Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antiphospholipid antibodies have been reported to occur in ischemic stroke patients, but there have been no previous reports linking these antibodies to spinal cord infarction. A case of spinal cord infarction associated with primary antiphospholipid syndrome in a 6-year-old boy is reported. Magnetic resonance imaging clearly demonstrated marked swelling of the thoracolumbar spinal cord with gadolinium-diethylenetriamine pentaacetic acid enhancement at an acute stage, followed later by cord atrophy. Serological study disclosed positive lupus anticoagulant and immunoglobulin G anticardiolipin antibody. It is suggested that the role of antiphospholipid antibodies as an etiological factor for spinal cord ischemia should be recognized among causes that might have been categorized as either spontaneous spinal cord infarction or myelitis.
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PMID:Spinal cord infarction associated with primary antiphospholipid syndrome in a young child. Case report. 836 Jul 45

We report a case of diffuse large cell non-Hodgkin's lymphoma with concomitant lupus anticoagulant at initial diagnosis. Progressive thrombosis occurred despite radiologically proven response of the lymphoma after chemotherapy treatment. Extraordinary bone scintigraphy with multiple "cold" lesions probably due to bone ischemia is described.
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PMID:Progressive thrombosis after treatment of diffuse large cell non-Hodgkin's lymphoma and concomitant lupus anticoagulant. 862 78

A 25-year-old Japanese woman who had been suffering from systemic lupus erythematosus (SLE) for 12 years was admitted to our hospital with a suspected diagnosis of peritonitis after suddenly developing severe abdominal pain and distention which could not be relieved by treatment with anodyne. Noninvasive examinations did not provide enough evidence to rule out acute appendicitis, bowel perforation, or ischemia due to vasculitis. Therefore, in consideration of the severity of her uncontrollable abdominal pain, an exploratory laparotomy was performed. The operative findings revealed nonbacterial peritonitis with a large amount of ascites and an edematous small bowel. No perforation of the intestine was found. On post-operative day (POD) 3, the severe abdominal pain redeveloped, but responded well to steroid pulse therapy. Based on the operative findings and her clinical course, the most likely diagnosis was thought to be acute lupus peritonitis. It is often difficult to ascertain whether abdominal pain in an SLE patients is due to lupus peritonitis or to an underlying cause requiring surgery. Thus, it is essential that continuous and careful assessment of the surgical abdomen is performed when a patient with SLE develops acute abdominal pain, and if a surgical condition cannot be ruled out, a laparotomy should be performed without delay.
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PMID:Lupus peritonitis mimicking acute surgical abdomen in a patient with systemic lupus erythematosus: report of a case. 888 45

Central nervous system involvement in neonatal lupus erythematosus (NLE) has not been previously reported. We report four patients with NLE, all with complete congenital heart block and three with cerebral ultrasound and color Doppler flow imaging (CDFI) studies demonstrating evidence of associated vasculopathy in the gangliothalamic vasculature. CDFI confirmed blood flow through the affected vessels, indicating that blood flow was not compromised at this early stage. Short-term follow-up revealed no signs of progression of the vasculopathy, focal ischemia, gangliothalamic atrophy, or neurological impairment. Nevertheless, the implications of this finding with respect to the natural history of NLE remain to be defined, particularly in cases in which the disease develops into systemic lupus erythematosus later in life. Besides specific diagnostic studies for NLE, cerebral ultrasound, and CDFI studies are mandatory in all cases of complete congenital heart block, regardless of whether mothers are diagnosed as having connective-tissue disease or not. Neonates with signs of vasculopathy in the gangliothalamic region should be examined for NLE.
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PMID:Central nervous system vasculopathy in neonatal lupus erythematosus. 888 46

Antiphospholipid antibodies (aPL) have been associated with a variety of neurological disorders, mostly linked to focal neuroparenchymal ischemia or infarction. Cerebral ischemia associated with the antiphospholipid syndrome (APS) occurs at a younger age than typical atherothrombotic cerebrovascular disease, is often recurrent, and high positive GPL values are usually linked to the presence of a lupus anticoagulant. When other features of the syndrome are not present and cerebral ischemia occurs only associated with anticardiolipin immunoreactivity, there appears to be no discerning features of these patients unless GPL > 40 for which recurrent thrombo-occlusive events appear to occur more frequently. Other neurological manifestations associated with aPL include cerebral venous sinus thrombosis, ocular ischemia, dementia, including ischemic encephalopathy, and chorea. The role of aPL in migrainous events is controversial and may not play a role in recent, large case-controlled studies. Most seizures in patients harboring aPL are associated with focal brain infarction.
Lupus 1996 Oct
PMID:Neurological aspects of antiphospholipid antibody syndrome. 890 59

