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Purpose: Idiopathic pulmonary fibrosis (IPF) is a type of interstitial lung disease found mostly in elderly persons, characterized by a high symptom burden and frequent encounters with health services. This study aimed to quantify the economic burden of IPF in Australia with a focus on resource utilization and associated direct costs. Methods: Participants were recruited from the Australian IPF Registry (AIPFR) between August 2018 and December 2019. Data on resource utilization and costs were collected via cost diaries and linked administrative data. Clinical data were collected from the AIPFR. A "bottom up" costing methodology was utilized, and the costing was performed from a partial societal perspective focusing primarily on direct medical and non-medical costs. Costs were standardized to 2021 Australian dollars ($). Results: The average annual total direct costs per person with IPF was $31,655 (95% confidence interval (95% CI): $27,723–$35,757). Extrapolating costs based on prevalence estimates, the total annual costs in Australia are projected to be $299 million (95% CI: $262 million–$338 million). Costs were mainly driven by antifibrotic medication, hospital admissions and medications for comorbidities. Disease severity, comorbidities and antifibrotic medication all had varying impacts on resource utilization and costs. Conclusion: This cost-of-illness study provides the first comprehensive assessment of IPF-related direct costs in Australia, identifies the key cost drivers and provides a framework for future health economic analyses. Additionally, it provided insight into the major cost drivers which include antifibrotic medication, hospital admissions and medications related to comorbidities. Our findings emphasize the importance of the appropriate management of comorbidities in the care of people with IPF as this was one of the main reasons for hospitalizations. [ABSTRACT FROM AUTHOR]

Purpose: Little is known about the impact of co-morbidities on health-related quality of life (HRQoL) for people with idiopathic pulmonary fibrosis (IPF). We aimed to investigate the relative contribution of co-morbidities to HRQoL of people with IPF. Methods: N = 157 participants were recruited from the Australian IPF Registry (AIPFR). Health state utilities (HSUs), and the super-dimensions of physical and psychosocial scores were measured using the Assessment of Quality of Life-8-Dimensions (AQoL-8D). The impact of co-morbidities on HRQoL was investigated using linear regression and general dominance analyses. Results: A higher number of co-morbidities was associated with lower HSUs (p trend = 0.002). Co-morbidities explained 9.1% of the variance of HSUs, 16.0% of physical super-dimensional scores, and 4.2% of psychosocial super-dimensional scores. Arthritis was associated with a significant reduction on HSUs (β = − 0.09, 95% confidence interval [CI] − 0.16 to − 0.02), largely driven by reduced scores on the physical super-dimension (β = − 0.13, 95% CI − 0.20 to − 0.06). Heart diseases were associated with a significant reduction on HSUs (β = − 0.09, 95% CI − 0.16 to − 0.02), driven by reduced scores on physical (β = − 0.09, 95% CI − 0.16 to − 0.02) and psychosocial (β = -0.10, 95% CI − 0.17 to − 0.02) super-dimensions. Conclusions: Co-morbidities significantly impact HRQoL of people with IPF, with markedly negative impacts on their HSUs and physical health. A more holistic approach to the care of people with IPF is important as better management of these co-morbidities could lead to improved HRQoL in people with IPF. [ABSTRACT FROM AUTHOR]

