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Rheumatology Advance Access originally published online on August 18, 2006
Rheumatology 2006 45(11):1328-1330; doi:10.1093/rheumatology/kel259
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


EDITORIALS

Eponymophilia in rheumatology

E. L. Matteson and A. Woywodt1

Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, MN, USA and 1Division of Nephrology, Hannover Medical School, Hannover, Germany

Correspondence to: Eric L. Matteson, Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. E-mail: matteson.eric{at}mayo.edu

An eponym is the name of a drug structure or a disease based on or derived from the name of a person. Eponyms are widely used in medicine to denote both specific disease states and to honour those who discovered, described or best characterized them. Despite the attempts of some editors and medical schools to rationalize medical terminology and expunge many eponyms, eponymophilia lives on, mainly for reasons of convenience and, as many medical students suspect, to serve as a means by which one can either shine on rounds or be shamed by not knowing an eponym important to the consultant.

The enthusiasm for particular eponyms has waxed and waned over time. Increasing medical knowledge and changes in classification have made some of them obsolete while new eponyms continue to appear. Political events have influenced the use of some eponyms while others just fell out of fashion. A few examples of eponyms’ use and abuse in rheumatology will serve to make the point that eponyms are often misapplied and falsely attributed. Some of them tend to excessively honour the eponymee while others appear quite simply arcane. Some eponyms are tendential and fraught with political or even jingoistic context. To make matters more complicated, eponyms are inconsistently applied across regions, countries and medical specialties, and some diseases have been linked to more than one name.

Despite best efforts to categorize them, there are, in fact, an unknown number of eponyms used in medicine. Many books in numerous languages list eponyms, some of which are very scholarly and give the student an insight into the person they seek to honour. Current English language books include Marcucci's Handbook of Medical Eponyms [1], Medical Acronyms, Eponyms, Mnemonics [2], Medical Acronyms, Eponyms, and Abbreviations [3] and the very learned Dictionary of Medical Eponyms by Ferkin and Whitworth [4]. In the web site, ‘whonamedit.com’, an effort is being made to catalogue more than 15 000 eponyms and more than 6000 persons. This effort currently stands at 7588 eponyms linked to 30 015 persons, with a distinctly male bias, as only 105 of the eponyms are linked to females.

In many cases, overlapping eponyms are used in different countries to honour the native son. Sometimes, these eponyms are strung together with rather unwieldy results. Ankylosing spondylitis is known variably as Bekhterev's syndrome, Bekhterev-Strümpell-Marie disease, Marie's disease, Marie–Strümpell arthritis, Pierre–Marie's disease, Pierre–Marie's syndrome and so on. Still worse, different ways of spelling add another level of complexity. In Germany, for instance, the disease is referred to as Bechterew's disease. The agreed upon general term, ‘ankylosing spondylitis’, when compared with these eponyms, represents a more concise and universally understandable description of the disease without the confusion of the eponym (or the many arcane synonyms such as spondylitis atrophica ligamentosa, spondylitis deformans, rheumatismal ossifying pelvospondylitis and rheumatoid spondylitis, which have been used to describe it).

A related disorder highlights both the problem of ‘first’ description and a damning social context. There is no consensus about the designation of a type reactive arthritis widely referred to as Reiter's disease in the British literature and generally as Reiter's syndrome in the American, with much inconsistency. Prominent authors such as Wright and Moll [5] used the term, ‘Reiter's disease’ in accordance with the designation of the Royal Committee on the Nomenclature of Diseases of the Royal College of Physicians of London. It has been suggested that the unwieldy designation of ‘syndrome of Stoll, Brodie, Fiessinger and LeRoy’ could justifiably (and somewhat tongue-in-cheek, given its unwieldy nature) be used instead, as these authors certainly describe the condition before Reiter [6]. However, it is the eponym ‘Reiter's disease’ or syndrome, which has prevailed.

