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Therapeutic and direct neurotoxic effects of gold therapy.

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LETTERS
1198
Therapeutic and direct neurotoxic effects of gold
therapy
To the Editor:
We were interested in the paper by Levine et al that
described their study of the neurotoxic effects of gold
therapy in rats (Levine JD, Goldstine J , Mayes M,
Moskowitz MA, Basbaum AI: The neurotoxic effects of gold
sodium thiomalate on the peripheral nerves of the rat:
insights into the antiinflammatory actions of gold therapy.
Arthritis Rheum 29:897-901, 1986). The authors’ main
finding, that gold has direct neurotoxic effects, is in keeping
with the results of a study that we published in 1980 (Katrack
SM, Pollock M, O’Brien CP, Nukada H, Allpress S, Calder
C, Palmer DG, Grennan DM, McCormack PL, Laurent MR:
Clinical and morphological features of gold neuropathy.
Brain 103:671-693, 1980). Since our study seems to have
escaped attention, we will briefly describe our main findings.
Our interest in this problem was stimulated by 3
patients who developed peripheral neuropathies while receiving gold therapy. Two of them had the unusual clinical
features of myokymia. Their cumulative doses of gold were
490 mg, 1,310 mg, and 1,350 mg, respectively. In parallel
experimental studies in hens, we found that gold produced a
dose-related neuropathy , with histologic findings of axonal
degeneration and segmental demyelination. Similar pathologic findings were noted in the sural nerve biopsy specimens from our 3 patients. We concluded that the
neuropathic effects of gold were probably the result of a
direct toxic effect.
Unlike Levine and coworkers, we did not find a
selective loss of unmyelinated nerve fibers, and we drew
no parallel between neurotoxicity and therapeutic effects
of gold.
D. M. Grennan, MD, FRCP
University of Manchester
Salford, U K
D. G . Palmer, MD, FRACP
M. Pollock, FRACP
University of Otago
Dunedin, NZ
Reply to letter by Casey et a1
To the Editor:
We read with interest the letter by Casey and coworkers regarding the beta-2-microglobulin (P2M) origin of
dialysis-related amyloid (1). When we published a report on
our first case of amyloid arthropathy in March 1985 ( 2 ) , we
suggested that when the potassium permanganate method
was used ( 3 ) , the amyloid deposits were of the AA type.
Admittedly, this is not specific enough to ascertain the type
of the protein subclass.
At that time, specific antibodies were not available to
further characterize these amyloid deposits. Since then, we
have tested the amyloid deposits in our 2 previously described patients (4), with specific antibodies directed against
P2M (Dakopatts, Copenhagen, Denmark). Positive results
were obtained in both cases, using an immunoperoxidase
(peroxidase-antiperoxidase) technique. This amyloid material has been shown to be related to P2M, and indeed,
confirms the findings of other investigators (5-7).
J. P. Huaux, MD
H. Noel, MD
J. M. Vandenbroucke, MD
C. van Ypersele de Strihou, MD
C. Nagant de Deuxchaisnes, MD
St-Luc University Hospital
Brussels, Belgium
I . Casey TT, Stone WJ, DiRaimondo CR, Page DL, Gorevic PD:
2.
3.
4.
5.
6.
To the Editor:
We appreciate the comments of Dr. Grennan and
colleagues. We were aware of their important light microscopy study of the neurotoxic effect of gold on myelinated
fibers in the hen. Our electron microscopy study, however,
was directed at the effects of gold on unmyelinated fibers
that contain neuropeptides. That we did not observe a
statistically significant effect of gold on myelinated afferents
may reflect the number of animals studied. Given the known
toxic effect of heavy metals on the peripheral nervous
system, it is likely that gold will exert some of its effects on
myelinated, as well as unmyelinated, fibers.
Jon Levine, MD, PhD
Allan Basbaum, PhD
University of California
San Francisco, CA
7.
Dialysis-related amyloid is amyloid of beta-2-microglobulin
origin (letter). Arthritis Rheum 29:1170, 1986
Huaux JP, Noel H, Bastien P, Malghem J , Maldague B,
Devogelaer JP, Nagant de Deuxchaisnes C: Amylose articulaire,
fracture du col fkmoral et hemodialyse periodique chronique.
Rev Rhum Ma1 Osteoartic 52:179-182, 1985
Wright JR, Calkins E, Humphrey RL: Potassium permanganate
reaction in amyloidosis. Lab Invest 36:274-281, 1977
Huaux JP, Noel H, Malghem J, Maldague B, Devogelaer JP,
Nagant de Deuxchaisnes C: Erosive azotemic osteoarthropathy:
possible role of amyloidosis (letter). Arthritis Rheum 28:
1075-1076, 1985
Gorevic PD, Casey TT, Stone WJ, DiRaimondo CR, Prelli FC,
Frangione B: Beta-2-microglobulinis an amyloidogenic protein in
man. J Clin Invest 76:2425-2429, 1985
Gejyo F, Yamada T, Odani S , Nakagawa Y, Arakawa M,
Kunitomo T, Kataoka H, Suzuki M, Hirasawa Y, Shirahama T,
Cohen AS, Schmid K: A new form of amyloid protein associated
with chronic hemodialysis was identified as beta 2-microglobulin.
Biochem Biophys Res Commun 129:701-706, 1985
Shirahama T, Skinner M, Cohen AS, Gejyo F, Arakawa M,
Suzuki M, Hirasawa Y: Histochemical and immunohistochemical characterization of amyloid associated with chronic hemodialysis as beta-2-microglobulin. Lab Invest 53:705-709, 1985
Eosinophilic synovitis and urticaria: an association
with symptomatic dermatographism or urticaria1
vasculitis?
To the Editor:
Brown and associates (1) have recently described an
interesting new subset of patients who have dermatographism
associated with eosinophilic synovitis and, in some cases,
elevated IgE levels. Warin and Champion (2) have identified
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effect, neurotoxins, direct, therapeutic, gold, therapy
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