Purpose: Idiopathic pulmonary fibrosis (IPF) is a progressive and debilitating chronic lung disease with a high symptom burden, which has a substantial impact on health-related quality of life (HRQoL). Our study aimed to assess the suitability of the EuroQol five-dimension (EQ-5D-5L) and the Assessment of Quality of Life- eight-dimension (AQoL-8D) questionnaires in measuring HRQoL as health state utility values (HSUVs) in an Australian IPF cohort. Methods: Data for estimation of health state utility values (HSUVs) were collected from participants of the Australian IPF Registry (AIPFR) using self-administered surveys which included the EQ-5D-5L and the AQoL-8D. Data on lung function and disease specific HRQoL instruments were collected from the AIPFR. Performance of the two instruments was evaluated based on questionnaire practicality, agreement between the two instruments and test performance (internal and construct validity). Results: Overall completion rates for the EQ-5D-5L and AQoL-8D were 96% and 85%, respectively. Mean (median) HSUVs were 0.65 (0.70) and 0.69 (0.72) for the EQ-5D-5L and AQoL-8D, respectively. There was reasonable agreement between the two instruments based on the Bland–Altman plot mean difference (−0.04) and intraclass correlation coefficient (0.84), however there were some fundamental differences. A larger range of values was observed with the EQ-5D-5L (−0.57–1.00 vs 0.16–1.00). The EQ-5D-5L had a greater divergent sensitivity and efficacy in relation to assessing HSUVs between clinical groupings. The AQoL-8D ,however, had a higher sensitivity to measure psychosocial aspects of HRQoL in IPF. Conclusion: The EQ-5D-5L demonstrated superior performance when compared to AQoL-8D in persons with IPF. This may be attributable to the high symptom burden which is physically debilitating to which the EQ-5D-5L may be more sensitive. [ABSTRACT FROM AUTHOR]

The chronic respiratory non-communicable diseases, asthma and chronic obstructive pulmonary disease (COPD) are among the leading causes of global mortality and morbidity. Individuals suffering from these diseases are particularly susceptible to respiratory infections caused by bacterial and/or viral pathogens, which frequently result in exacerbation of symptoms, lung function decline, frequent hospital emergency visits and increased socioeconomic burden. Human rhinoviruses (HRV) remain the major viral pathogen group implicated in exacerbations of both asthma and COPD. The rhinoviral entry into the host lung epithelium is facilitated primarily by the adhesion site ("receptor") intercellular adhesion molecule-1 (ICAM-1), coincidentally expressed on the respiratory epithelium in these conditions. Multiple observations of increased airway ICAM-1 protein in asthmatics, smokers and smoking-related COPD have been recorded in the literature. However, the lack of robust therapies for COPD in particular has triggered a renewed interest in assessing receptor antagonism-based anti-viral strategies for treatment of intercurrent viral infections in those with pre-existing chronic lung diseases. Given the crucial role ICAM-1 plays in facilitating HRV adhesion and, thus, transmissibility to the host respiratory system, as well as the up-regulation of ICAM-1 by smoking, we summarize the role of HRV in smoking-induced COPD and especially highlight the role of ICAM-1 in epithelial viral adhesion and chronic lung disease progression. Further, the review also sheds light specifically on evolving precision therapeutic strategies in blocking ICAM-1 for preventing viral adhesion and exacerbations of COPD. [ABSTRACT FROM AUTHOR]

Purpose: Idiopathic pulmonary fibrosis (IPF) is a progressive and universally fatal lung disease, characterised by increasing fibrosis of the lung parenchyma. In this study, we aimed to quantify the health state utility values (HSUVs) for Australians with IPF and to identify the factors affecting these HSUVs. Methods: Participants of the Australian IPF Registry (AIPFR), with data on EuroQoL five dimension—five level (EQ-5D-5L) profiles were included. Pulmonary function tests (PFTs) were used to assess disease severity using three IPF -based classification systems. Stepwise multivariable linear regression models assessed the relationship between HSUVs and important demographic and clinical parameters.Query Results: A total of 155 participants provided data for the analysis of HSUVs. For our base case, HSUVs ranged from − 0.57 to 1.00. Mean HSUVs for all participants was 0.65 (95% CI 0.61–0.70). In general, HSUVs decreased with increasing disease severity under all disease severity classification systems. Multivariable linear regression demonstrated a negative association between HSUVs, disease severity and having more than 2 comorbidities. Conclusions: Our study has shown that EQ-5D-5L has exhibited discriminatory sensitivity for the study population. We have demonstrated that disease severity and having more than two comorbidities was associated with lower HSUVs in Australians with IPF. Our findings support early diagnosis and appropriate evidence-based treatment to slow or prevent IPF progression; and identification and treatment of associated comorbidities to potentially improve health-related quality of life in people with IPF. [ABSTRACT FROM AUTHOR]

