PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “CARDIOLIPIN”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed2000

Cardiolipin is a normal component of human plasma lipoproteins.

Anticardiolipin (anti-CL) antibodies, diagnostic for antiphospholipid antibody syndrome, are associated with increased risks of venous and arterial thrombosis. Because CL selectively enhances activated protein C/protein S-dependent anticoagulant activities in purified systems and because CL is not known to be a normal plasma component, we searched for CL in plasma. Plasma lipid extracts [chloroform/methanol (2:1, vol/vol)] were subjected to analyses by using TLC, analytical HPLC, and MS. A plasma lipid component was purified that was indistinguishable from reference CL (M:1448). When CL in 40 fasting plasma lipid extracts (20 males, 20 females) was quantitated by using HPLC, CL (mean +/- SD) was 14.9 +/- 3.7 microgram/ml (range 9.1 to 24.2) and CL was not correlated with phosphatidylserine (3.8 +/- 1.7 microgram/ml), phosphatidylethanolamine (64 +/- 20 microgram/ml), or choline-containing phospholipid (1,580 +/- 280 microgram/ml). Based on studies of fasting blood donors, CL (>/=94%) was recovered in very low density, low density, and high density lipoproteins (11 +/- 5.3%, 67 +/- 11.0%, and 17 +/- 10%, respectively), showing that the majority of plasma CL (67%) is in low density lipoprotein. Analysis of relative phospholipid contents of lipoproteins indicated that high density lipoprotein is selectively enriched in CL and phosphatidylethanolamine. These results shows that CL is a normal plasma component and suggest that the epitopes of antiphospholipid antibodies could include CL or oxidized CL in lipoproteins or in complexes with plasma proteins (e. g., beta(2)-glycoprotein I, prothrombin, protein C, or protein S) or with platelet or endothelial surface proteins.

Antibodies, Antiphospholipid↗
PubMed2001

Anti-cardiolipin antibodies, Raynaud's phenomenon with digital ischemia, and non small cell carcinoma of the lung.

Raynaud's phenomenon, digital ischemia, antinuclear antibodies and anticardiolipin antibodies are uncommon features of malignancy. The association of all of these in a patient with malignancy has not previously been reported. We describe a 52 year old woman with non small-cell carcinoma of the lung who also had Raynaud's phenomenon, digital ischemia, anti-nuclear antibodies and anticardiolipin antibodies.

Antibodies, Antinuclear↗
PubMed2004

The association of antibodies to cardiolipin, beta 2-glycoprotein I, prothrombin, and oxidized low-density lipoprotein with thrombosis in 292 patients with familial and sporadic systemic lupus erythematosus.

OBJECTIVE: To determine the prevalence of antibodies to phospholipid-binding plasma proteins (aPL) and to oxidized low-density lipoprotein (OX-LDL), and to study the association of these antibodies with thrombosis and coronary heart disease (CHD) in patients with systemic lupus erythematosus (SLE). METHODS: Clinical data and sera from 89 Finnish patients with familial and 203 with sporadic SLE were available for the study. Enzyme-linked immunosorbent assays (ELISA) were used for antibody determination. RESULTS: The occurrence of thrombosis in our SLE patients was 13.7% (40/292) and of clinically diagnosed CHD was 1.4% (4/292). All antibody assays, except IgM-aCL, were significantly associated with thrombosis. IgG-aCL alone or in combination with anti beta 2-GPI or with anti OX-LDL were reasonably sensitive (38%, 48%, and 58%, respectively) and specific (87%, 80% and 72%, respectively) for a history of thrombosis. A high risk of arterial thrombosis (TIA or stroke) was associated with positivity of IgG-aCL, anti beta 2-GPI, and anti-prothrombin. Venous thrombosis was significantly associated with all other assays except IgM-aCL and anti-prothrombin. No test correlated with CHD, but the number of affected patients was small. There were three multiplex SLE families with two patients having a history of thrombosis: no consistent pattern of aPL or anti OX-LDL was found in these patients. CONCLUSION: IgG-aCL alone or in combination with anti beta 2-GPI or anti OX-LDL are sensitive and specific tests for detecting SLE patients at increased risk of thrombosis. The aetiopathogenesis of thrombosis in familial SLE appears to be multifactorial.

Adult↗