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PAI -1 (Plasminogen Activator Inhibitor-1)

Analyte: Plasminogen Activator Inhibitor 1

Specimen Type: Frozen Citrate or EDTA Plasma

Optimum Volume: 0.5 mL *

Stability:

2-8°C -20°C -70°C
Unstable* N.A.* N.A.*

Reporting units: ng/mL

Method: ELISA

Biological or Clinical Significance:

Plasminogen activator inhibitor-1 (PAI – 1) is the principal inhibitor of tissue plasminogen activator and urokinase, the activators of plaminogen and hence fibrinolysis.

PAI-1 is present in increased levels in various disease states (such as a number of forms of cancer), as well as in obesity and the metabolic syndrome. It has been linked to the increased occurrence of thrombosis in patients with these conditions. In inflammatory conditions in which fibrin is deposited in tissues, PAI-1 appears to play a significant role in the progression to fibrosis (pathological formation of connective tissue) and hence an acute phase reactant. Presumably, lower PAI levels would lead to less suppression of fibrinolysis and conversely a more rapid degradation of the fibrin.

The clinical interest in measuring PAI-l in plasma is based on studies in which high levels of PAI-1 activity are found in patients suffering from deep venous thrombosis, myocardial infarction and septicemia. Studies also show that PAI-1 activity correlates well with PAI-1 antigen in plasma samples. However, platelets contain large amounts of stored PAI-1 that is released in an inactive form hence affecting PAI-1 antigen values but not PAI-1 activity values. These findings indicate that platelet release should be avoided.

PAI-1 has diurnal variation, with higher concentration in the morning and decreased concentration in the afternoon.

Principle of Test Method:

The PAI-1 assay is a solid-phase ELISA that employs the quantitative sandwich enzyme immunoassay principle. *Note: Due to instability of the sample, two aliquots (0.5 mL each) are recommended in order to perform repeat analysis if needed.

*Please contact PBI for stability information.

References:

1. Mertens I, Van Gaal LF. Obesity, haemostasis and the fibrinolytic system. Obes Rev. 2002; 3: 85-101.
2. Shimomura I, Funahashi T, Takahashi M, Maeda K, Kotani K, Nakamura T, Yamashita S, Miura M, Fukuda Y, Takemura K, Tokunaga K, Matsuzawa Y. Enhanced expression of PAI-1 in visceral fat: possible contributor to vascular disease in obesity. Nat Med. 1996; 2: 800-803.
3. Wajchenberg BL. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome. Endocr Rev. 2000; 21: 697-738.
4. De Pergola G, De Mitrio V, Giorgino F, Sciaraffia M, Minenna A, Di Bari L, Pannacciulli N, Giorgino R. Increase in both pro-thrombotic and anti-thrombotic factors in obese premenopausal women: relationship with body fat distribution. Int J Obes Relat Metab Disord. 1997; 21: 527-535.
5. Giltay EJ, Elbers JM, Gooren LJ, Emeis JJ, Kooistra T, Asscheman H, Stehouwer CD. Visceral fat accumulation is an important determinant of PAI-1 levels in young, nonobese men and women: modulation by cross-sex hormone administration. Arterioscler Thromb Vasc Biol. 1998; 18: 1716-1722.
6. Ferguson MA, Gutin B, Owens S, Litaker M, Tracy RP, Allison J. Fat distribution and hemostatic measures in obese children. Am J Clin Nutr. 1998; 67: 1136-1140.
7. Gramling MW, Church FC. Plasminogen activator inhibitor-1 is an aggregate response factor with pleiotropic effects on cell signaling in vascular disease and the tumor microenvironment. Thromb Res. 2010; 125:377-381.
8. Cesari M, Pahor M, Incalzi RA. Plasminogen activator inhibitor-1 (PAI-1): a key factor linking fibrinolysis and age-related subclinical and clinical conditions. Cardiovasc Ther. 2010; 28:e72-e91.
9. Kluft C, Jie AF, Rijken DC, Verheijen JH. Daytime fluctuations in blood of tissue-type plasminogen activator (t-PA) and its fast-acting inhibitor (PAI-1).Thromb Haemost. 1988; 59: 329-332.

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