Influence of brain injury on early posttraumatic bone metabolism.
BACKGROUND
Various clinical studies and observations demonstrate enhanced osteogenesis in patients sustaining traumatic brain injury. It is presumed that the induction of this process starts early after trauma. The purpose of our study was to investigate humoral markers of bone metabolism during the early posttraumatic period, with special regard to traumatic brain injury.


METHODS
Serum concentrations of biochemical markers of bone metabolism (calcium, inorganic phosphorus, carboxyl-terminal propeptide of type 1 procollagen, pyridinoline cross-linked telopeptide domain of type 1 collagen, Ostase, osteocalcin, intact parathyroid hormone, and calcitonin) were measured in three different groups of 80 patients during the first posttraumatic week. Patients were categorized into three groups: group I, fractures only; group II, isolated traumatic brain injury; and group III, traumatic brain injury in combination with fractures.


RESULTS
Osteocalcin levels were significantly lower in the presence of traumatic brain injury (p < .05). Elevated pyridinoline cross-linked telopeptide domain of type 1 collagen levels expressed enhanced bone resorption in all groups, but levels were significantly higher in the absence of traumatic brain injury (p < .05). Intact parathyroid hormone levels were significantly higher on days 0 and 1 in the combined presence of traumatic brain injury plus fractures.


CONCLUSIONS
These results demonstrate an imbalance of bone formation and resorption parameters in patients with traumatic brain injury during the early posttraumatic period, suggesting a central regulation in bone formation. The lower levels of osteocalcin detected in this study may play an important role in patients with brain injury and the later development of posttraumatic heterotopic ossification.
Trentz
Omana A
OA
Research Division, Institute for Clinical Chemistry, University of Zurich, Zurich, Switzerland.
Handschin
Alexander E
AE
Bestmann
Lukas
L
Hoerstrup
Simon P
SP
Trentz
Otmar L
OL
Platz
Andreas
A
D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D016723:Bone Remodeling; D001842:Bone and Bones / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism*; D002116:Calcitonin / Q000097:blood; D002118:Calcium / Q000097:blood; D003094:Collagen / Q000097:blood; D024042:Collagen Type I; D005260:Female; D050723:Fractures, Bone / Q000150:complications; D006801:Humans; D008297:Male; D008875:Middle Aged; D009999:Ossification, Heterotopic / Q000175:diagnosis / Q000209:etiology; D010281:Parathyroid Hormone / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D010758:Phosphorus / Q000097:blood; D011347:Procollagen / Q000097:blood
D024042:Collagen Type I; D010281:Parathyroid Hormone; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C042813:procollagen type I carboxy terminal peptide; D010758:Phosphorus; D002116:Calcitonin; D003094:Collagen; D000469:Alkaline Phosphatase; D002118:Calcium