Pulmonary vasculitis: a clinical overview.

Vasculitides comprise a heterogeneous group of disorders characterized by necrotizing inflammation of blood vessels. Such inflammation may occur as part of a primary disease process or secondary to a variety of disorders. The lungs are frequently involved in both primary and secondary vasculitides. The aim of this review is to provide an overview on lung involvement in primary vasculitides based on articles written in English. While the clinical presentation may be quite unique for individual entities of primary vasculitis, overlapping features are frequently present. It is for this reason that the classification of primary vasculitides presents a challenge. The American College of Rheumatology published criteria for the classification of vasculitis in 1990 [1]. A committee of experts classified seven categories of primary vasculitis based on over 1,000 cases submitted by rheumatologists from 48 centers in the U.S., Canada and Mexico. The objective was to provide diagnostic categories for individual patients, and not the institution of a nomenclature system. An International Consensus Conference that convened in Chapel Hill, North Carolina, addressed this issue [2]. Based on the size of blood vessels involved, the conference adopted definitions for 10 different clinical entities. In our approach to primary vasculitis involving the lung, we adopt the nomenclature proposed by the Chapel Hill Conference with the addition of two entities: isolated pauciimmune pulmonary capillaritis [3] and BehcEet's disease [Table 1]. Pathogenesis There is general consensus about an immunopathogenic mechanism underlying vasculitis. Immune complexes formed in the bloodstream in the presence of antigen excess localize in the blood vessel wall. Increased vascular permeability enables immune complexes to be trapped along the basement membrane of the blood vessel wall, causing activation of complement and accumulation of complement-derived chemotactic factors. The polymorphonuclear neutrophils attracted to the area of immune complex deposition release lysosomal enzymes that damage the blood vessel wall. Neutrophil infiltration leads to fibrinoid necrosis, The acquisition of new information, the integration of newer diagnostic methods, and the use of new therapy have occurred with breathtaking rapidity during the past decade in pulmonology, as it has in medicine in general. In order to keep all of us informed, the periodic appearance of review articles written by authorities in the particular field has proven to be effective. The current article by Drs. Hatipoglu and Rubinstein is the first in a series dealing with pulmonary diseases that will appear in IMAJ. I believe this covers the specific area of pulmonary vasculitides in a comprehensive manner and sets a high standard for the subsequent articles to meet. A personal gift for me is that this first article is co-authored by a former student of mine, Dr. Rubinstein.

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