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APS - Neurology Related
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Antiphospholipid Antibodies and Stroke in Young Women |
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Stroke. 2002;33:2396. © 2002 American
Heart Association, Inc. Conclusions— The results from this
study support the importance of antiphospholipid antibodies
as an independent risk factor for stroke in young women. |
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Antiphospholipid Antibodies and Subsequent Thrombo-occlusive
Events in Patients With Ischemic Stroke |
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JAMA. 2004;291:576-584. |
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Antiphospholipid antibodies in cerebral ischemia. |
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Stroke. 1991 Jun;22(6):750-3. |
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Antiphospholipid antibodies in young adults with stroke. |
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J Thromb Thrombolysis. 2005
Oct;20(2):105-12. CONCLUSIONS: Antiphospholipid antibodies,
particularly Lupus Anticoagulant, is an independent risk
factor for first and possibly recurrent ischemic stroke in
young adults. The best therapeutic strategy for preventing
antiphospholipid antibody-associated recurrent stroke is not
clear. |
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ANTIPHOSPHOLIPID ANTIBODIES SYNDROME (APS) ASSOCIATED WITH
HYPERHOMOCYSTEINEMIA RELATED TO MTHFR GENE C677T AND A1298C
HETEROZYGOUS MUTATIONS IN A YOUNG MAN WITH IDIOPATHIC
HYPOPARATHYROIDISM (DIGEORGE SYNDROME) |
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Journal of Clinical Endocrinology &
Metabolism 2006, 10.1210/jc.2005-2782. Conclusions: APS,
revealed by anti-beta-2-glycoprotein (anti-2-GPI) and anti-prothrombin
(anti-PT) antibodies positivity, and moderate HHcy related
to heterozygous C677T and A1298C point mutations of the
MTHFR gene, were identified as a possible cause of
thrombotic disorder responsible for the widespread presence
of cutaneous and cerebral lesions. |
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Antiphospholipid antibodies syndrome in 'Stroke in young'. |
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Mehndiratta MM, Bhattacharya A, Gupta M,
Khawaja GK, Puri V. Antiphospholipid antibodies syndrome in
'Stroke in young'. Neurol India 1999;47:122-6 Promotes an
INR of greater than 3.0. |
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Antiphospholipid antibody syndrome manifested as a
postoperative cerebrovascular event in a child. |
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South Med J. 2000 Nov;93(11):1115-9. |
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Antiphospholipid syndrome and stroke |
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Rinsho Shinkeigaku. 2005
Nov;45(11):852-5. Antiphospholipid syndrome is characterized
by arterial or venous thrombosis, and the presence of
antiphospholipid antibodies (aPL). APL are considered to be
a cause of an acquired hypercoagulable state leading to
stroke and transient ischemic attack (TIA). We examined the
causes in 50 young patients with ischemic stroke. The most
prevalent cause was atherosclerosis and the incidence of APS
was 12.5%. APL comprise a heterogeneous group of
autoantibodies, such as beta2-glycoprotein I dependent
anticardiolipin antibody (beta2-GPIaCL), lupus anticoagulant
(LA), and other antiphospholid-protein antibodies. We
examined the incidence and the pathogenic role of
antiphospholipid protein antibodies. The subjects comprised
250 patients (155 male, 95 females) with ischemic stroke,
aged 26 to 92 years (mean 72 years). We measured beta2-GPI
aCL, IgG aCL, LA, phosphatidyserine dependent
antiprothrtombin antibody (PS-PT), antiphosphatidyl-serine
antibody (PS), antiphosphatidyl-inositol antibody (PI) in
each patient. The incidence of beta2-GPI aCL, IgG aCL, LA,
phosphatidyserine, PS-PT, PS, and PI was 2.8%, 12%, 9.2%,
7.2%, 9.6%, and 8.8%, respectively. The incidence of young
stroke patients under 50 years was 5.2%. Among 13 young
stroke patients, 5 had SLE. Among 23 patients with LA., 18
(78%) patients had PS-PT. Anti-PS-PT antibody is closely
related to LA. Antinuclear antibody was detected in 79% of
the patients with aPS and/or aPI. We compared the carotid
ultrasonographic findings in positive aPI or aPS patients
with those in negative ones. Increased IMT, plaque score and
carotid stenosis were more common in aPI and aPS-positive
patients than in negative ones Three of 5 patients who
showed positive beta2-GPI, aCL and LA, simulataneously, had
sysyemic lupus erythematosus as an immulological background.
Two of 3 patients with PI and/or PS and beta2-GPI and/or LA
were patients with SLE. Antiphospholipid antibody was
considered to be a risk factor of stroke, especially in SLE
and/or young female patients. The incidence of lupus
anticoagulant is more common than beta2-GPI aCL in ischemic
stroke. In SLE patients with stroke,
multi-antiphospholipid-protein antibodies was inclined to be
present. LA is closely related to ant-PS-PT and aPI and aPS
are associated with anti-nuclear antibody and precipitation
of atherosclerosis. |
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Antiphospholipid-Protein Antibodies and Ischemic Stroke |
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(Stroke. 1998;29:1755-1758.) © 1998
American Heart Association, Inc. |
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APS and MS |
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Association of antiphospholipid antibodies with central
nervous system disease in systemic lupus erythematosus. |
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Am J Med. 1995 Oct;99(4):397-401. |
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Brain vascular changes in the case of primary
antiphospholipid syndrome. |
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Folia Neuropathol. 1996;34(2):92-6.