Hans Conrad Julius Reiter [7] was born in 1881 in Leipzig, trained in medicine and, during the first World War, described the condition now named for him (an English translation appears in reference [5]. Reiter was an early convert to the Nazi Party, joining on August 31, 1931. He worked as the minister of hygiene in the District of Mecklenburg/Lübeck and was then the director of the Ministry of Hygiene and subsequently directed the Reichsgesundheitsamt (Department of Health). After 1933, he became the president of the German Health Ministry and, in this role, had direct oversight and complicity in the abusive activities of the Nazi Racial Hygiene Program. It has been appropriately, and with some success, suggested that his name be dropped as an eponym, an effort likely to be promoted by better understanding of the full spectrum of diseases termed ‘reactive arthritis’ [8]. The use of the eponym has declined, although no consensus has been achieved to abandon it altogether [9]. In Germany, the eponym became almost extinct after the publication of Wallace and Weisman [8], but to some extent is still in use elsewhere.

Three other examples serve to underscore that eponyms can, at times, be tendential, political or even nationalistic. One particularly egregious example is the introduction of the term ‘Takayasu arteritis’, to describe the inflammatory large vessel disease, which had been recognized by numerous physicians well before the time of Takayasu including Morgnani in 1761, Davy in 1839 and Savory in 1856 [10–12]. Makito Takayasu [13] presented the case of a young woman with retinal artery changes in the 12th Annual Meeting of the Japanese Society of Ophthalmology in 1908. It is apparent from Takayasu's description that he did not even recognize the peripheral artery changes of the disease [14]. Nevertheless, by 1941, Yasuvo Niimi [15] suggested that Takayasu be honoured by naming the disease for him, something that certainly must be seen in the context of the political climate at the time, at the height of Japanese imperial expansionism at the dawn of World War II.

A second example is that of Behçet's disease. In 1937, the Turkish dermatologist Hulusi Behçet [16] described in German two cases of patients with eye and ulcer features which characterize this condition. The condition was clearly described earlier, perhaps by Hippocrates as well as a number of other authors prior to Behçet, including Planner, Shigeta, Whitwell, and most particularly by Benedictos Adamantiades in 1931 [17, 18]. An English translation of the works of Adamantiades and Behçet may be found in reference [18]. The context of the debate about whose name, or even combination of names as often used in Europe, should be used was certainly fuelled by the just ended expulsion of the ethnic Greek population from Asia Minor by the Turks in the early 1920s. Indeed, Adamantiades himself was born in present day Bursa, Turkey [18].

A third eponym deriving from the period prior to World War II is that of ‘Wegener's granulomatosis’ [19]. Friedrich Wegener was an early member of the Nazi brownshirts and his mentor, Martin Staemmler, was an ardent supporter of the Nazi Racial Hygiene Program. At present, there is no direct evidence that Wegener participated in any way in war crimes, although he appears on a wanted list by the Polish Ministry for the Interior, which also transferred his file to the United Nations War Crimes Commission [20]. The condition described and reported by Wegener in 1936 had been described previously by others including Heinz Klinger [21], who had been Wegener's college roommate and reported on this disease entity in 1931. Interestingly, Wegener [22] himself did not refer to the disease as ‘Wegener's granulomatosis’, but, at most, referred to it as the ‘so-called Wegener's granulomatosis’, suggesting a certain personal distance to the designation.

At somewhat the opposite end of the eponymophilic spectrum is giant cell arteritis, which may have been described in Bagdad by Ali ibn Isa [23] around 1000 A.D. but certainly was credibly reported by the English physician, Jonathan Hutchinson [24] in 1890 as a ‘...’ peculiar form of thrombotic arteritis of the aged which is sometimes productive of gangrene’. It remained for Horton et al. [25] at Mayo Clinic to better characterize this disease both clinically and histopathologically, beginning in 1932. These authors were unaware of Hutchinson's previous work. The eponym ‘Horton's disease’ did not catch on in the United States, and is virtually unknown among many even at Mayo Clinic although it became widely used in other parts of the world; in France, it continues to be known as the ‘maladie de Horton’ and German physicians refer to it as ‘Morbus Horton’.

