Factors other than glucocorticoids are involved in the osteoblast activity decrease caused by tissue injury.
OBJECTIVE
Serum osteocalcin is a marker of bone formation. The concentration of osteocalcin is decreased with tissue injury. As glucocorticoids are known both to be increased in this situation and to diminish serum osteocalcin, we have hypothesized that they could be involved in this decrease.


METHODS
We compared osteocalcin levels in two groups of patients undergoing abdominal surgery, one receiving thiopental, and the other etomidate, a glucocorticoid synthesis blocker. For comparative reasons, another protein decreased by glucocorticoids (osteoprotegerin) was measured in patients anaesthetized with thiopental.


METHODS
Serum osteocalcin, cortisol and albumin were determined before and over the 24 h following surgery. Serum concentration of osteoprotegerin (OPG) and receptor activator of the nuclear factor kappaB ligand (RANKL) were also determined before and 24 h after surgery in a third group of nine patients who received thiopental for anaesthetic induction.


RESULTS
Cortisol levels were increased in the thiopental group, whereas, as expected, were decreased in etomidate patients. However, serum osteocalcin concentration decreased in a similar way in both groups. Serum OPG and RANKL levels were within the normal range at baseline and did not significantly change after surgery.


CONCLUSIONS
The decrease in serum osteocalcin induced by tissue injury is independent of the increase in cortisol secretion triggered by the latter. In addition, another pharmacologically proven effect of cortisol on bone metabolism, OPG inhibition, could not be demonstrated in the first 24 h following surgery, in spite of the physiological increase in endogenous cortisol secretion taking place in this period.
Department of Internal Medicine, Hospital Marques de Valdecilla, University of Cantabria, Santander, Spain.
J M
JM
Olmos
J A
JA
Amado
C
C
Valero
J L
JL
Hernández
J
J
González-Macías
D000005:Abdomen / Q000601:surgery; D000328:Adult; D018686:Anesthetics, Intravenous / Q000008:administration & dosage; D002352:Carrier Proteins / Q000097:blood; D005045:Etomidate / Q000008:administration & dosage; D005260:Female; D005938:Glucocorticoids / Q000502:physiology*; D006023:Glycoproteins / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood; D008875:Middle Aged; D010006:Osteoblasts / Q000502:physiology*; D015675:Osteocalcin / Q000097:blood*; D053244:Osteoprotegerin; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear / Q000097:blood; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D012709:Serum Albumin / Q000032:analysis; D013874:Thiopental / Q000008:administration & dosage; D014947:Wounds and Injuries / Q000097:blood / Q000503:physiopathology*
D018686:Anesthetics, Intravenous; D002352:Carrier Proteins; D005938:Glucocorticoids; D006023:Glycoproteins; D008562:Membrane Glycoproteins; D053244:Osteoprotegerin; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; D012709:Serum Albumin; C505686:TNFRSF11A protein, human; C506030:TNFRSF11B protein, human; C505688:TNFSF11 protein, human; D015675:Osteocalcin; D013874:Thiopental; D006854:Hydrocortisone; D005045:Etomidate