Article
Acute and prolonged changes of serum bone turnover marker and bone microarchitecture in male patients after severe burn injury
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Published: | March 9, 2015 |
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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.