Morphological picture of arterial fibromuscular dysplasia
(FMD) of carotid and cerebral arteries associated with
intracranial aneurysm and thrombotic small vessel
vasculopathy in a 34-year-old woman with primary
antiphospholipid syndrome (PAPS) is presented. The patient
died because of hemorrhage caused by aneurysm rupture. In
the walls of the aneurysm and aneurysmal dilatation of
middle cerebral artery dysplastic changes of FMD type were
found. The case fulfills the clinical and serological
criteria of antiphospholipid syndrome (APS). Microscopic
examination of the brain showed occlusion of small cerebral
vessels, characteristic for antiphospholipid syndrome. It
was caused by fibrin thrombi and endothelial proliferation
or fibrous webs in the vessel lumen. Neither features of
systemic lupus erythematosus (SLE) nor related autoimmune
diseases were observed in the morphological examination of
the brain, skin and internal organs. Therefore, it was
feasible to confirm the diagnosis of PAPS in the patient
with FMD of the large cephalic arteries. |
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Can neurologic manifestations of Hughes (antiphospholipid)
syndrome be distinguished from multiple sclerosis? Analysis
of 27 patients and review of the literature. |
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Medicine (Baltimore). 2000
Jan;79(1):57-68. |
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Central nervous system involvement in the antiphospholipid
(Hughes) syndrome |
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Rheumatology 2003; 42: 200-213. The
antiphospholipid (Hughes) syndrome (APS) is characterized by
arterial and/or venous thrombosis and pregnancy morbidity in
the presence of anticardiolipin antibodies and/or lupus
anticoagulant. APS can occur either as a primary disorder or
secondary to a connective tissue disease, most frequently
systemic lupus erythematosus. Central nervous system (CNS)
involvement is one of the most prominent clinical
manifestations of APS, and includes arterial and venous
thrombotic events, psychiatric features and a variety of
other non-thrombotic neurological syndromes. In this review
we focus on the common and some of the less common CNS
manifestations that have been reported in association with
antiphospholipid antibodies. |
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Cerebral microembolism, a disease marker for ischemic
cerebrovascular events in the antiphospholipid syndrome of
systemic lupus erythematosus? |
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Acta Neurol Scand. 1999 Jun;99(6):356-61.
CONCLUSION: MES may be related to disease activity in
patients with SLE and APS. Their detection may help to
assess individual cerebrovascular risk and contribute to
therapeutic decision making and therapeutic monitoring. |
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Cerebrovascular disease and antiphospholipid antibodies in
systemic lupus erythematosus, lupus-like disease, and the
primary antiphospholipid syndrome. |
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Am J Med. 1989 Apr;86(4):391-9. |
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Chorea and antiphospholipid antibodies: Treatment with
methotrexate |
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Neurology 2001;56:137-138. © 2001
American Academy of Neurology. |
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Cognitive Deficits in Patients With Antiphospholipid
Syndrome |
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Arch Intern Med. 2006;166:2278-2284.
Conclusions Cognitive deficits may often be found among
patients with APS, independent of any history of central
nervous system involvement. Livedo reticularis and the
presence of white matter lesions on brain magnetic resonance
imaging are associated with an increased risk for cognitive
dysfunction in APS. |
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Dementia associated with the antiphospholipid syndrome:
clinical and radiological characteristics of 30 patients |
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Rheumatology Advance Access originally
published online on September 14, 2004. Rheumatology 2005
44(1):95-99; doi:10.1093/rheumatology/keh408. |
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Factor V Leiden and Antiphospholipid Antibodies Are
Significant Risk Factors for Ischemic Stroke in Children |
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Stroke. 2000;31:1283. © 2000 American
Heart Association, Inc. |
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Features Associated with Epilepsy in the Antiphospholipid
Syndrome |
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J Rheumatol 2004;31:1344-8. Conclusion.
Epilepsy is common in APS and most of the risk seems to be
linked to vascular disease as manifested by extensive CNS
involvement, valvulopathy, and livedo reticularis and to the
presence of SLE. These factors, however, explain only part
of the increased occurrence of epilepsy in APS and other
causes such as direct immune interaction in the brain should
be investigated. |
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Hemidystonia symptomatic of primary antiphospholipid
syndrome in childhood. |
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Mov Disord. 1993 Jul;8(3):383-6. We
suggest that PAPS must always be considered when isolated or
recurrent focal cerebral ischaemia, and particularly
hemidystonia, occur in childhood. |
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Hypoperfusion of brain single photon emission computerized
tomography in patients with antiphospholipid antibodies. |
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J Dermatol Sci. 1997 Jan;14(1):20-8.
Hypoperfusion areas might be caused by microarterial
thrombosis, microvenous thrombosis or vascular spasms. Early
detection of cerebral abnormalities allows steps to be taken
to protect against irreversible progress of cerebral blood
flow. Therefore, brain SPECT should be performed in patients
with antiphospholipid antibodies. |
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Low dose aspirin after ischemic stroke associated with
antiphospholipid syndrome |
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Neurology 2003;61:111-114 © 2003 American
Academy of Neurology |
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Management of the neurological manifestations of APS--what
do the trials tell us? |
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Thromb Res. 2004;114(5-6):489-99.
CONCLUSIONS: (1) aPL are a risk factor for incident stroke
(Grade A, established as useful for the given condition in
the specified population). (2) The evidence to support the
role of aPL in recurrent stroke is conflicting and,
therefore, inconclusive. (3) Warfarin at moderate-intensity
doses is equally effective in preventing a recurrent
thrombotic event as warfarin at high-intensity doses in
patients with APS (Grade A evidence, established as useful
for the given condition in the specified population). (4)
Warfarin, at moderate-intensity doses is as effective as
aspirin (at a dose of 325 mg/day) in preventing recurrent
thrombotic events in patients who are aPL-positive at the
time of an initial stroke (Grade B evidence, probably useful
for the given condition in the given population). (5)
Currently there are no data to support the use of any
prophylactic therapy in patients with aPL and no clinical
manifestations for the purposes of preventing an incident
stroke. |
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Migraine in Hughes syndrome—heparin as a therapeutic trial? |
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Q J Med 2001; 94: 114-115 © 2001
Association of Physicians |
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Migraine, memory loss, and "multiple sclerosis ".
Neurological features of the antiphospholipid (Hughes’)
syndrome |
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Postgraduate Medical Journal
2003;79:81-83 © 2003 Fellowship of Postgraduate Medicine |
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Multiple sclerosis, neuropsychiatric lupus and
antiphospholipid syndrome: where do we stand? |
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Rheumatology Advance Access originally
published online on January 11, 2005 Rheumatology 2005
44(4):434-442; doi:10.1093/rheumatology/keh532 Rheumatology
Vol. 44 No. 4 © British Society for Rheumatology 2005. A
trial of anticoagulation might be worthwhile in some
patients with atypical MS and consistently positive aPL. |
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Neurological involvement as a poor prognostic factor in
catastrophic antiphospholipid syndrome: autopsy findings in
12 cases |
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Source: Lupus, Volume 12, Number 2, 1
February 2003, pp. 93-98(6) |
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Neurometabolite Markers of Cerebral Injury in the
Antiphospholipid Antibody Syndrome of Systemic Lupus
Erythematosus |
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Stroke. 1998;29:2254-2260. |
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Recurrent acute transverse myelopathy: Association with
antiphospholipid antibody syndrome |
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Shaharao V, Bartakke S, Muranjan MN,
Bavdekar MS, Bavdekar SB, Udani1 VP. Recurrent acute
transverse myelopathy: Association with antiphospholipid
antibody syndrome. Indian J Pediatr 2004;71:559-561 |
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Some considerations about the possible pathological
mechanisms at work in antiphospholipid syndrome and stroke |
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Rev Neurol. 2003 Oct 1-15;37(7):654-7.
