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Platelets in the synovial space.

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994
the normal range, but quantitative electromyography is
not yet, in the authors' opinion, as sensitive as careful
observation. These findings are substantiated in fact by
Rose and Willison (2), to whom Dr. Kaplan himself
referred.
Nerve conduction velocities were determined by
the techniques taught by the Mayo Clinic and accepted
by the American Association of Electromyography and
Electrodiagnosis. F-Wave studies were not performed
and the authors cannot see any indication for neuromuscular transmission studies in these patients.
The changes described were clear cut and unequivocal and were performed by an electromyographer
very well experienced in myopathies and myositis.
PHILIP
J . CLEMENTS,
M.D.
Assisrant Professor of Medicine
DAVIDS . CAMPION,
M.D.
Associate Professor of Medicine
UCLA School of Medicine
Los Angeles, California
As another approach to the question of the
presence of platelets in the joint, we have measured
the presence of a platelet-specific antigen, platelet
factor 4, in human synovial fluid. Synovial fluids
obtained at atraumatic arthrocentesis were stored at
-20°C until levels of platelet factor 4 antigen were
measured by a sensitive radioimmunoassay (12).
There are approximately 10 ng/ml of this material
in normal plasma (13,14), and as Figure I shows,
joint fluids from 3 patients with rheumatoid arthritis contained markedly elevated levels of this mate-
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REFERENCES
Clements PJ, Furst DE, Campion DS, Bohan A, Harris R,
Levy J, Paulus HE: Muscle disease in progressive systemic
sclerosis: diagnostic and therapeutic considerations. A rthritis Rheum 21:62-71, 1978
Rose AL, Willison RG: Quantitative electromyography
used in automatic analysis: studies in healthy subjects and
patients with primary muscle disease. J Neurol Neurosurg
Psychiat 30:403-410, 1967
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2 0.
Platelets in the Synovial Space
To the Editor:
Platelets are a potent source of mediators of
inflammation such as collagenase ( I ) , permeability enhancing factors (2), chemotactic factors (3,4), factors
which stimulate cellular proliferation (5-7), and prostaglandins and their intermediates (8). Materials such as
immune complexes (9) or monosodium urate crystals
(lo), which are known to be present in diseased joints
and to lead to inflammation there, stimulate platelets.
Thus the letter by Yaron and Djaldetti (11) suggesting that platelets gain entrance to the synovial
space provides an important additional link in the
chain of evidence indicating that platelets contribute
to the pathogenesis of certain forms of arthritis.
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Figure 1. Platelet Factor 4 antigen in human synovial fluid
Shaded area = mean f S D . Note the break in the ordinate.
995
rial. This indicates that platelet products were present in the synovial fluid from these patients. This
supports the concept that platelets may enter the
synovial space under certain circumstances and contribute to the pathogenesis of tissue injury there.
How platelets and their released products might enter
the joint and their role in various forms of arthritis
would thus appear to be questions for future investigation.
M.D.
MARKH. GINSBERG,
G. BRETH,M.D.
J. L. SKOSEY,
M.D.
Scripps Clinic and Research Foundation
La Jolla, California
University of Illinois School
of Medicine
Chicago, Illinois
REFERENCES
1. Chesney C, Harper E, Colman RW: Human platelet col-
lagenase. J Clin Invest 53:1647, 1974
2. Nachman R, Weksler BB, Ferris B: Increased vascular
permeability produced by human platelet granule cationic
extract. J Clin Invest 49:274, 1970
3. Weksler BB, Coupal C E Platelet-dependent generation of
chemotactic activity in serum. J Exp Med 137: 1419, 1973
4. Goetzl EJ, Woods J M , Gorman RG: Stimulation of human eosinophil and neutrophil polymorphonuclear leukocyte chemotaxis and random migration by 12-L-hydroxyl5,8,10,14-eicosa tetranoic acid. J Clin Invest 59: 179, 1977
5. Rutherford RB, Ross R: Platelet factors stimulate fibroblasts and smooth muscle cells quiescent in plasma serum
to proliferate. J Cell Biol 69:196, 1976
6. Yaron M, Yaron I, Herzberg M: Thrombocyte stimulation of hyaluronic acid production and proliferation rate
of human synovial fibroblasts. Scand J Rheumatol5:249,
1976
7. Castor CW, Ritchie JC, Scott ME, Whitney SL: Connective tissue activation. XI. Stimulation of glycosaminoglycan and D N A formation by a platelet factor. Arthritis Rheum 20:859, 1977
8. Smith JB, lngermain C, Kocsis JJ, Silver MJ: Formation
of prostaglandins during the aggregation of human platelets. J Clin Invest 52:965, 1973
9. Humphrey JH, Jaques R: The release of histamine and 5hydroxy-tryptamine (serotonin) from platelets by antigenantibody reactions (in vivo). J Physiol 128:9, 1955
10. Ginsberg MH, Kozin F, O’Malley M, McCarty DJ: Release of platelet constituents by monosodium urate crystals. J Clin Invest 60:999, 1977
1 I . Yaron M, Djaldetti M: Platelets in synovial fluid. Arthritis
Rheum 21:607, 1978
12. Ginsberg M H , Hoskins R, Sigrist P, Painter R: Purification of a heparin neutralizing protein from rabbit platelets
and its homology with human platelet factor four. Submitted for publication.
13. Bolton AE, Ludlam CA, Pepper DS, Moore S , Cash JD:
A radioimmunoassay for platelet factor 4. Thromb Res
8 5 1 , 1976
14. Ginsberg MH: Unpublished results
Severe Autoimmune Anemia and
Thrombopenia in Mixed Connective Tissue
Disease
To the Editor:
In mixed connective tissue disease (MCTD) mild
anemia is frequent, but Coombs’ positive hemolytic
anemia to the point of clinical significance has, we believe, only been reported once before ( 1 ). We observed
such a case simultaneously with autoimmune thrombopenia which subsided under corticosteroid therapy.
A 26-year-old woman had complained for 2 years
of arthalgias, proximal myalgias, and alopecia. Clinical
examination revealed non-deforming polyarthritis, sicca
syndrome, and skin trouble which included Raynaud’s
phenomenon with taut thick skin on fingers, livedo reticularis, and violaceous discoloration of eyelids. Temperature was 38°C and blood pressure 140/90 mm Hg.
A n ESR was 92 mm in the first hour, and hemoglobin level was 10.4 g/dl with normal blood cell count.
Coombs’ test for complement (type 111) on erythrocyte
surface was positive with no significant rate of circulating cold agglutinins. There was a polyclonal rise in
serum IgG reaching 47 g/l, antinuclear factors (ANF)
were positive up to 1 : 100,000 with speckled pattern.
Search for antibodies to extractable nuclear antigens
was positive only for the ribonuclease-sensitive antigen
(anti-RNP). LE cells and anti-dsDNA antibodies were
absent. Despite normal muscular enzyme levels, electromyogram revealed inflammatory myositis; the patient refused a muscle biopsy. Pulmonary function tests
and carbon monoxide diffusing capacity were restricted.
Histology confirmed Sjogren’s syndrome; cutaneous
and renal biopsies with immunofluorescence study
yielded no argument for systemic lupus erythematosus
(SLE). Diagnosis of MCTD was therefore retained and
the patient discharged under indomethacin treatment.
A month later, without any apparent reason,
marked pallor and intense asthenia set in. Physical examination revealed diffuse purpura with retina hemorrhage and splenomegaly. ESR was 98 mm/first hour,
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