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Gold-Induced ThrombocytopeniaResponse to Vincristine.

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(ESR) of 47 mm, a creatinine clearance of 56
ml/minute, a positive latex fixation test for rheumatoid
factor at a titer of 1 :2560, and a urinary sediment containing 12 to 15 erythrocytes and 5 leukocytes per highpower field, as well as hyaline, granular, and red cell
casts.
Roentgenograms revealed multiple bilateral pulmonary nodules averaging l .5 cm in diameter and bilateral maxillary and frontal sinus opacities. Pertinent normal laboratory findings included negative antinuclear
antibodies, Cslevels, and blood hemoglobin.
Review of the biopsy material from the previous
pulmonary segmental resection showed multiple noncaseating granulomata with numerous giant cells and
necrotizing vasculitis of small and medium-sized vessels
compatible with Wegener’s granulomatosis (Figure 2).
He was placed on cyclophosphamide therapy and
experienced prompt improvement of the chondritis and
gradual improvement of the other clinical manifestations.
Wegener’s granulomatosis accounted for most of
the clinical and laboratory findings in this patient. Besides the classic triad of pulmonary, paranasal sinus,
and renal involvement, he had arthritis, hearing loss,
granulomatous episcleritis, peripheral nerve involvement, leukocytosis, positive rheumatoid factor,
and elevated ESR, all of which occur frequently in
Wegener’s granulomatosis. Except for the high ESR,
these abnormalities rarely occur in relapsing polychondritis.
The swelling and redness of the ear were characteristic of relapsing polychondritis in that they did not
affect the ear lobe. Saddle-nose deformity in relapsing
polychondritis is due to inflammation, destruction, and
collapse of the nasal cartilage, whereas in Wegener’s
granulomatosis it is thought t o be due t o the granulomatous destructive lesion. The occurrence of chondritis elsewhere, although apparently uncommon, may
indicate that chondritis of the nasal cartilage can also
occur in Wegener’s granulomatosis and contribute to
the collapse of the nose.
Awareness of the possibility of chondritis of the
ear in Wegener’s granulomatosis is important both from
diagnostic and therapeutic standpoints because Wegener’s granulomatosis is preferably treated with immunosuppresive agents (2), whereas the treatment of choice
for relapsing polychondritis is corticosteroids (1 ).
REFERENCES
1. McAdam LP, O’Hanlan MA, Bluestone
R,et al: Relapsing
Arthritis and Rheumatism, Vol. 20, No. 6 (July-August 1977)
polychondritis: prospective study of 23 patients and review
of the literature. Medicine (Baltimore) 55:193-215, 1976
2. Fauci AS, Wolff SM: Wegener’s granulomatosis.Studies in
eighteen patients and review of the literature. Medicine
(Baltimore) 52:535-561, 1973
EFRAfN DfAZ-JOUANEN, M.D.
DONATO
ALARC~N-SEGOVIA,
M .D., F.A.C.P.
Department of Immunology and Rheumatology
Instituto Nacional de la Nutricihn
Mexico 22, D. F., Mexico
Gold-Induced Thrombocytopenia :
Response to Vincristine?
To the Editor:
Gold-induced thrombocytopenia may be transient and inconsequential or it may be lethal. Although
it has been compared to idiopathic thrombocytopenia,
data supporting immunopathogenesis are insubstantial,
and the rapid rise in platelet count sometimes noted
following treatment with dimercaprol is more suggestive
of direct platelet or bone marrow gold toxicity. Neither
corticosteroid nor dimercaprol treatment is always effective, and splenectomy, despite its obvious dangers in
severe thrombocytopenia, appears to have been indicated and effective at times.
Vincristine has been used to treat idiopathic
thrombocytopenia and some secondary (presumably
“immun,e”) thrombocytopenias resistant to corticosteroids, and in some instances, splenectomy. In 21 patients
with idiopathic thrombocytopenia given vincristine intravenously in small doses (2 mg for adults) every 7-10
days, the response in terms of rise in platelet count (to
normal, excellent; between 50,000 and 150,0OO, good;
and between 20,500 to 50,000, fair), was excellent in 6,
good in 7, fair in 3, and poor in 5 . Similar results
followed treatment of patients with secondary thrombocytopenia. A response was noted at times “within a
week.” The mode of action of vincristine in increasing
platelet count is unknown (1). Although immunosuppression has not been discounted, other effects may be
more important, as suggested by the observation that
low-dose vincristine is capable of inducing thrombocytosis in laboratory animals, and probably in man, with
normal platelet counts (2).