INTRODUCTION AND DEVELOPMENT: Over the last two decades
antiphospholipid syndrome (APS) has started to be recognized
from the association of apparently anionic
phospholipid-specific antibodies with thrombosis,
thrombocytopenia and recurrent foetal losses. This syndrome
affects patients with systemic lupus erythematosus and is
considered to be an important cause of thromboembolic
disease. Antiphospholipid antibodies are serum
immunoglobulins that react with negatively charged
phospholipids, albeit directly or by means of a cofactor,
affect the coagulation system, and promote thrombosis.
Recent research has been directed towards gaining an
understanding of the mechanisms by which these antibodies
are able to play a direct role in the pathophysiology of
thrombosis, and the extent to which certain risk factors,
such as smoking, high blood pressure, lipid disorders and so
on, exert an influence over the expression of phospholipids
in the cerebral endothelium. CONCLUSION: These antibodies
have no single mechanism of action; different authors have
described different pathological mechanisms, which help us
to understand the heterogeneous clinical manifestations of
APS. |
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Stroke and antiphospholipid syndrome: the treatment debate |
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Rheumatology Advance Access originally
published online on April 19, 2005 Rheumatology 2005
44(8):971-974; doi:10.1093/rheumatology/keh666 |
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The Antiphospholipid Syndrome and "Multiple Sclerosis" |
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The blood disease that mimics MS - Hughes Syndrome |
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How APS can mimic MS. |
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Thrombotic cerebral arteriopathy in patients with the
antiphospholipid syndrome. |
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Mod Pathol. 1993 Nov;6(6):644-53.
CONCLUSIONS: The cerebrovascular changes of the
antiphospholipid syndrome are derived from a chronic
thrombotic microangiopathy. The findings support the
hypothesis that antiphospholipid antibodies can cause
recurring episodes of intravascular thrombosis. |
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Top of Page |
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APS - Opthalmology Related
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A case of optic neuritis associated with anticardiolipin
antibodies |
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Rinsho Shinkeigaku. 1992 Mar;32(3):330-2.
We reported a case of optic neuritis with the persistence of
severe visual loss and central scotoma in a 26-year-old
woman who was proven to have biologic false positive test
for syphilis, and the elevated serum titres of IgG and IgM
anticardiolipin antibodies. C.S.F. findings showed the
absence of oligoclonal bands and the presence of IgM
anticardiolipin antibody. She was treated twice at intervals
of two weeks with methylprednisolone 1000 mg intravenously
daily for three days (pulse therapy), and was started on
oral prednisolone 60 mg daily which tapered gradually. After
the second treatment of the pulse therapy, her visual acuity
was improved remarkably and the titre of anticardiolipin
antibodies became normal. Her clinical course seemed to be
different from that of the optic neuritis of multiple
sclerosis, in which many of patients recover near normal
visual acuity after a first attack. We suggested that
antiphospholipid antibodies might play a role in the
etiology of her optic neuritis. |
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Antiphospholipid Antibody Syndrome |
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The most common ocular pathology is
thrombosis with resultant ischemia. This manifests as
central retinal vein or artery occlusion (CRVO or CRAO),
anterior ischemic optic neuropathy (AION), transient
ischemic attack (TIA), amaurosis fugax, isolated retinal
hemorrhages and cotton wool spots, and retinal
neovascularization. While these conditions typically occur
in the elderly, APAS patients may experience them earlier in
life. Besides the ocular manifestations, thrombi often
affect other systems. Venous thromboses of the arm and leg,
sagital, pelvic, mesenteric, portal and axillary vessels,
and pulmonary embolism have all been encountered in APAS.
With thrombosis in the arterial system, cerebrovascular
accidents have also occurred. Thrombocytopenia (reduced
platelet count) may also occur in these patients. |
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Bilateral retinal vascular occlusion during antiphospholipid
antibody syndrome: a case report |
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J Fr Ophtalmol. 2005 May;28(5):503-7
DISCUSSION AND CONCLUSION: Central retinal artery or vein
occlusion in a young patient must suggest the diagnosis of
antiphospholipid antibody syndrome. The bilateralism of
vascular occlusion is considered a severe factor because of
its consequence on functional ocular and vital prognosis,
where it can sound the alarm to the extension of thrombotic
events to other vessels in the body. Antiphospholipid
syndrome must be studied in cases of severe retinal vascular
occlusion in young patients. Its diagnosis is important
because the risk of recurrent thrombotic events may endanger
functional and vital prognosis. |
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Central retinal venous occlusion with co-existent thrombotic
thrombocytopenic purpura and antiphospholipid syndrome |
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British Journal of Ophthalmology
2003;87:658-659 © 2003 BMJ Publishing Group |
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Handbook of Ocular Disease Management Antiphospholipid
Syndrome |
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Patients with antiphospholipid antibody
syndrome (APAS) tend to be under age 50 and female. Up to 2%
of women may have antiphospholipid antibodies. Many will
also have lupus or other autoimmune diseases. |
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Ocular symptoms in association with antiphospholipid
antibodies. |
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Graefes Arch Clin Exp Ophthalmol. 1998
Sep;236(9):658-68 CONCLUSIONS: We did not find a clear
correlation between APA activity or the immunoglobulin
classes in the individual and the severity of the ocular
disease. The benefit from a therapy with the antiplatelet
agent acetylsalicylic acid was evident in a reduction of the
patients' transient visual disturbances and, in most cases,
no further progression of permanent visual field defects was
observed. |
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Ophthalmic signs in antiphospholipid syndrome. Patient
description |
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Klin Oczna. 2004;106(4-5):661-3
CONCLUSIONS: presented characteristic general and ophthalmic
signs point to APS. |
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Primary antiphospholipid antibody syndrome and retinal
occlusive vasculopathy. |
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Am J Ophthalmol. 1997 Jun;123(6):848-50
CONCLUSIONS: In retinal vascular occlusions of unexplained
origin, antiphospholipid antibodies may play an important
role in the pathogenesis. Detecting these antibodies in the
serum of patients with retinal vascular occlusion helps
determine the appropriate treatment with long-term oral
anticoagulants. |
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Retinal vein occlusion in two patients with primary
antiphospholipid syndrome. |
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Korean J Intern Med. 2001 Dec;16(4):274-6 |
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Review of severe vaso-occlusive retinopathy in systemic
lupus erythematosus and the antiphospholipid syndrome:
associations, visual outcomes, complications and treatment. |
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Clin Experiment Ophthalmol. 2004
Feb;32(1):87-100 Conclusion: Severe vaso-occlusive
retinopathy is a rare form of retinopathy in SLE often
associated with poor visual prognosis and
neovascularization. It may be a manifestation of the
antiphospholipid syndrome. Treatment is aimed at preventing
further thrombosis and complications arising from
neovascularization. |
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Sudden painless unilateral vision loss caused by branch
retinal artery occlusion: implications for the primary care
physician. |
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Am J Med Sci. 2004 Jan;327(1):44-6 |
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Visual disturbances and pathologic ocular findings in
primary antiphospholipid syndrome. |
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Ophthalmology. 1999 Aug;106(8):1537-40
CONCLUSIONS: Ocular involvement in PAS is uncommon.
