ARTHRITIS & RHEUMATISM

Vol. 52, No. 6, June 2005, pp 19491950

2005, American College of Rheumatology

LETTERS
ciated with systemic lupus erythematosus and antiphospholipid
syndrome (Macchi L, Rispal P, Clofent-Sanchez G, Pellegrin
JL, Nurden P, Leng B, et al. Anti-platelet antibodies in
patients with systemic lupus erythematosus and the primary
antiphospholipid antibody syndrome: their relationship with
the observed thrombocytopenia. Br J Haematol 1997;98:336
41) and are usually associated with thrombocytopenia. However, in some cases, antiplatelet antibodies have been shown to
induce acquired thrombopathy with normal platelet counts. In
the reported cases, results of in vitro aggregation tests are
usually abnormal. We think that sustained prolonged bleeding
time in our patient with LAC was related to an acquired
thrombopathy induced by antiplatelet antibodies. Repeated
ristocetin-dependent platelet agglutination tests showed abnormal in vitro aggregation. This could suggest that in vitro
tests for platelet aggregation studies may not always be sensitive enough to detect abnormal platelet function. Furthermore,
the presence of autoantibodies to platelet major membrane
glycoproteins may interfere (as in the case of endothelial cell
activation by antibodies causing LAC) with in vivo primary
hemostasis. We therefore propose that in patients with LAC
and a prolonged bleeding time, when results of platelet
aggregation tests are normal, a MAIPA should then be performed, followed by repeated platelet aggregation tests.

DOI 10.1002/art.21093

Monoclonal antibody immunospecific platelet assay in

patients with lupus anticoagulant and prolonged
bleeding time: comment on the article by Urbanus
et al
To the Editor:
We read with interest the report by Urbanus et al
(Urbanus RT, de Laat HB, de Groot PG, Derksen RH.
Prolonged bleeding time and lupus anticoagulant: a second
paradox in the antiphospholipid syndrome. Arthritis Rheum
2004;50:36059.) of their analysis about prolonged bleeding
time in patients with lupus anticoagulant (LAC). The authors
reported a prolonged bleeding time in 21 of 27 patients (78%)
with LAC. Of these 21 patients, 17 had a normal platelet count.
For all these patients, plasma levels of von Willebrand factor
and aggregation of platelets on the agonists ADP, collagen,
and arachidonic acid were normal, as was ristocetin-dependent
platelet agglutination. These results led the authors to postulate another mechanism for prolonged bleeding time in patients with LAC. They call it a second paradox in the
antiphospholipid syndrome when patients with prolonged
bleeding time do not display a bleeding tendency. Urbanus et
al hypothesize that antibodies causing LAC may activate
endothelial cells, leading to localized formation of nitric oxide
and prostacyclin, which are known inhibitors of platelet functioning. This would account for the paradox of prolonged
bleeding time in these patients despite the normal results of in
vitro platelet aggregation studies.
We noticed that autoantibodies against platelets were
not analyzed in these patients. We would like to suggest
another mechanism that we observed in 1 patient with LAC.
We performed laboratory tests on blood obtained from a
young woman who was found during presurgical testing to have
a prolonged bleeding time (12 minutes). Her platelet count
(215 109/liter), mean platelet volume (7.4 fl), and platelet
morphology were normal. Further investigation because of a
prolonged thromboplastin time revealed LAC associated with
antiphospholipid antibodies and the presence of antinuclear
antibodies at a titer of 1:300. The patients history was
unremarkable except for a mild and transitory postpartum
thrombocytopenia (90 109/liter) 3 years previously. We
performed a monoclonal antibody immunospecific platelet
assay (MAIPA) and a platelet aggregation test to search for
acquired thrombopathy. The MAIPA revealed significant titers of antiglycoprotein IIb-IIIa (antiGPIIb-IIIa), anti
GPIa-IIa, and antiGPIb-IX. Despite these results, in vitro
aggregation of platelets on the agonists ADP, collagen, adrenaline, and arachidonic acid was normal, as was ristocetindependent platelet agglutination. The results of platelet aggregation tests 2 months later were normal, except for the
ristocetin-dependent platelet agglutination test, which showed
marked hypoaggregation.
It is well known that antiplatelet antibodies are asso-

N. Schleinitz, MD
L. Camoin, PharmD, PhD
E. Bernit, MD
D. Reviron, MD
V. Veit, MD
J. R. Harle, MD
University Hospital CHU la Conception
Marseille, France

