Skip to main content
Journal of Clinical Pathology logoLink to Journal of Clinical Pathology
. 1988 Jun;41(6):615–618. doi: 10.1136/jcp.41.6.615

Acquired dysfibrinogenaemia masquerading as disseminated intravascular coagulation in acute pancreatitis.

J T Wilde 1, W E Thomas 1, D A Lane 1, M Greaves 1, F E Preston 1
PMCID: PMC1141540  PMID: 3384995

Abstract

Acquired dysfibrinogenaemia as the cause of coagulation abnormalities occurred in a case of acute pancreatitis. Initial coagulation studies showed a prolonged thrombin time and increased concentrations of serum fibrinogen/fibrin degradation products and plasma D-dimer. Further studies on purified fibrinogen showed evidence of degradation of the C-terminal ends of the A-alpha chains, which, it is suggested, resulted from the action of circulating pancreatic proteases. Fibrin polymerisation was thus shown to be impaired, which explains the prolongation of the thrombin time. There was a temporal relation between increased amylase activities and the prolonged thrombin time, both of which returned to normal three weeks after admission. Acquired dysfibrinogenaemia may be an underrecognized phenomenon in acute pancreatitis and may lead to misinterpretation of coagulation test abnormalities.

Full text

PDF
615

Images in this article

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Belitser V. A., Varetskaja T. V., Malneva G. V. Fibrinogen-fibrin interaction. Biochim Biophys Acta. 1968 Feb 19;154(2):367–375. doi: 10.1016/0005-2795(68)90051-2. [DOI] [PubMed] [Google Scholar]
  2. Green G., Thomson J. M., Dymock I. W., Poller L. Abnormal fibrin polymerization in liver disease. Br J Haematol. 1976 Nov;34(3):427–439. doi: 10.1111/j.1365-2141.1976.tb03589.x. [DOI] [PubMed] [Google Scholar]
  3. Lane D. A., Scully M. F., Thomas D. P., Kakkar V. V., Woolf I. L., Williams R. Acquired dysfibrinogenaemia in acute and chronic liver disease. Br J Haematol. 1977 Feb;35(2):301–308. doi: 10.1111/j.1365-2141.1977.tb00586.x. [DOI] [PubMed] [Google Scholar]
  4. Lasson A., Ohlsson K. Consumptive coagulopathy, fibrinolysis and protease-antiprotease interactions during acute human pancreatitis. Thromb Res. 1986 Jan 15;41(2):167–183. doi: 10.1016/0049-3848(86)90227-6. [DOI] [PubMed] [Google Scholar]
  5. Marder V. J., Shulman N. R. High molecular weight derivatives of human fibrinogen produced by plasmin. II. Mechanism of their anticoagulant activity. J Biol Chem. 1969 Apr 25;244(8):2120–2124. [PubMed] [Google Scholar]
  6. Martinez J., Palascak J. E., Kwasniak D. Abnormal sialic acid content of the dysfibrinogenemia associated with liver disease. J Clin Invest. 1978 Feb;61(2):535–538. doi: 10.1172/JCI108964. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Soria J., Soria C., Ryckewaert J. J., Samama M., Thomson J. M., Poller L. Study of acquired dysfibrinogenaemia in liver disease. Thromb Res. 1980 Jul 1;19(1-2):29–41. doi: 10.1016/0049-3848(80)90401-6. [DOI] [PubMed] [Google Scholar]
  8. Southan C., Thompson E., Lane D. A. Direct analysis of plasma fibrinogen-derived fibrinopeptides by high-performance liquid chromatography. Thromb Res. 1986 Jul 15;43(2):195–204. doi: 10.1016/0049-3848(86)90060-5. [DOI] [PubMed] [Google Scholar]
  9. Weber K., Osborn M. The reliability of molecular weight determinations by dodecyl sulfate-polyacrylamide gel electrophoresis. J Biol Chem. 1969 Aug 25;244(16):4406–4412. [PubMed] [Google Scholar]

Articles from Journal of Clinical Pathology are provided here courtesy of BMJ Publishing Group

RESOURCES