Study seeks to identify genetic, proteomic and clinical biomarkers that distinguish rapidly progressive fibrotic phenotypes from stable phenotypes irrespective of aetiology. This manuscript presents baseline insights from the recruited cohort. METHODS: In this prospective, longitudinal study, participants with fibrotic ILDs, including idiopathic pulmonary fibrosis (IPF), fibrotic hypersensitivity pneumonitis, rheumatoid arthritis-associated ILD, asbestosis and unclassifiable ILD, were enrolled from 24 UK sites. Participants underwent comprehensive baseline evaluation including demographics, exposure history, lung function testing, 6-min walk tests, blood sampling and standardised questionnaires to assess symptoms and quality of life. RESULTS: A total of 272 participants were recruited, predominantly older white males with a smoking history. Baseline lung function showed comparable forced vital capacity (mean 89.0% predicted), diffusion of carbon monoxide (mean 57.9% predicted) and 6-min walk distance (mean 302 m) across ILD subtypes. Hypertension was the most prevalent comorbidity, affecting 40.8% of participants, with no significant differences across subtypes. Anxiety and depression were notably lower in IPF than non-IPF (4.5%; 21.0%). Previous occupational exposure was reported in 68.8% of participants, with asbestos exposure the most prevalent (36%). Bird exposure was reported by 40.4% of participants, with no significant differences across subtypes. No significant differences in health-related quality of life scores were observed across subtypes. CONCLUSIONS: Despite varied aetiologies, fibrotic ILDs exhibit demographic and functional similarities, including lung function and health-related quality of life suggesting commonalities in disease mechanisms. TRIAL REGISTRATION
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Journal articleRowbotham NJ, Jeanpierre M, Bush A, et al., 2026,
New pathogenic PTPN2 variant leading to childhood interstitial lung disease.
, ThoraxProtein tyrosine phosphatase non-receptor type 2 (PTPN2) is a tyrosine phosphatase involved in T cell receptor signal transduction and cytokine response. Loss of function variants have previously been linked with immune mediated diseases such as inflammatory bowel disorders, rheumatoid arthritis and type 1 diabetes. We present a case of childhood interstitial lung disease with a newly identified pathogenic (PTPN2) gene variant in a boy aged 4 years.
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Journal articleRidd MJ, Brown SJ, Beattie P, et al., 2026,
Reply to Comment on 'Food Allergy Test-Guided Dietary Advice for Children With Atopic Dermatitis: A Consensus Study'.
, Pediatr Dermatol -
Journal articleKarp T, Merid SK, Kermani NZ, et al., 2026,
Nasal gene expression shows a distinct signature in type 2-high asthma but not in type 2-low disease.
, J Allergy Clin ImmunolBACKGROUND: Type 2 (T2)-low asthma is defined by low levels of T2 inflammation and is associated with resistance to inhaled corticosteroids. Its molecular mechanisms are mostly unknown, and treatment options are limited. We previously showed that nasal brush transcriptomes differ between asthma and controls, reflecting disease-relevant biology. OBJECTIVE: We explored nasal gene expression related to T2-low asthma in the ATLANTIS cohort. METHODS: We compared nasal brush RNA sequencing data between 82 T2-low and 63 T2-high asthma patients and 57 controls. T2-low asthma was defined as blood eosinophil counts < 0.15 × 109/L and Feno < 25 ppb and T2-high as blood eosinophil counts > 0.3 × 109/L and Feno > 25 ppb. Weighted gene coexpression network analysis (WGCNA) was applied to identify gene modules associated with T2-low asthma. The BAMSE and U-BIOPRED cohorts were used for replication analyses. RESULTS: Although differentially expressed genes were found in patients with T2-high asthma across all 3 cohorts, no differentially expressed genes were observed in individuals with T2-low disease compared to controls in ATLANTIS, nor consistently across other cohorts. Our assessment of molecular heterogeneity could not attribute this result to greater intersample variability within the T2-low group. WGCNA in ATLANTIS identified "black" and "purple" gene modules linked to T2-low asthma, with genes enriched in T-cell immunity and ribosomal RNA biology pathways, respectively. The "black" module was replicated in U-BIOPRED and showed the same direction in BAMSE. CONCLUSION: T2-high asthma shows a distinct nasal gene expression signature compared to healthy controls, while patients with T2-low asthma exhibit no consistent changes. Future studies should explore T-cell immunity in T2-low asthma and integrate lower airway multiomics data.