We describe a case of a verrucous non-bacterial endocarditis on the native mitral valve in a patient with polymyositis. This case, to our knowledge, represents the first report in the literature we could get. The case reached our attention after an episode of acute limb ischemia which lead to an echocardiographic examination that showed vegetations on the valve. No cardiac signs or symptoms were evident. We discuss the possible relation between the two disorders. The possibility of autoimmune diseases, other than lupus or lupus-related disorders, to produce this kind of lesions should be confirmed by a systematic echocardiographic study of these patients even if they have no evidence of cardiac involvement.
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PMID:[Verrucous abacterial endocarditis and polymyositis. A possible association?]. 903 27

There are only few data available regarding the immunological mechanisms for cerebral infarction. The aim of this study was to find out the humoral and cell-mediated immunity under the conditions of focal brain ischemia (CI). As a method for humoral immunity, the complement consumption test against a panel of 8 antigens, quantitative analysis of immunoglobins and fractionized sedimentation of erythrocytes were used in the group of pts with CI, and the group of atherosclerotics (AS) and hypertonics (VH), potential victims of focal brain ischemia. It was found that the occurrence of antibodies against the whole panel of antigens in the group of CI is significantly higher as compared with the healthy controls, but it is lower than that in the group of AS and VH. The occurrence of antibodies exclusively against only brain antigens and that in CSF is similar. No correlation to the location of ischemic lesion and the degree of neurological deficit score was found. These findings didn't change in 2 and 4 weeks as well as in 1 year after the onset of CI. The quantitative analysis of immunoglobins revealed statistically higher levels of IgA and lower levels of IgM in comparison with the controls. IgG were higher, but without statistical significance. Statistically significant higher levels of all immunoglobins in CSF were found. As similar trend of changes found also in the group of AS and VH. These results of humoral immunity confirmed by the results of fractionized sedimentation of erythrocytes with EP. The results can be interpreted as a possible change or disorder of central regulation of immunizing processes due to the latent (in AS and VH) of manifest (in CI) lesions of the brain. But the quality and quantity of this response might have been affected by the entire case history of the patients who survived cerebral infarction. The changes in immunity response of the organism in CI was shown also in cell-mediated immunity. The results a statistically significant increase in stimulatory (SI) as well as in immunoregulatory (IRI) indices in stroke patients under the age of 40. These findings didn't change 2 and 4 weeks after the onset of CL. An increase in IRI was due to the increase in Th lymphocytes. In the immune response of the organism in CI, the antiphospholipid antibodies (aPLs = anticardiolipin antibodies (aCL) and lupus anticoagulant--LA) play an important role. aCLs were present in 9.8% of the first stroke pts when compared to 4.3% in controls. The most common isotype of the antibodies we IgG. Of all first-stroke pts who were aCL positive only 8% had no other stroke risk factors (atrial fibrillation, diabetes, hypertension and other). aCLs are an important risk factor for the first stroke, mainly in the young, but also in the elderly. The presence of aCLs increases the risk for recurrent strokes. aPLs are not necessarily associated with the specific location of clinical stroke syndrome but they are in significant correlation to the occurrence of multiple strokes on CT (30:18%). None of the initially aCL-negative patients became aCL-positive during the time course of CI. These data support the idea that aCLs play a causal role in stroke (PROPTER HOC changes) rather than vice versa (POST HOC changes). From the therapeutic point of view, currently there do not exist any good treatment guidelines for preventing the second stroke. The analysis of HLA. antigen showed an increase in some HLA (A2, A28 etc.) and a decrease in others (A3, A9 etc.) in comparison with the controls. This might refer to the participation of genetic factors in the onset of CI.
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PMID:[Cerebral infarct and the immune response]. 933 23

