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Serve reversible thrombocytopenia associated with meclofenamate.

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LETTERS
indomethacin treatment (26.0 5 15.6%; P < 0.005).
When PBL were obtained from the patient during
periods of medication or from the healthy control, in
vitro addition of indomethacin did not cause a significant change in generation of Con A-SC. These data
showing that the reduced generation of Con A-SC
activity during drug-free periods could also be reversed by in vitro addition of indomethacin to the
generation cultures indicate that the changes observed
in vivo were from the effect of the drug on lymphocyte
function and were not a nonspecific manifestation of
the clinical improvement. Since in vivo indomethacin
treatment of some patients with decreased Con A-SC
generation can affect the results of this assay, it is clear
that treatment with antiinflammatory drugs must be
considered in any study that attempts to relate Con ASC function to disease activity.
Acknowledgments. Supported in part by NIH
grants AM26696 and AM28395 and the Minnesota
Chapter of the Arthritis Foundation.
LARSSKOLDSTAM,
MD
University of Linkoping
Linkoping, Sweden
DAVIDZOSCHKE,
MD
Hennepin County Medical Center
Minneapolis, M N
RONALDMESSNER,MD
University of Minnesota School of Medicine
Minneapolis, M N
1. Strelkauskas AJ, Callery RT, McDowell J, Bore1 Y,
Scholossman SF: Direct evidence for loss of human
suppressor cells during active autoimmune disease. Proc
Natl Acad Sci USA 755150-5154, 1978
2. Abdou NI, Pascual E, Racela L: Suppressor T cell (ST)
dysfunction and anti-ST antibody in active early rheumatoid arthritis (abstract). Arthritis Rheum 22586, 1979
3. Chattopadhyay C, Chattopad yay H, Natvig JB, Michaelsen TE, Mellbye OY: Lack of suppressor cell activity in
rheumatoid synovial lymphocytes. Scand J Immunol
19:309-316, 1979
4. Keystone EC, Gladman DD, Buchanan R, Cane D,
Poplonski L: Impaired antigen-specific suppressor cell
activity in patients with rheumatoid arthritis. Arthritis
Rheum 23:124&1250, 1980
5. Wolinski SI, Goodwin YS, Messner RP, Williams RC:
Role of prostaglandin in the depressed cell-mediated
immune response in rheumatoid arthritis. Clin Immunol
Immunopathol 17:31-37, 1980
6. Goodwin JS: Modulation of Concanavalin A-induced
suppressor cell activation of prostaglandin Ez. Cell Immunol49:421-425, 1980
359
7. Skoldstam L, Zoschke DC, Messner RP: Prostaglandin
Ez and induction of Concanavalin-A-induced suppressor
cells. Clin Res 28:790A, 1980
8. Huskisson ED: Assessment for clinical trials. Clin Rheum
Dis 2:37-49, 1976
Severe, reversible thrombocytopenia
associated with meclofenamate
To the Editor:
Several nonsteroidal antiinflammatory drugs
have been introduced recently for the treatment of
arthritis and other musculoskeletal complaints. These
agents have generally been well tolerated, but at least
one (sulindac) has been associated with significant
hematologic toxicity (1,2). We report here a case of
severe, reversible thrombocytopenia associated with
meclofenamate, the most recent addition to the approved antiinflammatory medications.
The patient is an 80-year-old woman with a long
history of hypertension, arteriosclerotic cardiovascular disease, chronic urinary tract infection, and degenerative joint disease. During the 9 months before her
admission, she was treated with alpha-methyldopa,
trimethopridsulfamethoxazol, naproxen, buffered aspirin, and acetaminophen with codeine. Four weeks
before her admission, meclofenamate, 100 mg 3 times
daily, was added to the previous regimen. One day
before admission the patient noted numerous red skin
lesions and on the following day she was admitted to
the hospital (day 0). There was no personal or family
history of easy bruisability, prolonged bleeding, or
other blood dyscrasias.
The results of the physical examination showed
that the patient was afebrile and that there were
numerous petechiae and other purpuric lesions on the
trunk and all 4 extremities. Results of tests on a stool
sample were positive for occult blood. Other laboratory studies revealed a hematocrit of 25.5% and a
platelet count of 10,000/mm3 compared with 37.9%
and 149,000/mm3 respectively 5 weeks earlier. The
prothrombin time was 10.4 seconds (control 10.4 seconds), and the partial thromboplastin time was 26.1
seconds (control 24.1 seconds). Findings from direct
and indirect Coombs tests were negative.