Long-acting β2-agonists (LABAs) such as formoterol and salmeterol are used for prolonged bronchodilatation in asthma, usually in combination with inhaled corticosteroids (ICSs). Unexplained paradoxical asthma exacerbations and deaths have been associated with LABAs, particularly when used without ICS. LABAs clearly demonstrate effective bronchodilatation and steroid-sparing activity, but long-term treatment can lead to tolerance of their bronchodilator effects. There are also concerns with regard to the effects of LABAs on bronchial hyperresponsiveness (BHR), where long-term use is associated with increased BHR and loss of bronchoprotection. A complicating factor is that formoterol and salmeterol are both chiral compounds, usually administered as 50:50 racemic (rac-) mixtures of two enantiomers. The chiral nature of these compounds has been largely forgotten in the debate regarding LABA safety and effects on BHR, particularly that (S)-enantiomers of β2-agonists may be deleterious to asthma control. LABAs display enantioselective pharmacokinetics and pharmacodynamics. Biological plausibility of the deleterious effects of β2-agonists (S)-enantiomers is provided by in vitro and in vivo studies from the short-acting β2-agonist (SABA) salbutamol. Supportive clinical findings include the fact that patients in emergency departments who demonstrate a blunted response to salbutamol are more likely to benefit from (R)-salbutamol than rac-salbutamol, and resistance to salbutamol appears to be a contributory mechanism in rapid asthma deaths. More effort should therefore be applied to investigating potential enantiospecific effects of LABAs on safety, specifically bronchoprotection. Safety studies directly assessing the effects of LABA (S)-enantiomers on BHR are long overdue. [ABSTRACT FROM AUTHOR]

The complete correct name should read as follows Dinesh Kumar Chellappan The original article has been corrected. Correction to: Inflammopharmacology (2022) 30:725-735 https://doi.org/10.1007/s10787-022-0096... The 7th author name has been incorrectly published in the original publication. [Extracted from the article]

We have established that EMT is an active process throughout the airway tree in smokers and even more so in airways in COPD. (Comment on: Proliferation Genes Repressed by TGF- Are Downstream of Slug/Snail2 in Normal Bronchial Epithelial Progenitors and are Deregulated in COPD. EMT in basal epithelial cells was first postulated as active in human airways disease in lung transplant recipients as part of the development of Bronchiolitis Obliterans Syndrome (BOS) in chronic lung allograft dysfunction/rejection [[2]]. [Extracted from the article]

Asthma phenotypes based on age-of-onset may be differently influenced by the interaction between variation in toll-like receptor (TLR)/CD14 genes and environmental microbes. We examined the associations between single-nucleotide polymorphisms (SNP) in the TLR/CD14 genes and asthma, and their interaction with proxies of microbial exposure (childhood farm exposure and childhood rural environment). Ten SNPs in four genes (TLR2, TLR4, TLR6, CD14) were genotyped for 1,116 participants from the Tasmanian Longitudinal Health Study (TAHS). Using prospectively collected information, asthma was classified as never, early- (before 13 years) or late-onset (after 13 years). Information on childhood farm exposure/childhood rural environment was collected at baseline. Those with early-onset asthma were more likely to be males, had a family history of allergy and a personal history of childhood atopy. We found significant interaction between TLR6 SNPs and childhood farm exposure. For those with childhood farm exposure, carriers of the TLR6-rs1039559 T-allele (p-interaction = 0.009) and TLR6-rs5743810 C-allele (p-interaction = 0.02) were associated with lower risk of early-onset asthma. We suggest the findings to be interpreted as hypothesis-generating as the interaction effect did not withstand correction for multiple testing. In this large, population-based longitudinal study, we found that the risk of early- and late-onset asthma is differently influenced by the interaction between childhood farming exposure and genetic variations. [ABSTRACT FROM AUTHOR]