Transient visual disturbances are common, although most of
them are related to central nervous system rather than
ocular ischemia. Pathologic ophthalmic findings are unlikely
to be found in asymptomatic patients or in patients with
transient visual disturbances. Routine retinal
fluoroangiography performed on patients with PAS is
unproductive. |
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Top of Page |
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APS - Other
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A cross-sectional study of clinical thrombotic risk factors
and preventive treatments in antiphospholipid syndrome |
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Rheumatology 2002; 41: 924-929 © 2002
British Society for Rheumatology. Conclusion. While
traditional risk factors were similar between groups,
pregnancy and surgical procedures increased the risk of
thrombosis. Hypertension and smoking were associated with
arterial events. Possessing a combination of risk factors
may increase the occurrence of arterial thrombosis but not
venous thrombosis. Use of aspirin and/or hydroxychloroquine
may be protective against thrombosis in asymptomatic
aPL-positive individuals. |
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Abdominal Thrombotic and Ischemic Manifestations of the
Antiphospholipid Antibody Syndrome: CT Findings in 42
Patients1 |
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Radiology. 2001;218:768-771. CONCLUSION:
Patients who have circulating antiphospholipid antibodies
are at risk for major abdominal vascular thromboses and
organ infarction. Radiologists must be familiar with this
syndrome; they may be the first physicians to suggest the
diagnosis on the basis of findings of unusual or recurrent
sites of thrombosis, especially in young patients. |
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Adrenal failure followed by status epilepticus and hemolytic
anemia in primary antiphospholipid syndrome |
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Thrombosis Journal 2005, 3:6.
doi:10.1186/1477-9560-3-6. Published: 18 April 2005.
Conclusion: Adrenal failure is a rare complication of APS in
children with only five cases reported to date. As shown in
our patient, this syndrome can manifest in a diverse set of
simultaneously occurring symptoms. |
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An unusual cause of acute abdominal pain – A case
presentation |
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BMC Blood Disorders 2006, 6:1
doi:10.1186/1471-2326-6-1. Conclusion: This case presented
to us as an acute abdominal pain. Subsequent investigations
revealed the presence of splenic infarction. Coagulation
risk factors for thrombosis proved negative. Haematological
investigations revealed the presence of anticardiolipin
antibodies at the first instance but subsequent
determinations were negative. Hence, it mimicked Hughes
syndrome initially but the criteria for temporal persistence
of anticardiolipin antibody was not fulfilled. Unusual
surgical presentation of a thrombotic abnormality as
abdominal pain due to splenic infarction. |
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Anti-phospholipid reactivity against cardiolipin metabolites
occurring during endothelial cell apoptosis |
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Arthritis Research & Therapy 2006, 8:R180
doi:10.1186/ar2091. We have recently shown that cardiolipin
(CL) and its metabolites move from mitochondria to other
cellular membranes during death receptor-mediated apoptosis.
In this study we investigate the immunoreactivity to CL
derivatives occurring during endothelial apoptosis in
patients with antiphospholipid syndrome (APS) and systemic
lupus erythematosus (SLE). We compared the serum
immunoreactivity to CL to that of its derivatives
monolysocardiolipin (MCL), dilysocardiolipin (DCL), and
hydrocardiolipin (HCL), by means of both enzyme-linked
immunosorbent assay and thin layer chromatography (TLC)
immunostaining. In addition, we investigated the composition
of phospholipid extracts from the plasma membrane of
apoptotic endothelial cells and the binding of patients'
sera to the surface of the same cells by using high
performance TLC and immunofluorescence analysis. The average
reactivity to MCL was comparable to that of CL and
significantly higher than that for DCL and HCL in patients
studied, both in the presence or in the absence of
beta2-Glycoprotein I. Of relevance for the pathogenic role
of these autoantibodies, IgG from patients' sera showed an
increased focal reactivity with the plasma membrane of
endothelial cells undergoing apoptosis. Interestingly, the
phospholipid analysis of these light membrane fractions
showed an accumulation of both CL and MCL. Our results
demonstrated that a critical number of acyl chains in CL
derivatives is important for the binding of
anti-phospholipid antibodies and that MCL is an antigenic
target with immunoreactivity comparable to CL in APS and
SLE. Our finding also suggests a link between apoptotic
perturbation of CL metabolism and the production of these
antibodies. |
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Antiphospholipid antibodies in patients with sensorineural
hearing loss. |
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Eur Arch Otorhinolaryngol. 2005
Aug;262(8):622-6. Sensorineural hearing loss can be
associated with autoimmune diseases and the presence of
antiphospholipid antibodies. Sixty patients (mean age 47
years, range 18-76 years) with sudden sensorineural hearing
loss were studied with audiograms, stapedial thresholds,
otoacoustic emissions, positional and caloric testing. The
serologic testing included antibodies against
phosphatidylserine and beta(2)-glycoprotein. Additionally, a
group of 34 patients (mean age 65 years, range 31-81 years)
with normal tension glaucoma was examined because in a
previous study these patients were reported to have elevated
concentrations of antiphospholipid antibodies with a
coincidence of progressive sensorineural hearing loss. The
baseline for antiphospholipid antibody levels was
established in a control group of 40 healthy blood donors.
