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Thromb Haemost 1996; 76(01): 069-073
DOI: 10.1055/s-0038-1650524
Original Article
Schattauer GmbH Stuttgart

Liver Steatosis and Its Relation to Plasma Haemostatic Factors in Apparently Healthy Men - Role of the Metabolic Syndrome

M Cigolini
1   The Institute of Clinical Medicine, Verona, Italy
,
G Targher
2   The Division of Endocrinology and Metabolic Diseases, University of Verona, Verona, Italy
,
G Agostino
1   The Institute of Clinical Medicine, Verona, Italy
,
M Tonoli
1   The Institute of Clinical Medicine, Verona, Italy
,
M Muggeo
2   The Division of Endocrinology and Metabolic Diseases, University of Verona, Verona, Italy
,
G De Sandre
1   The Institute of Clinical Medicine, Verona, Italy
› Institutsangaben
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Publikationsverlauf

Received: 26. Oktober 1995

Accepted after resubmission03. April 1996

Publikationsdatum:
10. Juli 2018 (online)

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Summary

The relationship between liver steatosis, evaluated by ultrasonography, and various plasma haemostatic factors was examined in 64 apparently healthy males, aged 38 years. Plasma levels of factor VII clotting activity (F-VIIc), plasminogen activator inhibitor-1 (PAI-1) activity and antigen, tissue-type plasminogen activator (t-PA) activity significantly differed in men with liver steatosis (n = 31) as compared with those without steatosis (n = 33). No significant differences were found in t-PA antigen and F-VII antigen. The men with liver steatosis also had significantly higher body mass index (BMI), plasma triglyceride and 2 h post-load insulin concentrations. While the differences in plasma haemostatic factors were substantially unchanged after adjustment for BMI, they totally disappeared when further allowance was made for plasma triglyceride and 2 h insulin concentrations. In conclusion, these results indicate that liver steatosis correlates specifically with increased PAI-1, F-VIIc and decreased t-PA levels, and suggest that such a relation is largely mediated by concomitant alterations in plasma triglyceride and insulin concentrations.

 

