| 1. |
- Cullinan, Paul, et al.
(författare)
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Occupational lung diseases : from old and novel exposures to effective preventive strategies
- 2017
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Ingår i: The Lancet Respiratory Medicine. - 2213-2600 .- 2213-2619. ; 5:5, s. 445-455
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Tidskriftsartikel (refereegranskat)abstract
- Occupational exposure is an important, global cause of respiratory disease. Unlike many other non-communicable lung diseases, the proximal causes of many occupational lung diseases are well understood and they should be amenable to control with use of established and effective approaches. Therefore, the risks arising from exposure to silica and asbestos are well known, as are the means of their prevention. Although the incidence of occupational lung disease has decreased in many countries, in parts of the world undergoing rapid economic transition and population growth-often with large informal and unregulated workforces-occupational exposures continue to impose a heavy burden of disease. The incidence of interstitial and malignant lung diseases remains unacceptably high because control measures are not implemented or exposures arise in novel ways. With the advent of innovative technologies, new threats are continually introduced to the workplace (eg, indium compounds and vicinal diketones). In developed countries, work-related asthma is the commonest occupational lung disease of short latency. Although generic control measures to reduce the risk of developing or exacerbating asthma are well recognised, there is still uncertainty, for example, with regards to the management of workers who develop asthma but remain in the same job. In this Review, we provide recommendations for research, surveillance, and other action for reducing the burden of occupational lung diseases.
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| 2. |
- Moitra, Subhabrata, et al.
(författare)
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Effect of asthma on the development of obesity among adults : Results of the European Community Respiratory Health Survey (ECRHS)
- 2018
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Ingår i: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Introduction: Obesity has been associated with asthma, however the reverse relation has recently been observed among children.Objective: To investigate whether asthma contributes to obesity incidence in adults.Methods: The ECRHS is a cohort study with two follow-ups around, 10-years (ECRHS-II) and 20-years (ECRHS-III) after enrolment. Participants with obesity (BMI>30kg/m2) at baseline were excluded (n=957), leaving 8618 non-obese subjects who participated in at least one follow-up. Asthmatics were described if the subjects reported ever having asthma and had an asthma attack or woke up by an attack of shortness of breath in last 12 months or on current asthma medication. We evaluated the association between: (1) asthma at baseline (ECRHS-I) and obesity at ECRHS-II; and (2) newly reported asthma at ECRHS-II and obesity at ECRHS-III.Results: 10.2% of asthmatics at baseline developed obesity after 10 years compared to 7.7% of non-asthmatics (Age, sex & country-adjusted relative risk: 1.26; 95% confidence interval: 1.03-1.55). Further adjustment for BMI at baseline slightly reduced this risk (RR:1.2; 95%CI: 1.0-1.4). Obesity risk was highest for those developing asthma in adulthood (RR:1.37; 95%CI: 1.01-1.86) compared to those with childhood onset asthma (RR: 1.13; 95%CI: 0.83-1.53). Asthmatics who were non-atopic at baseline had a higher risk of developing obesity at 1st follow up (RR: 1.47; 95%CI: 1.15-1.86). Similar trend was observed in newly reported asthmatics in ECRHS-II and increased obesity risk at the final follow up ECRHS-III (RR: 1.22; 95%CI: 0.86-1.73).Conclusion: These results suggest that asthmatics are at a higher risk of developing obesity.
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| 3. |
- Pyasi, Kanchan, et al.
(författare)
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Evaluating the role of leukotriene-modifying drugs in asthma management : Are their benefits ‘losing in translation’?
- 2016
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Ingår i: Pulmonary Pharmacology and Therapeutics. - : Elsevier BV. - 1094-5539. ; 41, s. 52-59
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Forskningsöversikt (refereegranskat)abstract
- Leukotrienes (LTs) initiate a cascade of reactions that cause bronchoconstriction and inflammation in asthma. LT-modifying drugs have been proved very effective to reduce inflammation and associated exacerbation however despite some illustrious clinical trials the usage of these drugs remains overlooked because the evidence to support their utility in asthma management has been mixed and varied between studies. Although, there are plenty of evidences which suggest that the leukotriene-modifying drugs provide consistent improvement even after just the first oral dose and reduce asthma exacerbations, the beneficial effect of these drugs has remained sparse and widely debated. And these beneficial effects are often overlooked because most of the clinical studies include a mixed population of asthmatics who do not respond to LT-modifiers equally. Therefore, in the present era of personalized medicine, it is important to properly stratify the patients and non-invasive measurements of biomarkers may warrant the possibility to characterize biological/pathological pathway to direct treatment to those who will benefit from it. Endotyping based on individual's leukotriene levels should probably ascertain a subgroup of patients that would clearly benefit from the treatment even though the trial fails to show overall significance. In this article, we have methodically evaluated contemporary literature describing the efficacy of LT-modifying drugs in the management of asthma and highlighted the importance of phenotyping the asthmatics for better treatment outcomes.
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| 4. |
- Stenberg, Henning, et al.
(författare)
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Club cell protein (CC16) in plasma, bronchial brushes, BAL and urine following an inhaled allergen challenge in allergic asthmatics
- 2018
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Ingår i: Biomarkers. - 1354-750X. ; 23:1, s. 51-60
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Tidskriftsartikel (refereegranskat)abstract
- Background: Club cell protein (CC16) is a pneumoprotein secreted by epithelial club cells. CC16 possesses anti-inflammatory properties and is a potential biomarker for airway epithelial damage. We studied the effect of inhaled allergen on pulmonary and systemic CC16 levels. Methods: Thirty-four subjects with allergic asthma underwent an inhaled allergen challenge. Bronchoscopy with bronchoalveolar lavage (BAL) and brushings was performed before and 24 h after the challenge. CC16 was quantified in BAL and CC16 positive cells and CC16 mRNA in bronchial brushings. CC16 was measured in plasma and urine before and repeatedly after the challenge. Thirty subjects performed a mannitol inhalation challenge prior to the allergen challenge. Results: Compared to baseline, CC16 in plasma was significantly increased in all subjects 0–1 h after the allergen challenge, while CC16 in BAL was only increased in subjects without a late allergic response. Levels of CC16 in plasma and in the alveolar fraction of BAL correlated significantly after the challenge. There was no increase in urinary levels of CC16 post-challenge. Mannitol responsiveness was greater in subjects with lower baseline levels of CC16 in plasma. Conclusions: The increase in plasma CC16 following inhaled allergen supports the notion of CC16 as a biomarker of epithelial dysfunction.
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