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Nail pigmentation after parenteral gold therapy for rheumatoid arthritis Вgold nails.

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LETTERS
119
>2,000 unitsfliter (normal 20-140 unitdliter). High-dose
prednisone was continued and symptomatic treatment for
pancreatitis begun. The patient subsequently developed
Staphylococcus aureus sepsis. An open lung biopsy revealed
intraalveolar hemorrhage. Liver function test results were
elevated, and there was severe central nervous system
involvement characterized by seizures and psychosis.
After 5 days her renal, pancreatic, and pulmonary
problems improved or resolved, but the central nervous
system (CNS) manifestations progressed to involve mental
function and, clinically, the basal ganglia. Prednisone was
initially maintained at 80 mg per day, then tapered to 50 mg
per day. A trial of pulse Soh-Medrol was given without CNS
improvement, and she was discharged on a regimen of
Haldol and 50 mg prednisone daily.
Oppenheimer and Boitnoff autopsied children who
had been treated with corticosteroids for the nephrotic
syndrome of various etiologies; they found evidence of
pancreatitis in many of these subjects (3). However, the
effects of serum calcium levels or immunosuppressive agents
administered were not examined, and pancreatitis was attributed to steroid ingestion. Reynolds et al (4) reviewed a
series of patients who were receiving steroid therapy and
had pancreatitis. They found SLE to be the overwhelming
primary diagnosis and emphasized an association between
SLE and pancreatitis. Additionally, the patients with SLE
and pancreatitis generally had lupus activity in more than 4
organ systems.
Our patient had SLE activity in multiple organ
systems at the time of diagnosis of pancreatitis, had not
received any recent prior medications associated with pancreatitis, and had resolution of her pancreatitis with continued use of high-dose corticosteroids. Her case, like those
described by Croft et al (2) and Reynolds et a1 (41, suggests
that pancreatitis is another organ system manifestation of
SLE, a disease generally associated with multiple organ
system involvement.
Nail pigmentation after parenteral gold therapy for
rheumatoid arthritis: “gold nails”
To the Editor:
We recently noted yellowish pigmentation of toenails
in a patient with rheumatoid arthritis (RA) treated with gold.
Published reviews of chrysotherapy make no mention of this
occurrence (1).
A 59-year-old man with seropositive nodular rheumatoid arthritis (RA)of 14 years’ duration was treated with
gold for 3 years beginning in 1976. He was managed with
salicylates and low-dose prednisone until June 1976 when
gold sodium thiomalate (GST) was added for progressive
articular disease. He received 2 test doses of 10 and 25 mg
GST, a series of 20 weekly intramuscular injections of GST
for a total of 1,000 mg, followed by monthly intramuscular
doses of 50 mg GST. In June 1979 he developed a severe
dermatitis, and gold was discontinued after a total cumulative dose of 2,500 mg had been administered. Subsequent to
withdrawal of gold, he noted yellowish discoloration of
toenails which had gradually been growing out. There was
no history of local trauma, industrial exposure, psoriasis,
fungal infection. or other nail disorders.
The toenails, particularly those of the great toes.
showed a distal band of yellowish discoloration (Figure I).
The dkcolored section was thickened and sharply demarcated by a linear ridge from the proximal, normal-looking
portion. The fingernails were clear. Bacterial and fungal
cultures of nail scrapings were negative. Determination of
gold in great toenail clippings by carbon-furnace atomicabsorption spectrometry (2) showed traces of the metal; 2 pg
Au/gm dry weight tissue (compared with <0.6 pg Au/gm
tissue in nail clippings from 3 normal controls).
The yellow band moved slowly distally with growth
of the nail plate, and the entire nail was replaced by new
growth within 8 months.
Pigmentation of skin by gold, or dermal chrysiasis, is
Catherine Marino, MD
Esther Lipstein-Kresch. MD
Queens Hospital Center
Long Island Jewish-Hillside Medical Center
Jamaica, N Y
I . Mallory A. Kern F: Drug-induced pancreatitis: a critical review.
Gastroenterology 7 8 3 13-820, 1980
2. Croft SP, Jarrett MP. Craig R , Perlman SG: Pancreatitis and
systemic lupus erythematosus: a case report Iletter). Arthritis
Rheum 26:238-239. 1983
3. Oppenheimer EH. Boitnoff JK: Pancreatitis in children following
adrenocorticosteroid therapy. Bull Johns Hopkins Hosp 107:297.
1 %O
4. Reynolds JC. Inrnan RD. Kimberly RP, Chuong JH.Kovacs JE,
Walsh MB: Acute pancreatitis in SLE: report of twenty cases
and a review of the literature. Medicine 61:25-32. 1982
Figure 1. Right great toenail showing a distal band of yellowish
discoloration.
LETTERS
120
a rare side effect of chrysotherapy (3). It presents as a bluegray, slate-colored, or occasionally yellowish pigmentation
most pronounced in the exposed parts of the body (3,4). The
complication is dose-dependent, occurring in patients who
received more than about 150 mg of gold/kg of body weight
(3). It was described clearly during the days of frequent
chrysotherapy for tuberculosis (3,4). Although deposition of
gold in skin is common after chrysotherapy for RA (4-61,
smaller amounts of gold are usually administered to patients
with arthritis, and clinical hyperpigmentation is extremely
rare (4).
