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Infants of mothers receiving gold therapy.

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LETTERS
104
Podagra and a low grade polyarthritis persisted
until the patient was seen in 1977 with an acutely painful right knee effusion. At that time a right olecranon
nodule was found. Knee joint aspiration revealed
slightly turbid synovial fluid with normal viscosity and
good much clot formation. Microscopy showed a white
blood cell count (WBC) of 6.0 X lo9 with polymorphonuclear leukocytes 49% and monocytes 51% with a
moderate number of negatively birefringent needle
shaped crystals. Other investigations revealed hemoglobin 128 gm/100 ml, ESR 122 mm/hr, uric acid 0.72
mmol/100 ml, RA latex 1/500, and Rose Waaler 1/320.
Allopurinol was begun and no further attacks of acute
gout were recorded.
During the next 2 years, low grade polyarthritis
persisted. Therapy included indomethacin, allopurinol,
and intraarticular corticosteroid injections. When seen
in April 1980, there was marked synovitis of the patient’s MCP and PIP joints, wrists, and elbows, with
flexor tenosynovitis of both hands. A nodule was present on the right olecranon. Investigations were as follows: hemoglobin 115 gm/100 ml, ESR 117 mm/hr,
uric acid 0.36 mmol/l00 ml, RA latex l/320, Rose
Waaler 1/320, and ANA 1 : 10 (normal 1 : 10). X-rays
showed that during the previous 2 years there had been
further cartilage loss and new erosions of the MCP and
wrist joints. Excisional biopsy of the olecranon nodule
showed a classic rheumatoid nodule. Microscopic examination showed a central area of necrosis surrounded by
palisading mononuclear cells.
The acute synovitis slowly responded to bedrest,
intraarticular corticosteroids, indomethacin, and the
reintroduction of low dose gold therapy. Allopurinol
was continued.
Wallace (1) raised two important questions
which may be answered by our case: 1) Are rheumatoid
factor-coated crystals less inflammatory? For at least 5
of the 9 years that our patient had uncontrolled gout, he
was rheumatoid factor-positive. There was no difference in the frequency or severity of gout attacks, either
before or after the onset of the rheumatoid arthritis.
Thus, the presence or absence of rheumatoid factor does
not seem to have influenced the episodes of gout. 2) Are
uric acid crystals immunosuppressive? While hyperuricemic, our patient developed wrist and elbow joint
damage with a rheumatoid nodule. During the 3 years
that he has been normouricemic, his rheumatoid arthritis has been moderately progressive. Certainly introducing allopurinol has not dramatically influenced
the course of the RA, and hyperuricemia per se does not
seem to have been in any way protective.
The mutual exclusion of rheumatoid arthritis
and gout may be related to genetic susceptibility rather
than to any biochemical or immunologic factor.
RODNEYF. WATERWORTH,
FRACP
Wellington Regional Rheumatic Diseases Unit
Hutt Hospital
Wellington 2, New Zealand
REFERENCES
1. Wallace DJ, Klinenberg JR, Morhaim D, et al: Coexistent
gout and rheumatoid arthritis. Arthritis Rheum 22:8 1-86,
1979
2. Jessee EF, Toone E, Owen DS, Irby R. Coexistent rheumatoid arthritis and chronic tophaceous gout. Arthritis
Rheum 23:244247, 1980
Infants of mothers receiving gold therapy
To the Editor:
Gold salts are commonly used in the management of refractory rheumatoid arthritis, and the therapeutic efficacy of gold has been well established (1). In
addition, gold is frequently associated with a wide range
of toxicities including dermatitis, mucous membrane reactions, glomerulitis with hematuria or nephrotic syndrome, bone marrow suppression, and anaphylactic reactions. Little information exists, however, concerning
the usage of gold salts during pregnancy and the subsequent potential toxicity or teratogenicity in the fetus.
We recently cared for an infant whose mother received
gold thiomalate throughout her pregnancy, and thus
had the opportunity to study the pharmacology and toxicity of gold in the neonate.
A 21-year-old woman was diagnosed as having
rheumatoid arthritis in 1974. Gold therapy was begun
in 1976. At the time of conception and throughout her
pregnancy, the patient received 100 mg of gold sodium
thiomalate monthly by intramuscular injection. When
pregnancy was confirmed she was advised to discontinue gold therapy but refused. Her last dose of gold
during pregnancy was 3 days prior to delivery.
.The pregnancy was otherwise uncomplicated,
and the patient delivered at term a 2,970 gm female
with no obvious major or minor congenital anomalies.
Maternal venous serum gold level at delivery was 19.9
pmole/liter (392 &lo0 ml) with a simultaneous umbilical cord serum level of 11.4 pmole/liter (225 pg/lOO
ml), clearly demonstrating the transplacental passage of
“therapeutic” concentrations of gold in a term neonate,
At 2% weeks the infant’s venous serum gold level was
2.6 pmole/liter (52 pg/lOO ml), consistent with the de-
LETTERS
105
crease of serum concentration commonly seen in arthritis patients following cessation of gold therapy (1). Serial urine analyses and blood counts were within normal
limits.
