In 1770, Dr. Ezekiel Hersey, a wealthy physician practicing in Hingham, Mass., bequeathed £1,000 to Harvard College for the support of a Professor of Anatomy and Physic. This would become the university’s first endowed chair in the medical sciences. However, it was 12 years before Harvard acted on Hersey’s bequest to establish a professorship and build a medical school. This delay was due to the insufficient funding of the initial endowment and the monetary inflation created by the American Revolutionary War, which eroded Harvard’s finances. Eventually, other Hersey family members pledged support, and the professorship was established. More than two centuries later, this august epithet continues to be bestowed upon the incumbent physician-in-chief at my hospital. How quaint! I find this title amusing, befitting an alchemist or anatomist, but not a physician scientist. After all, the term physic conjures up images of William Shakespeare’s King Lear, reciting: “Take physic, pomp. Expose thyself to feel what wretches feel.” Even the venerable Oxford English Dictionary considers physic, whose origins date to the late Middle English era, nearly obsolete. Yet in the rarified halls of academia, where tradition trumps the trendy, physic lives on.
For many years, the ACR had taken a similar line of reasoning with its use of the antediluvian term, rheumatism. Since its inception in 1958, our flagship publication, Arthritis & Rheumatism (A&R), had sported this word on its masthead. Over the centuries, physicians and patients alike have used it to characterize an exceedingly vague array of aches and pains. Unlike beauty, rheumatism is not in the eye of the beholder. Is it a serious ache or a transient pain of little consequence? Though the lack of any corresponding physical signs should have, in theory, limited its utility in clinical practice, this was hardly the case. To paraphrase Macbeth, rheumatism is a word full of sound and fury, signifying nothing.
I once saw a patient who, on the advice of his general practitioner in London, had been told to consume several grams of aspirin daily to treat his rheumatism. Years later, following his first leg amputation, his medical team wanted some insight as to why the arteries in his amputated extremity showed the classical histopathologic features of giant cell arteritis.1 A few months later, he lost his other leg to the same disease. Were his longstanding complaints of rheumatism obscuring an undetected case of polymyalgia rheumatica (PMR)? Would timely corticosteroid therapy to treat PMR have prevented this tragic outcome? As is often the case, rendering a diagnosis of rheumatism enables the practitioner to falsely claim insight and knowledge about a condition, to briefly commiserate with the patient, and then to shoo them away. This approach may be only marginally better than Sir William Osler’s advice for physicians to exit through the back door when an arthritic patient enters through the front door.
Rheum: An Evolution
An obvious problem facing rheumatology has been the lack of having an identifiable organ system that we could all rally around. The multisystem diseases that we manage can be fairly untidy, straying into many organs and tissues, requiring rheumatologists to be skilled in a variety of disciplines. In contrast, other specialists can limit their range of interest. For example, neurologists can focus all of their attention on the nervous system, cardiologists can keep their trained eyes on the beating heart and its attendant plumbing, and gastroenterologists can stay busy probing the various abdominal viscera.
These and other disciplines share the envious circumstance of being well defined and circumscribed. That is not our reality. Where is our focus of interest? Some consider it to be the musculoskeletal system. Possibly, but muscles and joints are not always our prime focus. When evaluating patients for systemic diseases such as vasculitis or systemic lupus erythematosus (SLE), the emphasis may lie far from bone and joints.
To be a rheumatologist is to be a medical jack-of-all-trades and a master or mistress of them all. How did our specialty acquire its name? The term rheuma is derived from the Greek word that describes something that flows. Hippocrates attributed many illnesses, especially those causing muscle achiness to the abnormal flow of body rheums or humors. The influential 1st century botanist and founding author of De Materia Medica, Pedanios Dioscorides, concluded that arthritis was caused by, “a defluxion of rheum or a humour, bilious, sanguineous, melancholic, but usually pituitrous and crude.”2 Since then, rheumatism has served as the all-encompassing explanation for everything that ached. However, rheumatism was facing some competition from another novel term—gout.
Around the time of the fall of the Roman Empire, most medical scribes concurred that all joint pain could be divided into two basic categories—gout and everything else.3 In fact, this simple dichotomy persisted beyond the next millennium. Beginning in the 16th century, a great debate ensued. Were gouty attacks, such as podagra, actually helpful to the patient by providing an “exit pathway” through which the body could discharge potentially lethal humors? This concept was hotly debated for some time. Some authorities believed that treating gouty attacks as opposed to letting them run their natural course was harmful to the patient. Allowing these peccant humours to be released from the body via the big toe or the foot was considered to be in the best interest of the patient’s health.3 Let the rheums flow! Fortunately, this inane approach was finally laid to rest following Carl Wilhelm Scheele’s discovery of urate crystals and Alfred Garrod’s critical insights into the pivotal role of urate in the pathogenesis of gout.
