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Serum gold levels.

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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.
1. Schlosstein L, Terasaki PI, Bluestone R, et al: High as-
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
DUNCAN S. OWEN, JR., hf.D., F.A.C.P.
Medical College of Virginia
Virginia Commonwealth University
Richmond, Virginia
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).
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,
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
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
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.
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