Anticardiolipin antibodies (ACA) are most often not associated with lupus‐like anticoagulant (LLAC) in human immunodeficiency virus (HIV) infection

Capel, Paul D.; Janssens, A; Clumeck, Nathan; Gérard, M.; Feremans, Walter; Vandevelde, Dianne; Fondu, Pierre

doi:10.1002/ajh.2830370404

Cited by 11 publications

(8 citation statements)

References 16 publications

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“…Other investigations have found that in several stages of the disease, the prevalence of one isotype over the others may vary. For example, the prevalence of IgG aCL was 24-94% and IgM aCL was 0-50% (20,22,23). We found 6.3% of aPT and 6.3% of anti-b 2 GPI, as expected.…”

Section: Prevalence Of Antiphospholipid and Antiplatelet Antibodiessupporting

confidence: 86%

“…IgG and IgM aCL were found in 12.9% of HIVinfected patients. In other studies, the prevalence of aCL has shown a wider range (8-75%) (9,(20)(21)(22). Other investigations have found that in several stages of the disease, the prevalence of one isotype over the others may vary.…”

Section: Prevalence Of Antiphospholipid and Antiplatelet Antibodiesmentioning

confidence: 91%

“…In HIV-infected patients the prevalence of aCL has been reported from 8-75% (9,(20)(21)(22), but generally their presence is not associated with thrombotic events (22)(23)(24)(25). The prevalence of aPlt in HIV-infected patients is 6.5-50% (26,27).…”

Section: Introductionmentioning

confidence: 99%

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Prevalence of antiphospholipid and antiplatelet antibodies in human immunodeficiency virus (HIV)‐infected Chilean patients

Palomo

Alarcón

Sepúlveda

et al. 2003

Clinical Laboratory Analysis

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Antiphospholipid (aPL) and antiplatelet (aPlt) antibodies, found in patients with autoimmune diseases, are also detected in infectious diseases. The purpose of this study was to examine the prevalence of these antibodies in HIV patients and to evaluate an association of these antibodies with thrombocytopenia and/or thrombosis. Sixty-three HIV-seropositive patients and 52 normal controls were studied. Anti-cardiolipin (aCL), anti-beta(2) glycoprotein I (anti-beta(2)GPI), and antiprothrombin (aPT) antibodies were determined and the lupus anticoagulant (LA) test was performed. Antiplatelet antibodies (aPlt) were also determined. Seven out of 63 (12.7%) HIV patients were positive for aCL, four of 63 (6.3%) for anti-beta(2)GPI, and five of 63 (7.9%) for aPT. No patients studied were LA positive. Six out of 63 (9.5%) patients were positive for aPlt. One of them showed weak reactivity for GPIb-IX. The platelet count of patients (202+/-63 x 10(3) platelets/microL) was significantly lower than in the controls (343+/-6 x 10(3) platelets/microL) (P<0.001). There was no correlation between the presence of aPL and/or aPlt and thrombocytopenia. Of the HIV-infected patients, 22.2% presented aPL and 9.4% aPlt antibodies. In this study, the presence of aPL and aPlt antibodies was not associated with the development of thrombosis and/or thrombocytopenia.

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Section: Prevalence Of Antiphospholipid and Antiplatelet Antibodiessupporting

confidence: 86%

Section: Prevalence Of Antiphospholipid and Antiplatelet Antibodiesmentioning

confidence: 91%

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Prevalence of antiphospholipid and antiplatelet antibodies in human immunodeficiency virus (HIV)‐infected Chilean patients

Palomo

Alarcón

Sepúlveda

et al. 2003

Clinical Laboratory Analysis

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“…Anticardiolipin antibodies have been commonly reported in HIV-positive patients, with a prevalence of 7.7-94%. 27,28,[37][38][39][40][41][42][43][44][45] There are two different types of anticardiolipin antibodies, immunoglobulin (Ig) G and IgM. The literature reports the IgG anticardiolipin antibody to be positive in 41-94% of patients with HIV 38,39,40,42,46 compared with the IgM anticardiolipin antibody, which is reported to be positive in only 7% of patients with HIV.…”

