Antiphospholipid Antibodies and
Arterial Thrombosis

Case Reports and a Review of the Literature
Gregory S. McGee, MD; William H. Pearce, MD; Leena Sharma, MD;
David Green, MD, PhD; James S. T. Yao, MD, PhD

Antiphospholipid antibodies are a relatively heterogeimmunoglobulins with binding specificities for
negatively charged or neutral phospholipids. Currently, the
most commonly detected antiphospholipid antibodies include the anticardiolipin antibody, the lupus anticoagulant,
and an antibody implicated in false-positive VDRL testing.
Recently, a clinical syndrome of vaso-occlusive disorders
associated with antiphospholipid antibodies has been identified and may result from immune-mediated disruption of
endothelial function. This clinical syndrome encompasses
\s=b\

neous mix of

arterial and venous thrombosis, recurrent fetal loss, neurologic dysfunction (eg, migraine, chorea, and encephalopathy), systemic and pulmonary arterial hypertension, and
endocardial disease. Although most commonly associated
with systemic lupus erythematosus, the antiphospholipid
antibody syndrome also has been identified in patients with
vaso-occlusive disease without systemic lupus erythematosus. Recently, identification of antiphospholipid antibodies
has been facilitated by the development of a more sensitive
assay for anticardiolipin antibody. In this article, case histories of three patients with arterial thrombosis and associated anticardiolipin antibodies, including the first associated case of terminal aortic thrombosis, are reviewed and
the subject of the antiphospholipid antibody syndrome is
discussed.

(Arch Surg. 1992;127:342-346)
antibodies have been detected since
Wassermann et used complement fixation in 1906
to detect reagin in the serum of patients with syphilis. The
first antigens were saline extracts of liver from fetuses
with syphilis, followed by alcohol extracts of various nor-

Antiphospholipid al1

Accepted for publication September 22, 1991.
From the Department of Surgery, Division of Vascular Surgery

(Drs McGee, Pearce, and Yao), and the Department of Medicine,
Divisions of Rheumatology (Dr Sharma) and Hematology/Oncology
(Dr Green), Northwestern University Medical School, Chicago, Ill.

Reprint requests to Division of Vascular Surgery, Northwestern
University, 251 E Chicago Ave, Suite 626, Chicago, IL 60611 (Dr
Pearce).

mal tissues. Pangborn2 in 1942 noted that the antigen re¬

sponsible for reagin reactivity was an acidic phospholipid
extracted from a bovine heart muscle, which was subse¬
quently named cardiolipin. Following the development of
the more specific treponemal immobilization test in 1949,
many patients were found who were either transiently or
chronically false positive using the VDRL (cardiolipin)
antigen. These patients had a higher prevalence of
autoimmune disease and other antibodies in their serum.3
Thrombotic complications have long been associated
with systemic lupus erythematosus (SLE). The occurrence
of thromboembolic events in patients with SLE was first
noted by Baehr et al4 in 1935, and the association between
circulating anticoagulants, false-positive VDRL test re¬
sults, and SLE was reported by Conley and Hartmann5 in
1952. These lupuslike anticoagulants have been found to
be antibodies to procoagulant phospholipids, which pro¬
long the activated partial thromboplastin time, thromboplastin (factor III), and properties of viper venom testing.
Diagnosis of lupus anticoagulants requires correction of
the activated partial thromboplastin time and phospho¬
lipid, with care taken to remove platelet debris from sam¬
ples before testing. In 1963, Bowie et al6 first reported four
cases of thrombotic complications in patients with both
SLE and circulating anticoagulants. This apparent para¬
dox of circulating anticoagulants and thrombosis was ini¬
tially misinterpreted as a compensatory phenomenon as¬
sociated with increased thromboplastin generation in
these patients with SLE and anticoagulants.
Laurell and Nilsson7 demonstrated in 1957 that cardio¬

lipin in syphilitic assays would remove lupus anticoagu¬
lant activity, and in 1980, Thiagarajan et al8 confirmed the
presence of specific antiphospholipid antibodies (APLA)
in patients with the lupus anticoagulant. The lupus anti¬
coagulant and the anticardiolipin antibody appear to be
similar immunoglobulins with different binding specific¬
ities. Inhibition of endothelial prostacyclin secretion by
these circulating immunoglobulins was proposed by Car¬
reras et al9 to explain the increased thrombotic complica¬
tions in patients with lupuslike antibodies. Other possi¬
ble mechanisms suggested to account for excessive

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Fig 1. —Case 2. Carotid angiogram demonstrates occlusion of the
right internal carotid artery distal to the bifurcation.