  • References

  • 1 Asplund-Carlson A, Hamsten A, Wiman B, Carlson LA. Relationship between plasma plasminogen activator inhibitor-1 activity and VLDL triglyceride concentration, insulin levels and insulin sensitivity: studies in randomly selected normo- and hypertriglyceridaemic men. Diabetologia 1993; 36: 817-825
    CrossrefPubMedGoogle Scholar
  • 2 Bruckert E, Ankri A, Jung M, Turpin G, De Gennes JL. Mild liver abnormalities associated with elevated plasma factor VII and protein C in hypertriglyceridaemic patients. Eur J Med 1993; 8: 461-465
    PubMedGoogle Scholar
  • 3 Bruckert E, Ankri A, Giral P, Turpin G. Relation between plasminogen activator inhibitor-1 and hepatic enzyme concentrations in hyperlipidemic patients. Thromb Haemost 1994; 72: 434-437
    Artikel in Thieme ConnectPubMedGoogle Scholar
  • 4 Cigolini M, Targher G, Seidell JC, Schiavon R, Manara F, Zenti MG, Mattioli C, De Sandre G. Relationships of plasminogen activator inhibitor-1 to anthropometry, serum insulin, triglycerides and adipose-tissue fatty acids in healthy men. Atherosclerosis 1994; 106: 139-146
    CrossrefPubMedGoogle Scholar
  • 5 Cigolini M, Targher G, De Sandre G, Muggeo M, Seidell JC. Plasma fibrinogen in relation to serum insulin, smoking habits and adipose-tissue fatty acids in healthy men. Eur J Clin Invest 1994; 24: 126-130
    CrossrefPubMedGoogle Scholar
  • 6 Cigolini M, Targher G, Tonoli M, Manara F, Muggeo M, De Sandre G. Hyperuricaemia: relationships to body fat distribution and other components of the insulin resistance syndrome in 38-yr-old healthy men and women. Int J Obes 1995; 19: 92-96
    PubMedGoogle Scholar
  • 7 Gossink BB, Lemon SK, Scheible W, Leopold GR. Accuracy of ultrasonography in diagnosis of hepatocellular disease. Am J Roentgenol 1979; 133: 19-23
    CrossrefPubMedGoogle Scholar
  • 8 Dawson S, Henney A. The status of PAI-1 as a risk for arterial and thrombotic disease: a review. Atherosclerosis 1992; 95: 105-117
    CrossrefPubMedGoogle Scholar
  • 9 Hamsten A. The hemostatic system and coronary heart disease. Thromb Res 1993; 70: 1-38
    CrossrefPubMedGoogle Scholar
  • 10 Hamsten A, Wiman B, De Faire U, Blomback M. Increased plasma levels of rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction. N Engl J Med 1985; 313: 1557-1563
    CrossrefPubMedGoogle Scholar
  • 11 Meade TW, Brozovic M, Chakrabarti RR, Haines AP, Imeson JD, Mellows S, Miller GJ, North WRS, Stirling Y, Thompson SG. Haemostatic function and ischaemic heart disease: principal results of the Northwick Park Heart Study. Lancet 1986; 533-537
    PubMedGoogle Scholar
  • 12 Clain DJ, Lefkowitch JH. Fatty liver disease in morbid obesity. Gastroenterol Clin North Am 1987; 16: 239-252
    PubMedGoogle Scholar
  • 13 Braillon A, Capron JP. Foie et obesite. Gastroenterol Clin Biol 1983; 7: 627-634
    PubMedGoogle Scholar
  • 14 Seidell JC, Cigolini M, Deslypere JP, Charzewska J, Ellsinger BM, Cruz A. Body fat distribution in relation to serum lipids and blood pressure in 38-year-old European men. The European Fat Distribution Study. Atherosclerosis 1991; 86: 251-260
    CrossrefPubMedGoogle Scholar
  • 15 Seidell JC, Cigolini M, Deslypere JP, Charzewska J, Ellsinger BM, Cruz A. Body fat distribution in relation to physical activity and smoking habits in 38-year-old European men. The European Fat Distribution Study Am J Epidemiol 1991; 133: 257-265
    CrossrefPubMedGoogle Scholar
  • 16 Reaven GM. Banting lecture: Role of insulin resistance in human disease. Diabetes 1988; 37: 1595-1607
    CrossrefPubMedGoogle Scholar
  • 17 De Fronzo RA, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidaemia, and atherosclerotic cardiovascular disease. Diabetes Care 1991; 14: 173-194
    CrossrefPubMedGoogle Scholar
  • 18 Juhan-Vague I, Alessi MC, Vague P. Increased plasma plasminogen activator inhibitor 1 levels. A possible link between insulin resistance and atherothrombosis. Diabetologia 1991 34. 457-462
    PubMedGoogle Scholar
