Goodpasture's 1919 article on the etiology of influenza-the historical road to what we now call Goodpasture Syndrome.

Ernest W. Goodpasture is known to most physicians from the syndrome that bears his name: rapidly progressive (crescentic) glomerulonephritis and pulmonary hemorrhage due to anti-glomerular basement membrane (GBM) antibodies. The term “Goodpasture’s Syndrome” was first used in 1957 in the title of an article by Stanton and Tange1 out of Melbourne, Australia describing 9 cases of glomerulonephritis with pulmonary hemorrhage. They credit Goodpasture with the discovery of the syndrome in his 1919 article on the etiology of influenza.2 It is amazing that these authors would choose to name this syndrome after Goodpasture because of the clinicopathologic description of the second of 2 patients whom he considered to have died of influenza in an article published 38 years earlier. Collins3 in his excellent book, Earnest William Goodpasture: Scientist, Scholar, Gentleman, suggests that Nobel laureate Sir Macfarlane Burnet (also in Melbourne), an admirer of Goodpasture and his work,4 may have been responsible. Collins goes on to say that Goodpasture himself believed that the use of his name for this syndrome was inappropriate. The eponym, however, stuck. In 1965, Sturgill and Westervelt,5 using the relatively new technique of immunofluorescence, described the linear staining for gamma globulins along the pulmonary and glomerular capillaries in a patient with Goodpasture syndrome. Lerner et al6 in 1967 showed that these anti-GBM antibodies were pathogenic. It was in 1971 that Martinez and Kohler7 recommended that the term Goodpasture’s syndrome be restricted to those patients with pulmonary-renal vasculitic syndrome mediated by antibodies to the GBM. Anti-GBM antibodies are responsible for a minority of cases of vasculitic pulmonary-renal syndrome. Most cases are due to antineutrophil cytoplasmic antibodies (ANCA). Indeed, the histopathologic description of Goodpasture’s second patient is more compatible with ANCA-related disease than with Goodpasture syndrome. The splenic lesions and the intestinal lesions would be unlikely in a case of anti-GBM–mediated disease. Therefore, are we to abandon the use of the term Goodpasture syndrome? Ernest Goodpasture never intended to describe this entity, and the entity he did describe is most likely not what we now call Goodpasture syndrome. The use of eponyms can be problematic and some people actively discourage their use. A particularly striking example of the problem with eponyms is the ongoing controversy concerning the use of the term Wegener granulomatosis for ANCAassociated granulomatous vasculitis (coincidently another cause of pulmonary-renal vasculitis).8 Wegener was a Nazi before and during World War II and may or may not have been involved with atrocities committed during this period. Patients themselves have objected to this eponym.9 Although there is no doubt that Friedrich Wegener described the disease named after him, there is doubt whether the medical community should honor him. In contrast, Ernest Goodpasture, whether or not he described his eponymous syndrome, was a widely respected scientist, educator, and administrator deserving of honor by the medical community. Besides, Goodpasture syndrome is a lot easier to say than “antiglomerular basement membrane-mediated glomerulonephritis and pulmonary capillaritis.”