Fig 2. —Case 2. Upper-extremity angiogram reveals occlusion of the
right proximal brachial artery.

thrombosis in patients with lupus and APLA include
prekallikrein inhibition,10 tissue factor induction,11 thrombomodulin neutralization,12 alteration in protein C and S
activity,1314 and lowered functional antithrombin III ac¬

gram was obtained and showed no recurrence of the thrombus.
Aspirin therapy was substituted for warfarin. She did well for
the next 5 months, but then had a first trimester spontaneous
abortion. At this writing, she is asymptomatic and continues as¬

tivity.15
Following the standardization of the anticardiolipin
antibody enzyme-linked immunosorbent assay for this
APLA in 1985,16 increasing numbers of patients with
thrombotic complications with and without autoimmune
diseases tested positively for anticardiolipin antibodies.
This report documents the clinical histories and outcomes
of three patients presenting to a vascular surgical service
with arterial thrombosis and positive APLA. The anticar¬
diolipin antibody test used was a solid phase enzyme immunoassay (EL-ACA, Thera Test Laboratories Ine, Chi¬
cago, 111).
REPORT OF CASES
CASE 1.—A 25-year-old white woman was examined because
of the sudden, transient loss of sight in a sector of the right vi¬
sual field. She had no history of neurologic events, no other
known medical illnesses, and no family history of thrombotic or
connective tissue disorders. Laboratory studies revealed normal
values for proteins C, S, fibrinogen, and antithrombin III; how¬
ever, she tested positively for the antinuclear antibody, and her
erythrocyte sedimentation rate and rheumatoid factor were ele¬
vated. There was no clinical evidence of SLE or scleroderma, and
the results of her lupus erythematosus cell preparation were
negative. Her initial platelet count was 155xl09/L, her prothrombin time was 12 seconds, and her partial thromboplastin
time was 35 seconds. The results of tests for the anticardiolipin
antibody (strong positive IgG, weakly positive IgA, and negative
IgM) and the lupus anticoagulant were positive.
The results of the carotid duplex examination were normal,
and a cerebral angiogram failed to demonstrate extracranial oc¬
clusive disease or evidence of intracranial vasculitis. The transesophageal echocardiogram revealed a mass in the left atrium
near the mitral valve that was thought to be consistent with a
myxoma. The preoperative diagnosis was an atrial myxoma, yet,
during thoracotomy, a large intra-atrial thrombus was found and
removed. A therapeutic postoperative regimen of warfarin
sodium was begun, but after 5 months, the patient again expe¬
rienced a transient episode of visual loss. A second echocardio-

pirin therapy.

Case 2.—A 26-year-old woman was seen for evaluation of
thigh and buttock claudication. The patient had suffered a right
hemispheric stroke 4 months before admission, and a cerebral
arteriogram revealed an occluded right internal carotid and right
brachial artery (Figs 1 and 2). The angiogram showed no
evidence of aortitis. A transesophageal echocardiogram revealed
a small residual ventriculoseptal defect from a repair done at age

22 months, and no intracardiac thrombus was seen. The results
of tests for erythrocyte sedimentation rate, antinuclear antibody,
and lupus erythematosus preparation were normal; however,
the results of her IgG anticardiolipin antibody test were moder¬
ately positive, and she was given aspirin and warfarin sodium.
A mild residual upper and lower extremity weakness persisted,
and an ambulatory rehabilitation program was initiated. In the
ensuing 3 months, her walking improved, but she developed
claudication that progressed from left calf pain at five blocks to
bilateral buttock cramping after walking one half block.
Her surgical history included a ventricular septal defect repair
at age 22 months and a left femoral thrombectomy with vein
patch angioplasty 3 years before admission. She denied having