  • 19 Eliasson M, Asplund K, Evrin PE, Lindahl B, Lundblad D. Hyperinsulin-aemia predicts low tissue plasminogen activator activity in a healthy population. The Northern Sweden MONICA Study. Metabolism 1994; 43: 1579-1586
    PubMedGoogle Scholar
  • 20 Juhan-Vague I, Thompson SG, Jespersen J. on behalf of the ECAT Angina Pectoris Study Group. Involvement of the hemostatic system in the insulin resistance syndrome. A study of 1500 patients with angina pectoris. Arterioscler Thromb 1993 13. 1865-1873
    PubMedGoogle Scholar
  • 21 Mykkanen L, Ronnemaa T, Mamiemi J, Haffner SM, Bergmann R, Laakso M. Insulin sensitivity is not an independent determinant of plasma plasminogen activator inhibitor-1 activity. Arterioscler Thromb 1994; 14: 1264-1271
    CrossrefPubMedGoogle Scholar
  • 22 Mehta J, Mehta P, Lawson D, Saldeen T. Plasma tissue plasminogen activator inhibitor levels in coronary artery disease: correlation with age and serum triglyceride concentrations. J Am Coll Cardiol 1987; 9: 263-268
    CrossrefPubMedGoogle Scholar
  • 23 Raccah D, Alessi MC, Seelies V, Menard C, Juhan-Vague I, Vague P. Plasminogen activator inhibitor activity in various types of endogenous hypertriglyceridemia. Fibrinolysis 1993; 7: 171-176
    PubMedGoogle Scholar
  • 24 Miller GJ, Martin JC, Mitropoulos KA, Reeves RL, Thompson RL, Meade TW, Cooper JA, Cruickshank JK. Plasma factor VII is activated by postprandial triglyceridemia, irrespective of dietary fat composition. Atherosclerosis 1991; 86: 163-171
    CrossrefPubMedGoogle Scholar
  • 25 Mitropoulos KA, Miller GJ, Reeves RL, Wilkes HC, Cruickshank JK. Factor VII coagulant activity is strongly associated with the plasma concentration of large lipoprotein particles in middle-aged men. Atherosclerosis 1989; 76: 203-208
    CrossrefPubMedGoogle Scholar
  • 26 Folsom AR, Wu RR, Davis CE, Conlan MG, Sorlie PD, Szklo M. Population correlates of plasma fibrinogen and factor VII, putative cardiovascular risk factors. Atherosclerosis 1991; 91: 191-205
    CrossrefPubMedGoogle Scholar
  • 27 Moor E, Hamsten A, Karpe F, Bavenholm P, Blomback M, Silveira A. Relationship of tissue factor pathway inhibitor activity to plasma lipoproteins and myocardial infarction. Thromb Haemost 1994; 71: 707-712
    Artikel in Thieme ConnectPubMedGoogle Scholar
  • 28 Mitropoulos KA, Esnouf MP. The autoactivation of factor XII in the presence of long-chain saturated fatty acids: a comparison with the potency of sulphatides and dextran sulphate. Thromb Haemost 1991; 66: 446-452
    Artikel in Thieme ConnectPubMedGoogle Scholar
  • 29 Mitropoulos KA, Martin JC, Reeves BEA, Esnouf MP. The activation of the contact phase of coagulation by physiological surfaces in plasma: the effect of large negatively charged liposomal vescicles. Blood 1989; 73: 1523-1533
    PubMedGoogle Scholar
  • 30 Stiko-Rahm A, Wiman B, Hamsten A, Nilsson J. Secretion of plasminogen activator inhibitor-1 from cultured human umbilical vein endothelial cells is induced by very low density lipoprotein. Arteriosclerosis 1990; 10: 1067-1073
    CrossrefPubMedGoogle Scholar
  • 31 Mussoni L, Mannucci L, Sirtori M, Camera M, Madema P, Sironi L, Tremoli E. Hypertriglyceridemia and regulation of fibrinolytic activity. Arterioscler Thromb 1992; 12: 19-25
    CrossrefPubMedGoogle Scholar
  • 32 Alessi MC, Juhan-Vague I, Kooistra T, Declerck PJ, Collen D. Insulin stimulates the synthesis of plasminogen activator inhibitor-1 by the human hepatocellular cell line Hep G2. Thromb Haemost 1988; 60: 491-494
    Artikel in Thieme ConnectPubMedGoogle Scholar
  • 33 Schneider DJ, Sobel BE. Augmentation of synthesis of plasminogen activator inhibitor type 1 by insulin and insulin-like growth factor type implications for vascular disease in hyperinsulinemic states. Proc Natl AcadSci USA 1991; 88: 9959-9963
    CrossrefPubMedGoogle Scholar
  • 34 Tran-Than C, Fasel-Felley J, Pralong G, Hofstette JR, Bachmann F, Kruithof EKO. Plasminogen activators and plasminogen activator inhibitors in liver deficiencies caused by chronic alcoholism or infectious hepatitis. Thromb Haemost 1989; 62: 651-653
    Artikel in Thieme ConnectPubMedGoogle Scholar