Rheumatism continued to battle gout for preeminence in the nomenclature of musculoskeletal pain disorders. There was room for little else. The situation changed in the early 19th century when Augustin Jacob Landré-Beauvais, a resident physician at the Saltpêtrière asylum in France, described a new form of arthritis afflicting some of his patients. His cohort at the asylum consisted of poor women, previously ignored by other physicians who often chose to treat more affluent male patients suffering from gout. He referred to this polyarthritis, which is now called rheumatoid arthritis (RA), as primary asthenic gout.4
Fast forward another 50 years to Alfred Garrod, who ingeniously fused gout and rheumatism together to create a new moniker, rheumatic gout, to replace Landré-Beauvais’ label for RA. Realizing that rheumatic gout was a distinct disease, Alfred Garrod’s son, Archibald, caused a stir some 40 years later, when he extricated this disorder from the clutches of gout. He did not stray far, selecting another rheum variant, rheumatoid arthritis. Since this disease has kept its name constant for well over a century, it has assured the long-term survival of the term rheum in our lexicon.
Like a virus embedded in our DNA, rheum continues to pass from one generation to the next. Has the definition of all things rheum gotten any clearer? After all, what is the meaning of rheumatology? Of course, readers of this publication understand the breadth of a rheumatologist’s practice, but have you ever tried to explain your métier to a stranger at a cocktail party?
From Blumberg B S. History of arthritis and rheumatism. Arthritis Rheum. 1960;3:421-422.
In The Company of Wolves
It wasn’t just RA and gout that sowed such confusion. What about the red wolf? The characteristic facial rash of SLE is considered to have first been described by a monk named Herbenus, who lived in Tours, France, more than 1,000 years ago. He chose lupus, or wolf in Latin. After studying many images of wolves on Google, I doubt that I would have chosen this canine. Centuries later, other authors described the facial rash of lupus as having a butterfly appearance, though its Latin translation, papilio, never caught on as a medical term. There were a number of challengers to the name lupus, including the interesting Latin descriptor, noli mi tangere, or touch me not. This phrase has its derivation in the New Testament where it describes what Jesus said to Mary Magdalene when she approached him following his resurrection.5
The prolific Hungarian dermatologist Moritz Kaposi is credited with making some sense of all these diverse lupus-related skin lesions. He subdivided the cutaneous features of lupus into discoid and systemic forms. He also introduced the concept of lupus as being a systemic disease with a potentially fatal outcome. Though William Osler is heaped with praise for his work in defining SLE, his contributions may be overstated. For example, over a decade, he published a series of seminal papers describing 29 cases of various skin disorders that he referred to as the erythema group of diseases. These included a variety of lesions that were not typical for lupus, such as purpura and angioneurotic edema.6 In fact, among the series there were only two definite cases of SLE. Yet this fact has not prevented Sir William from being showered with accolades for his writings on cutaneous lupus. Based on his dismissive approach to managing patients with osteoarthritis and his paltry collection of cutaneous lupus cases, Osler’s contributions to rheumatology may have been exaggerated.
Around the time of the fall of the Roman Empire, most medical scribes concurred that all joint pain could be divided into two basic categories—gout and everything else.
Star Wars Meets Rheumatology
What if rheumatologists had an about-face and followed the baseball metaphor of calling diseases the way they see them? In 1985, Dan McCarty, MD, professor emeritus at the Medical College of Wisconsin in Milwaukee and a past president of the ACR, described a series of 10 older patients who developed the sudden onset of symmetrical polyarthritis involving their hands and feet.7 He noted that their seronegative synovitis was also associated with marked, pitting edema of the hands and feet. Over time, the clinical and laboratory signs of inflammation along with their extremity edema gradually resolved. Being a modern man, Dr. McCarty shunned the Classics and the animal world when he named this condition, remitting seronegative symmetrical synovitis with pitting edema. Finally, rheumatologists could describe an illness whose name said it all. Perhaps Dr. McCarty was influenced by the blockbuster movie of that era, Star Wars, when he promoted the use of the mnemonic RS3PE to describe this form of arthritis.
Needless to say, I was delighted to hear of the recent demise of the word rheumatism. For those of you who may be unaware, our lead journal, A&R, is now referred to as Arthritis & Rheumatology. I wish I could say that the word lived beyond its usefulness, but I doubt that it ever served any useful purpose. Rheumatology has replaced rheumatism. Hallelujah! Are we making progress? I need to ruminate on this development for a while.
Dr. Helfgott is physician editor of The Rheumatologist and associate professor of medicine in the division of rheumatology, immunology, and allergy at Harvard Medical School in Boston.
References
- Helfgott SM. Pedal gangrene caused by giant cell arteritis. Arthritis Rheum. 1987;30:1078-1079.
- Parish LC. A historical approach to the nomenclature of rheumatoid arthritis. Arthritis Rheum. 1963;6:138-158.
- Rodnan GP. Growth and development of rheumatology in the United States—a bicentennial report. Arthritis Rheum. 1977;20:1149-1168.
- Kahn MF. Landré-Beauvais. Joint Bone Spine. 2001;68:143.
- Smith CD, Cyr M. The history of lupus erythematosus. From Hippocrates to Osler. Rheum Dis Clin North Am. 1988;14:1-14.
- Savin, JA. Osler and the skin. Brit J Derm. 2000;143:1-8.
- McCarty D, O’Duffy D, Pearson L, Hunter J. Remitting seronegative symmetrical synovitis with pitting edema. RS3PE syndrome. JAMA. 1985;254:2763-2767.
