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APS - Neurology Related

 
Antiphospholipid Antibodies and Stroke in Young Women  
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.
 
Antiphospholipid Antibodies and Subsequent Thrombo-occlusive Events in Patients With Ischemic Stroke  
JAMA. 2004;291:576-584.
 
Antiphospholipid antibodies in cerebral ischemia.  
Stroke. 1991 Jun;22(6):750-3.
 
Antiphospholipid antibodies in young adults with stroke.  
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.
 
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)  
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.
 
Antiphospholipid antibodies syndrome in 'Stroke in young'.  
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.
 
Antiphospholipid antibody syndrome manifested as a postoperative cerebrovascular event in a child.  
South Med J. 2000 Nov;93(11):1115-9.
 
Antiphospholipid syndrome and stroke  
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.
 
Antiphospholipid-Protein Antibodies and Ischemic Stroke  
(Stroke. 1998;29:1755-1758.) © 1998 American Heart Association, Inc.
 
APS and MS  
 
Association of antiphospholipid antibodies with central nervous system disease in systemic lupus erythematosus.  
Am J Med. 1995 Oct;99(4):397-401.
 
Brain vascular changes in the case of primary antiphospholipid syndrome.  
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.
 
Can neurologic manifestations of Hughes (antiphospholipid) syndrome be distinguished from multiple sclerosis? Analysis of 27 patients and review of the literature.  
Medicine (Baltimore). 2000 Jan;79(1):57-68.
 
Central nervous system involvement in the antiphospholipid (Hughes) syndrome  
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.
 
Cerebral microembolism, a disease marker for ischemic cerebrovascular events in the antiphospholipid syndrome of systemic lupus erythematosus?  
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.
 
Cerebrovascular disease and antiphospholipid antibodies in systemic lupus erythematosus, lupus-like disease, and the primary antiphospholipid syndrome.  
Am J Med. 1989 Apr;86(4):391-9.
 
Chorea and antiphospholipid antibodies: Treatment with methotrexate  
Neurology 2001;56:137-138. © 2001 American Academy of Neurology.
 
Cognitive Deficits in Patients With Antiphospholipid Syndrome  
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.
 
Dementia associated with the antiphospholipid syndrome: clinical and radiological characteristics of 30 patients  
Rheumatology Advance Access originally published online on September 14, 2004. Rheumatology 2005 44(1):95-99; doi:10.1093/rheumatology/keh408.
 
Factor V Leiden and Antiphospholipid Antibodies Are Significant Risk Factors for Ischemic Stroke in Children  
Stroke. 2000;31:1283. © 2000 American Heart Association, Inc.
 
Features Associated with Epilepsy in the Antiphospholipid Syndrome  
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.
 
Hemidystonia symptomatic of primary antiphospholipid syndrome in childhood.  
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.
 
Hypoperfusion of brain single photon emission computerized tomography in patients with antiphospholipid antibodies.  
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.
 
Low dose aspirin after ischemic stroke associated with antiphospholipid syndrome  
Neurology 2003;61:111-114 © 2003 American Academy of Neurology
 
Management of the neurological manifestations of APS--what do the trials tell us?  
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.
 
Migraine in Hughes syndrome—heparin as a therapeutic trial?  
Q J Med 2001; 94: 114-115 © 2001 Association of Physicians
 
Migraine, memory loss, and "multiple sclerosis ". Neurological features of the antiphospholipid (Hughes’) syndrome  
Postgraduate Medical Journal 2003;79:81-83 © 2003 Fellowship of Postgraduate Medicine
 
Multiple sclerosis, neuropsychiatric lupus and antiphospholipid syndrome: where do we stand?  
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.
 
Neurological involvement as a poor prognostic factor in catastrophic antiphospholipid syndrome: autopsy findings in 12 cases  
Source: Lupus, Volume 12, Number 2, 1 February 2003, pp. 93-98(6)
 
Neurometabolite Markers of Cerebral Injury in the Antiphospholipid Antibody Syndrome of Systemic Lupus Erythematosus  
Stroke. 1998;29:2254-2260.
 
Recurrent acute transverse myelopathy: Association with antiphospholipid antibody syndrome  
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
 
Some considerations about the possible pathological mechanisms at work in antiphospholipid syndrome and stroke  
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.
 
Stroke and antiphospholipid syndrome: the treatment debate  
Rheumatology Advance Access originally published online on April 19, 2005 Rheumatology 2005 44(8):971-974; doi:10.1093/rheumatology/keh666
 
The Antiphospholipid Syndrome and "Multiple Sclerosis"  
 
The blood disease that mimics MS - Hughes Syndrome  
How APS can mimic MS.
 
Thrombotic cerebral arteriopathy in patients with the antiphospholipid syndrome.  
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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APS - Opthalmology Related

 
A case of optic neuritis associated with anticardiolipin antibodies  
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.
 
Antiphospholipid Antibody Syndrome  
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.
 
Bilateral retinal vascular occlusion during antiphospholipid antibody syndrome: a case report  
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.
 
Central retinal venous occlusion with co-existent thrombotic thrombocytopenic purpura and antiphospholipid syndrome  
British Journal of Ophthalmology 2003;87:658-659 © 2003 BMJ Publishing Group
 
Handbook of Ocular Disease Management Antiphospholipid Syndrome  
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.
 
Ocular symptoms in association with antiphospholipid antibodies.  
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.
 
