Supplement Article |
OP1. HISTORY OF GIANT CELL ARTERITIS (GCA) AND POLYMYALGIA RHEUMATICA (PMR)
Mayo Clinic College of Medicine, USA
Whether GCA and PMR existed in antiquity, or are conditions of modern times is unknown. Hutchinson's report in 1890 of an elderly man with "red streaks" on his forehead appears to be the first detailed case. In 1930, Schmidt discussed a patient with symptoms of GCA but attributed them to an aneurysm. In 1932, Horton et al. reported 2 patients whose temporal artery biopsies showed arteritis. In 1937, these workers summarized 7 cases who manifested systemic symptoms, headache, fever, anemia and jaw claudication. Temporal artery biopsies showed granulomatous inflammation with giant cells. The authors considered this a new vasculitis calling it "temporal arteritis".
Over the next decade occasional cases were published describing many of the symptoms of GCA. In 1938, Jennings observed a patient with visual loss. In the 1941, Gilmour reported autopsy findings in 3 older patients with inflammation in large vessels that appeared similar to temporal arteritis. He suggested the name "giant cell arteritis". In 1946, Kilbourne and Wolff, noted involvement of multiple cranial vessels and offered the name "cranial arteritis".
PMR was also described in the late 19th century, by Bruce in 1888. Some physicians (e.g. Copeman, Slocumb, Hamrin) stated that PMR was recognized as a clinical syndrome in the 1930's or even before, although not written about. However, it wasn't until the 1940's and early 1950's that reports on this condition started to appear under a variety of names such as secondary fibrositis, periarthrosis humeroscapularis, peri-extraarticular rheumatism, myalgic syndrome of the aged, pseudo-polyarthrite rhizomelique, and anarthritic rheumatoid disease. Barber's article in 1957 in which he coined the term "polymyalgia rheumatica" caught the attention of many, and this name was eventually adopted. In the 1950s, shortly after the discovery of the potent anti-inflammatory properties of cortisone, Birkhead and colleagues showed that GCA responded well to this drug. Later, low doses were found also to be very effective in PMR.
The link between GCA and PMR wasn't recognized immediately. But, in the 1940's and 1950's, several authors noted that some patients with GCA had findings of PMR. The reports by Paulley and Hughes, Alestig and Barr, Hamrin, and others in the 1960's, led to a wider appreciation of a close connection between PMR and GCA. Modern research on these conditions has increased our understanding substantially. However, much more knowledge is needed and only waits to be discovered by the skilled, inquiring, and dedicated scientist.