Hamostaseologie 2011; 31(02): 94-104
DOI: 10.5482/ha-1134
Review
Schattauer GmbH

Coagulation and inflammation

Molecular insights and diagnostic implicationsGerinnung und EntzündungMolekulare Erkenntnisse und diagnostische Implikationen
S. Lipinski
1   Institut für Klinische Molekularbiologie, Christian-Albrechts-Universität, Kiel
,
L. Bremer
1   Institut für Klinische Molekularbiologie, Christian-Albrechts-Universität, Kiel
,
T. Lammers
2   I. Medizinische Klinik, Universitätsklinikum Schleswig-Holstein, Campus Kiel
,
F. Thieme
2   I. Medizinische Klinik, Universitätsklinikum Schleswig-Holstein, Campus Kiel
,
S. Schreiber
1   Institut für Klinische Molekularbiologie, Christian-Albrechts-Universität, Kiel
2   I. Medizinische Klinik, Universitätsklinikum Schleswig-Holstein, Campus Kiel
,
P. Rosenstiel
1   Institut für Klinische Molekularbiologie, Christian-Albrechts-Universität, Kiel
› Author Affiliations
Further Information

Publication History



09 December 2010

Publication Date:
28 December 2017 (online)

Summary

Overwhelming evidence has linked inflammatory disorders to a hypercoagulable state. In fact, thromboembolic complications are among the leading causes of disability and death in many acute and chronic inflammatory diseases. Despite this clinical knowledge, coagulation and immunity were long regarded as separate entities. Recent studies have unveiled molecular underpinnings of the intimate interconnection between both systems. The studies have clearly shown that distinct pro-inflammatory stimuli also activate the clotting cascade and that coagulation in turn modulates inflammatory signaling pathways.

In this review, we use evidence from sepsis and inflammatory bowel diseases as a paradigm for acute and chronic inflammatory states in general and rise hypotheses how a systematic molecular understanding of the “inflammation-coagulation” crosstalk may result in novel diagnostic and therapeutic strategies that target the inflammation-induced hypercoagulable state.

Zusammenfassung

Seit langem ist bekannt, dass systemische Entzündungen mit einer gesteigerten Blutgerinnung einhergehen. Tatsächlich besteht für Patienten mit akuten oder chronischen Entzündungserkrankungen ein erhöhtes Morbiditäts- und Sterberisiko durch thrombo- embolische Komplikationen. Entgegen dieser klinischen Befunde wurden Hämostase und Immunität in der Vergangenheit i. d. R. als unabhängige Prozesse betrachtet. Aktuelle Studien zeigen nun molekulare Verbindungen auf und bestätigen das enge Zusammenspiel beider Systeme. Immunzellen wie auch bestimmte pro-entzündliche Botenstoffe führen zu einer Aktivierung der Gerinnungskaskade – und umgekehrt beeinflussen Faktoren der Blutgerinnung die Entzündungsantwort.

Dieser Artikel fasst am Beispiel von Sepsis und chronisch-entzündlichen Darmerkrankungen, stellvertretend für akute und chronische Entzündungen, aktuelle Erkenntnisse zusammen und leitet daraus neue diagnostische und therapeutische Strategien ab, die die entzündungsvermittelte pathologische Gerinnungsaktivierung in Zukunft gezielt unterbinden könnten.

 
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