Sarcoidosis and Wegener's granulomatosis (WG) share membership in the
family of granulomatous diseases. Both are systemic processes that hav
e major expressions in common sites, such as the respiratory tract, ki
dneys, skin, nervous system, eye and orbit, musculoskeletal system, an
d heart. In spite of these common features, they are sharply divergent
in clinical course and pathology, sarcoidosis being a more benign, in
dolent disease of low mortality, in contrast to the highly lethal more
dramatic course of WG. Both entities respond to glucocorticoids, but
WG frequently requires cytotoxic agents such as cyclophosphamide. The
current concepts of pathogenesis suggest sarcoidosis to involve mainly
T-cell mediated mechanisms, whereas in the case of WG the presence of
antineutrophil cytoplasmic autoantibodies (ANCA) points toward humera
l mechanisms, although T-cells may also be involved.