In 12 of the 60 patients with sudden sensorineural hearing
loss, levels of antiphospholipid antibodies were elevated.
Antiphosphatidylserine IgM antibodies were significantly
lower compared to controls and patients with the combination
of hearing loss and normal tension glaucoma (Fisher's exact
two-sided test, P < 0.01). Our data suggest that antibodies
against beta2-glycoprotein seem to coincidence with an acute
event, such as sudden sensorineural hearing loss, whereas
antibodies against phosphatidylserine IgG are detectable in
the prolonged sequel, such as in patients with progressive
sensorineural hearing loss and normal tension glaucoma. |
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Antiphospholipid antibody in localised scleroderma |
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Annals of the Rheumatic Diseases
2003;62:771-774. Conclusions: These results suggest that aCL
and LAC are the major autoantibodies in patients with
generalised morphoea. |
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Antiphospholipid antibody syndrome complicated by Grave's
disease. |
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J Dermatol. 2002 Dec;29(12):776-80. The
report describes a woman with primary antiphospholipid
antibody syndrome complicated with Grave's disease.
Developing symptoms included a small cutaneous nodule on her
finger and subsequently ecchymotic purpura on the cheeks,
ears, buttocks and lower legs. Histological examinations
showed thrombosed vessels in the dermis without or with
hemorrhage, respectively. Laboratory investigation revealed
positive lupus anticoagulant and immunogenic hyperthyroidism
due to Grave's disease. There is a close relationship
between the cutaneous manifestation of antiphospholipid
antibody syndrome and the activities of Grave's disease and
a possible link of antiphospholipid antibody syndrome with
Grave's disease was suggested both by the etiology of the
disease as well as the disease activity. |
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Antiphospholipid antibody syndrome in a six-year-old female
patient. |
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Am J Ophthalmol. 2003 Apr;135(4):542-4
CONCLUSIONS: Although uncommon, retinovascular thrombosis in
children can occur in APA syndrome. Testing for ACA and
lupus anticoagulant should be considered. |
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Antiphospholipid Antibody Syndrome Ulcers |
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© 1996-2005, American College of
Physicians. All rights reserved. |
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Antiphospholipid antibody syndromes and the Internet. |
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Lupus. 1996 Oct;5(5):418-24. Information
regarding the antiphospholipid antibody syndrome is
accessible on the Internet, and encompasses both physician
specific and patient specific files. The quantity and
quality of data available at these sites, however, varies
greatly and both search-refining and data manipulating
protocols and software need improvement. |
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Antiphospholipid inner ear syndrome. |
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Laryngoscope. 2005 May;115(5):879-83.
CONCLUSIONS: These data support the hypothesis that
antiphospholipid antibodies are involved in the pathogenesis
of some forms of inner ear dysfunction, presumably by
causing microthrombus formation in the labyrinthine
vasculature. Basic science studies are required to better
understand the mechanisms by which antiphospholipid
antibodies mediate inner ear dysfunction. Clinical studies
to evaluate the efficacy of anticoagulation in this group of
patients are also required. |
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Antiphospholipid Syndrome Has Many Faces |
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04/18/2002 By Anne MacLennan Review of
Arthritis & Rheumatism Volume 46, Issue 4, 2002. Pages:
1019-1027. |
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Asymptomatic sensorineural hearing loss in patients with
systemic lupus erythematosus. |
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J Clin Rheumatol. 2006 Oct;12(5):217-20.
CONCLUSION: If it can be established how often this ASNHL
progresses to a clinical problem, it can be important that,
as part of initial studies, patients with SLE undergo
audiometric tests. |
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Colonic ulcers in propylthiouracil induced vasculitis with
secondary antiphospholipid syndrome |
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Postgraduate Medical Journal
2005;81:338-340. A 48 year old white woman was admitted to
the hospital because of several bouts of migratory
polyarthritis, weight loss, fever, and abdominal pain over a
period of 15 months. She had been taking propylthiouracil
100 mg daily for three years for hyperthyroidism treatment.
A test for antineutrophil cytoplasmic autoantibodies (ANCA)
was positive with a perinuclear pattern of staining.
Antiphospholipid antibodies were also detected. Colonoscopy
showed several ulcers on intestinal mucosa and the biopsy
specimen showed intense microscopic vasculitis. The patient
is well after methylprednisolone pulse therapy and eight
months of oral azathioprine. A surveillance colonoscopy
showed complete healing of intestinal ulcers. No recurrence
of symptoms has occurred and autoantibodies are negative, 10
months after treatment finished. The sequence of events
suggests a propylthiouracil induced vasculitis p-ANCA
positive and an antiphospholipid syndrome. This is the first
report of colonic ulcers diagnosed and successfully treated
in such circumstances. |
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Endocrinologic manifestations of the antiphospholipid
syndrome. |
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Lupus. 2006;15(8):485-9. Clinicians
should keep a high index of suspicion for adrenal
insufficiency in patients with APS. |
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Genomics and targeting antithrombotic therapy in
antiphospholipid syndrome |
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Blood, 15 February 2006, Vol. 107, No. 4,
pp. 1249. |
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HCV and HIV may trigger antiphospholipid syndrome |
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Last Updated: 2004-04-16 12:25:03 -0400
(Reuters Health) |
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Infectious origin of the antiphospholipid syndrome |
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Annals of the Rheumatic Diseases
2006;65:2-6; doi:10.1136/ard.2005.045443 |
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Ischemic Colitis due to Antiphospholipid Antibody Syndrome |
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Comments: This 69 year old lady presented
to the hospital with sudden onset of left lower quadrant
pain and bloody diarrhea. She described having experienced
similar episodes over the past 25 years occurring every
several years but recently with increasing frequency. The
episodes have typically lasted several days before resolving
without sequella. A CT scan on this admission showed marked
wall thickening of the distal transverse colon, the splenic
flexure, and the descending colon. Inflammatory changes were
seen in the surrounding pericolic fat. The wall thickening
had a somewhat nonspecific appearance, although increased
mucosal and serosal enhancement raised the possibility of
ischemia. On the basis of this study, the differential
diagnosis included either an infectious or an inflammatory
process. Colonoscopy was then performed. The right and
transverse colon was normal but the splenic flexure down to
the sigmoid was diffusely abnormal with marked ulceration
and mucosal edema. The broad segments of ulceration favored
the diagnosis of an ischemic etiology and the prior history
of periodic occurrence of these events made an infectious
etiology less likely. Biopsies were performed and these
showed focal ulceration with acute inflammatory exudates
adjacent to intact mucosa. Other areas show crypt dropout,
with regeneration seen in the remaining crypts and fibrin
deposition in the lamina propria. These features were most
suggestive of ischemic colitis. Cultures for C. diff and
other pathogens were negative. At four week follow-up,
complete healing was demonstrated in the affected areas.