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Journal articleLayhadi JA, Starchenka S, De Kam P, et al., 2026,
Modulation of cellular, molecular, and humoral responses by PQ Grass 27,600 SU for the treatment of seasonal allergic rhinitis: a randomised double blind placebo control exploratory field study
, Allergy, Vol: 81, Pages: 232-247, ISSN: 0105-4538Background:A short-course pre-seasonal subcutaneous injection of PQ Grass is clinically effective for the treatment of allergic rhinitis, though its mechanism remains unclear. The aim of the study was to interrogate immunological mechanisms induced by PQ Grass conventional and extended regimens.Methods:A RDBPC exploratory field study involving participants that either received injections of PQ Grass with a cumulative dose of 27,600 SU conventional (six once weekly injections) or extended regimen (three once weekly injections followed by three once monthly injections) or placebo containing microcrystalline tyrosine (MCT) (placebo + MCT) or saline (placebo) was performed. Humoral, cellular, and molecular responses were assessed at baseline (V1), end of treatment, prior to grass pollen season (V12) and end of pollen season (V15). Immunoglobulin analyses and cellular/gene microarray analyses were performed in the sub-study cohort consisting of PQ Grass Conventional (n = 25 and n = 10, respectively), PQ Grass Extended (n = 26 and n = 10, respectively), Placebo with MCT (n = 13 and n = 5, respectively), and Placebo (saline; n = 12 and n = 5, respectively).Results:Both PQ Grass regimens, conventional and extended, were associated with improvement in total combined scores (TCS) with a relative difference of −35.0% (p = 0.03) and −40.8% (p = 0.01) against placebo with MCT, respectively. Both PQ Grass treatment regimens were associated with increases in the sIgG4/sIgE ratio (all, p < 0.05) and induction of IgA1 (all, p < 0.05) and IgA2 (all, p < 0.01) compared to placebo groups. Nasal fluid (p < 0.01) and serum (p < 0.05) blocking antibodies are functional and have the capacity to inhibit allergen-IgE complex formation and binding to B cells i
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Journal articleChan R, Horn NE, Siddiqui S, 2026,
Precision Medicine for Asthma: Tailored to its Severity and Endotype/Phenotype.
, Allergy Asthma Immunol Res, Vol: 18, Pages: 19-38, ISSN: 2092-7355Asthma is a chronic respiratory disease affecting more than 300 million people globally and remains a major cause of morbidity, mortality, and healthcare burden. Traditionally, asthma has been managed using a stepwise treatment algorithm focused on inhaled corticosteroids, bronchodilators, and add-on therapies. While this approach provides a broad framework for care, it does not adequately account for the heterogeneity of the disease, which encompasses diverse clinical phenotypes, underlying endotypes, and variable treatment responses. Many patients with moderate-to-severe asthma continue to experience poor control, frequent exacerbations, and impaired quality of life despite standard therapies. Precision medicine offers an alternative strategy by identifying and targeting specific "treatable traits" across pulmonary, extrapulmonary, and behavioral domains. Advances in biomarker profiling-including blood eosinophils, fractional exhaled nitric oxide, volatile organic compounds, and transcriptomics-have enabled more accurate risk prediction and patient stratification. Imaging techniques, such as high-resolution computed tomography and hyperpolarized magnetic resonance imaging, are improving the ability to detect small airways dysfunction, mucus plugging, and other key disease mechanisms. Biologic therapies directed at type 2 inflammation pathways, including anti-immunoglobulin E, anti-interleukin (IL)5, anti-IL4Rα, and anti-thymic stromal lymphopoietin agents, have significantly reduced exacerbation rates and improved lung function, although biomarker variability, high treatment costs, and limited accessibility remain barriers to widespread use. Emerging oral, inhaled, and long-acting biologics further expand the therapeutic landscape. Looking forward, the integration of multi-omics, deep phenotyping, and artificial intelligence promises to transform asthma management by enabling personalized therapy tailored to individual patient profiles. This narrat
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Journal articlePhelan AK, Infante S, Barni S, et al., 2026,
Reply to "Some observations on systematic review of Phelan et al".
