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Results for “CARDIOLIPIN”

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At least 1,135 records · Page 63Linked to original sources
PubMed1992

Monoclonal autoantibodies to cardiolipin derived from SLE mice.

The objective of this study was to clarify the specificity of anticardiolipin antibodies (aCL). Eighteen monoclonal hybridoma aCL from systemic lupus erythematosus (SLE)-prone MRL/Mp-lpr/lpr mice were established, and the reactivity of monoclonal aCL to phospholipids, DNA, nuclei of human epithelial cells, platelets, vascular endothelial cells, heparin, protein C and thrombomodulin was examined. All the 18 monoclonal aCL reacted with phosphatidylserine and some showed reactivity to phosphatidylinositol and phosphatidylcholine. Six of 16 monoclonal aCL were demonstrated to have the property of lupus anticoagulant. Monoclonal aCL were classified into three categories, in terms of DNA-binding specificity. Ten of 18 aCL had characteristics of antinuclear antibodies. Six of 11 aCL reacted with platelets. Three of 18 aCL were bound to vascular endothelial cells and to heparin. No monoclonal aCL reacted with protein C or thrombomodulin. Therefore, the conclusion was made that monoclonal aCL from SLE mice showed a polyspecific nature.

Animals↗
PubMed1999

Serum cardiolipin antibodies in cancer patients with thromboembolic events.

This study was undertaken to investigate a possible association of anticardiolipin antibodies (ACLAs) in cancer patients with thromboembolic events. Twenty-five patients with solid tumors complicated with acute thrombosis, 36 cancer patients without any thrombotic events, and a group of 20 healthy volunteers without thrombosis or malignancy were included. The mean age of the cancer patients with and without thrombosis and healthy subjects were 50 years (range 20-75), 45 years (range 23-66), and 40 years (range 20-68), respectively. Deep venous thrombosis (n = 16) and thrombosis of the central venous port-catheter systems (n = 9) were confirmed by Doppler sonography in all patients. IgG and IgM isotypes of ACLAs were quantitated by enzyme-linked immunosorbent assay with normal levels of < 23 GPL and < 11 MPL, respectively. Mean values of IgG ACLAs were found similar in cancer patients with acute thrombosis (13.8 +/- 4.9 GPL), without thrombosis (12.8 +/- 5.4 GPL) or in healthy subjects (14.8 +/- 5.5 GPL). Although the mean values of IgM ACLAs were within normal limits in all groups, cancer patients with thrombotic events had higher levels of IgM ACLAs (mean = 10.5 +/- 2.2 MPL) than cancer patients without thrombosis (mean = 4.6 +/- 2.4 MPL) (p = .01). Healthy subjects also had lower levels of IgM ACLAs (mean = 7.1 +/- 3.2 MPL) than cancer patients with thrombosis (p = .16). In addition, a higher percentage of cancer patients with or without thrombosis had IgM and IgG ACLA levels above normal limits compared with healthy controls. In conclusion, our study suggests an association between ACLAs or IgG and particularly IgM isotypes and venous thrombosis in malignancy. Identification of cancer patients who are at higher risk for developing thromboembolic events might lead to a better selection of patients for prophylactic anticoagulant therapy.

Adult↗
PubMed2000

Autoantibody responses to cardiolipin and DNA in infancy: association with lymphocytic panniculitis.

We report an infant with anticardiolipin (aCL) antibodies who presented with erythematous nodular skin lesions and elevated liver enzyme levels. The cutaneous manifestation was histologically lymphocytic lobular panniculitis with vasculitic and hemorrhagic changes. The infant also had low levels of anti-double stranded DNA (dsDNA) and anti-single stranded DNA (ssDNA) antibodies. There were no detectable antibodies to small nuclear ribonucleoproteins including Ro/SSA and La/SSB. His mother was consistently seronegative for any of these antibodies. Without corticosteroid therapy, cutaneous lesions resolved and anticardiolipin antibodies, but not anti-dsDNA and ssDNA antibodies, normalized within 16 months after the onset of the disease. Our patient demonstrated an uncommon presentation of aCL related cutaneous manifestation, the presentation with panniculitis being only the third such patient reported in the literature. Of great interest was the appearance of aCL antibodies and skin lesions during very early infancy.

Adult↗
PubMed1999

Antibodies to cardiolipin and beta2-glycoprotein-1 in HTLV-1-associated myelopathy/tropical spastic paraparesis.

Anticardiolipin and anti-beta2GP1 antibodies were measured in 50 patients with HTLV-1-associated Myelopathy-Tropical Spastic Paraparesis (HAM-TSP) and the results were compared with those obtained for 34 HTLV-1-positive and 35 HTLV-1-negative controls, as well as 128 SLE patients. aCL but not anti-beta2GP1 was associated with HTLV-I infection. aCL was more prevalent than anti-beta2GP1 (32% vs. 8%) and was not associated with anti-beta2GP1 in HAM-TSP. IgA was the dominant isotype of aCL and anti-beta2GP1. The data suggest that tin HAM-TSP, IgA aCL are frequent and are associated with HTLV-1 infection.

Antibodies, Anticardiolipin↗
PubMedDate not supplied

[Activated protein C resistance and cardiolipin antibodies in leg ulcers].

