Diffuse interstitial fibrosis

Katjalainen A, Anttila S, Heikkila L. 1993b. Ix)be of origin of lung cancer among asbestos-exposed patients with or without diffuse interstitial fibrosis. Scand J Work Environ Health 19(4) 102-107. 

Figure 9-8 is the chest radiograph of a 60-year-old male 8 hours postexposure to HC it shows diffuse, dense, peripheral pulmonary infiltrates. The patient presented with moderately severe resting dyspnea and diffuse coarse crackles on auscultation. Taken 14 weeks postexposure, Figure 9-9 is a section from an open lung biopsy from the same patient. Diffuse interstitial fibrosis with inflammatory cells are evident. This patient presented with a persistent, moderate resting dyspnea. At this point, the patient had not been treated with steroids. 

Fig. 9-9. A section from an open lung biopsy of the patient whose chest radiograph is shown in Figure 9-8, 14 weeks postexposure to zinc oxide (HC). He had persistent moderate dyspnea at rest and a Po2 of 61 mm Hg breathing room air. Steroids had not been used. The section shows diffuse interstitial fibrosis with few inflammatory cells. Hematoxylin and eosin stain original magnification x 400.

Diffuse interstitial fibrosis-type nonasbestos pneumoconiosis had an exceedingly high concurrence of lung cancers when compared with pneumoconiosis without diffuse interstitial fibrosis (Ka-TABAMi etal. 2000). Squamous cell carcinomas of... 

Hamman L, Rich AR. Fulminating diffuse interstitial fibrosis of the lungs. Trans Am Clin Climat Assoc 1935 51(1) 154-163. 

Progressive massive fibrosis Diffuse interstitial fibrosis Pleural fibrosis... 

Microscopic diagnosis of asbestosis requires (a) diffuse interstitial fibrosis and (b) the presence of asbestos bodies in ordinary 5-pm paraffin sections (Hourihane and McCaughey 1966 Hinson et al. 1973 Craighead et al. 1982 Churg and Green 1998). Early asbestosis starts around the respiratory bronchioles and spreads through the interstitium from bron-... 

Fig. 2.1.17. Autopsy lung showing asbestosis (diffuse interstitial fibrosis) in the lower zones, along with a large lung cancer (arrow). The presence of asbestosis allows one to attribute the lung cancer to asbestos exposure. From Churg and Green (1998), used with permission...

Fig. 2.1.18. Microscopic view of a case of relatively mild asbestosis. Note the pattern ofpaucicellular diffuse interstitial fibrosis. Asbestos bodies cannot be seen at this low magnification...

Fig. 2.1.19. Asbestos bodies from another case of asbestosis. Both diffuse interstitial fibrosis and asbestos bodies are required for the pathological diagnosis of asbestosis...

As is true of most forms of diffuse interstitial fibrosis (ATS/ERS 2002), transbronchial biopsies are totally unsuitable for diagnosing asbestosis. At a minimum, a large open or thoracoscopic biopsy is required. 

Traditionally, chest radiographic features of diffuse interstitial fibrosis have been regarded as crucial for the diagnosis of asbestosis (American Thoracic Society 1986 Weill 1987). Characteristically, a bilateral basal reticulonodular pattern is seen (Parkes 1994). Small irregular opacities, which may differ in size, are seen in early disease and are denoted by the symbols s, t and u of the International Labour Office (ILO) classification (International Labour Office 2002) (Fig. 7.1a,b), although mixed irregular and rounded opacities are sometimes... 

Although exposure to aluminum metal and its oxides in the workplace is very common, pneumoconioses attributable to these agents are rare. In early studies, pulmonary fibrosis in relation to aluminum exposure has been reported almost exclusively in workers involved in bauxite smelting (Shaver s disease) (Shaver andRiDDELL 1947 Wyatt and Riddell 1948) or in those exposed to finely divided aluminum powders, especially of the flake variety (pyro powder), in the fireworks and explosives industry (Mitchell et al. 1961 Jordan 1961). Subsequently, diffuse interstitial fibrosis has been reported in workers making aluminum oxide abrasives (Bellot et al. 1984 Jederlinic et al. 1990) and in aluminum arc welders (Vallyathan et al. 1982 Herbert etal. 1982). 

Pneumocystis pneumonia occurs in patients with congenital or acquired immunodeficiency, for instance transplant patients and others who are receiving immunosuppressive therapy. Not infrequently, Pneumocystis pneumonia coexists with other pulmonary infections. The infection may be diffuse or focal, with a propensity to affect the lower lobes. In contrast with several other forms of pneumonia, there is no fibrinous pleurisy. The alveolar septa are increased in thickness and infiltrated with plasma cells and lymphocytes. The characteristic feature is the intra-alveolar exudate. This is foamy and strongly periodic acid-Schiff (PAS) positive, being composed of parasitic cysts. An intra-alveolar eellular reaction to the exudate is absent, and a few areas of hyaline membrane formation may be found. The diagnosis may be obtained by lung biopsy material. The organism may also be seen in sputum. In some instances, diffuse interstitial fibrosis may be the end result. 

Fibrosis of the walls of small airways and diffuse interstitial fibrosis are both associated with particle exposure. Several different mechanisms are probably operative. There is some evidence that exposure to asbestos and possibly other types of mineral particles causes increased permeability of the epithelium to small molecules (33) this process may allow particle-evoked, alveolar macrophage-derived growth factors and other cytokines to reach interstitial fibroblasts (30). The mechanism of increased permeability is disputed, with data extant that both support and deny a role for AOS (34,35). 

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