Colonic ischemia most frequently involves the splenic
flexure and the left colon and can mimic inflammatory bowel
disease or malignancy. While full thickness injury and acute
perforation can occur, the mucosal changes usually resolve
within 2 weeks. Stricture formation is rare. Usually no
cause for the event can be determined. E coli O157 is a
pathogen frequently associated with colonic ischemia. During
her workup she was found to have an ANA positive at 1:2560
in a homogeneous and speckled pattern and a positive
antiphospholipid antibody titer on two consecutive studies,
thus establishing the diagnosis of antiphospholipid antibody
syndrome as the cause of her recurrent ischemic events.
Antiphospholipid antibody syndrome is caused by a class of
antibodies which includes lupus anticoagulant and anti
cardiolipin antibodies and appear to be directed against a
spectrum of plasma proteins bound to phospholipids involved
in the clotting cascade. Anti-phospholipid antibody syndrome
more commonly is associated with pregnancy loss, recurrent
CVAs, thrombophlebitis, pulmonary emboli and deep venous
thrombosis. Prospective studies report rates of recurrent
thromboembolic events in the range of 7-10% per patient per
year. Anticoagulation therapy with warfarin reduces the rate
of recurrent thrombotic events. Contributed by: Alexandra
Gutierrez, M.D. G.I. Fellow Massachusetts General Hospital |
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Management of antiphospholipid antibody syndrome: a
systematic review. |
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JAMA. 2006 Mar 1;295(9):1050-7.
CONCLUSIONS: In patients with APS, moderate-intensity
warfarin is effective for preventing recurrent venous
thrombosis and perhaps also arterial thrombosis. Aspirin
appears to be as effective as moderate-intensity warfarin
for preventing recurrent stroke in patients with prior
stroke and a single positive test result for
antiphospholipid antibody. The optimal treatment of other
thrombotic aspects of APS needs to be addressed in
well-designed prospective studies. |
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Neuroendocrine manifestations of phospholipid antibody
disease identified by long-term follow-up study of patients
with phospholipid antibodies. |
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Ann N Y Acad Sci. 2006 Jun;1069:386-90.
In conclusion: (1) Inflammatory disease may develop in some
patients with aPL and appears to be set off by pregnancy, a
known trigger for clinical thrombotic events in aPL
patients. (2) Thyroid cancer may be associated with aPL, and
this association warrants further study with larger number
of patients. |
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Perioperative medical management of antiphospholipid
syndrome: hospital for special surgery experience, review of
literature, and recommendations. |
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J Rheumatol. 2002 Apr;29(4):843-9.
Patients with antiphospholipid syndrome (APS), who are
predisposed to vascular thrombotic events, are at additional
risk for thrombosis when they undergo surgery. Serious
perioperative complications (recurrent thrombosis,
catastrophic exacerbation, or bleeding) occur despite
prophylaxis. We describe our perioperative experience with
APS patients who underwent a variety of surgeries, review
the literature, and discuss strategies that may guide other
physicians in their perioperative evaluation and management
of patients with APS. Recommendations: perioperative
strategies should be clearly identified before surgical
procedure; pharmacological and physical antithrombosis
interventions vigorously employed; periods without
anticoagulation kept to a minimum; and any deviation from a
normal course should be considered a potential disease
related event. |
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Spectrum of vascular pathology affecting patients with the
antiphospholipid syndrome. |
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|
Hum Pathol. 1995 Jul;26(7):716-24. A
thrombotic microangiopathy that is identified in patients
with the antiphospholipid syndrome (APS) represents only a
part of the vascular pathology that can be associated with
antiphospholipid antibodies (aPL). Tissues from two
autopsies, four renal biopsies, two skin biopsies, and one
amputated leg were obtained from six patients who met
criteria for the diagnosis of APS. Three patients had
systemic lupus erythematosus (SLE), one had lupus-like
disease, and two had a primary APS. Five of the patients
were hypertensive. Arteries of three patients disclosed
fibrin thrombi along with widespread obstruction by
recanalized intimal connective tissue. Small renal,
leptomeningeal, and pulmonary arteries showed concentric
cellular and fibrous intimal hyperplasia indistinguishable
from hypertensive vascular disease. Glomerular capillary and
afferent arteriolar thrombi were found in renal biopsies
from two SLE patients. One of these SLE patients required a
leg amputation in which the popliteal artery demonstrated
thrombosis, intimal hyperplasia, and acute inflammation. The
findings support clinical and experimental data that
indicate aPLs cause thrombosis but suggest diversity in the
pathogenetic mechanisms aPLs are capable of promoting.
Inflammation seems to be rare and to accompany thrombosis.
Intimal hyperplasia is particularly common. Its involvement
of renal arteries may contribute to hypertension that
develops in some APS patients. |
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Spontaneous recovery of sudden sensorineural hearing loss:
possible association with autoimmune disorders. |
|
|
J Am Acad Audiol. 2006
Jul-Aug;17(7):498-505. |
| |
|
Superior mesenteric artery thrombosis associated with
antiphospholipid syndrome. |
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|
West J Med. 1991 August; 155(2): 174–176. |
| |
|
The Antiphospholipid Story |
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|
© 2003. The Journal of Rheumatology
Publishing Company Limited. |
| |
|
The systemic nature of the antiphospholipid syndrome. |
|
|
Scand J Rheumatol. 2004;33(6):365-72.
Antiphospholipid syndrome (APS, Hughes' syndrome) is a
systemic autoimmune disorder characterized by arterial
and/or venous thrombosis and recurrent foetal loss,
accompanied by mild to moderate thrombocytopaenia and
elevated titres of antiphospholipid antibodies (aPLs): lupus
anticoagulant (LAC) and/or anticardiolipin (aCL) antibodies.