Ophthalmic signs in antiphospholipid syndrome. Patient description  
Klin Oczna. 2004;106(4-5):661-3 CONCLUSIONS: presented characteristic general and ophthalmic signs point to APS.
 
Primary antiphospholipid antibody syndrome and retinal occlusive vasculopathy.  
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.
 
Retinal vein occlusion in two patients with primary antiphospholipid syndrome.  
Korean J Intern Med. 2001 Dec;16(4):274-6
 
Review of severe vaso-occlusive retinopathy in systemic lupus erythematosus and the antiphospholipid syndrome: associations, visual outcomes, complications and treatment.  
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.
 
Sudden painless unilateral vision loss caused by branch retinal artery occlusion: implications for the primary care physician.  
Am J Med Sci. 2004 Jan;327(1):44-6
 
Visual disturbances and pathologic ocular findings in primary antiphospholipid syndrome.  
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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APS - Other

 
A cross-sectional study of clinical thrombotic risk factors and preventive treatments in antiphospholipid syndrome  
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.
 
Abdominal Thrombotic and Ischemic Manifestations of the Antiphospholipid Antibody Syndrome: CT Findings in 42 Patients1  
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.
 
Adrenal failure followed by status epilepticus and hemolytic anemia in primary antiphospholipid syndrome  
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.
 
An unusual cause of acute abdominal pain – A case presentation  
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.
 
Anti-phospholipid reactivity against cardiolipin metabolites occurring during endothelial cell apoptosis  
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.
 
Antiphospholipid antibodies in patients with sensorineural hearing loss.  
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.
 
Antiphospholipid antibody in localised scleroderma  
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.
 
Antiphospholipid antibody syndrome complicated by Grave's disease.  
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.
 
Antiphospholipid antibody syndrome in a six-year-old female patient.  
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.
 
Antiphospholipid Antibody Syndrome Ulcers  
© 1996-2005, American College of Physicians. All rights reserved.
 
Antiphospholipid antibody syndromes and the Internet.  
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.
 
Antiphospholipid inner ear syndrome.  
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.
 
Antiphospholipid Syndrome Has Many Faces  
04/18/2002 By Anne MacLennan Review of Arthritis & Rheumatism Volume 46, Issue 4, 2002. Pages: 1019-1027.
 
Asymptomatic sensorineural hearing loss in patients with systemic lupus erythematosus.  
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.
 
Colonic ulcers in propylthiouracil induced vasculitis with secondary antiphospholipid syndrome  
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.
 
Endocrinologic manifestations of the antiphospholipid syndrome.  
Lupus. 2006;15(8):485-9. Clinicians should keep a high index of suspicion for adrenal insufficiency in patients with APS.
 
Genomics and targeting antithrombotic therapy in antiphospholipid syndrome  
Blood, 15 February 2006, Vol. 107, No. 4, pp. 1249.
 
HCV and HIV may trigger antiphospholipid syndrome  
Last Updated: 2004-04-16 12:25:03 -0400 (Reuters Health)
 
Infectious origin of the antiphospholipid syndrome  
Annals of the Rheumatic Diseases 2006;65:2-6; doi:10.1136/ard.2005.045443
 
Ischemic Colitis due to Antiphospholipid Antibody Syndrome  
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
 
Management of antiphospholipid antibody syndrome: a systematic review.  
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.
 
Neuroendocrine manifestations of phospholipid antibody disease identified by long-term follow-up study of patients with phospholipid antibodies.  
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.
 
Perioperative medical management of antiphospholipid syndrome: hospital for special surgery experience, review of literature, and recommendations.  
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.
 
Spectrum of vascular pathology affecting patients with the antiphospholipid syndrome.  
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.
 
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.  
West J Med. 1991 August; 155(2): 174–176.
 
The Antiphospholipid Story  
© 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.
 
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

 
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.
 
Antiphospholipid antibodies and pregnancy loss  
 
Antiphospholipid antibodies and pregnancy rates and outcome in in vitro fertilization patients  
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.
 
Antiphospholipid Antibodies in Predicting Adverse Pregnancy Outcome  
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  
7/28/2003
 
Antiphospholipid Antibody Syndrome and Pregnancy Article by Stella Nowicki, DDS  
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
 
Antiphospholipid Syndrome (aPL)  
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)  
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.
 
Antiphospholipid syndrome and pregnancy  
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.
 
Antiphospholipid Syndrome in Pregnancy: A Randomized, Controlled Trial of Treatment  
Obstetrics & Gynecology 2002;100:408-413 © 2002 by The American College of Obstetricians and Gynecologists
 
Antiphospholipid syndrome in pregnancy: a randomized, controlled trial of treatment.  
Obstet Gynecol 2002; 100:408-13.
 
Clearance of Antiphospholipid Antibodies in Pregnancies Treated With Heparin  
Obstetrics & Gynecology 2001;97:394-398 © 2001 by The American College of Obstetricians and Gynecologists
 
Management of thrombosis in antiphospholipid syndrome and systemic lupus erythematosus in pregnancy.  
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.
 
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)
 
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.
 
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

 
*SERONEGATIVE ANTIPHOSPHOLIPID ANTIBODY SYNDROME (SNAPS)…AND SNAPPING TO IT!!  
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).
 
Antiphospholipid syndrome without antiphospholipid antibodies at the tim