gms | German Medical Science

33. Jahrestagung der Deutschsprachigen Arbeitsgemeinschaft für Verbrennungsbehandlung (DAV 2015)

14.01. - 17.01.2015, Leogang, Österreich

Acute and prolonged changes of serum bone turnover marker and bone microarchitecture in male patients after severe burn injury

Meeting Abstract

  • G. K. Muschitz - Division of Plastic and Reconstructive Surgery, Department of Surgery, Medical University Vienna, Vienna, Austria
  • H. Moussalli - St. Vincent Hospital – Medical Department II – Academic Teaching Hospital of Medical University of Vienna, Vienna, Austria
  • C. Muschitz - St. Vincent Hospital – Medical Department II – Academic Teaching Hospital of Medical University of Vienna, Vienna, Austria
  • E. Maurer - University Clinic of Plastic and Reconstructive Surgery, Medical University of Innsbruck, Austria, Innsbruck, Austria
  • R. Kocijan - St. Vincent Hospital – Medical Department II – Academic Teaching Hospital of Medical University of Vienna, Vienna, Austria
  • A. Kaider - Center for Medical Statistics, Informatics and Intelligent Systems, Medical University of Vienna, Vienna, Austria
  • H. Resch - St. Vincent Hospital – Medical Department II – Academic Teaching Hospital of Medical University of Vienna, Vienna, Austria
  • W. Happak - Division of Plastic and Reconstructive Surgery, Department of Surgery, Medical University Vienna, Vienna, Austria
  • T. Rath - Division of Plastic and Reconstructive Surgery, Department of Surgery, Medical University Vienna, Vienna, Austria
  • P. Pietschmann - Department of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Vienna, Austria

Deutschsprachige Arbeitsgemeinschaft für Verbrennungsbehandlung. 33. Jahrestagung der Deutschsprachigen Arbeitsgemeinschaft für Verbrennungsbehandlung (DAV 2015). Leogang, Österreich, 14.-17.01.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc15dav05.12

doi: 10.3205/15dav45, urn:nbn:de:0183-15dav458

Veröffentlicht: 9. März 2015

© 2015 Muschitz et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Introduction: Patient enduring severe burn injury have acute elevations of bone metabolism, triggered by inflammatory processes. This study tests the hypothesis that early changes of bone metabolism cause prolonged cortical and trabecular bone deterioration.

The primary objective was to investigate changes of bone turnover marker (BTM: P1NP, CTX, sclerostin, vitamin D) in the acute phase in stratum I and in stratum II.

Secondary objectives included the evaluation of bone microarchitecture after a mean period of 2 years assessed by high-resolution peripheral quantitative computed tomography (HR-pQCT; in vivo resolution 82 µm) of radius and tibia in stratum II.

Patients and methods: In stratum I 21 male otherwise healthy and untreated Caucasian patients (45.6±20.0 years; 18.7±16.1 days of immobilization) with burn injury grade IIb–III and a TBSA of 37.2±14.8% were included. BTM were evaluated after 48 hours, at days 7, 21, 56.

In stratum II 20 male Patients (40.2±11.3 years; TBSA 43.9±12.3%; 27.5±2.9 months after trauma) were compared to 45 age matched healthy controls (HC).

Results: In stratum I a rapid and prolonged increase of BTM without changes of low calcium and vitamin D levels was found: (CTX: Δ +178%, P1NP Δ +389%, p<0.0001 for both). All BTMs in stratum II were still severely altered compared to HC: CTX: Δ +71%, P1NP Δ -43%, sclerostin +91%; p<0.001 for all. At both, the radius and the tibia, a significant detoriation of bone microarchitecture was observed compared to HC: Trabecular bone volume, cortical porosity, cortical and trabecular parameters; endocortical perimeter; p<0.001 for all.

Conclusions: We observed an early and sustained increase in BTM and structural alterations in bone microarchitecture after severe thermal trauma. These detoriations are likely due to the impaired early and ongoing changes in bone metabolism after trauma and could increase the individual risk for fragility fractures.