186 One week later the patient showed marked symptomatic improvement in his right eye, but the painful swelling of his joints persisted. Visual acuity was 20/50 OD and applanation tension was 18 mm Hg. T h e cornea was clear and the anterior chamber revealed 4+ flare and 2f cells. T h e vitreous, seen clearly for the first time, revealed a 4+ cellular reaction. Because of the heavy vitreous reaction prednisone (80 mg every other day) was instituted. By the end of October the visual acuity was 20/30 OD and improvement was noted in both chambers. Over the ensuing 3 weeks the uveitis and arthritis resolved and visual acuity returned to normal in his right eye. Topical and systemic adrenocorticosteroids were gradually decreased over that period ancl finally discontinued nearly 2 months after the initial ophthalmology visit. Subsequent musculoskeletal and ocular examinations have been normal. Whether the presence of HL-A 27 in our patient is related to the rheumatic disorder or the uveitis, or both conditions, is unclear. He has developed neither spondylitis nor.sacroiliitis, and the peripheral arthritis and uveitis completely resolved. T h e severe involvement of the vitreous is unusual in Reiter’s syndrome or ankylosing spondylitis, but was a prominent feature in our patient necessitating the use of systemic corticosteroids. T h e marked vitreous involvement suggests that posterior, as well as anterior, uveitis may accompany rheumatic diseases. REFERENCES 1. Schlosstein L, Terasaki PI, Bluestone R, et al: High as- 2. 3. 4. 5. 6. sociation of an HL-A antigen, W 27, with ankylosing spondylitis. N Engl J Med 288:704-706, 1973 Morris R, Metzger AL, Bluestone, et al: HL-A W 27-a clue to the diagnosis and pathogenesis of Reiter’s syndrome. N Engl J Med 290:554-556, 1974 Rachelsfsky GS, Terasaki PI, Katz R, et al: Increased prevalence of W 27 in juvenile rheumatoid arthritis. N Engl J Med 290:892-893, 1974 Ah0 K, Ahvonen P, Lassus A, et al: HL-A antigen 27 and reactive arthritis. Lancet 2: 157, 1973 Brewerton DA, Caffrey M, Nicholls A, et al: Reiter’s disease and HL-A 27. Lancet 2:996-998, 1973 Brewerton DA, Caffrey M, Nicholls A, et al: Acute anterior uveitis and HL-A 27. Lancet 2:994-996, 1973 b1.D. M.D. DUNCAN S. OWEN, JR., hf.D., F.A.C.P. Medical College of Virginia Virginia Commonwealth University Richmond, Virginia WILLIAM M. EDWARDS, JAMES FERGUSON, Serum Gold Levels T o T h e Editor: Dr. Gottlieb and his associates have presented new and interesting material in their recent paper on gold (1). One of their conclusions, however - that their findings “will help dispel the notion serum gold levels are a valuable guide to improve crysotherapy,” is open to question. If one reviews the data they originally published (2), i t seems that the 8 patients labelled least improved showed considerable improvement in such objective criteria as number of involved and painful joints, ESR, walking time, and latex fixation titer. Indeed, these changes were of equal magniture to those shown by the most improued group. Furthermore, in looking at Figure 2 of their more recent paper (l), it appears that the mean serum gold level (measured 1 week after injection), was at or about 300 pg/lOO ml after the fifth week of therapy. Lorber et a1 have shown that patients who consistently achieve levels of 300 pg/lOO ml fare better than patients who do not (3). Krusius and his associates have reported similar findings in patients who achieve such levels after 5 weeks of treatment (4). Our own findings presented in a preliminary communication agree with this (5). T h e hypothesis that to achieve serum gold levels of 300 pg/lOO ml or higher, early during crysotherapy, may influence the outcome favorably does not seem to be contradicted by Dr. Gottlieb’s data. One might argue with some justification that Dr. Gottlieb’s good therapeutic results were due to the achievement of high serum gold levels. I t is only at such levels that considerable binding to plasma proteins other than albumin occurs (6). As Lorber has suggested, this may be important in facilitating entry of gold into phagocytosing cells and interfering with cell-mediated and cell-dependent inHammatory reactions (6). REFERENCES 1. Gottlieb NL, Smith PM, Smith EM: Pharmacodynamics 197Au and 193Au labeled aurothiomalate in blood: correlation with course of rheumatoid arthritis, gold toxicity and gold excretion. Arthritis Rheum 17:171-183, 1974 2. Gottlieb NL, Smith PM, Smith EM: Gold excretion correlated with clinical course during chrysotherapy in rheumatoid arthritis. Arthritis Rheum 15:582-592, 1972 3. Lorber A, Atkins CJ, Chang CC, et al: Monitoring 187 serum gold values to improve chrysotherapy in rheumatoid arthritis. Ann Rheum Dis 32:133-139, 1973 4. Krusius F-E, Markkanen A, Peltola P: Plasma levels and urinary excretion of gold during routine treatment of rheumatoid arthritis. Ann Rheum Dis 29: 232-235, 1970 5. Harth M, Thompson JM: Relation of serum gold levels (SAu) to clinical response in patients with rheumatoid arthritis (RA). Ann RC Physicians Surg Cana p. 60 January 1973 (abstr) 6. Lorber A, Bovy RA, Chang CC: Relation between serum gold contents and distribution to serum immunoglobulins and complement. Nature (New Biol) 236:250252. 1972 M.D., F.A.C.P.(C), Rheumatic Diseases Unit University of Western Ontario M. HARTH, The History of Rheumatoid Arthritis T o the Editor: T h e paper by Dr. Charles L. Short entitled “The Antiquity of Rheumatoid Arthritis” (ARTHRITIS RHEUM 17:193-205, 1974) is a valuable contribution to the study of the history and evolution of the disease. T h e first good description was done by Sir Alfred Baring Garrod in 1859, but there are several other early descriptions of rheumatic diseases that could well be rheumatoid arthritis. Figure 1 is a photograph of a painting that hangs in the Royal National Hospital for Rheumatic Diseases, Bath, and clearly illustrates on the left a patient with a typical rheumatoid hand. This painting, by William Hoare, is dated 1742. Incidentally, Fig 1. From the Royal National Hospital for Rheumatic Diseases, Bath, England.