diabetes, myocardial infarction, hyperlipidemia, or hyperten¬

sion, although she had a 10-year history of migrainelike head¬
aches. She denied the use of tobacco, alcohol, oral contracep¬
tives, or illegal drugs, and was taking warfarin, ranitidine
hydrochloride and aspirin on admission. She had no family his¬
tory of autoimmune disease or premature atherosclerosis.
On physical examination, she was an alert, normotensive
white woman without a facial rash or masklike facies. She had
strong and symmetric carotid pulses without temporal artery
tenderness. A holosystolic cardiac murmur was heard, while her
abdomen was without masses, tenderness, or bruits. The results
of an extremity examination revealed nonpalpable right brachial,
ulnar, and radial pulse and decreased left leg strength. Palpable
pulses were absent in both lower extremities, with ankle-brachial
indexes less than 0.3 bilaterally. Laboratory values on admission
included a hemoglobin of 134 g/L, platelet count of 185 x 109/L,
prothrombin time of 17 seconds, partial thromboplastin time of
27 seconds, fibrinogen of 2.55 g/L, and normal renal and hepatic
profiles. Her erythrocyte sedimentation rate was 19 mm/h, and
the results of tests for anti-double-stranded DNA, antiribonu-

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to posterior tibial bypass with reversed saphenous vein was
performed. Anticoagulation with heparin sodium was contin¬
ued after the surgical procedure, and she was discharged with
a regimen of nifedipine, warfarin, enteric-coated
aspirin, and
prednisone. The graft was patent 2 years later.

Fig 3. —Case 2. A translumbar aortogram reveals terminal aortic oc¬

clusion.

cleoprotein, lupus erythematosus preparation, and rheumatoid
factor were negative. The results of her protein C and S levels as

well as her antithrombin III levels were normal. The results of the
tests for anticardiolipin antibody were positive (IgG positive and
IgM negative), and the results of tests for lupus anticoagulant
and VDRL were negative.
A translumbar aortogram revealed occlusion of her infrarenal
aorta (Fig 3), and aortobifemoral grafting was performed with
normalization of distal pulses. The patient did well after the sur¬
gical procedure and was to continue aspirin and warfarin sodium

therapy at discharge.
Case 3. —A 36-year-old white woman with SLE was examined
for complaints of recurrent right-foot ischemia. She had a history
of lower extremity Raynaud's phenomenon and had been
treated with prednisone, cyclophosphamide, nifedipine, and
Bier's Block anesthesia with transient symptomatic relief. Two
months before admission, she had undergone a short-segment
right tibial to tibial bypass for rest pain resulting from focal tibial
vessel occlusion, and had been given warfarin sodium after sur¬
gery. She returned with recurrent rest pain.
Her medical history was significant for SLE of 18 years' dura¬
tion. She did not have hypertension, diabetes, stroke, myocardial infarction, or hyperlipidemia. She denied the use of tobacco,
oral contraceptives, or illegal drugs. She had no family history

of premature atherosclerosis or autoimmune disease.
On examination, she was normotensive with symmetrically
strong brachial and radial pulses. She had no cervical bruits, and
the results of cardiopulmonary and abdominal examinations
were normal. She had symmetric and strong femoral and
popliteal pulses, with palpable left posterior tibial and dorsalis
pedis pulses. She had a cyanotic right foot with no audible right
pedal pulses. She had evidence of polyarthritis and a peripheral

neuropathy.
Her laboratory data demonstrated a hemoglobin of 121 g/L,
hematocrit of 0.35, a platelet count of 351 x 109/L, a prothrombin
time of 12.6 seconds, and a partial thromboplastin time of 30
seconds. She had a normal renal and hepatic profile, and normal
antithrombin III and protein C and S levels. Her sedimentation
rate was elevated at 83 mm/h, and the results of tests for lupus
erythematosus cell preparation and IgM and IgG anticardiolipin
antibodies were positive. Results of the lupus anticoagulant and
VDRL testing were negative.
An angiogram confirmed occlusion of her tibial bypass.
Thrombolytic therapy was used to recanalize her tibial vein graft,
which appeared diffusely sclerotic angiographically. A popliteal

