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Background: Many patients with chronic spontaneous urticaria (CSU) do not achieve complete control of their symptoms with current available treatments. In a dose-finding phase 2b study, ligelizumab improved urticaria symptoms in patients with H1-antihistamine (H1-AH) refractory CSU. Here, we report the efficacy and safety outcomes from two ligelizumab phase 3 studies., Methods: PEARL-1 and PEARL-2 were identically designed randomised, double-blind, active-controlled and placebo-controlled parallel-group studies. Patients aged 12 years or older with moderate-to-severe H1-AH refractory CSU were recruited from 347 sites in 46 countries and randomly allocated in a 3:3:3:1 ratio via Interactive Response Technology to 72 mg ligelizumab, 120 mg ligelizumab, 300 mg omalizumab, or placebo, dosed every 4 weeks, for 52 weeks. Patients allocated to placebo received 120 mg ligelizumab from week 24. The primary endpoint was change-from-baseline (CFB) in weekly Urticaria Activity Score (UAS7) at week 12, and was analysed in all eligible adult patients according to the treatment assigned at random allocation. Safety was assessed throughout the study in all patients who received at least one dose of the study drug. The studies were registered with ClinicalTrials.gov, NCT03580369 (PEARL-1) and NCT03580356 (PEARL-2). Both trials are now complete., Findings: Between Oct 17, 2018, and Oct 26, 2021, 2057 adult patients were randomly allocated across both studies (72 mg ligelizumab n=614; 120 mg ligelizumab n=616; 300 mg omalizumab n=618, and placebo n=209). A total of 1480 (72%) of 2057 were female, and 577 (28%) of 2057 were male. Mean UAS7 at baseline across study groups ranged from 29·37 to 31·10. At week 12, estimated treatment differences in mean CFB-UAS7 were as follows: for 72 mg ligelizumab versus placebo, -8·0 (95% CI -10·6 to -5·4; PEARL-1), -10·0 (-12·6 to -7·4; PEARL-2); 72 mg ligelizumab versus omalizumab 0·7 (-1·2 to 2·5; PEARL-1), 0·4 (-1·4 to 2·2; PEARL-2); 120 mg ligelizumab versus placebo -8·0 (-10·5 to -5·4; PEARL-1), -11·1 (-13·7 to -8·5; PEARL-2); 120 mg ligelizumab versus omalizumab 0·7 (-1·1 to 2·5; PEARL-1), -0·7 (-2·5 to 1·1; PEARL-2). Both doses of ligelizumab were superior to placebo (p<0·0001), but not to omalizumab, in both studies. No new safety signals were identified for ligelizumab or omalizumab., Interpretation: In the phase 3 PEARL studies, ligelizumab demonstrated superior efficacy versus placebo but not versus omalizumab. The safety profile of ligelizumab was consistent with previous studies., Funding: Novartis Pharma., Competing Interests: Declaration of interests MM is or recently was a speaker, an adviser for, or has received research funding from Amgen, Allakos, Aralez, AstraZeneca, Celldex, FAES, Genentech, GI Innovation, Kyowa Kirin, Leo Pharma, Menarini, Novartis, Moxie, MSD, Roche, Sanofi, Third Harmonic, UCB, and Uriach. LFE is or recently was a speaker or adviser for Novartis, Sanofi, and AbbVie, and has received research support from Novartis and Sanofi. AMG-A reports roles as a medical adviser for Uriach Pharma, Sanofi, Genentech, Novartis, FAES, GSK, AMGEN, Thermo Fisher, and has received research grants supported by Uriach Pharma, Novartis, and Instituto Carlos III- FEDER; she also participates in educational activities for Uriach Pharma, Novartis, Genentech, Menarini, LEO-PHARMA, GSK, MSD, Almirall, AVENE, and Sanofi. GS has received research support from Aimmune, Amgen, AstraZeneca, DBV technologies, Genentech, Kedrion, Leo Pharma, Novartis, Nuvo Pharmaceuticals, Sanofi, Stallergenes, Merck, and Schering-Plough; and is a medical adviser or has received payment for lectures from Merck, Novartis, CSL Behring, Pfizer, Anaphylaxis Canada, the Allergy Asthma and Immunology Society of Ontario, and the Canadian Hereditary Angioedema Network. MH has received lecture or consultation fees from TAIHO Pharmaceutical, Novartis, MSD, Teikoku Seiyaku, Mitsubishi Tanabe Pharma, Kaken Pharmaceutical, Kyorin Pharmaceutical, Uriach, Sanofi, and Kyowa-Kirin and GI Innovation. SS received grant, research, or clinical trial support from the National Institutes of Health, ITN, Novartis, Regeneron, and is a consultant or advisery board member for Genentech, Novartis, Medimmune, AstraZeneca, Pfizer, Allakos, Eli Lily, and Gossamer Bio. CG has