Section: Antiphospholipid Antibodiesmentioning

confidence: 99%

Risk Factors for Venous Thromboembolism in Patients with Human Immunodeficiency Virus Infection

Kiser

Badowski

2010

Pharmacotherapy

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Prevention and treatment of venous thromboembolism are gaining attention in the lay and medical communities because of an increase in frequency, cost, and risk factors. Evidence shows that patients with human immunodeficiency virus (HIV) have multiple risk factors and a 2-10-fold increased risk for venous thromboembolism compared with the general population. A higher rate of venous thromboembolism also occurs in patients with HIV who are younger than 50 years (3.31% vs 0.53% in age-matched healthy controls, p<0.0001), have a CD4(+) cell count less than 200 cells/mm³, or have a diagnosis of acquired immunodeficiency syndrome. Both protein S and C deficiencies--disorders that may predispose individuals to thrombotic disease--are considered risk factors; in addition, the use of protease inhibitors and the presence of active opportunistic infections or antiphospholipid antibodies may be associated with venous thromboembolism. It is imperative that all risk factors for venous thromboembolism be identified and incorporated into medical decision making for high-risk patients, including those with HIV. The classification and mechanism of these risk factors are not well understood. Long-term, prospective studies assessing the factors associated with venous thromboembolism in patients with HIV are needed. Risk stratification systems or screening tools, as well as effective preventive measures, must be developed.

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“…High numbers in the peripheral blood were also reported in rheumatoid arthritis [21], Sjögren's syndrome [22], and recent-onset insulin-dependent diabetes mellitus [23]. In the setting of HIV infection there are few reports concerning the number and the role of CD5 þ B lymphocytes in relation to the development of autoimmune phenomenon, lymphoid neoplasia or disease progression [24,25].…”

Section: Introductionmentioning

confidence: 99%

Anti-phospholipid antibodies and CD5+ B cells in HIV infection

Grünewald¹,

Schüler-Maué³

et al. 1999

Clinical and Experimental Immunology

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This cross-sectional study evaluates the correlation between anti-phospholipid antibodies and CD5+ B cells in 110 patients infected with HIV-1. There were 89.1% of the patients who had IgG antibodies against cardiolipin and phosphatidylserine. The prevalence of IgM and IgA antibodies was < 22%. AIDS was associated with lower frequencies of IgM antibodies against cardiolipin (P = 0.05) and IgG-antibodies against cardiolipin and phosphatidylserine (P = 0.011). Drug users had higher IgM antibodies against phospholipids than patients from other risk groups (P = 0.02). A history of thromboembolic events was not accompanied by higher levels of anti-phospholipid antibodies (P > 0.2). No correlation between anti-phospholipid antibodies and CD5+ B cells was detected. Percentage part of CD5+ B lymphocytes was elevated in all patients and absolute CD4+ T lymphocyte counts and HIV p24 antigen were inversely correlated. In advanced disease a significant reduction of anti-phospholipid antibodies was contrasted with persistent elevation of CD5+ B lymphocytes. These observations may reflect immunological dysfunction involving apoptosis and endothelial damage rather than polyclonal B cell hyperstimulation. A possible explanation would be that in HIV infection an increased rate of spontaneous apoptosis in peripheral blood lymphocytes is accompanied by functional and structural changes of mitochondria. Therefore, structurally altered mitochondrial phospholipids could serve as antigen to induce specific humoral immune responses.

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Anticardiolipin antibodies (ACA) are most often not associated with lupus‐like anticoagulant (LLAC) in human immunodeficiency virus (HIV) infection

Cited by 11 publications

References 16 publications

Prevalence of antiphospholipid and antiplatelet antibodies in human immunodeficiency virus (HIV)‐infected Chilean patients

Prevalence of antiphospholipid and antiplatelet antibodies in human immunodeficiency virus (HIV)‐infected Chilean patients

Risk Factors for Venous Thromboembolism in Patients with Human Immunodeficiency Virus Infection

Anti-phospholipid antibodies and CD5+ B cells in HIV infection

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