BACKGROUND: We conducted a prospective study to determine the prevalence of activated protein C resistance and anticardiolipin antibodies in leg ulcers, whatever venous, arterial or arteriovenous. PATIENTS AND METHODS: One hundred fifteen patients hospitalized for leg ulcers, without antiphospholipid syndrome were included. The vascular abnormalities were studied by clinical examination, Doppler, duplex Doppler and, when required, arteriography. Activated protein C resistance was isolated by a "classic" test (normalized APTT ratio in PCa presence or absence) and by a "second generation test" (by preliminary dilution with deficient factor V plasma). All patients with abnormal results on the second test were screened for the factor V Leiden (by PCR amplication with use of restriction enzymes). Anticardiolipin antibodies were investigated with an ELISA method with Harris standards as reference, in which the positive threshold was established at 20 units. RESULTS: Among these 115 patients, 50 venous (43.5 p. 100), 23 arterial (20 p. 100), 42 arteriovenous (36.5 p. 100) leg ulcers were identified. Activated protein C resistance was isolated in 12 cases (10.4 p. 100) (heterozygous carriers): 7 venous ulcers, 3 arteriovenous, 2 arterial. Anticardiolipin antibodies were measured at significant level in 49 cases (42.6 p. 100): 21 venous ulcers, 18 arteriovenous, 10 arterial. DISCUSSION: In this study, there was no statistical difference between the activated protein C resistance prevalence in leg ulcers when compared with Lorraine population (p=0.27). Factor V Leiden or anticardiolipin antibodies abnormalities were isolated in 56 cases (48.7 p. 100) without statistical difference between the 3 types of ulcers. Finally, the pathophysiology of venous, arterial and arteriovenous leg ulcers remains complex, suggesting several coagulation perturbations.

Activated Protein C Resistance↗
PubMedDate not supplied

Functional protein C and anti-cardiolipin antibody in children with portal vein thrombosis.

BACKGROUND: Portal vein thrombosis (PVT) is a common cause of portal hypertension in children from developing countries. Deficiencies of proteins C and S and elevated anticardiolipin antibody (aCL) levels have been shown to predispose to venous thrombosis. We studied these factors in children with idiopathic PVT. METHODS: 19 children with PVT (mean [SD] age 5.7 [2.1] y; 15 boys) were studied; all had had variceal bleeding, and had PVT on ultrasonography. Functional protein C activity was measured using a clotting assay; if it was normal, a clotting assay for functional protein S activity was performed. IgG aCL levels were measured in all sera using an in-house standardized solid-phase ELISA. RESULTS: Protein C functional activity ranged from 4% to 109%. Eight children had activity below 70%, the lower cut-off of the normal range. Protein S assay, done in 10 of the 11 children with normal protein C activity levels, was normal (above the cut-off level of 65% of the normal range). IgG aCL levels were abnormally elevated (>mean + 2SD of 16 healthy control children) in nine children; of these, three had associated protein C deficiency. Thus, of the 19 children with idiopathic PVT, 14 had abnormality in one or more tests. CONCLUSION: A majority of children with PVT of unknown etiology have functional protein C deficiency or abnormally elevated levels of aCL antibodies.

Antibodies, Anticardiolipin↗
PubMed2004

Splenic infarction associated with anti-cardiolipin antibody: a report of two cases.

There are few cases of splenic infarction associated with antiphospholipid antibody reported in the literature. We present two cases of splenic infarction associated with anticardiolipin antibody, one complicated by the development of a splenic pseudocyst. Clinical diagnostic features of splenic infarction are described. In addition, a review of the literature on thrombotic manifestations of antiphospholipid syndrome is presented.

Adult↗
PubMedDate not supplied

Discordance between anti-beta2-glycoprotein-I and anti-cardiolipin antibodies in patients with clinical criteria of antiphospholipid syndrome.

OBJECTIVES: Clinical and immunological features of patients with clinical manifestations of the antiphospholipid syndrome (APS) with anti-beta2-glycoprotein-I antibodies (anti-beta2-GP-I) but without anticardiolipin antibodies (aCL) or any other autoimmune condition are not well documented. We sought to determine the clinical significance of positive anti-beta2-GP-I with negative aCL. METHODS: From July 2002 through July 2003, 1,179 serum samples obtained in our hospital from the Community of Madrid were tested for anti-beta2-GP-I and aCL by enzyme-linked immunosorbent assay. Clinical records of patients with discordant anti-beta2-GP-I and aCL were retrospectively analysed. RESULTS: A total of 56 patients with discordant anti-beta2-GP-I and aCL were identified. By logistic regression analysis, after adjusting for age, sex and risk factors of thrombosis, the risk for developing APS criteria associated with anti-beta2-GP-I was significant [odds ratio 3.88; 95% confidence interval (CI): 1.05-14.27; p = 0.04). 15 out of 56 patients (26.8%) had positive anti-beta2-GP-I and negative aCL. 5 out of 15 anti-beta2-GP-I-positive patients had clinical APS without serological nor clinical evidence of any autoimmune disease. CONCLUSION: Determination of anti-beta2-GP-I should be considered in individual cases with clinical manifestations of primary APS and repeated negative results on conventional antiphospholipid antibody test.

Aged↗
PubMed2006

[Inhibition of cardiolipin binding antibodies from synovial fluids of patients with arthritis by endotoxin].

In the presented study was prooven that aCl antibodies cross-reacting with LPS (endotoxin) from arthritic synovial fluids are part of the aPL antibodies pool and correlated with presence in joints bacterial cell wall components like LPS-showing endotoxin presence in synovial fluids and they may be usefull in differential diagnosis of the different kind of arthritis and also in explanation of their aetiology at all--especially in cases of early, undifferentiated arthritis.

Antibodies, Anticardiolipin↗