recently been an adviser for Celltrion and has participated in an advisery board for Sanofi. DF is, or recently was, a speaker or adviser for Novartis, Sanofi, AbbVie, Takeda, AstraZeneca, CSL Behring, and Roche. DR received fees as lecturer and advisery board member for Novartis, Leo, Lilly, MSD, UCB, Janssen, Sanofi, Menarini, Genesis pharma, and AbbVie. FB has received payment or honoraria as speaker fees from Novartis. GWC reports having received research grants, as well as being a lecturer or having received advisery board fees, from Menarini, Alk-Abello', Allergy Therapeutics, AstraZeneca, Boehringer Ingelheim, Chiesi Farmaceutici, Genentech, Guidotti-Malesci, GSK, Hal Allergy, Mylan, Merck, Merck Sharp & Dome, Mundipharma, Novartis, Regeneron, Roche, Sanofi-Aventis, Sanofi-Genzyme, Stallergenes-Greer, UCB Pharma, Uriach Pharma, Valeas, and Vibor-Pharma. HR reports receiving speaker's fees, advisery board fees or funds for research to the institution from Novartis Pharma, Pharming, Sanofi-Genzyme, Third Harmonic, and Leo Pharma. CI reports having received research or clinical trial support, or fees for lectures from Novartis, Sanofi, AstraZeneca, Takeda, and Stallergenes Greer. JCS reports receiving fees for being consultant or advisery board member for Leo Pharma, Novartis, Pfizer, Sanofi-Genzyme, Trevi, UCB, and Vifor; for being speaker for AbbVie, Almirall, Alvotech, Janssen-Cilag, Eli-Lilly, Leo Pharma, Novartis, Pfizer, and Sanofi-Genzyme; for being the investigator in clinical trials for AbbVie, Almirall, Amgen, AnaptysBio, BMS, Boehringer Ingelheim, Celtrion, Galderma, Galapagos, Helm, Kliniksa, Incyte, InfraRX, Janssen-Cilag, Leo Pharma, Medimmune, Menlo Therapeutics, Merck, Novartis, Pfizer, Regeneron, UCB, Teva, and Trevi. JAB reports grants and personal fees from Novartis, AstraZeneca, Allakos, Amgen, Celldex, Genentech, and Sanofi Regeneron outside the submitted work. JGP has received travel support, speakers' honoraria, and educational grants from Novartis, Sanofi Regeneron, Takeda, Pharming, and CSL Behring. KK is or recently was a speaker or adviser for Novartis, Sanofi, Takeda, and A Menarini, and has received research grants from Novartis. LA is or recently was a speaker, adviser, or has received research funding from AstraZeneca, GSK, Novartis, OM-Pharma, Regeneron, Shire, Takeda, and Sanofi-Genzyme. PS is or recently was a speaker, adviser, or has received research funding from AbbVie, Allergika, Almirall, Amgen, Beiersdorf, Biocryst, Biogen, BMS, Boehringer-Ingelheim, Celgene, CSL-Behring, Eli-Lilly, Galderma, Hexal, Janssen, Klinge, Klosterfrau, LEO-Pharma, LETI-Pharma, L'Oreal, Medice, Novartis, Octapharma, Pfizer, Pflüger, Pharming, Pierre Fabre, Regeneron, Shire, Takeda, Regeneron, Sanofi-Genzyme, und UCB Pharma. RS is Director and Founder of Samson Medical Pty, and serves on the pharmaceutical advisery board of Eli Lilly, Pfizer, Leo Pharmaceutical, and reports being on the speaker bureau of Pfizer, AbbVie, and Novartis. He has also been principal investigator in clinical trials for AbbVie, Aerotech, Akesobio, Amgen, Arcutis, Arena, Ascend AstraZeneca, Bayer, Biotherapeutics Boehringer Ingelheim, Bristol Myer Squibb, Celgene, Coherus BioSciences, Connect, Demira, Eli Lilly, Galderma, GSK, F. Hoffman–La Roche, Janssen, MedImmune, Merck, Merck Sharpe & Dohme, Novartis, Oncobiologics, Pfizer, Principia, Regeneron, Roche, Reistone Biopharma, Samson Clinical, Sanofi-Genzyme, Sun Pharma UCB, Valeant, and Zai Labs. He is President of the Australasian Hair and Wool Research Society, Vice President of the International Society of Dermatology, and The International Academy of Dermatology. SG has consulted or advised for Novartis and IgGenix. SFT is or recently was a speaker, adviser for, or has received research funding from AbbVie, Almirall, Boehringer Ingelheim, CSL, Eli Lilly, Janssen, Leo Pharma, Novartis, Sanofi, Pfizer, UCB, and Union Therapeutics. TT received clinical trial support from Novartis, AstraZeneca, Celldex Therapeutics, Genentech, and GSK. YMY has received research or clinical trial support from Novartis, Amgen, Yuhan, Takeda, and Daewoong ABa, DM, and ES are employees of Novartis Pharmaceuticals, East Hanover, New Jersey, NJ, USA. EH is an employee of Novartis Institutes for Biomedical Research, China. VV is an employee of Novartis Healthcare Private, Hyderabad, India. ABu, KL, MP, and TS are employees of Novartis Pharma, Basel, Switzerland. KG, JL, and OU report no conflicts of interest., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