Despite the historical inaccuracies and confusion of eponymic usage, even in rheumatology, their creation and use continues to be enthusiastically propagated in some quarters. A recent example is the attempt to introduce antiphospholipid antibody syndrome as ‘Hughes syndrome’ by students of Graham Hughes [26]. Doubtless, Hughes deserves recognition for his comprehensive description of the antiphospholipid syndrome. In the early and mid-1980s, Hughes and his group crystallized the clinical features and relationship of antiphospholipid antibody syndrome to lupus erythematosus based on extensive observations and investigations [27, 28]. However, this work did not occur in a vacuum and was contributed to by not only many co-workers but was preceded by important observations dating back to even 20 years before; for example, that of Bowie et al. [29] at Mayo Clinic and many others who contributed important clinical observations as well as laboratory work which led to the elucidation of this syndrome. While an honour to one investigator, introduction of such an eponym is arcane and a disservice to the medical community and the work of many who have contributed to the understanding of this as well as many other diseases both in and outside the field of rheumatology.

Some may argue that the eponyms are a convenient short cut; for example, even the term ‘Reiter's syndrome’ is pleomorphic, and better and more appropriate terminology including specific descriptions of reactive arthritis must be used. Along the same line, the eponym ‘Wegener's granulomatosis’ should be replaced by a more suitable descriptor, such as ANCA-associated granulomatous vasculitis. Improved classification may be desirable and the new term should be better capable of characterizing a condition that is ‘limited’ in some and systemic in others.

Some eponyms will certainly be difficult to replace, but better understanding of the pathophysiology of diseases and proper appreciation of the work of many investigators who have contributed to advancing medical science provide an overwhelming rationale for discontinuing their use. This is not a question of fastidiousness, but a recognition of the need for terms of universality, consistency and perhaps even a reflection of changing the practice of medicine with emphasis on its scientific foundations. In papers on medical history and reviews, we can still refer to people, acknowledge their respective contributions and describe the historical or even political context of their work. It is our duty to keep medical practice free of political, tendential or jingoistic context. Consider, for instance, someone who lost relatives during the genocide. What will he or she think of our profession if we label him or her with an eponym, such as ‘Reiter's syndrome’ or ‘Wegener's granulomatosis’?

Because of the extensive use of English as an international language of medicine, English language publications have a particular responsibility to eliminate eponym use and standardize medical terminology. It is time to leave eponyms behind and confine them to their deserved places in the archives of medical history.

