Asbestos-related bilateral diffuse pleural thickening: natural history of radiographic and lung function abnormalities.

We evaluated whether restrictive lung function among asbestos-exposed individuals with pleural fibrosis was caused by radiographically inapparent parenchymal inflammation and/or parenchymal fibrosis. All 24 study participants were sheet metal workers who were nonsmokers with normal parenchyma on posteroanterior chest radiograph. These subjects had either normal pleura (n = 7), circumscribed plaques (n = 9), or diffuse pleural thickening (n = 8). After controlling for age, years in the trade, and pack-years of smoking, we found that sheet metal workers with diffuse pleural thickening had a lower forced vital capacity (P less than 0.001), total lung capacity (P less than 0.01), and CO-diffusing capacity of the lung (P less than 0.05) than those with normal pleura. Similarly, sheet metal workers with circumscribed plaques were found to have a reduced forced vital capacity; however, because of the small number of study subjects, this difference (regression coefficient = -11.0) was only marginally significant (P = 0.06). Although circumscribed plaque and diffuse pleural thickening were both associated with a lymphocytic alveolitis and a higher prevalence of parenchymal fibrosis on high-resolution computerized tomography (HRCT) scan, neither a lymphocytic alveolitis nor the finding of parenchymal fibrosis on HRCT scan influenced the relationship between pleural fibrosis and restrictive lung function. We conclude that pleural fibrosis is associated with restrictive lung function and abnormally low diffusion that appears to be independent of our measures of parenchymal injury (chest X-ray, bronchoalveolar lavage, and HRCT scan).(ABSTRACT TRUNCATED AT 250 WORDS)

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Natural history of pleural thickening after exposure to crocidolite.

Occupational and Environmental Medicine ◽

10.1136/oem.46.7.461 ◽

1989 ◽

Vol 46 (7) ◽

pp. 461-467 ◽

Cited By ~ 1

Author(s):

N H de Klerk ◽

W O Cookson ◽

A W Musk ◽

B K Armstrong ◽

J J Glancy

Keyword(s):

Natural History ◽

Pleural Thickening ◽

History Of

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Investigating the Natural History of Lung Function

CHEST Journal ◽

10.1378/chest.08-1750 ◽

2009 ◽

Vol 135 (5) ◽

pp. 1330-1341 ◽

Cited By ~ 20

Author(s):

Robab Kohansal ◽

Joan B. Soriano ◽

Alvar Agusti

Keyword(s):

Lung Function ◽

Natural History ◽

History Of

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Development and validation of the Evaluation Platform In COPD (EPIC): a population-based outcomes model of COPD for Canada

10.1101/401745 ◽

2018 ◽

Author(s):

Mohsen Sadatsafavi ◽

Shahzad Ghanbarian ◽

Amin Adibi ◽

Kate Johnson ◽

J Mark FitzGerald ◽

...

Keyword(s):

Risk Factors ◽

Lung Function ◽

Natural History ◽

External Validation ◽

Population Based ◽

Source Population ◽

Occupational Risk Factors ◽

Open Population ◽

History Of ◽

Evaluation Platform

AbstractBackgroundWe report the development, validation, and implementation of an open-source population-based outcomes model of Chronic Obstructive Pulmonary Disease (COPD) for Canada.MethodsEvaluation Platform in COPD (EPIC) is a discrete event simulation model of Canadians 40 years of age or older. Three core features of EPIC are its open-population design (incorporating projections of future population growth, aging, and smoking trends), its incorporation of heterogeneity in lung function decline and burden of exacerbations, and its modeling of the natural history of COPD from inception. Multiple original data analyses, as well as values reported in the literature, were used to populate the model. Extensive face validity as well as internal and external validity evaluations were performed.ResultsThe model was internally validated on demographic projections, mortality rates, lung function trajectories, COPD exacerbations, and stability of COPD prevalence over time within strata of risk factors. In external validation, it moderately overestimated rate of overall exacerbations in two independent trials, but generated consistent estimates of rate of severe exacerbations and mortality.LimitationsIn its current version, EPIC does not consider uncertainty in the evidence. Several components such as additional (e.g., environmental and occupational) risk factors, treatment, symptoms, and comorbidity will have to be added in future iterations.ConclusionsEPIC is the first multi-purpose outcome- and policy-focused model of COPD for Canada. By modeling the natural history of COPD from its inception, it is capable of modeling the outcomes of decisions across the entire care pathway of COPD. Platforms of this type have the capacity to be iteratively updated to incorporate the latest evidence and to project the outcomes of many different scenarios within a consistent framework.