The real-world efficacy of biologics may be insufficiently assessed through common drug survival studies. The objective was thus to examine the real-world performance of biologics in the treatment of psoriasis using the composite endpoint of either discontinuation or off-label dose escalation. Using a prospective nationwide registry (DERMBIO, 2007-2019), we included patients with psoriasis treated with adalimumab, secukinumab, and/or ustekinumab, which have all been used as first-line therapy during the inclusion period. The primary endpoint was a composite of either off-label dose escalation or discontinuation of treatment, whereas the secondary outcomes were dose escalation and discontinuation, respectively. Kaplan-Meier curves were used for the presentation of unadjusted drug survival curves. Cox-regression models were used for risk assessment. In 4,313 treatment series (38.8% women, mean age 46.0 years, and 58.3% bio-naivety), we found that the risk of the composite endpoint was lower for secukinumab when compared with ustekinumab (hazard ratio [HR] 0.66, 95% confidence interval [CI] 0.59-0.76), but higher for adalimumab (HR 1.15, 95% CI 1.05-1.26). However, the risk of discontinuation was higher for secukinumab (HR 1.24, 95% CI 1.08-1.42) and adalimumab (HR 2.01, 95% CI 1.82-2.22). For bio-naive patients treated with secukinumab, the risk of discontinuation was comparable to that of ustekinumab (HR 0.95, 95% CI 0.61-1.49)., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Little is known about how the spirometric definition of airway obstruction affects the association between COPD and comorbidities and whether these associations might be due to genetic predisposition., Aim: 1) To examine the impact of the spirometric definition on the associations between COPD and its comorbidities and 2) To examine whether these associations can be explained by shared genetic or environmental factors., Methods: 11,458 twins, aged 40-80 years, from the Danish Twin Registry were recruited who completed a questionnaire on medical history, life style factors and had a clinical examination. COPD was defined by respiratory symptoms (RS) plus airway obstruction according to either GOLD (FR-COPD) or ERS/ATS guidelines (LLN-COPD). Self-reported physician diagnoses were used to identify comorbidities., Results: The mean age of participants was 58.4 years ±SD 9.7, mean BMI was 26.6 kg/m 2  ± SD 4.4, 52% were female and the prevalence of LLN2.5-COPD and FR-COPD was 2.5% and 6.3%, respectively. Among eight major comorbidities, multivariate logistic regression showed COPD was only associated with heart failure, whereas RS alone were associated with 6 out of 8 comorbidities after Bonferroni-correction. There was an increased risk of heart failure, ischemic heart disease, depression and pulmonary embolism in twin individuals with RS compared with the co-twin without RS., Conclusions: COPD was only associated with an increased risk of heart failure. Discordant COPD-individuals (FR-COPD+/LLN5-COPD-) were at increased risk of heart failure. Sub-analyses showed that RS, but not airway obstruction were associated with an increased risk of comorbidities., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Spondyloarthritis (SpA) is an umbrella term describing a family of chronic inflammatory rheumatic diseases. These diseases are characterised by inflammation of the axial skeleton, peripheral joints, and entheseal insertion sites throughout the body which can lead to structural joint damage including formation of axial syndesmophytes and peripheral osteophytes. Genetic evidence, preclinical and clinical studies indicate a clear role of interleukin (IL)- 23 and IL-17 as mediators in SpA pathogenesis. Targeting the IL-23/-17 pathways seems an efficient strategy for treatment of SpA patients, and despite the remaining challenges the pathway holds great promise for further advances and improved therapeutic opportunities. Much research is focusing on serological markers and imaging strategies to correctly diagnose patients in the early stages of SpA. Biomarkers may facilitate personalised medicine tailored to each patient's specific disease to optimise