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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 28-year-old man suffered from recurrent facial exanthema, arthritis and stomatitis for ten years and died six months after a catatonic episode with terminal cerebral convulsions. Three years before his death high KBR-Antititers to Herpes simplex- and cytomegalic virus were observed, while Lupus-Erythematosus-Tests (LE-Tests) only became positive in the last months. At autopsy, changes compatible with Systemic Lupus Erythematosus (SLE) were found in the mitral valves, the spleen, and the kidneys. The brain displayed hemorrhagic infarction of the striate bodies and thrombophlebitis of the internal cerebral veins, the wall of which exhibited circumscribed infiltrations with numerous hematoxilin bodies and LE cells. This seems to be the first observation of LE-specific changes in the brain. The importance of cerebral vein affection in SLE involving the nervous system is stressed and a hypothesis submitted proposing the viral etiology of SLE.
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PMID:[Thrombophlebitis of internal cerebral veins in a case of systemic lupus erythematosus (author's transl)]. 738 48

We have previously demonstrated that patients with cirrhosis may be positive for lupus anticoagulant and anticardiolipin antibodies. The prevalence and clinical value of antiphospholipid antibodies in cirrhosis have never been described. Besides, it has not yet been determined if serum levels of beta-2-glycoprotein I, which is synthesized by the liver and mediates the interaction between cardiolipin and anticardiolipin antibodies affects lupus anticoagulant detectability in cirrhosis. We evaluated the prevalence of lupus anticoagulant in 63 patients with cirrhosis and related it to beta-2-glycoprotein I serum levels. We also analyzed whether lupus anticoagulant and anticardiolipin antibodies were associated with previous thrombotic complications. Eleven patients (18%) were lupus anticoagulant positive; 14 (22%) had high values of anticardiolipin antibodies. Fourteen patients had a previous history of splanchnic venous thrombosis (n = 9) or thrombophlebitis (n = 5). A significant association between lupus anticoagulant (p = 0.0001), anticardiolipin antibodies (p = 0.0001) and venous thrombosis was found. Patients with severe liver failure had significantly lower beta-2-glycoprotein I levels than those with moderate (p < 0.01) or low (p < 0.001) hepatic insufficiency. Among 14 anticardiolipin antibodies positive patients, six with severe liver failure were lupus anticoagulant negative and had beta-2-glycoprotein I values below 100 micrograms/ml. In four of these, basal values of dilute activated partial thromboplastin time were not modified by the addition of 50 micrograms/ml of exogenous beta-2-glycoprotein I. This study shows that antiphospholipid antibodies are relatively frequent in cirrhosis and that beta-2-glycoprotein I levels are not so low as to affect lupus anticoagulant detectability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of lupus anticoagulant in patients with cirrhosis: relationship with beta-2-glycoprotein I plasma levels. 769 32

A clinical case of syndrome of antiphospholipid antibodies is reported. The patient is a 10-year-old girl with thrombophlebitis of the right leg associated with the presence of lupus-like anticoagulant antibodies. No secondary pathologies were found. It is not possible, anyway, to make a definitive differential diagnosis between primary and secondary forms of syndrome of antiphospholipid antibodies because of intermediate situations where antiphospholipid antibodies are associated with 2 or 3 ARA criteria for the diagnosis of lupus (lupus-like syndrome). A long term follow-up is therefore necessary.
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PMID:[The clinical syndrome associated with antiphospholipid antibodies. A diagnosis to be confirmed after a long follow-up]. 779 7

The antiphospholipid antibodies (aPL), namely, the lupus anticoagulant and the anticardiolipin antibodies, are a family of autoantibodies directed predominantly against negatively charged phospholipids. Many studies have confirmed that patients with these antibodies are prone to repeated episodes of thrombosis, fetal losses, and thrombocytopenia. The association of aPL with these clinical events has been termed the antiphospholipid syndrome. Several skin lesions have been found in patients with this syndrome, including livedo reticularis, livedoid vasculitis, thrombophlebitis, cutaneous infarctions and gangrene of digits, ulcerations, lesions resembling vasculitis (nodules, macules), cutaneous necrosis/infarctions, subungual splinter hemorrhages, and, less commonly, discoid lupus and Degos' disease (malignant atrophic papulosis). In this article, we review the main immunologic and clinical aspects of this syndrome with special emphasis on the dermatologic features.
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PMID:Antiphospholipid syndrome. 842 86

The antiphospholipid syndrome may present itself to virtually all medical specialties. It can be as non-threatening as thrombophlebitis or mild thrombocytopenia or as severe as cerebral arterial infarct or the so called "catastrophic APS". In order to diagnose it properly, it is important to be aware of its clinical manifestations and laboratory peculiarities. The primary form of APS seems to be more common than the SLE related one. Because any artery or vein may be involved, the spectrum of clinical manifestations of APS is so wide that they include virtually all medical specialties.
Lupus 1996 Oct
PMID:Clinical manifestations of the aPL syndrome. 890 68

