Circulating anticoagulant in patients seropositive for human immunodeficiency virus

Taillan, B.; Roul, C.; Fuzibet, J. G.; Vinti, H.; Pesce, A.; Bayle, J; Cassuto, Jill‐Patrice; Dujardin, P

doi:10.1016/s0002-9343(89)80708-9

Cited by 10 publications

(6 citation statements)

References 4 publications

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“…For example, Non Nucleoside Reverse Transcriptase Inhibitors are known to induce an elevation of dGT [41] and protease inhibitors increase the amount of dyslipidemia [42]. Hyperbilirubinemia may also be a consequence of antiretroviral treatments such as Atazanavir or Indinavir [43], affecting the interpretation of bilirubin-based scores such as Fibrotest Ò or Hepascore Ò .…”

Section: Discussionmentioning

confidence: 99%

Performance of 11 biomarkers for liver fibrosis assessment in HIV/HBV co-infected patients

Bottéro

Lacombe

Guéchot

et al. 2009

Journal of Hepatology

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Section: Discussionmentioning

confidence: 99%

Performance of 11 biomarkers for liver fibrosis assessment in HIV/HBV co-infected patients

Bottéro

Lacombe

Guéchot

et al. 2009

Journal of Hepatology

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“…87,88 About 10% of patients with SLE have the lupus anticoagulant; however, the entity is commonly seen in other conditions, including cancer, lymphoproliferative disorders, and viral infections, especially in association with the human immunodeficiency virus. [89][90][91] Most commonly the lupus anticoagulant develops in otherwise healthy individuals (primary lupus anticoagulant thrombosis syndrome). There is also an association with drug ingestion; commonly associated drugs include chlorpromazine, procainamide, quinidine, hydralazine, phenytoin, and Fansidar.…”

Section: Lupus Anticoagulantmentioning

confidence: 99%

Antiphospholipid and Thrombosis Syndromes

Bick

Baker²

1994

Semin Thromb Hemost

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ACAs and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism or mechanisms whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories, as previously discussed, have been advanced. The most common thrombotic events associated with ACAs are DVT and PE (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), cerebrovascular or retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). The relative frequency of ACAs in association with arterial and venous thrombosis strongly suggests that these should be looked for in any patient with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through IV) should be defined, if possible, because this may dictate both type and duration of both immediate and long-term anticoagulant therapy. Unlike those with ACAs, patients with primary lupus anticoagulant thrombosis syndrome usually have venous thrombosis. Since the aPTT is unreliable in patients with lupus anticoagulant and is not usually prolonged in patients with ACAs, definitive tests (ELISA for ACA and the dRVVT for lupus anticoagulant) should be immediately ordered when suspecting antiphospholipid syndrome or in patients with otherwise unexplained thrombotic or thromboembolic events.

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“…286 LA is also seen in patients with other disorders, including malignancy, lymphoproliferative disorders, 286 and viral infections, particularly human immunodeficiency virus infection. 287 In addition, LA may be associated with use of the same drugs that induce the formation of ACLAs. [288][289][290] Even patients with drug-induced LA (usually gamma M immunoglobulin [IgM] idiotype) exhibit an increased risk of thrombosis.…”

Section: Lupus Anticoagulantmentioning

confidence: 99%

Treatment of Hereditary and Acquired Thrombophilic Disorders

Baker¹,

Bick²

1999

Semin Thromb Hemost

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The treatment of hereditary and acquired thrombophilic disorders is based on an understanding of the disease pathophysiology, prevalence, associated morbidity and mortality, and available therapeutic options. Genetic mutations are identified that result in activated protein C (APC) resistance and hyperhomocyst(e)inemia. The underlying etiologies are less well-defined; however, the disorders of factor XII deficiency, dysfibrinogenemia, Wien-Penzing platelet defect, and sticky platelet syndrome (SPS) are treatable inherited thrombophilias. Antithrombin deficiency, protein C and protein S deficiencies, and plasminogen deficiency are disorders both inherited and acquired. Antiphospholipid antibodies, myeloproliferative syndromes, and Trousseau's syndrome are acquired. Treatment for acute arterial thrombosis or venous thromboembolism is the same or similar for all thrombophilic disorders. Long-term management is based on the risk of a primary or recurrent acute thrombotic event, compared with the risk of the proposed therapy. Few blinded, controlled studies are available to validate treatment recommendations. When long-term anticoagulation is advised, careful consideration should be given to the risk associated with therapy. Bleeding risk, variable efficacy, and the risk of cutaneous necrosis limit the use of warfarin. Fixed low-dose unfractionated porcine heparin and low-molecular-weight heparins (LMWH) offer significant advantages for long-term management. These recommendations are derived from an analysis of the pertinent medical literature and are expected to change with the progress of clinical and laboratory investigation.

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Circulating anticoagulant in patients seropositive for human immunodeficiency virus

Cited by 10 publications

References 4 publications

Performance of 11 biomarkers for liver fibrosis assessment in HIV/HBV co-infected patients

Performance of 11 biomarkers for liver fibrosis assessment in HIV/HBV co-infected patients

Antiphospholipid and Thrombosis Syndromes

Treatment of Hereditary and Acquired Thrombophilic Disorders

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