Gold sodium thiomalate has been shown to be
teratogenic in rats and rabbits, but the dosages and
treatment schedules employed in those studies greatly
exceed the guidelines established by the manufacturer
for use in humans (2,3). Human fetal experience is
sparse and anecdotal because no controlled studies are
available. Hollander discusses a series of uneventful
pregnancies in women receiving gold salt therapy, but
no long-term followup of the offspring has been reported (4). Miyamoto reported no gross deformities in
the offspring of 26 patients who received gold therapy
throughout pregnancy. An additional 43 patients had
discontinued gold salts in early to mid pregnancy, and
except for 2 cases of hip anomalies, the offspring were
normal (5). Rocker was able to demonstrate the transplacental passage of gold by detection of gold deposits
in the placenta, liver, and kidney of a 20-week abortus
which had no gross internal or external malformations
(6)The present report demonstrates the transplacental passage of gold salts in quantities sufficient to
establish in the term neonate serum levels of gold commonly encountered in patients undergoing aurotherapy.
It furthermore demonstrates a normal decrement of the
serum gold level over the first few weeks of life.
The accumulating evidence suggests that gold
therapy in pregnancy can be safely continued in selected patients whose rheumatoid arthritis is of such
severity to warrant it. However, since no long-term
followup of offspring born to mothers receiving
aurotherapy is available, it would seem prudent in most
cases to avoid the use of gold salts until its safety has
been unequivocally established.
DANIELL. COHEN,MD
JOSEPH
ORZEL,MD
USAF Hospital, RA F Lakenheath
APO N Y 091 79
ANDREWTAYLOR,MSc
Department of Biochemistry
University of Surrey
Guildford, England
REFERENCES
1. Zvaifier NJ: Gold and antimalarial therapy, Arthritis and
Allied Conditions. Edited by DJ McCarty. Philadelphia,
Lea & Febiger, 1979, p 355
2. Szabo KT, Guemero FJ, Kang VJ: The effects of gold containing compounds on pregnant rabbits and their fetuses.
Vet Pathol lS(Supp1 5):89, 1978
3. Szabo KT, DiFebbo ME, Phelan DG: The effects of gold
containing compounds on pregnant rabbits and their fetuses. Vet Pathol 15(Suppl 5):97, 1978
4. Hollander JL: Gold therapy for rheumatoid arthritis, Arthritis and Allied Conditions. Edited by JL Hollander.
Philadelphia, Lea & Febiger, 1972, p 479
5. Miyamoto T, Miyaji S, Horiuchi Y, Hara M, Ishihara K:
Gold therapy in bronchial asthma-special emphasis upon
blood levels in gold and its teratogenicity. Nippon Noika
Gakkai Zaashi 63:1190, 1974
6. Rocker I, Henderson WJ: Transfer of gold from mother to
fetus. Lancet ik1246, 1976
Retinol-binding protein in rheumatoid arthritis
To the Editor:
Low plasma retinol-binding protein (RBP) may
indicate protein-energy malnutrition (PEM) (1).
Chronic inflammatory disease, such as rheumatoid arthritis (RA), may be one of the many causes of PEM.
Using radial immunodiffusion in plates (supplied
by Behring-Werke, Marburg, West Germany), we measured RBP in 17 patients who have classic or definite
RA. Thirteen of the patients were women and 4 were
men, ranging in age between 35 and 62, with a mean of
46.3 years. We also determined RBP for a control group
of 19 osteoarthritis patients who are comparable in regard to age and sex.
We found that RBP levels were significantly
lower in RA (3.04 0.19 mg/100 ml, mean k standard
error; ranges 1.23 to 4.27 mg/100 ml) than in osteoarthritis (5.97 f 0.36 mg/100 ml, ranges 4.32 to 9.21
mg/100 ml; t = 6.869; P < 0.001) (Figure 1).
This reduced RBP may have diagnostic value in
distinguishing between RA and osteoarthritis. It may
also indicate PEM in RA. Conversely, the PEM might
be caused by corticosteroids often given to RA patients,
since corticosteroids decrease the synthesis and enhance
the catabolism of proteins (2). However, 6 of the RA patients who were not receiving corticosteroids also had
low retinol binding protein.
In the interpretation of these results, the strict
relationship between RBP, vitamin A, and zinc must
also be considered. RBP is a specific transport protein,
and its plasma levels reflect the amount of vitamin A
available to the tissues. In malnourished children, both
RBP and vitamin A are low (3). Furthermore, plasma
vitamin A depression follows zinc deficiency in rats (4).
Because zinc is depressed in RA patients ( 5 ) , it has been
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