DOI 10.1002/art.21217

Reply
To the Editor:
We thank Dr. Schleinitz and colleagues for their letter,
in which they support our finding of an association between
LAC and a prolonged bleeding time in the presence of normal
platelet counts and normal platelet aggregation test results.
Since we did not perform a MAIPA, we cannot exclude the
possibility that our patients had autoantibodies against specific
glycoproteins on the platelet membrane that can prolong the
bleeding time but that simultaneously do not interfere with
traditional tests for platelet function. It remains hard to explain
why the ristocetin-dependent platelet agglutination was normal at the initial screening and abnormal during followup in
the patient described by Schleinitz et al. In this regard, it would
be of interest to know whether the LAC and MAIPA findings
1949

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LETTERS

were also positive at the time of the abnormal result of

theristocetin-dependent platelet agglutination test.
R. T. Urbanus

P. G. de Groot, PhD
R. H. W. M. Derksen, MD, PhD
University Medical Center
Utrecht, The Netherlands

DOI 10.1002/art.21057

Clinical Images: Tuberculous rice bodies of the wrist

The patient, a 21-year-old man, presented with a 2-year history of a gradually increasing mass on the ulnar aspect of his right wrist.
Physical examination revealed a movable mass on the volar and ulnar aspects of the right wrist. Results of chest radiography were
normal. Sagittal (A) and axial (B) T2-weighted magnetic resonance imaging (MRI) revealed multiple nodules (small arrows in A
and B) of low signal intensity within the distended ulnar bursa (large arrow in A and B) and flexor tendon sheaths. These nodules
extended through the carpal tunnel to the digits. The MRI appearance of the nodules was consistent with that of rice bodies (13).
Surgical excision was performed and showed multiple polished white rice bodies (small arrows in C) and thickened synovium (C)
in the distended bursa and flexor tendon sheaths. Histologic examination of the specimens showed caseating granulomas with
Langerhans-type giant cells. Acid-fast bacilli were not seen on Ziehl-Neelsen staining of the surgical specimen, but Mycobacterium
tuberculosis was grown after 8 weeks of incubation, which confirmed the diagnosis of tuberculous tenosynovitis and bursitis.
Microscopic observation revealed that the rice bodies consisted of an inner amorphous cord of eosinophilic material which was
surrounded by collagen and fibrin (36). The patient was treated with ethambutol, isoniazid, and rifampin for 9 months, and he
had no recurrence. The appearance and composition of rice bodies in tuberculosis are similar to those in rheumatoid arthritis,
seronegative inflammatory arthropathies, chronic synovial inflammation, and other chronic, low-grade synovial infections such as
those that result from mycobacteria (36). The etiology of rice body formation remains unclear. Some hypotheses are synovial
microinfarction and de novo formation within the synovial fluid, followed by fibrin aggregation (5,6).
1. Hsu CY, Lu HC, Shih TT. Tuberculous infection of the wrist: MRI features.
AJR Am J Roentgenol 2004;183:6238.
2. Chau CL, Griffith JF, Chan PT, Lui TH, Yu KS, Ngai WK. Rice-body
formation in atypical mycobacterial tenosynovitis and bursitis: findings on
sonography and MR imaging. AJR Am J Roentgenol 2003;180:14559.
3. Lee EY, Rubin DA, Brown DM. Recurrent mycobacterium marinum tenosynovitis of the wrist mimicking extraarticular synovial chondromatosis on
MR images. Skeletal Radiol 2004;33:4058.
4. Popert J. Rice-bodies, synovial debris, and joint lavage. Br J Rheumatol
1985;24:12.
5. Cheung HS, Ryan LM, Kozin F, McCarty DJ. Synovial origins of rice bodies
in joint fluid. Arthritis Rheum 1980;23:726.
6. Popert AJ, Scott DL, Wainwright AC, Walton KW, Williamson N, Chapman
JH. Frequency of occurrence, mode of development, and significance of rice
bodies in rheumatoid joints. Ann Rheum Dis 1982;41:10917.

Guo-Shu Huang, MD
Chian-Her Lee, MD
Cheng-Yu Chen, MD
Departments of Radiology
and Orthopedic Surgery
Tri-Service General Hospital
Taipei, Taiwan, Republic of China