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Acquired protein S deficiency.

B Kemkes-Matthes1

  • 1Zentrum für Innere Medizin, Justus Liebig Universität Giessen.

The Clinical Investigator
|June 1, 1992
PubMed
Summary

Hereditary and acquired deficiencies of protein S, a coagulation inhibitor, increase the risk of blood clots. Acquired deficiencies in conditions like nephrotic syndrome and malignancy contribute to this risk.

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Area of Science:

  • Coagulation science
  • Hematology
  • Thrombosis research

Background:

  • Hereditary deficiencies in coagulation inhibitors (antithrombin III, protein C, protein S) are linked to increased thromboembolic events.
  • Acquired protein S deficiencies have been identified in various disease states associated with frequent thromboembolic complications.
  • These acquired deficiencies can be as significant as hereditary ones.

Purpose of the Study:

  • To discuss disease states characterized by acquired protein S deficiency.
  • To explore the mechanisms underlying acquired protein S alterations.
  • To highlight the role of acquired protein S deficiency in thromboembolic complications.

Main Methods:

  • Literature review of disease states with acquired protein S deficiency.
  • Analysis of mechanisms causing protein S alterations in specific conditions.
  • Correlation of acquired protein S deficiency with thromboembolic incidence.

Main Results:

  • Acquired protein S deficiency is observed in nephrotic syndrome, acute phase reactions, malignancy, and pregnancy.
  • These deficiencies contribute to the occurrence of thromboembolic complications in affected patients.
  • The extent of acquired protein S deficiency can rival that of hereditary forms.

Conclusions:

  • Acquired protein S deficiency is a significant factor in thromboembolic complications across various diseases.
  • Understanding these acquired deficiencies is crucial for managing thrombotic risk.
  • Further research into the mechanisms and management of acquired protein S deficiency is warranted.

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