The antiphospholipid syndrome is an acquired multisystem disorder of hypercoagulation, which may be primary or secondary to underlying diseases. Serologic markers for the syndrome are the lupus anticoagulant and anticardiolipin antibodies. Clinical features include recurrent thrombotic events (arterial or venous), repeated fetal loss, and thrombocytopenia. Cutaneous manifestations may occur as the first sign of antiphospholipid syndrome. These include livedo reticularis, necrotizing vasculitis, livedoid vasculitis, thrombophlebitis, cutaneous ulceration and necrosis, erythematous macules, purpura, ecchymoses, painful skin nodules, and subungual splinter hemorrhages. Antiphospholipid syndrome may also be associated rarely with anetoderma, discoid lupus erythematosus, cutaneous T-cell lymphoma, or disorders that closely resemble Sneddon or Degos syndromes. Noninflammatory vascular thrombosis is the most frequent histopathologic feature observed. Prophylaxis and treatment of thrombosis in patients with antiphospholipid syndrome relies principally on anticoagulant and antiplatelet agents.
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PMID:Antiphospholipid syndrome and the skin. 920 65

Antiphospholipid syndrome is characterized by thromboses, fetal losses and antiphospholipid antibodies. This group of antibodies includes lupus anticoagulant, false positive syphilitic reaction, anionic (such as anticardiolipin) and neutral phospholipids antibodies, and anti-phospholipid/cofactors antibodies (such as anti-beta 2-glycoprotein 1). Dominant manifestations are recurrent thrombophlebitis and pulmonary embolism, arterial occlusive disease of young people, obstetrical complications such as fetal losses, livedo, and thrombocytopenia. Warfarin is presently the main treatment.
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PMID:[Antiphospholipid antibodies syndrome]. 978 Nov 33

The antiphospholipid syndrome is characterized by clinical evidence of arterial or venous thrombosis, thrombocytopaenia, recurrent fetal loss and repeated positivity of antiphospholipid autoantibodies. The association of antiphospholipid syndrome with the development of adrenal failure has been reported in more than 40 patients in the last 20 years, mostly due to bilateral cortical haemorrhage or thrombosis of adrenal vessels. The presence of antibodies against adrenal cortex was never documented in these patients. Here we report a case of recurrent thrombophlebitis, acute adrenal failure, and chronic hepatitis occurring in a young man found to have antiphospholipid antibodies and lupus anticoagulant. Autoantibodies against adrenal cortex were detected and abdominal ultrasonography showed morphologically normal adrenals. Mild thrombocytopaenia, Coomb's positive anaemia, increase in alanine- and aspartate-aminotransferases and increase in urinary protein excretion were found. Autoantibodies against liver/kidney microsomes were positive and liver biopsy was compatible with autoimmune hepatitis. The patient was treated with cortisone acetate, fludrocortisone and warfarin. Dilated cardiomyopathy was revealed one year later and coronarography did not document any occlusive coronary disease. Three years later, titres of autoantibodies, including those directed towards the adrenal cortex, were increased and others, previously absent, were detected. Nevertheless, the patient's clinical conditions seemed unchanged. At this time, an abdominal CT scan showed adrenal dysmorphisms with bilateral annular calcifications and central hypodensities suggesting previous bilateral adrenal haematomas. The hypercoagulable state that occurs in antiphospholipid syndrome can induce a localized inflammatory response generated by tissue injury, with a consequent release of intracellular antigens and antibodies production. Consequently, tissue-specific autoantibodies positivity may persist until the cells involved in antigen production are completely destroyed.
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PMID:Antiphospholipid syndrome, adrenal failure, dilated cardiomyopathy and chronic hepatitis: an unusual manifestation of multiorgan autoimmune injury? 991 71

The outcome of collagen vascular diseases after treatment with plasmapheresis was studied in 9 patients with polyarteritis nodosa (PN), in 2 patients with Wegener's granulomatosis (WG), in 1 patient with allergic granulomatous angitis (AGA), and in 20 patients with systemic lupus erythematosus (SLE) associated with antiphospholipid syndrome (APS). Improvement after treatment with plasmapheresis was observed in 41.7% of the patients with PN, WG, and AGA. On the other hand, with the exception of 1 patient with thrombocytopenia and 1 patient with renal failure, all of the clinical manifestations, including thrombocytopenia, central nervous system (CNS) lupus, thrombophlebitis, lung infarction, and recurrent abortions in the SLE patients with APS, improved after plasmapheresis. Plasmapheresis is thought to be an influential strategy of treatment for patients with collagen vascular diseases.
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PMID:Outcome of collagen vascular diseases by treatment with plasmapheresis. 1022 53

We describe a 50-year-old woman who developed severe pain of the left lower limb after an episode of thrombophlebitis. Bone scintigraphy and thermography showed results indicative of reflex sympathetic dystrophy. Laboratory analysis revealed the presence of the lupus anticoagulant. The patient was diagnosed as antiphospholipid syndrome complicated with reflex sympathetic dystrophy of the left lower limb. To our knowledge, this is the first report of a patient with reflex sympathetic dystrophy with underlying antiphospholipid syndrome.
Lupus 1999
PMID:Reflex sympathetic dystrophy in a patient with the antiphospholipid syndrome. 1048 17


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