APS was defined originally in 1983 in systemic lupus
erythematosus (SLE) patients, but later it was found that
APS can be primary or secondary to other autoimmune diseases
or malignancy. During the past 20 years many organs have
been reported to be involved in this syndrome and the
clinical manifestations are seen in every medical field.
Moreover, many aPLs have been found in APS besides aCLs and
LACs, which bind to the autoantigen beta-2-glycoprotein I
(beta2GPI). Treatment for APS, based on antiplatelet and
anticoagulation drugs, is dependent on various parameters,
including whether SLE is also present, classical vs
non-classical manifestations of the diseases, women with APS
based on pregnancy morbidity, the presence of elevated aCL
antibody titres in the absence of clinical manifestations,
and catastrophic APS. |
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|
Urologic damage of the primary antiphospholipid syndrome |
|
|
Arch Esp Urol. 2004 Sep;57(7):707-23. The
antiphospholipid syndrome is an acquired autoimmune systemic
disease generating a permanent hypercoagulability status
with recurrent multiorgan thrombotic events due to
circulating antiphospholipid antibodies. It may be secondary
to a heterogeneous group of diseases (mainly lupus) and
drugs, or primary if it appears isolated without any
demonstrable systemic disease or concomitant medication. It
is mainly characterized by venous or arterial recurrent
thrombosis, recurrent abortion, thrombocytopenia, and
circulating antiphospholipid auto-antibodies. Treatment with
anticoagulants and correction of the hypercoagulable status
contributing factors, arterial or venous thrombosis, and
vascular risk aim to avoid new thrombosis episodes.
Genitourynary system may be affected in any of its parts,
generally by arterial or venous thrombosis. Kidney is the
most frequently affected organ, in addition to transplanted
kidney grafts, adrenal glands, bladder and testicles. There
is a relationship between antiphospholipid syndrome and
infertility. For the first time, we describe bladder
involvement presenting as hyperreflexic neurogenic bladder
with detrusor-sphincter dyssynergia after spontaneous spinal
cord thrombosis in an asymptomatic adolescent with primary
antiphospholipid syndrome which was unknown before. |
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APS - Pregnancy
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A Multicenter, Placebo-Controlled Pilot Study of Intravenous
Immune Globulin Treatment of Antiphospholipid Syndrome
During Pregnancy |
|
|
The American Journal of Obstetrics and
Gynecology 01/01/2000 (Volume 182, Number 1) |
| |
|
A study of sixty pregnancies in patients with the
antiphospholipid syndrome. |
|
|
Clin Exp Rheumatol. 1996
Mar-Apr;14(2):131-6. |
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|
Antiphospholipid antibodies and pregnancy loss |
|
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|
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Antiphospholipid antibodies and pregnancy rates and outcome
in in vitro fertilization patients |
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|
Authors: A. Denis, M. Guido, R. Adler, P.
Bergh, C. Brenner, R. Scott, Jr. Source: Fertility and
Sterility: June, 1997 (Vol. 67) Pages 1084-1090. |
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Antiphospholipid Antibodies in Predicting Adverse Pregnancy
Outcome |
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|
Annals of Internal Medicine. 15 March
1994 | Volume 120 Issue 6 | Pages 470-475 |
| |
|
Antiphospholipid Antibody Syndrome |
|
|
by Sara Marder, M.D. Instructor and
Fellow in Maternal and Fetal Medicine Department of
Obstetrics and Gynecology Yale University School of Medicine |
| |
|
Antiphospholipid Antibody Syndrome (APS) or Hughes and
Pregnancy |
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|
7/28/2003 |
| |
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Antiphospholipid Antibody Syndrome and Pregnancy Article by
Stella Nowicki, DDS |
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|
Background: Antiphospholipid syndrome
(APS) is a recently recognized autoimmune condition that may
manifest with fetal loss, thrombosis, or autoimmune
thrombocytopenia. Women with these clinical features should
be tested for lupus anticoagulant (LAC) and anticardiolipin
(aCL) antibodies; most patients with APS have both LAC and
aCL immunoglobulin G (IgG) antibodies. The diagnosis of APS
requires the presence of both clinical and biological
features. Systemic lupus erythematosus (SLE) is a chronic
systemic disease with diverse clinical and laboratory
manifestations. LAC (and aCL) predisposes to clotting in
vivo, predominantly by interfering with the antithrombotic
role of phospholipids (PLs); therefore, it is associated
with clinical thrombosis, not bleeding. The antiphospholipid
(aPL) autoantibodies bind moieties on negatively charged PLs
or moieties formed by the interaction of negatively charged
PLs with other lipids, PLs, or proteins. aPL antibodies
belong to the large family of antibodies that react with
negatively charged PLs, including cardiolipin,
phosphatidylglycerol, phosphatidylinositol,
phosphatidylserine, phosphatidylcholine, and phosphatidic
acid. Last Updated: September 4, 2005 |
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Antiphospholipid Syndrome (aPL) |
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|
Because of the higher risks for stroke,
pregnancy loss, and other complications with aPL, mothers
need close monitoring of the disease. More frequent prenatal
visits are often needed. |
| |
|
Antiphospholipid Syndrome (aPL) |
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|
Antiphospholipid syndrome is an
autoimmune disease in which the body produces large amounts
of antiphospholipid antibodies. Phospholipids are a special
type of fat containing phosphate that makes up the outer
walls of the body's cells. Antiphospholipid antibodies
attack the phospholipids. This causes many different
problems including increased blood clotting. Cardiolipin is
one type of phospholipid and specific anticardiolipin
antibodies may develop. |
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Antiphospholipid syndrome and pregnancy |
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|
Akush Ginekol (Sofiia). 2004;43(1):36-42.
The antiphospholipid antibody syndrome (APLS) is
multisystem, autoimmune disease, which is characterized by:
thrombosis, obstetrics complications and thrombocytopenia.
The two most clinically significant antiphospholipid
antibodies (APLa) that are associated with recurrent
pregnancy loss and thrombosis are anticardiolipin antibodies
(ACL) and lupus anticoagulant (LA). The laboratory diagnosis
is based on the presence of moderate to high positive ACL
and/or LA. The inhibitory effect of antiphospholipid
antibodies /APLa/ on trophoblast intercellular fusion,
hormone production and invasion may cause pregnancy loss.