treatment efficacy and to monitor therapeutic response. This narrative review focuses on the IL-17 pathway in SpA-related diseases with emphasis on its role in pathogenesis, current approved IL-17 inhibitors, and the need for biomarkers reflecting core disease pathways for early diagnosis and measurement of disease activity, prognosis, and response to therapy., (Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: Although smoking is the major risk factor for chronic obstructive pulmonary disease (COPD) many patients with obstructive lung function suggesting COPD are never-smokers. Therefore, other lifestyle factors have been suggested as risk factors., Aims: i) To examine the association between self-reported intake of fruit and vegetables and risk of COPD and ii) to examine whether the association between these traits are due to underlying genetic factors., Methods: 12,449 twins, aged 40-80, from the Danish Twin Registry were recruited. The participants completed a questionnaire on medical history and lifestyle factors and participated in clinical examination. COPD was defined according to ATS/ERS recommendations. Multivariate logistic regressions were used to estimate the risk of COPD in individuals with a low intake of fruit and vegetables. Co-twin control analyses were performed to examine whether the association between fruit and vegetables and COPD is explained by genetic factors. Self-reported physician-diagnosed asthmatic individuals were excluded., Results: Of the 11,458 individuals were included in the analyses, 48% of the participants were males. Mean age was 58.9 (years)±SD 9.6, mean BMI (kg/m 2 )26.6 ± SD 4.4. A multivariate logistic regression, including sex, age and BMI showed that both smoking, no and heavy drinking and physical inactivity were independent predictors of COPD. There was a significant frequency-pendent association between intake of fruit and vegetables and increased risk of COPD. Conditional logistic regression analyses showed that the association might be controlled by genetic factors., Conclusions: This study shows that low intake of fruit and vegetables is associated with an increased risk of COPD and the association might be under influence of genetic factors., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Introduction: Omalizumab is a humanized monoclonal anti-IgE antibody, which is widely used for patients with severe uncontrolled asthma. Treatment with omalizumab is known to decrease the number of exacerbations and GETE score (Global Evaluation of Treatment Effectiveness) - but little is known about which patients benefit the most. Moreover, the time to discontinuation of the treatment with omalizumab has yet to be investigated. In this real-life study on a Danish population we explore these important issues., Method: In a retrospective real-life study, 54 patients treated with omalizumab at a specialized outpatient asthma clinic were included. Change in GETE score, time to discontinuation of treatment and associated risk factors were analysed., Results: As a result of omalizumab treatment, most patients improved in GETE score from poor/worsening to excellent. Women were treated for a median time of 31 months (95% CI: 4.6-57.4) and approximately 50% of patients discontinued treatment after 500 days whilst, for men, 50% discontinued treatment after 1500 days. Eosinophil count above 300 cells/μL at treatment initiation was positively related to the discontinuation of omalizumab (HR 4.3 95%CI (1.22-15.28) p = 0.023)., Conclusion: In conclusion, female gender and an eosinophil count above 300 cells/μL may predict a better treatment response, leading to a shorter treatment time than the current guideline recommendation of maximum 48 months. Additionally, the GETE score improves with omalizumab. More real-life studies are needed to determine which patients will benefit the most from the treatment., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Asthma may be associated with polycystic ovary syndrome (PCOS), and possibly patients with PCOS have a more severe type of asthma. The purpose of this systematic literature review is to summarize evidence of a coexistense of PCOS and asthma using the available literature. The search was completed on 01.01.2016. English language articles were retrieved using the search terms 'Asthma' AND 'PCOS', 'Asthma' AND 