All her medications were discontinued at the
time of admission, and clonidine, 0.2 mg twice daily,
was instituted for control of hypertension. The platelet
count increased from 10,000/mm3 on day 0 to
195,000/mm3 on day 4. Since trimethoprim/sulfamethoxazol was the suspected cause of the thrombo-
360
cytopenia ( 3 ) , meclofenamate was restarted at 100 mg
3 times daily on day 3. The patient was discharged to a
nursing home and clonidine and meclofenamate were
prescribed.
On day 8 the patient complained of fatigue,
malaise, and nausea. There was no evidence of new
bleeding. Laboratory studies at that time revealed a
platelet count of 5,000. The patient was readmitted,
and the meclofenamate was promptly discontinued.
On day 9 the patient received 6 units of platelets. From
day 8 to day 13 the platelet count increased steadily
from 5,000/mm3 to 198,000/mm3. When she was discharged on day 13, she was receiving clonidine and
was subsequently restarted on aspirin. Five weeks
after her discharge from the hospital, her followup
platelet count was 210,000/mm~.
We believe that this is the first report of thrombocytopenia associated with the use of meclofenamate. However, there are at least 5 reports of thrombocytopenia associated with the use of flufenamic
acid-related compounds (3). Coombs positive hemolytic anemia and marrow suppression with hypoplasia
have also been reported (4). Meclofenamate has only
recently been made available for widespread use in
rheumatic conditions and has not previously been
associated with blood dyscrasias.
LETTERS
The mechanism of thrombocytopenia in our
patient is unclear. It seems unlikely that marrow
suppression would explain the rapid onset of thrombocytopenia with the second administration and rapid
recoveries after discontinuation. Since Coombs positivity with hemolysis (4) occurs with related compounds, an immunologically mediated peripheral consumption with decreased platelet survival time may be
a more likely explanation.
F. SCHIMIZZI,
MD
GREGORY
PHILLIP
M. GRAEHL,MD
MD
JOSEPHP. MICHALSKI,
Veterans Administration Medical Center
Long Beach, C A
University of California
Irvine, C A
Morris EL, Hochberg MC, Dorsch CA: Agranulocytosis
and sulindac. Arthritis Rheum 24:752-753, 1981
Rosenbaum JT, O’Connor M: Thrombocytopenia associated with sulindac. Arthritis Rheum 24:753-754, 1981
Swanson M, Cool R: Drugs, Chemicals and Blood Dyscrasias. Hamilton, IL, Drug Intelligence, Inc., 1977, p 601
Mills JA: Nonsteroidal anti-inflammatory drugs (Part 11).
N Engl J Med 290:1002-1004, 1974
BOOK REVIEW
Progress in Clinical Immunology. Volume 4 . Edited by
Robert S . Schwartz, MD, New York, Grune and
Stratton, Inc., 1980. 179 pages. Illustrated. $23.50.
The fourth volume of this series contains
articles on “Drug-Induced
Systemic Lupus
Erythematosus” by Arthur Weinstein; “Immune
Responses of Human Lymphocytes In Vitro” by
Barton F. Haynes, Paul Katz, and Anthony S. Fauci;
“Evaluation and Clinical Significance of Circulating
Immune Complexes” by A. N . Theofilopoulos;
“Autoantibodies to the Insulin Receptor: Clinical
Significance and Experimental Applications” by Len
C . Harrison and C. Ronald Kahn; “Prospects for the
Clinical Control of IgE Synthesis” by David H. Katz;
and “Lymphocytotoxic Antibodies” by Raphael J.
DeHoratius.
Each review summarizes in moderate detail the
most recent results in the respective areas. Particular
emphasis is placed on the potential clinical applications of the experimental data. The references are
complete through 1979. However, rapid change in
clinical immunology will probably render many of
these reviews obsolete within a few years. Thus,
although the volume is well worth reading for rheumatologists with a particular interest in the subject matter, it is not a good investment for a personal library.
Moreover, a few of the articles are duplicated in other
immunology review series.
DENNISCARSON,MD
Scripps Clinic and Research Foundation
La Jolla, CA 92037
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