COMMENT
are acquired autoantibodantibodies
Antiphospholipid
ies (IgG, IgM, and IgA) that are often found in patients
with SLE and other autoimmune disorders. Various
names have been given to these antibodies, including the
lupus anticoagulant, the anticardiolipin antibody, and the
antibody responsible for the false-positive syphilis
(VDRL) test. The lupus anticoagulant derives its name
from its ability to prevent the formation of the prothrombin activator complex required for converting prothrombin to thrombin, resulting in prolongation of the activated
partial thromboplastin time and Russell's viper time.
Cardiolipin is the phospholipid antigen used in screening
tests for syphilis, and thus arises the correlation between
anticardiolipin antibodies and false-positive VDRL tests.
Although a recent study demonstrated separation of lu¬
pus anticoagulant and anticardiolipin activity,17 little ev¬
idence exists to confirm these as distinct antibodies,1819
and they might be best characterized as having different
specificities with overlapping reactivities.
Studies of APLA have reported wide ranges in their
prevalence. In patients with SLE, the prevalence of anti¬
cardiolipin antibody is 21% to 63%, and the prevalence of
the lupus anticoagulant is 6% to 73%.19-20"24 In normal
young adults, the prevalence of anticardiolipin antibodies
ranges from 0% to 7.5% .18'20 Patients with APLA are more
likely to be female (in a 4:1 ratio) and younger if they have
SLE than patients with non-SLE disorders.25-26 In patients
with non-SLE disorders, the prevalence of APLA ranges
from 4% to 87%,18 and includes elderly patients and pa¬
tients with acute infections, arthritis (both osteo and

rheumatoid), syphilis, scleroderma, systemic lupus
erythematosus, drug-induced (chlorpromazine) lupus,
Guillain-Barré syndrome, and patients infected with the

human immunodeficiency virus.27"31 The apparent in¬
crease in the prevalence of APLA syndrome is partially
related to improved assays for the detection of anticardi¬
olipin antibody. The use of enzyme-linked immunosorbent assays or solid-phase radioimmunoassay tech¬
niques, introduced in 1983,32 has made the detection of
anticardiolipin antibody the most specific and the most
sensitive of the tests for APLA syndrome.
Although originally described in patients with bleeding
disorders, APLA such as the lupus anticoagulant are
rarely related to hemorrhage. Much more germane is the
risk of both arterial and venous thrombosis and abortion
in patients with APLA. The etiology of these clinical
events may involve one of several mechanisms. Adher¬
ence of the antibody to lipid to the platelet surface
may
initiate platelet aggregation and attachment,33 or it may
inhibit endothelial cell production of the vasodilator
prostacyclin.34 Defects in fibrinolysis may result from a
decrease in plasminogen activator release or from dimin¬
ished protein C, thrombomodulin, or antithrombin III ac¬
tivity in patients with APLA syndrome.10"15,35 Although
several studies have suggested that high antibody titer
and specific antibody isotype (IgG and IgA) may be asso¬
ciated with an increased risk of thrombosis,36-37 no firm
consensus on this subject has been reached.

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The clinical disorders in which APLA have been re¬
ported are varied and include recurrent midterm miscar¬

riage, pulmonary hypertension, endocardial disease,

thrombocytopenia, avascular necrosis, transverse myeli¬
tis, migraine, chorea, Guillain-Barré syndrome, seizures,
livedo reticularis, chronic leg ulcers, arterial thrombosis
(cerebral, coronary, retinal, and peripheral), and venous
thrombosis (recurrent iliofemoral deep vein thrombosis,

renal vein, vena cava, and retinal vein). Patients who test
positive for both lupus anticoagulant and APLA have a
ninefold increased risk of arteriovenous thrombosis. The
first patient had many of the classic stigmata of APLA

syndrome, including unexplained thromboses, neuro¬
logic dysfunction, thrombocytopenia, and spontaneous