Gold is also deposited in minute quantities in nail
plates (2,5) and cornea (7) of RA patients receiving gold. A
causal relationship between gold therapy and toenail pigmentation in our patient was suggested by a number of
observations. First, pigmentation appeared de novo after
chrysotherapy and slowly resolved after withdrawal of gold
and regrowth of the nail plate. Second, nail pigmentation did
not recur after discontinuation of gold; the duration of
followup was 4 years. Third, other causes of nail discoloration (8) such as fungal or bacterial infections, psoriasis,
external dyes and stains, drugs (9), or yellow-nail syndrome,
were carefully excluded. Nail gold levels are probably of
limited diagnostic value; traces of the metal are present in
nails of normal adults who have not received gold compounds (5,lO). levels of up to 4. I pg Adgm tissue have been
recorded in normal-appearing nails during chrysotherapy (2),
and gold levels in skin, hair, or nails do not seem to correlate
with gold toxicity (5).
We suggest that nail pigmentation due to gold, or
"onychochrysiasis," should be included as a rare manifestation of prolonged gold therapy for RA. The complication is
probably analogous to nail discoloration produced by arsenic
(Mees' stripes), silver (argyria), thallium, and other heavy
metals (9).
Adel G. Fam, MD
Thomas W. Paton, PharmD
University of Toronto
Toronto. Ontario, Canada
1. Gibbons RB: Complications of chrysotherapy: a review of
recent studies. Arch Intern Med 139:343-346, 1979
2. Kame1 H, Brown DH, Ottaway JM, Smith WE: Determination
of gold in tissues by carbon-furnace atomic-absorption spec-
trometry. Talanta 24:309-313, 1977
3. Schmidt OEL: Chrysiasis. Arch Dermatol Syphil 44446-452,
1941
4. Cox AJ. Marich KW: Gold in the dermis following gold therapy
for rheumatoid arthritis. Arch Dermatol 108:655-657, 1973
5. Gottlieb NL, Smith PM, Penneys NS, Smith EM: Gold concentrations in hair, nail, and skin during chrysotherapy. Arthritis
Rheum 17:56-62, 1974
6. Ghadially FN. DeCoteau WE, Huang S, Thomas 1: Ultrastructure of the skin of patients treated with sodium aurothiomalate.
J Pathol 124:77-82. 1978
7. Hashimoto A. Maeda Y ,It0 H, Okazaki M, Hara T: Corneal
chrysiasis, a clinical study in rheumatoid arthritis patients
receiving gold therapy. Arthritis Rheum 15:309-312. 1972
8. Samman PD: Principal nail symptoms: discoloration, The Nails
in Disease. Third edition. London, William Heinemann Medical
Books, 1978. pp 18-24
9.
Samman PD: Miscellaneous acquired nail disorders: abnormalities of the nails due to drugs. The Nails in Disease. Third
edition. London, William Heinemann Medical Books, 1978, pp
86-103, 98-100
10.
Kanabrocki E, Case LF, Graham LA, Fields T, Oester YT,
Kaplan E: Neutron-activation studies of trace elements in
human fingernail. J Nucl Med 9:478-481. 1968
Giant cell arteritis in two Chinese patients
To the Editor:
Giant cell arteritis occurs predominantly in whites.
There have been a few cases reported in black women; 1 in
an American Indian, and 1 in a Mexican-American (King
DT, Freed JF: Giant cell arteritis in an elderly black woman.
Arthritis Rheum 22902-203. 1979). Biopsy-documented
temporal arteritis has been reported in Japanese patients, but
is rare. (Takasuge K, Nishihara R: Polymyalgia rheumatica
with temporal arteritis: a survey of reported cases in Japan,
1977 Annual Report of the Research Committee on Vascular
Lesions of Collagen Diseases. Edited by Y Shiokawa. Tokyo, The Ministry of Health and Welfare, 1978, pp 229-238
[Jap]). We report the first 2 cases of biopsy-proven giant cell
arteritis in patients of Chinese extraction.
An 82-year-old woman, born in China of Chinese
parents, was seen at her home in Manila, Philippine Islands,
in 1980. She complained of morning stiffness and pain on
shoulder and hip motion, pain in her jaw while chewing, and
right temporal headache. Her erythrocyte sedimentation rate
(ESR) was 122 mndhour. Biopsy of the right temporal artery
demonstrated giant cell arteritis.
A 79-year-old seaman, born in San Francisco of
Chinese parents, was brought to Virginia Mason Hospital in
1981 because of memory impairment and inability to care for
himself. Tests showed a hematocrit of 28% and ESR of 129
mmlhour. A computed tomography brain scan showed small
infarcts in both hemispheres and cerebral atrophy. Although
he had no localizing symptoms or signs, a temporal artery
biopsy was performed because of the very rapid sedimentation rate. The histologic picture was that of marked granulomatous arteritis.
While the preponderance of whites among patients
with giant cell arteritis is still striking, it is occasionally seen
in patients of other races, now including the Chinese.
Kenneth R. Wilske, MD
Louis A. Healey, MD
S. Rockwell Fredrickson, MD
The Mason Clinic
Seattle, W A
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nail, вgold, gold, arthritis, pigmentation, parenteral, therapy, rheumatoid
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