Deficient t-PA release and elevated PA inhibitor levels in patients with spontaneous or recurrent deep venous thrombosis
- PMID: 3109059
Deficient t-PA release and elevated PA inhibitor levels in patients with spontaneous or recurrent deep venous thrombosis
Abstract
The fibrinolytic system was investigated in 120 patients with spontaneous or recurrent deep vein thrombosis (DVT) without any known organic disease able to explain by itself the occurrence of a thrombosis and without any known defect of antithrombin III, Heparin Cofactor II, Protein C, or Protein S. The assays included: Euglobulin fibrinolytic activity (EFA), tissue-type plasminogen activator related antigen (t-PA-Ag) and plasminogen activator inhibitor activity (PA inhibitor), which were measured before and after 10 min of venous occlusion (V.O.). On the basis of the results, the patients could be classified in 3 groups: good responders with an at least two-fold increase of EFA after venous occlusion (n = 76), poor responders with a lesser increase of EFA due to deficient release of t-PA (n = 12), and poor responders with a normal t-PA release but an increased level of PA-Inhibitor (n = 32). The poor responders due to deficient t-PA release (10% of total) had a higher incidence of recurrence of deep vein thrombosis, than the other groups (p less than 0.01). An overall correlation was found between the level of PA-Inhibitor activity and the triglyceride level (r = 0.40, p less than 0.01), suggesting that these elevations may be due to a common cause, at least in some of the patients. It is concluded that a poor fibrinolytic response to venous occlusion occurs in 35 percent of DVT patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Similar articles
-
Hypofibrinolysis in patients with a history of idiopathic deep vein thrombosis and/or pulmonary embolism.Thromb Haemost. 1992 Apr 2;67(4):397-401. Thromb Haemost. 1992. PMID: 1631786
-
Age dependence of blood fibrinolytic components and the effects of low-dose oral contraceptives on coagulation and fibrinolysis in teenagers.Thromb Haemost. 1988 Dec 22;60(3):361-4. Thromb Haemost. 1988. PMID: 3149043
-
[Decreased fibrinolytic capacity in coronary patients by increased plasminogen activator inhibitor activity].Helv Chir Acta. 1992 Jan;58(4):503-8. Helv Chir Acta. 1992. PMID: 1582860 German.
-
Fibrinolysis in patients with acute ischaemic heart disease. With particular reference to systemic effects of tissue-type plasminogen activator treatment on fibrinolysis, coagulation and complement pathways.Dan Med Bull. 1993 Sep;40(4):383-408. Dan Med Bull. 1993. PMID: 8222763 Review.
-
Pathophysiology of thrombophilic states.Folia Haematol Int Mag Klin Morphol Blutforsch. 1988;115(3):243-52. Folia Haematol Int Mag Klin Morphol Blutforsch. 1988. PMID: 2465210 Review.
Cited by
-
Insulin resistance and polycystic ovary syndrome.Curr Diab Rep. 2002 Feb;2(1):71-6. doi: 10.1007/s11892-002-0061-y. Curr Diab Rep. 2002. PMID: 12643125 Review.
-
Tissue-type plasminogen activator. A review of its pharmacology and therapeutic use as a thrombolytic agent.Drugs. 1989 Sep;38(3):346-88. doi: 10.2165/00003495-198938030-00003. Drugs. 1989. PMID: 2509190 Review.
-
Identification of polyclonal and monoclonal antibodies against tissue plasminogen activator in the antiphospholipid syndrome.Arthritis Rheum. 2005 Dec;52(12):4018-27. doi: 10.1002/art.21485. Arthritis Rheum. 2005. PMID: 16320350 Free PMC article.
-
Effect of oral defibrotide on tissue-plasminogen activator and tissue-plasminogen activator inhibitor balance.Eur J Clin Pharmacol. 1992;42(4):379-83. doi: 10.1007/BF00280122. Eur J Clin Pharmacol. 1992. PMID: 1516602 Clinical Trial.
-
Proteomic biomarkers of sleep apnea.Sleep. 2020 Nov 12;43(11):zsaa086. doi: 10.1093/sleep/zsaa086. Sleep. 2020. PMID: 32369590 Free PMC article.
MeSH terms
Substances
LinkOut - more resources
Other Literature Sources