abortion. She had evidence of an ill-defined autoimmune
disease, and thus would be considered to have secondary
APLA syndrome. The second patient had no evidence of
SLE or other autoimmune disorders, and would be clas¬
sified as having primary APLA syndrome. The most
common site of thrombosis in patients with non-SLE
APLA syndrome is in the cerebral vessels, often resulting
in neurologic dysfunction and stroke.38 As in the first two
patients described, the diagnosis should be suspected
from a history of thrombotic complications in patients
without atherosclerotic risk factors such as age, hyper¬
tension, and smoking, and should be confirmed with a
test for anticardiolipin antibody and lupus anticoagulant.
The association of thrombosis with the lupus anticoag¬
ulant in patients with SLE was first described in 1963.6 Of
patients with SLE and anticardiolipin antibody, as in the
third patient in this series, almost one third will have
thrombotic events, while in patients with SLE and throm¬
bosis, almost two thirds will test positively for the
anticardiolipin antibody.18 Again, the cerebral circulation
is most commonly affected,38 with sporadic reports of ax¬
illary, retinal, digital, and mesenteric thrombosis.39"41 Pe¬
ripheral arterial disease in patients with SLE who are an¬
tiphospholipid antibody-negative is rare, occurring in
fewer than 1.5% of patients.42 Therefore, patients with
SLE who manifest symptoms of extremity hypoperfusion,
as in the third patient described, should be tested using
the lupus anticoagulant and the anticardiolipin antibody
enzyme-linked immunosorbent assay. Antibody titers
have been shown to fall during active thrombosis, mak¬
ing exclusion of the diagnosis difficult during the acute
phase.43 Antibody titers should be rechecked in 4 to 6
weeks to confirm or exclude the diagnosis.
The treatment of patients with APLA is determined by
the presence of an associated autoimmune disorder
and/or thrombotic events. In asymptomatic cases de¬
tected with screening studies, no treatment is recom¬
mended. In patients with an associated autoimmune dis¬
ease (eg, SLE) and clinical manifestations of APLA
syndrome (eg, fetal wastage, arteriovenous thrombosis),
appropriate immunosuppression and long-term antico¬
agulation are necessary to prevent recurrent thrombosis.
In patients without an autoimmune disease and mani¬
festing clinical evidence of APLA, long-term anticoagulation is also recommended. In one study, discontinuation
of oral anticoagulation resulted in recurrent thrombosis,44
leading some authors to recommend either indefinite anticoagulation or treatment until the results of APLA tests
were

negative.45

In summary, antiphospholipid antibodies are a group
of heterogeneous autoantibodies frequently associated

with autoimmune disease and thrombotic events. Their
presence may be suspected after finding a false-positive
syphilis test result, the lupus anticoagulant, an elevated
partial thromboplastin time, or thrombocytopenia. The
diagnosis is best confirmed with the enzyme-linked
immunosorbent assay or solid phase anticardiolipin test,
with treatment designed to control the autoimmune dis¬
ease and prevent recurrent thromboembolism.
This study was supported in part by the Alyce F. Salerno Foun¬

dation, Chicago, III.

References
1. Wassermann A, Neisser A, Bruck C. Eine serodiagnostische reaktion bei syphilis. Dtsch Med Wochenschr. 1906;32:745-746.
2. Pangborn MC. Isolation and purification of serologically active
phospholipid from beef heart. J Biol Chem. 1942;143:247-256.
3. Moore JE, Mohr CF. Biologically false positive serologic tests for
syphilis: type, incidence, and cause. JAMA. 1952;150:467-473.
4. Baehr G, Klemperer P, Schifrin A. A diffuse disease of the peripheral circulation (usually associated with lupus erythematosus and
endocarditis). Trans Assoc Am Physicians. 1935;50:139-155.
5. Conley CL, Hartmann RC. A hemorrhagic disorder caused by circulating anticoagulant in patients with disseminated lupus erythematosus. J Clin Invest. 1952;31:621-622.
6. Bowie WEJ, Thompson JH, Pasacuzzi CA, Owen CA. Thrombosis
in systemic lupus erythematosus despite circulating anticoagulants. J

Lab Clin Med. 1963;62:416-430.
7. Laurell A, Nilsson IM. Hypergammaglobulinemia, circulating anticoagulant and biologically false positive Wassermann reaction: a study
of two cases. J Lab Clin Med. 1957;49:694-707.
8. Thiagarajan P, Shapiro SS, DeMarco L. Monoclonal immunoglobulin M-lambda coagulation inhibitor with phospholipid specificity:
mechanism of a lupus anticoagulant. J Clin Invest. 1980;66:397-405.
9. Carreras LO, Vermylen JG. 'Lupus' anticoagulant and thrombosis:
possible role of inhibition of prostacyclin secretion. Thromb Haemost.