A patient with a history of recurrent late fetal loss associated with multiple placental infarcts and cerebrovascular ischemia at the age of 36, followed a year later by a myocardial infarction, was referred for further investigation. Coronary angiography was normal. Antinuclear factor, lupus anticoagulant, anticardiolipin antibodies, and other thrombophilia parameters were negative, but there was moderate hyperthyroidism with positive thyroid peroxidase antibodies. Platelet numbers and von Willebrand factor (vWF) were normal. Her platelets showed spontaneous aggregation that disappeared with aspirin intake. However, aggregation still was induced by low levels of ristocetin (0.3 to 0.5 mg/mL). The low-dose ristocetin aggregation in patient platelet-rich plasma (PRP) was completely blocked by neutralizing antiglycoprotein Ib (GPIb) and anti-vWF antibodies. The monoclonal anti-Fc gamma RII receptor antibody IV.3 inhibited partly, which suggests that PRP aggregation by low-dose ristocetin was elicited by vWF-immunoglobulin (Ig) complexes. Upon addition to washed human platelets, with vWF (10 micrograms/mL), purified patient Igs dose-dependently enhanced ristocetin (0.15 mg/mL)-induced aggregation between 0 and 500 micrograms/mL, an effect that disappeared again above 1 mg/mL. Aggregation was dependent on the vWF concentration and was blocked by IV.3 or neutralizing anti-GPIb or anti-vWF antibodies. The spontaneous aggregation of normal platelets resuspended in patient plasma could be inhibited totally by IV.3 and partially by neutralizing anti-GPIb or anti-vWF antibodies. Perfusion with normal anticoagulated blood, enriched with 10% of control or patient plasma, over surfaces coated with vWF showed increased platelet adhesion and activation in the presence of patient antibodies. Treatment of the patient with the antithyroid drug thiamazol and temporary corticosteroids, aspirin, and ticlopidine did not correct the platelet hypersensitivity to ristocetin. These observations suggest that some autoantibodies to vWF may both enhance vWF binding to platelets and cause platelet activation through binding to the Fc gamma RII receptor, and thereby may be responsible for a new form of antibody-mediated thrombosis.
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PMID:Recurrent arterial thrombosis linked to autoimmune antibodies enhancing von Willebrand factor binding to platelets and inducing Fc gamma RII receptor-mediated platelet activation. 953 91

The purpose of this study was to determine the clinical characteristics of chronic renal failure patients who developed hand ischemia in the limb carrying the dialysis angioaccess. A retrospective review of the charts of 352 patients who underwent 409 upper extremity arteriovenous access, and who were subsequently diagnosed as steal syndrome, was performed at the Emory University Hospital between February 1992 and January 1997. Hand ischemia occurred after 13 of 299 arteriovenous grafts (4.3%) and after 2 of 110 direct forearm arteriovenous fistulas (1.8%). Six patients developed ischemic manifestations immediately postoperatively, 2 in the first week, 4 after 1 month, and 1 after 1 year. Thirteen occurred in association with the primary access procedure. Two cases occurred following graft thrombectomy and outflow dilatation. Seven patients were mildly symptomatic with dialysis-induced pain, coldness, or numbness; 8 patients developed severe ischemic manifestations in the form of sensory loss in 3, severe intolerable pain with impalpable pulse in 3, and digital gangrene and amputation in 2, one of whom developed an unhealed amputation stump and required a higher amputation level with satisfactory healing of the revised stump. Three patients were treated conservatively, 6 by banding, 4 by ligation, 1 by embolization, and 1 by distal ligation and bypass operation. Clinical characteristics of patients with hand ischemia included long-standing insulin-dependent diabetes (10), chronic hypertension (12), peripheral arterial disease (14; 93.3%), coronary artery disease (8), and systemic lupus erythematosis (1). Severe peripheral arterial diseases are commonly found and may be markers for risk of hand ischemia after access surgery.
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PMID:Incidence and characteristics of patients with hand ischemia after a hemodialysis access procedure. 953 65

Pneumonia is the most common serious complication of varicella infection in adults. A variety of thrombotic complications including purpura fulminans and disseminated intravascular coagulation have been reported in children with varicella but not in adults. Two men with varicella pneumonia who had profound lower extremity ischemia caused by thrombosis of the profunda femoris and tibial arteries are reported. Both patients had free protein S deficiency and vascular thrombosis in association with varicella pneumonia without overt evidence of disseminated intravascular coagulation or purpura fulminans. Antiphospholipid immunoglobulin G and immunoglobulin M antibodies were present in one, whereas the other had evidence of the lupus anticoagulant. The proposed pathogenesis and management options including intraarterial thrombolytic therapy with urokinase and the need for long-term anticoagulation are discussed.
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PMID:Spontaneous tibial artery thrombosis associated with varicella pneumonia and free protein S deficiency. 954 47


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