These concepts were considered in dealing with
the problems of a 39-year-old woman with rheumatoid
arthritis who received a total of 335 mg of gold sodium
thiomalate over 8 weeks. The last 50-mg injection was
1289
given despite decreased platelets. This treatment was
followed by heavy menstrual flow, gingival bleeding,
and melena, and she was hospitalized on 1/21/77.
Hematocrit was 22, white blood count 7,200, and
platelet count 7,000. Because of bleeding, hypertension,
and a headache, she was given 8 units of platelets. The
platelet count immediately after platelet transfusion was
3,500. Ten additional units also had no effect on the
count, and the hematocrit fell to 16, necessitating transfusion with packed red blood cells. During the first day
she received 140 mg of methylprednisolone, and 60 mg
of prednisone daily thereafter. Dimercaprol was begun
at the same time, and was given to a total of 5700 mg
over I0 days. Vincristine was given in 2-mg intravenous
doses on the morning of 1/29/77. Serial platelet counts
were as follows:
1/21 :7,000 and 3,500
1/22 :7,000
1 /23 : 3,000
1/24 :3,000
1/25 : 1,000
1/26 :2,000
1/27 :6,000
1/28 :2,000
1/29: 1,OOO
1/30:9,000
1/3 1 :35,000
2/01 :94,000
2/03 : 358,000
2/04: 357,000
2/09: 346,000
The increase in platelets may have been a response to corticosteroids or dimercaprol or both, rather
than to vincristine. Nevertheless, their recovery suggests
that further trials with vincristine may be warranted in a
seriously compromised patient. Vincristine is not without side effects, especially those reflecting neurotoxicity,
and the dose is critical: large doses may “paradoxically”
cause thrombocytopenia.
GENEV. BALL,M.D.
University of Alabama in Birmingham
School of Medicine
University Station
Birmingham, Alabama 35294
REFERENCES
I . Ahn ‘S, Iarrington WJ, Seelman RC, Eytel CS: Vincristine therapy of idiopathic and secondary thrombocytopenias. N Engl J Med 291:376-380, 1974
2. Robertson JH, Crozier EH, Woodend B E Vincristine therapy of thrombocytopenias. N Engl J Med 292:108, 1975
(letter)
Arthritis and Rheumatism, Vol. 20, No. 6 (July-August 1977)
Intrapericardial Steroids in Treatment of
Rheumatoid Pericardial Tamponade
To the Editor:
Pericardial tamponade is a rare but catastrophic
complication of rheumatoid arthritis. A review of the
literature reveals only 22 cases of these associated entities (1-3). We present a case of Felty’s syndrome with
pericardial tamponade treated by pericardiocentesis and
instillation of intrapericardial steroids.
A 62-year-old white male was admitted to the
hospital complaining of shortness of breath and anterior
pleuritic chest pain. For 8 years before admission he had
severely deforming rheumatoid arthritis for which he
took occasional aspirin. The patient was noted to have
absolute neutropenia and splenomegaly 1.5 years before
hospitalization. Table 1 lists pertinent laboratory data.
A ssmTcsulfur colloid scan demonstrated hepatosplenomegaly. The patient did well until several days before
admission, when he noted gradually increasing shortness of breath and sharp anterior pleuritic chest pain.
Physical examination revealed an alert thin
male in moderate respiratory distress. Blood pressure
was 132/90 with a 14-mm pulsus paradoxus. The pulse
measured 100 beats per minute, respirations 32, and
temperature 98.4. The lung was dull to percussion at the
right base, and there were rales in that region. The
precordium was inactive, The liver span was 12 cm in
the midclavicular line, and the spleen was palpated three
finger-breadths below the left costal margin. Marked
rheumatoid deformities of the hand and feet were present. Multiple rheumatoid nodules were also noted.
Kussmaul’s sign and pericardial friction rubs were absent. Table 1 includes initial laboratory data. Chest
X-ray showed new cardiomegaly and a loculated right
pleural effusion. ECG was of low voltage. An emergency
echocardiogram confirmed the presence of a large pericardial effusion.
A percutaneous in-dwelling pericardial catheter
was inserted, and 600 cm9 of serosanguinous fluid were
withdrawn; the patient’s dyspnea improved markedly.
Table 1 shows the pericardial fluid analysis. Fluid studied by Dr. Gene Ball at the University of Alabama
revealed the presence of y-globulin complexes which
could be precipitated by monoclonal rheumatoid factor.
Before the pericardial catheter was removed, 60 mg of
methylprednisolone acetate was introduced into the pericardial sac. Subsequently the patient did well and was
discharged on 20 mg of prednisone every other day. He
has remained free of symptoms for 6 months without
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