1982;48:28-40.

10. Sanfelippo MJ, Drayana CJ. Prekallikrein inhibition associated
with the lupus anticoagulant: a mechanism of thrombosis. Am J Clin
Pathol. 1982;77:275-279.
11. Tannenbaum SH, Finko R, Cines DB. Antibody and immune
complexes induce tissue factor production by endothelial cells. J
Immunol. 1986;137:1532-1537.
12. Freyssinet JM, Wiesel ML, Gauchy J, Boneu B, Cazenave JP. An
IgM lupus anticoagulant that neutralizes the enhancing effect of phospholipid on purified endothelial thrombomodulin activity: a mechanism for thrombosis. Thromb Haemost. 1986;55:309-313.
13. Freyssinet JM, Cazenave JP. Lupus-like anticoagulants' modulation of the protein C pathway and thrombosis. Thromb Haemost.

1987;58:679-681.
14. Walker TS, Triplett DA, Javed N, Musgrave K. Evaluation of lupus
anticoagulants: antiphospholipid antibodies, endothelium-associated
immunoglobulins, endothelial prostacyclin secretion, and antigenic
protein S levels. Thromb Res. 1988;51:267-281.
15. Cosgriff TM, Martin BA. Low functional and high antigenic
antithrombin III level in a patient with the lupus anticoagulant and recurrent thrombus. Arthritis Rheum. 1981;24:94-96.
16. Loizou S, McCrea JD, Rudge AC,
Reynolds R, Boyle CC, Harris EN.
Measurement of anticardiolipin antibodies by an enzyme-linked immunosorbent assay (ELISA): standardization and quantitation of results.
Clin Exp Immunol. 1985;62:738-745.
17. Exner T, Sahman N, Trudinger B. Separation of anticardiolipin
antibodies from lupus anticoagulant on a phospholipid-coated polystyrene column. Biochem Biophys Res Commun. 1988;155:1001-1007.
18. Love PE, Santoro SA. Antiphospholipid antibodies: anticardiolipin and the lupus anticoagulant in systemic lupus erythematosus (SLE)
and in non-SLE disorders. Ann Intern Med. 1990;112:682-698.
19. Meyer O, Cyna L, Bourgeois P, Kahn MF, Ryckewaert A. Profile
and cross-reactivities of antiphospholipid antibodies in systemic lupus
erythematosus and syphilis. Clin Rheumatol. 1987;6:369-377.
20. Manoussakis MN, Gharavi AE, Drosos AA, Kitridou RC, Moutsopoulous HM. Anticardiolipin antibodies in unselected autoimmune
rheumatic disease patients. Clin Immunol Immunopathol. 1987;44:297\x=req-\

307.
21. Meyer O, Piette JC, Bourgeois P, et al. Antiphospholipid antibodies: a disease marker in 25 patients with autoimmune antibody

negative systemic lupus erythematosus (SLE): comparison with a group
of 91 patients with antinuclear antibody positive SLE. J Rheumatol.
1987;14:502-506.
22. Regan MG, Lackner H, Karpatkin S. Platelet function and coagu-

lation profile in lupus erythematosus. Ann Intern Med. 1974;81:462-468.
23. Exner T, Rickard KA, Kronenberg H. A sensitive test demonstrat-

Downloaded From: http://archsurg.jamanetwork.com/ by a Oakland University User on 06/15/2015

ing lupus anticoagulant and its behavioral patterns. Br J Haematol.
1978;49:141-143.
24. Rosner E, Pauzner R, Lusky A, Modan M, Mang A. Detection and
quantitative evaluation of lupus circulating activity. Thromb Haemost.
1987;57:144-147.
25. Schleider MA, Nachman RL, Jaffe EA, Coleman M. A clinical study
of the lupus anticoagulant. Blood. 1976;48:499-509.
26. Triplett DA, Brandt JT, Musgrave KA, Orr CA. The relationship
between lupus anticoagulants and antibodies to phospholipid. JAMA.