References

  1. Marcucci L. (2002) Marcucci's Handbook of Medical Eponyms(Lippincott Williams & Wilkins, Philadelphia).
  2. Jones KN. (1999) Medical Acronyms, Eponyms, Mnemonics(Wysteria Publishers, Bellmore, New York).
  3. Belong MF. (2002) Medical Acronyms, Eponyms, and Abbreviations(Practice Management Information Corporation, Los Angeles).
  4. Ferkin BG and Whitworth JA. (2001) Dictionary of Medical Eponyms 2nd Lancaster UK Parthenon Publishing Group Ltd.
  5. Wright V and Moll JMH. (1976) Seronegative Polyarthritis(North Holland Publishing Company, Amsterdam) pp. 237–69.
  6. Iglesias-Gammara A, Restrepo JF, Valle R, Matteson EL. (2005) A brief history of Stoll–Brodie–Fiessinger–LeRoy syndrome (Reiter's Syndrome) and reactive arthritis. Cur Rheumatol Rev 1:71–9.
  7. Reiter H. (1916) Über eine bisher unerknnte Spirochäteninfektion (Spirochaetosis Arthritica). Dtsch med Wchschr 42:1535–6.
  8. Wallace DJ and Weisman MH. (2000) Should a war criminal be awarded with eponyms? The double-life of Hans Reiter (1881–1969). J Clin Rheumatol 6:49–54.
  9. Lu DW and Katz KA. (2005) Declining use of the eponym "Reiter's syndrome" in the medical literature, 1998–2003. J Am Acad Dermatol 53:720–3.[CrossRef][Web of Science][Medline]
  10. Morgnani GB. (1761) De sedibus, et causis morborum per anatomen indagatis(Remondiniana, Venetia) Vol. 5:.
  11. Davy J. (1839) Researches, physiological and anatomical(Smith, Elder and Company, London).
  12. Savory WS. (1856) Case of a young woman in whom the main arteries of both upper extremities and of the left side of the neck were throughout completely obliterated. Med Chir Tr 39:205–19.
  13. Takayasu M. (1908) Case with unusual changes of the central vessels in the retina. Acta Soc Ophthalmol Jpn 12:554–5.
  14. Judge RD, Currier RD, Gracie WA, Figley MM. (1962) Takayasu's arteritis and the aortic arch syndrome. Am J Med 32:379–92.[CrossRef][Web of Science][Medline]
  15. Niimi Y. (1941) A case of Dr. Takayasu's disease. J Gen Ophthalmol 35:1404–5.
  16. Behçet H. (1937) Über rezidivierende, aphthöse, durch ein Virus verursachte Geschwüre am Mund, am Auge und an den Genitalien. Dermat Wchnschr 105:1152–7.
  17. Adamantiades B. (1931) Sur un cas d’iritis a hypopion récidivant. Ann Ocul 168:271–8.
  18. Matteson EL and Calamia KT. (2002) Behçet's Disease(Mayo Foundation for Medical Education and Research, Rochester, MN).
  19. Wegener F. (1936) Über generalizierte, septische Gefässserkrankungen. Verh deut Pathol Ges 29:202–10.
  20. Woywodt A, Haubitz M, Haller H, Matteson EL. (2006) Wegener's granulomatosis. Lancet 367:1362–6.[CrossRef][Web of Science][Medline]
  21. Klinger H. (1931) Grenzformen der Periarteriitis nodosa. Frankfurt Ztschr Pathol 42:455–80.
  22. Wegener F. (1967) Die pneumogene allgemeine Granulomatose - sog. Wegenersche Granulomatose. In Staemmler M and Kaufman E (Eds.). Lehrbuch der speziellen pathologischen Anatomie(De Gruyter, Berlin) vol. 1:Suppl, pp. 225–99.
  23. Isa AI. (1936) Tadhkirat. In Wood CA (Ed.). Memorandum Book of a Tenth-Century Oculist for the Use of Modern Ophthalmologists(Northwestern University Press, Chicago) pp. 225–6.
  24. Hutchinson J. (1890) On a peculiar form of thrombotic arteritis of the aged which is sometimes productive of gangrene. Arch Surg 1:323–9.
  25. Horton BT, Magath TB, Brown GE. (1932) Undescribed form of arteritis of temporal vessels. Proc Staff Meet Mayo Clin 7:700–1.
  26. Khamashta MA. (2000) Hughes Syndrome, Antiphospholipid Syndrome(Springer-Verlag, London).
  27. Hughes GRV. (1984) The Prosser-White oration 1983: Connective tissue disease and the skin. Clin Exp Dermatol 9:535–44.[CrossRef][Web of Science][Medline]
  28. Hughes GRV. (1983) Thrombosis, abortion, cerebral disease, and the lupus anticoagulant. Br Med J 287:1088–9.[Free Full Text]
  29. Bowie EJW, Thompson JH Jr, Pascuzzi CV, Owen CA. (1963) Thrombosis in systemic lupus erythematosus despite circulating anticoagulant. J Lab Clin Med 62:416–30.[Web of Science][Medline]

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