'systemic inflammation', 'Asthma' AND 'metabolic syndrome', 'asthma' AND 'gynaecology', 'PCOS' AND 'systemic inflammation', 'PCOS' AND 'metabolic syndrome', 'PCOS' AND 'allergy'. Five papers meeting prespecified search criteria were found of which two were registry studies of relevance. The current literature supports a coexistense of PCOS and asthma and gives us an indication of the causes for the possible link between PCOS and asthma. Further research in the area must be conducted to determine the exact nature and magnitude of the association., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Background: Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality and is associated with several systemic diseases, such as type 2 diabetes. It has been suggested that comorbidity between COPD and type 2 diabetes is due to shared genetic factors., Aim: To examine the relationship between type 2 diabetes and chronic bronchitis and COPD in adult twins, and to examine to what extent comorbidity between these diseases is explained by shared genetic or environmental factors., Methods: Questionnaire data on chronic bronchitis and hospital discharge data on diagnosed COPD in 13,649 twins, aged 50-71 years, from the Danish Twin Registry were cross-linked with hospital discharge diagnosis data on type 2 diabetes from the Danish National Patient Registry., Results: The risk of type 2 diabetes was higher in persons with symptoms of chronic bronchitis than in those without symptoms (3.5 vs. 2.3%), OR = 1.57 (1.10-2.26), p = 0.014, and in individuals with diagnosed COPD than in those without the diagnosis (6.6 vs. 2.3%), OR = 2.62 (1.63-4.2), p < 0.001. The results were significant after adjusting for age, sex, smoking, and BMI. Correlations between genetic effects on chronic bronchitis and type 2 diabetes, and between genetic effects on diagnosed COPD and type 2 diabetes, respectively, were 0.33 (0.00-0.79), p = 0.103, and 0.43 (0.00-0.98), p = 0.154. Non-shared environmental correlations between chronic bronchitis and type 2 diabetes were -0.13 (-0.43 to 0), p = 0.498 and diagnosed COPD and type 2 diabetes -0.12 (-0.48 to 0), p = 0.665., Conclusions: Patients with chronic bronchitis or COPD have an increased risk of type 2 diabetes independent of sex, age, smoking and BMI. The genetic correlation between type 2 diabetes and chronic bronchitis was 33% and type 2 diabetes and COPD was 43%, however neither were statistically significant. The increased risk of type 2 diabetes should be accommodated in the management of patients with chronic bronchitis or COPD., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Aim: To examine the association between early menarche and risk of post-menarcheal asthma., Methods: Using data from two multidisciplinary questionnaire surveys, conducted eight years apart, we prospectively studied 10,648 female twins, 12-41 years of age, from the nationwide Danish Twin Registry. Early menarche was defined as menarche before 12 years of age. We performed a cohort analysis and a co-twin control analysis including twin pairs discordant for incident asthma., Results: Early menarche was observed in 9.3% of the individuals. The eight-year cumulative incidence of asthma was higher in girls with early menarche compared to girls without early menarche (7.4 vs. 4.5%), OR = 1.71 (1.31-2.22), p < 0.001; also after adjustment for BMI, current age, physical activity, education, and smoking, OR = 1.53 (1.15-2.04), p = 0.003. The unadjusted risk of asthma was increased by 8% (1-15%), p = 0.041 per year earlier menarche occurred. Among 167 twin pairs discordant for incident asthma, there was a non-significant tendency towards early menarche being more common in the asthmatic than the non-asthmatic co-twin (12.0 vs. 9.6%), OR = 1.57 (0.61-4.05), p = 0.350. The risk of asthma was not uniform in discordant monozygotic and dizygotic twins., Conclusion: Early menarche is associated with increased risk of asthma among Danish female twins independently of BMI, age, physical activity, educational level and smoking. Results indicate a complex relationship possibly mediated through innate and non-genetic effects., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: Smoking is a major risk factor for lung diseases and lower respiratory symptoms, but since not all smokers develop chronic bronchitis and since chronic