1988;259:550-554.

27. Derkson RHWM, Bouma BN, Kater L. The prevalence and clinical
association of the lupus anticoagulant in systemic lupus erythematosus.
Scand J Rheumatol. 1987;16:185-192.
28. Harris EN, Gharavi AE, Hughes GRV. Antiphospholipid antibodies. Clin Rheumatol Dis. 1985;11:591-609.
29. Espinoza LR, Hartman RL. Significance of the lupus anticoagulant.
Am J Hematol. 1986;22:331-337.
30. Fort JG, Chowchock S, Abruzzo JL, Smith JB. Anticardiolipin antibodies in patients with rheumatic diseases. Arthritis Rheum.

1987;30:752-760.
31. Johansson EA, Lasus A. The occurrence of circulating anticoagu-

lants in patients with syphilitic and biologically false positive antilipoidal antibodies. Ann Clin Res. 1974;6:105-108.
32. Harris EN, Boey ML, Mackworth-Young CG, et al. Anticardiolipin
antibodies: detection by radioimmunoassay and association with
thrombosis in systemic lupus erythematosus. Lancet. 1983;2:1211-1214.
33. Mueh JR, Herbst KD, Rapaport SI. Thrombosis in patients with the
lupus anticoagulant. Ann Intern Med. 1980;92:156-159.
34. Carreras LO, Defreyn G, Machin SJ, Vermylen JG, Van Assche A.
Arterial thrombosis, intrauterine death, and lupus anticoagulant: detection of an immunoglobulin interfering with prostacyclin formation.
Lancet. 1981;1:244-246.
35. Chu P, Russell N, Cater D, Harris R, Powell R. Mechanisms of de-

fective fibrinolysis in systemic lupus erythematosus. Arthritis Rheum.
Abstract.
36. Kalunian KC, Peter JB, Middlekauff HR, et al. Clinical significance
of a single test for anticardiolipin antibodies in patients with systemic
lupus erythematosus. AmJ Med. 1988;85:602-608.
37. Harris EN, Chan JK, Asherson RA, Aber VA, Gharavi AE, Hughes
GR. Thrombosis, recurrent fetal loss, and thrombocytopenia: predictive value of the anticardiolipin antibody test. Arch Intern Med.

1987;30(suppl):69.

1986;146:2153-2156.
38. Levine SR, Welch KMA. The spectrum of neurologic disease associated with antiphospholipid antibodies. Arch Neurol. 1987;4:876\x=req-\

883.
39. Asherson RA, Harris EN, Gharavi AE. Aortic arch syndrome associated with anticardiolipin antibodies and the lupus anticoagulant:
comment on Ferrante paper. Arthritis Rheum. 1985;38:594.
40. Asherson RA, Morgan SH, Harris EN, Gharavi AE, Krausz T,
Hughes GRV. Arterial occlusion causing large bowel infarction: a
reflection of a clotting diathesis in SLE. Clin Rheumatol. 1985;5:102-106.
41. Hall S, Buettner H,Luthra HS. Occlusive retinal vascular disease
in systemic lupus erythematosus. J Rheumatol. 1984;11:846-850.
42. Asherson RA, Berkson RHWM, Harris EN, et al. Large vessel occlusion and gangrene in systemic lupus erythematosus and lupus-like
disease: a report of six
cases.JRheumatol. 1986;13:740-747.
43. Drenkard C, Sanchez-Guerrero J, Alarcon-Segovia D. Fall in antiphospholipid antibody at time of thromboocclusive episodes in

systemic lupus erythematosus. J Rheumatol. 1989;16:614-617.

44. Asherson RA, Chan JKH, Harris EN, Gharavi AE, Hughes GRV
Anticardiolipin antibody, recurrent thrombosis, and warfarin with-

drawal. Ann Rheum Dis. 1985;44:823-825.
45. Case records of the Massachusetts General Hospital weekly clinical pathological exercises: a 38-year-old woman with fever, skin
lesions, thrombocytopenia, and venous thromboses. N Engl J Med.

1990;322:754-769. Case 11-1990.

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