, J Allergy Clin Immunol Pract, Vol: 14, Pages: 322-323 -
Journal articleBoyle RJ, Shamji MH, 2026,
Getting the Basics Right in Allergy Care.
, Clin Exp Allergy, Vol: 56, Pages: 4-6 -
Journal articleNicholson AG, Adegunsoye A, Piciucchi S, et al., 2026,
Reply: From the authors of the ERS/ATS statement on the international multidisciplinary classification of the interstitial pneumonias.
, Eur Respir J, Vol: 67 -
Journal articleCourse CW, Bush A, Kotecha S, 2026,
Looking beyond bronchopulmonary dysplasia: prematurity-associated lung disease and its phenotypes.
, Lancet Respir Med, Vol: 14, Pages: 60-71Preterm birth is increasingly recognised as a determinant of chronic respiratory disease across the life course. In this Series on prematurity-associated lung disease (PLD), we introduce the concept of PLD as a unifying framework for the diverse pulmonary consequences of preterm birth. Historically, most attention has focused on extremely preterm infants (<28 weeks of gestation) who develop bronchopulmonary dysplasia (BPD), yet not all infants with BPD have long-term morbidity. Conversely, those born very (28-31 weeks), moderate (32-33 weeks), or late (34-36 weeks) preterm also have increased risk for developing lung disease. Multiple factors beyond BPD-including gestational age and intrauterine growth restriction-contribute to PLD development. Recently described PLD phenotypes include prematurity-associated obstructive lung disease, prematurity-associated preserved ratio impaired spirometry, and prematurity-associated dysanapsis. Each phenotype reflects distinct early-life exposures and mechanisms, with differing implications for prognosis. Defining these phenotypes provides a foundation for personalised monitoring and targeted therapeutic strategies.
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Journal articleAvitzur N, Knaub M, Thornton-Wood F, et al., 2026,
The impact of pulmonary fibrosis on sex and sexual function: a multinational mixed methods study.
, Eur Respir J, Vol: 67BACKGROUND: Sex is an important part of life for many adults, yet sexual function may be impacted by chronic respiratory diseases such as pulmonary fibrosis (PF). This multinational study sought to characterise the impact of PF on sex and sexual function, using mixed quantitative and qualitative methodology. METHODS: We analysed data from a patient registry, a clinical study, an online survey and patient interviews to accomplish our objective and develop a conceptual framework for describing the effects of PF on sex-related quality of life. These cohorts used three distinct questionnaires, University of California, San Diego Shortness of Breath Questionnaire (UCSD-SOBQ), Sheffield Profile for Assessment and Referral to Care (SPARC) questionnaire, and Changes in Sexual Function Questionnaire (CSFQ), to assess sexual dysfunction, respectively. Individual patient interviews were conducted and qualitatively evaluated using thematic analysis. RESULTS: Dyspnoea with sexual activity affected 2054/2759 (74%) of registry patients, associated with male sex, lower forced vital capacity (FVC) % predicted, lower diffusing capacity of the lung for carbon monoxide (D LCO) % predicted and worse cough. Distress due to the effect of PF on their sex life was reported in 52/225 (23%) of the clinical cohort, associated with younger age, male sex, lower D LCO % predicted and worse cough. Sexual dysfunction was common, affecting 56/67 (83%) female and 63/73 (86%) male survey respondents. Qualitative analysis of patient interviews identified several themes, including sex life limitations, changes in interpersonal relationships and quality of life. All patients wanted to discuss sex with trusted healthcare providers. CONCLUSIONS: In this multinational study, patients with PF reported engaging in sex and sexual activities but were adversely impacted by the effect of PF on their sex life, with both physical and psychological limitations. Sexual dysfunction was common, driven by multiple disea
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