Once placentation is established their thrombogenic action
leads to decreased placental perfusion and subsequent
infarction. The APLa--mediated inhibition of trophoblastic
invasion and APLa--mediated vasculopathy in the placental
bed arteries result in abnormal uterine artery /UA/ Doppler
waveforms. The association between APLa and high resistance
index /RI/ and/or diastolic notch /DN/ in the Doppler
waveforms is high predictive for adverse pregnancy outcome,
including pre-eclampsia/eclampsia, intrauterine growth
retardation, placental abruption, intrauterine fetal death.
Maternal treatment and careful monitoring of fetal
well-being are mandatory in the management of these
high-risk pregnancies. |
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Antiphospholipid Syndrome in Pregnancy: A Randomized,
Controlled Trial of Treatment |
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|
Obstetrics & Gynecology 2002;100:408-413
© 2002 by The American College of Obstetricians and
Gynecologists |
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Antiphospholipid syndrome in pregnancy: a randomized,
controlled trial of treatment. |
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Obstet Gynecol 2002; 100:408-13. |
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Clearance of Antiphospholipid Antibodies in Pregnancies
Treated With Heparin |
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|
Obstetrics & Gynecology 2001;97:394-398 ©
2001 by The American College of Obstetricians and
Gynecologists |
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Management of thrombosis in antiphospholipid syndrome and
systemic lupus erythematosus in pregnancy. |
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|
Ann N Y Acad Sci. 2005 Jun;1051:606-12.
Pregnancy is a high risk period for thrombosis in women with
antiphospholipid syndrome (APS) and systemic lupus
erythematosus (SLE) with antiphospholipid antibodies (aPL).
Thrombosis may affect the mother, both in the venous and
arterial beds, and also have a role in pregnancy loss.
Thromboprophylaxis thus is warranted in most of these women.
However, specific regimens containing low-dose aspirin,
unfractionated heparin (UH), low molecular weight heparin
(LMWH), and even dicumarinics in some circumstances after
the first trimester are still a matter of controversy. Women
with previous thrombosis should receive full antithrombotic
doses of UH or LMWH during the whole pregnancy. Treatment of
pregnancy losses is more debated, consisting of low-dose
aspirin with or without associated heparin. The choice of
treatment for a given patient must always take into account
the woman's opinion after a careful discussion with the
treating physician. Peripartum thromboprophylaxis with LMWH
in women receiving aspirin-only regimens and prevention of
osteoporosis in those treated with heparin are considered
essential in the medical management of these patients. |
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Obstetric Implications of Antiphospholipid Antibodies:
Pregnancy Loss and Other Complications |
|
|
Clinical Obstetrics and Gynecology:
Volume 44(1) March 2001 pp 2-10 |
| |
|
Pregnancy Loss in the Antiphospholipid-Antibody Syndrome — A
Possible Thrombogenic Mechanism |
|
|
N Engl J Med 1997;337 (154-160) |
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|
TNF- Is a Critical Effector and a Target for Therapy in
Antiphospholipid Antibody-Induced Pregnancy Loss |
|
|
The Journal of Immunology, 2005, 174:
485-490. The antiphospholipid syndrome (APS) is
characterized by recurrent fetal loss, intrauterine growth
restriction, and vascular thrombosis in the presence of
antiphospholipid (aPL) Abs. Our studies in a murine model of
APS induced by passive transfer of human aPL Abs have shown
that activation of complement and recruitment of neutrophils
into decidua are required for fetal loss, and emphasize the
importance of inflammation in aPL Ab-induced pregnancy loss.
In this study, we examine the role of TNF- in pregnancy
complications associated with aPL Abs in a murine model of
APS. We show that aPL Abs are specifically targeted to
decidual tissue and cause a rapid increase in decidual and
systemic TNF- levels. We identify the release of TNF- as a
critical intermediate that acts downstream of C5 activation,
based on the fetal protective effects of TNF- deficiency and
TNF blockade and on the absence of increased TNF- levels in
C5-deficient mice treated with aPL Abs. Our results suggest
that TNF- links pathogenic aPL Abs to fetal damage and
identify TNF blockade as a potential therapy for the
pregnancy complications of APS. |
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Use of the Low-Molecular-Weight Heparin Nadroparin During
Pregnancy: A Review |
|
|
from Current Medical Research and Opinion
Posted 04/02/2003. Summary: Antithrombotic therapy is often
used during pregnancy for the treatment and prevention of
venous thromboembolism, the prevention of systemic embolism
in patients with heart valve prostheses and the prevention
of foetal loss in patients with antiphospholipid syndrome.
Low-molecular-weight heparins (LMWHs), including nadroparin,
have largely replaced unfractionated heparin as the
anticoagulant of choice. The use of the LMWH nadroparin in
pregnant women at an increased risk of thromboembolism or
foetal loss is discussed in this review. Deep vein
thrombosis can be effectively treated or prevented with
nadroparin without any serious adverse events. Nadroparin
0.1 ml/10 kg sc once daily prevents thromboembolic
complications in pregnant women with heart valve prostheses.
Nadroparin is also effective in preventing foetal loss,
through contributing to normal placental development and in
decreasing the risk of premature delivery in pregnant women
with antiphospholipid syndrome or women with herpes and
antiphospholipid syndrome. These results demonstrate
nadroparin is effective, easy to administer and associated
with a low incidence of foetal and maternal complications.
The use of nadroparin at a prophylactic dose of 0.3 ml (2850
IU AXa, 95 IU/kg) (for high-risk patients, 0.3-0.6 ml) sc
once daily, and a therapeutic dose of 0.1 ml/10 kg (95
IU/kg) sc twice daily, is in line with the latest
international guidelines of the American College of Chest
Physicians. |
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APS - Seronegative APS - SNAPS
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*SERONEGATIVE ANTIPHOSPHOLIPID ANTIBODY SYNDROME (SNAPS)…AND
SNAPPING TO IT!! |
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|
By: Gale McCarty, MD, FACR, FACP “You
don’t have the syndrome because your tests are low level or
negative…” or “You have livedo, a heart valve problem, and
thrombocytopenia, but these aren’t listed as criteria for
diagnosis” are comments made frequently by healthcare
providers from many specialties to patients with clinical
features suggesting the Antiphospholipid Antibody Syndrome
(APS). |
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Antiphospholipid syndrome without antiphospholipid
antibodies at the tim |
