No correlation was found between the degree of RB/DIP-like changes and pulmonary function parameters, including TLC (r = — 0.22, p = 0.45), Dlco (r = — 0.42, p = 0.13), or FEV1 (r = 0.11, p = 0.71). Although both index patients had restrictive impairment on lung function testing, the extent of RB/DIP-like changes on biopsy did not correlate with the presence or absence of restrictive physiology in the whole group (Table 1). Although smoking is associated with COPD and lung cancer, the link between smoking and certain ILDs is less well recognized. Cigarette smoking causes a variety of nonneoplastic histologic and radiographic changes in the lung (Fig 3). so
In some smokers, combinations of these patterns of injury can be identified in the same individual, as demonstrated in this study (Fig 3). Smoking-related ILD is a term used to describe the relationship between RB-ILD, DIP, and PLCH as interstitial disorders that are etiologically linked to cigarette smoking. Our study provides additional insight into the overlap between these diseases, demonstrating that in biopsy-proven PLCH, coexistent RB/DIP-like abnormalities are ubiquitous, and correlate with the amount of cigarettes consumed. In addition, we demonstrate that in some individuals, the extent of RB/DIP injury on lung biopsy may be very extensive, cause ground-glass attenuation on HRCT, and result in radiographic patterns that are suggestive of alternative diagnoses.
Several descriptive histopathologic studies document the association of nonspecific DIP-like changes in biopsy specimens of patients with PLCH, It is generally accepted that a diagnosis of DIP is made following the systematic exclusion of other lung diseases that may be accompanied by such a DIP-like reaction. Similarly, the discovery of RB on lung biopsy is not equivalent to a diagnosis of RB-ILD. Figure 3. Nonproportional Venn diagram illustrating the spectrum of airways and interstitial injury associated with cigarette smoking. The larger outer circle represents the virtually universal occurrence of RB in smokers. Emphysema will develop in approximately 20% of these smokers during their lifetime. ILD will develop in a small proportion of smokers due to DIP or PLCH. In a significant proportion of those in whom DIP or PLCH develops (or overlaps of both), there is accompanying emphysema (as in the current series). RB-ILD develops when a smoker has an exaggerated RB reaction associated with ILD.