bronchitis is also diagnosed in never-smokers, it has been suggested that some individuals are more susceptible to develop chronic bronchitis due to genetics., Objective: To study the relative influence of genetic and environmental factors on the variation in the susceptibility to chronic bronchitis., Methods: In a population-based questionnaire study of 13,649 twins, 50-71 years of age, from the Danish Twin Registry, we calculated sex-specific concordance rates and heritability of chronic bronchitis. The response rate was 75%., Results: The prevalence of chronic bronchitis was 9.3% among men and 8.5% among women. The concordance rate for chronic bronchitis was higher in monozygotic twins than in dizygotic twins among women; 0.30 vs. 0.17, but not among men; 0.15 vs. 0.18. The heritability of chronic bronchitis adjusted for smoking and age was 55% (36-71%) in women, whereas the susceptibility to chronic bronchitis in men for 25% (8-41%) was ascribable to familial environment but not to genetic factors., Conclusions: Chronic bronchitis shows a moderate familial aggregation, particularly in women. Increased susceptibility to respiratory disease among female smokers relative to male smokers may have a genetic origin., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Aim: To examine the association between intake of alcohol and risk of adult-onset asthma., Methods: Using data from two multidisciplinary questionnaire surveys we prospectively studied 19,349 twins, 12-41 years of age, from the nationwide Danish Twin Registry., Results: The eight-year incidence of asthma was 4.3%. After adjustment for sex, age, BMI, physical activity, educational level and smoking, the risk of new-onset asthma was significantly related to overall alcohol intake in a U-shaped manner with the lowest risk observed in the group with a moderate weekly intake of alcohol (1-6 units/week), p = 0.006. The highest risk of asthma was observed in rare/never drinkers (<1 unit/month), OR = 1.59 (1.25-2.02), p = 0.000, whereas the risk of asthma in heavy daily drinkers (≥4 units/day) was also increased, however not statistically significant, OR = 1.13 (0.54-2.36), p = 0.747. The risk of new-onset asthma was lower for subjects with wine preference (3.3%) compared with beer preference (4.3%) or no preference (4.4%). After multivariable adjustment, wine preference was inversely related to incident asthma compared with beer preference. However, this finding was not statistically significant, OR = 0.87 (0.51-1.46), p = 0.590., Conclusion: Alcohol intake is associated with new-onset asthma in adults with a U-shaped association between amount of alcohol intake and the risk of asthma., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Background: Over the past decades the prevalence of asthma has increased in most parts of the world, and widespread changes in lifestyle and environment have been postulated as the primary cause for this. We examined whether the extent to which genetic and environmental factors influence susceptibility to asthma has changed between 1994 and 2003., Methods: Two different cohorts of twins (n = 3393 and n = 2813 pairs), both 12-20 years of age, from the Danish Twin Registry, participated in questionnaire studies nine years apart. Prevalence of asthma and resemblance between twins for asthma was compared between the two cohorts., Results: The prevalence of asthma increased from 7.1% in 1994 to 10.8% in 2003, p < 0.001. The change was significant both in males (7.7 vs. 12.4%, p < 0.001); and females (6.6 vs. 9.2%, p < 0.001). The best-fitting model, which included additive genetic and non-shared environmental effects, showed that the heritability of asthma increased significantly from 79% in 1994 to 91% in 2003, p = 0.005., Conclusions: This result could indicate that environmental changes over the past years have increased the expression of genes and thus have lead to a higher heritability in the succeeding cohort. This is consistent with the hypothesis that changes in the environment, particular in childhood, are the cause of the increase in the prevalence of asthma over the past decades., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Background: Respiratory syncytial virus (RSV) bronchiolitis has been associated with later development of asthma, wheezing, abnormal pulmonary function, and sensitization. Our aim