Phlebologie 2013; 42(01): 13-18
DOI: 10.12687/phleb2123_1_2013
Review
Schattauer GmbH

Endocrine mechanisms in the pathogenesis of primary varicosis

Endokrine Mechanismen in der Pathogenese der primären Varikose
Ch. Busch
1   Department of Dermatology, University of Tuebingen, Germany
,
S. Schnabl
1   Department of Dermatology, University of Tuebingen, Germany
,
A. Strölin
1   Department of Dermatology, University of Tuebingen, Germany
› Author Affiliations
Further Information

Publication History

Eingereicht: 15 November 2013

Angenommen: 16 January 2013

Publication Date:
30 December 2017 (online)

Summary

Introduction: Varicose veins affect up to 40 % of men and up to 51 % of women. The patho-physiology of primary varicosis (chronic venous insufficiency, CVI) is poorly understood. Here, the available data on possible endocrine mechanisms in healthy and varicose veins are reviewed.

Methods: An extensive literature search was conducted in PubMed using the following key words: Chronic venous insufficiency, CVI, chronic venous disease, CVD, varicosis, saphenous vein, pathogenesis, hormone.

Results: Several theories ranging from incompetence of the valves to functional, biological or morphologic changes in different layers of the vein wall have been proposed. However, an increasing body of evidence suggests that endocrine mechanisms might be involved in the pathogenesis of primary varicosis. In this respect a growing number of hormones (e.g. estrogen, progesterone, relaxin-2, and oxytocin) and their receptors have been linked to primary varicosis in experimental, pharmacological and histological studies.

Conclusion: In summary, endocrine-based mechanisms seem to play a role in the pathogenesis of primary varicosis. This opens up the perspective for pharmacological treatments targeting the various described endocrine regulatory networks.

Zusammenfassung

Einleitung: Die chronische Venenerkrankung (chronisch-venöse Insuffizienz, CVI) betrifft bis zu 40 % aller Männer und bis zu 51 % aller Frauen. Trotz ihrer hohen Prävalenz und den schweren klinischen Verlaufsformen bis hin zum venösen Ulcus cruris oder dem arthrogenen Stauungssyndrom ist die Pathophysiologie der primären Varikose bis heute ungeklärt. Im vorliegenden Übersichtsartikel wurden mittels Literaturrecherche die aktuelle Datenlage sowie die bestehenden Hypothesen aufgeführt und beschrieben.

Methode: Eine intensive Literaturanalyse wurde in PubMed durchgeführt mit folgenden Schlüsselwörtern: Chronisch-venöse Insuffizienz, CVI, chronische venöse Erkrankung, CVD, Varicosis, Vena saphena magna, Pathogenese, Hormone.

Ergebnisse: Hierzu bestehen unterschiedliche Theorien, welche von einer anlagebedingten Klappeninsuffizienz bis zu biologischen und morphologischen Veränderungen in den verschiedenen Schichten der Venenwand rei-chen. Gleichzeitig findet sich in der Literatur eine wachsende Anzahl von Arbeiten, die sich mit dem möglichen Einfluss von Hormonen auf die Entstehung der CVI, bzw. einem pathologisch veränderten endokrinologischen System in der Vena saphena magna (VSM) von CVI-Patienten beschäftigen. So wurden in zahlreichen Studien unterschiedliche Muster der Exprimierung von Hormonen (u.a. Östrogen, Progesteron, Relaxin-2, Oxytocin) und ihren jeweiligen Rezeptoren nachgewiesen. Eine unterschiedliche Ansprechbarkeit in Bezug auf Vasokonstriktion und Vasodilatation von Patienten mit gesunden und varikös veränderten VSM-Präparaten konnte in pharmakologischen Studien nachgewiesen werden.

Schlussfolgerung: Zusammenfassend lässt sich feststellen, dass endokrinologische Mechanismen eine Rolle in der Pathogenese der CVI zu spielen scheinen. Dies eröffnet theoretisch erstmals pharmakologische Therapieoptionen für die Behandlung der CVI. In Anbetracht des noch relativ jungen Forschungsgebietes der “Phlebo-Endokrinologie” und der interessanten wissenschaftlichen Erkenntnisse der letzten Jahre ist eine vertiefte Grundlagenforschung dennoch unabdingbar, um die genaue Rolle der einzelnen Hormone bzw. ihres komplexen Zusammenspiels in der Pathogenese der CVI zu eruieren.

 
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