Progressive massive fibrosisprogressive massive fibrosis, progressive massive fibrosis and life expectancy
Progressive Massive Fibrosis PMF, characterized by the development of large conglomerate masses of dense fibrosis usually in the upper lung zones, can complicate silicosis1 and coal worker's pneumoconiosis2 Conglomerate masses may also occur in other pneumoconioses, such as talcosis,3 berylliosis CBD,3 kaolin pneumoconiosis,4 and pneumoconiosis from carbon compounds,4 such as carbon black, graphite, and oil shale Conglomerate masses can also develop in sarcoidosis,5 but usually near the hilae and with surrounding paracitricial emphysema
The disease arises firstly through the deposition of silica or coal dust or other dust within the lung, and then through the body's immunological reactions to the dust
According to the International Labour Office ILO, PMF requires the presence of large opacity exceeding 1 cm by x-ray By pathology standards, the lesion in histologic section must exceed 2 cm to meet the definition of PMF6 In PMF, lesions most commonly occupy the upper lung zone, and are usually bilateral The development of PMF is usually associated with a restrictive ventilatory defect on pulmonary function testing PMF can be mistaken for bronchogenic carcinoma and vice versa PMF lesions tend to grow very slowly, so any rapid changes in size, or development of cavitation, should prompt a search for either alternative cause or secondary disease
Pathogenesis and causesedit
The pathogenesis of PMF is complicated, but involves two main routes - an immunological route, and a mechanical route
Immunologically, disease is caused primarily through the activity of lung macrophages, which phagocytose dust particles after their deposition These macrophages seek to eliminate the dust particle through either the mucociliary mechanism, or through lymphatic vessels which drain the lungs Macrophages also produce an inflammatory mediator known as interleukin-1 IL-1, which is part of the immune systems first line defenses against infecting particles IL-1 is responsible for 'activation' of local vasculature, causing endothelial cells to express certain cell adhesion molecules, which help the cells of the bodies immune system to migrate into tissues Macrophages exposed to dust have been shown to have markedly decreased chemotaxis Production of inflammatory mediators - and the tissue damage that ensues as an effect of this, as well as reduced motility of cells, is fundamental to the pathogenesis of pneumoconiosis and the accompanying inflammation, fibrosis, and emphysema
There are also some mechanical factors involved in the pathogenesis of Complex Pneumoconiosis that should be considered The most notable indications are the fact that the disease tends to develop in the upper lobe of the lung - especially on the right, and its common occurrence in taller individuals
- ^ Ziskind M, Jones RN and Weill H Silicosis: State of the Art Am Rev Resp Dis, 1976;113:643-665
- ^ Hurley JF, Alexander WP, Hazledine DJ, Jacobsen M, Maclaren WM October 1987 "Exposure to respirable coalmine dust and incidence of progressive massive fibrosis" British journal of industrial medicine 44 10: 661–72 PMC 1007898 PMID 3676119 doi:101136/oem4410661
- ^ a b Chong S et al Pneumoconiosis: Comparison of Imaging and Pathologic Findings RadioGraphics, 2006;26:59-77
- ^ a b Glazer CS and Newman LS Occupational Interstitial Lung Disease Clinics Chest Med, 2004;25:467-478
- ^ Pipavath S and Godwin JD Imaging of Interstitial Lung Disease Clinics Chest Med, 2004;25:455-465
- ^ Craighead JE et al Diseases Associated with Exposure to Silica and Nonfibrous Silicate Minerals Arch Pathol Lab Med, 1988;112:673-720
Occupational Lung Diseases, 3rd Edition, Morgan and Seaton http://pimmedicinedalca/il1htm
|Lower RT/lung disease
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