was to determine the differential effect within monozygotic (MZ) twin pairs discordant for severe RSV bronchiolitis in infancy on the subsequent development of asthma, pulmonary function, and allergy., Methods: Thirty-seven MZ twin pairs discordant for RSV hospitalization in infancy (mean age 10.6 months) were compared at the mean age of 7.6 years for lung function, bronchial responsiveness, fractional exhaled nitric oxide (Feno), asthma diagnosis, use of asthma medication, and skin prick test to common inhalant allergens., Results: There were no differences within MZ twin pairs discordant for RSV hospitalization in infancy with respect to pulmonary function, Feno, asthma prevalence, asthma medication use, or sensitization (P > .1 for all comparisons)., Conclusions: We found no differential effect from severity of RSV infection on the development of asthma and allergy in MZ twin pairs discordant for RSV hospitalization in infancy. This argues against a specific effect of severe RSV infection in the development of asthma and allergy. Because of the small sample size, this study must be considered as a hypothesis-generating study.

Background: Poor adherence to asthma treatment is a well-recognised challenge and is associated with increased morbidity, mortality and consumption of health care resources. This study examined the impact of receiving a daily text message reminder on one's cell phone on adherence to asthma treatment., Methods: A total of 26 subjects aged 18-45 years, with a clinical history of asthma and a positive methacholine challenge test (PD(20)

Background: The susceptibility to develop hay fever is putatively the result both of genetic and environmental causes. We estimated the significance and magnitude of genetic and environmental contributions to hay fever among young adult twins., Methods: From the birth cohorts 1953-82 of The Danish Twin Registry 11,750 twin pairs were identified through a nationwide questionnaire survey. Subjects were regarded hay fever cases when responding affirmatively to the question 'Do you have, or have you ever had hay fever?' Latent factor models of genetic and environmental effects were fitted to the observed data using maximum likelihood methods., Results: The overall cumulative prevalence of hay fever was 12.6%. Identical twins were significantly more likely to be concordant for hay fever than were fraternal twins (P<0.001). Additive genetic effects accounted for 71% and non-shared environmental effects accounted for 29% of the individual susceptibility to hay fever. The same genes contributed to the susceptibility to hay fever both in males and in females. In families with asthma, the susceptibility to develop hay fever was, in addition to genes, to a great extent ascribable to family environment, whereas the aetiology of 'sporadic' hay fever was mainly genetic., Conclusions: The susceptibility to develop hay fever is attributable to major genetic influences. However, effects of family environment and upbringing are also of importance in families where asthma is present. These results indicate that different sub-forms of hay fever may have different aetiologies.

Respiratory morbidity in Inuit children is high. However, little is know regarding lung function measures in this population. The forced expiratory volumes in one second (FEV(1)) and forced vital capacity (FVC) in 888 Greenlandic Inuits (N=888) and Danes (N=477) aged 6-18 years were compared. Furthermore, associations between level of lung function and atopy and lifestyle factors were estimated in Greenlanders. The effect of height on FEV(1) and FVC was significantly different in Greenlanders and Danes, this difference in lung function increased with increasing height, and could not be explained by differences in age weight and BMI. Thus, Greenlanders taller than 130 cm had up to 300-400 ml higher FEV(1) and FVC compared with Danes of the same height. Among Greenlanders, those living in settlements had the highest levels of both FEV(1) and FVC. Greenlanders had elevated levels of FEV(1) and FVC compared with Danes. The Inuit having a shorter limb length in relation to trunk height may account for these differences. However, our finding that Greenlanders living in settlements had the highest lung function level also suggests a possible role of factors in the traditional Greenlandic lifestyle.