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Infantile Lobar Hyperinflation: Expectant Treatment

PEDIATRICS ◽

10.1542/peds.59.6.1012 ◽

1977 ◽

Vol 59 (6) ◽

pp. 1012-1018

Author(s):

Daniel C. Shannon ◽

I. David Todres ◽

Fergus M. B. Moylan

Keyword(s):

Lung Function ◽

Natural History ◽

Distress Syndrome ◽

Blood Gases ◽

Arterial Blood Gases ◽

Expectant Treatment ◽

Arterial Blood ◽

Regional Lung Function ◽

Regional Lung ◽

History Of

Arterial blood gases and regional lung function, measured with a 133xenon technique, were used to evaluate the physiological defects and follow the natural history of 16 infants with lobar hyperinflation ("emphysema"). Hypoxemia was due to V/Q inequality at rest. Worsening of hypoxemia (mean PaO2 Δ -26 mm Hg) with crying was due to shunting as a consequence of cessation of ventilation in the involved lobe. Surgery was necessary in three patients. Two deaths were caused by bronchopulmonary dysplasia after respiratory distress syndrome (RDS). In 12 of 14 infants, lung function was normal between the ages of 5 days and 1 year.

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Diffuse pleural thickening in asbestos workers: disability and lung function abnormalities.

Thorax ◽

10.1136/thx.39.8.604 ◽

1984 ◽

Vol 39 (8) ◽

pp. 604-607 ◽

Cited By ~ 47

Author(s):

C R McGavin ◽

G Sheers

Keyword(s):

Lung Function ◽

Pleural Thickening ◽

Diffuse Pleural Thickening

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Natural history of systemic sclerosis–related interstitial lung disease: How to identify a progressive fibrosing phenotype

Journal of Scleroderma and Related Disorders ◽

10.1177/2397198319889549 ◽

2019 ◽

Vol 5 (2_suppl) ◽

pp. 31-40 ◽

Cited By ~ 5

Author(s):

Elizabeth R Volkmann

Keyword(s):

Systemic Sclerosis ◽

Interstitial Lung Disease ◽

Lung Function ◽

Natural History ◽

Lung Disease ◽

Disease Progression ◽

Rapid Progression ◽

History Of ◽

Rate Of Decline ◽

Patients Experience

The natural history of interstitial lung disease in patients with systemic sclerosis is highly variable. Historical observational studies have demonstrated that the greatest decline in lung function in systemic sclerosis occurs early in the course of the disease; however, not all patients experience a decline in lung function even in the absence of treatment. Furthermore, among patients who do experience a decline in lung function, the rate of decline can be either rapid or slow. The most common clinical phenotypes of systemic sclerosis–related interstitial lung disease are, therefore, as follows: (1) rapid progressors, (2) gradual progressors, (3) stabilizers, and (4) improvers. This review summarizes the features of systemic sclerosis–related interstitial lung disease patients who are more likely to experience rapid progression of interstitial lung disease, as well as those who are more likely not to experience interstitial lung disease progression. Understanding the clinical, biological, and radiographic factors that consistently predict interstitial lung disease–related outcomes in systemic sclerosis is central to our ability to recognize those patients who are at heightened risk for interstitial lung disease progression. With new options available for treating patients with systemic sclerosis–related interstitial lung disease, it is more important than ever to accurately identify patients who may derive the most benefit from aggressive systemic sclerosis–related interstitial lung disease therapy. Early therapeutic intervention in patients with this progressive fibrosing phenotype may ultimately improve morbidity and mortality outcomes in patients with systemic sclerosis–related interstitial lung disease.

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