RESUMO
Objective:To investigate the effect of somatostatin receptor ligands (SRLs) on bone metabolism in patients with acromegaly.Methods:Retrospective analysis of clinical data of acromegaly patients( n=100) received surgery or SRLs alone for 3 months. The changes of growth hormone (GH), insulin-like growth factor-1 (IGF-1), osteocalcin (OC), N-mid fragment of osteocalcin (N-MID), amino-terminal peptide of type I procollagen (P1NP) and C-terminal peptide degradation product of type I collagen(CTX) were compared before and after treatment. Patients were divided into drug treatment group and surgical group according to treatment methods. According to the decline of GH after medication, patients in the drug treatment group were further divided into drug sensitive group and drug insensitive group. Results:The average dynamic GH and IGF-1 indexes in the drug treatment group were significantly decreased after treatment compared with before treatment (both P<0.05), and CTX was also significantly decreased after treatment [1.25 (0.67, 1.40) ng/mL vs 1.34 (0.57, 1.68) ng/mL, P<0.05]. The mean dynamic GH, IGF-1 index, OC, N-MID, P1NP, and CTX in surgical group were significantly decreased after treatment compared with before treatment (all P<0.01). In the surgical group, there was a positive correlation between GH difference (ΔGH) and N-mid difference (ΔN-MID; r=0.454, P=0.026), and there was a positive correlation between IGF-1 index difference (ΔIGF-1 index) and CTX difference (ΔCTX; r=0.339, P=0.036). After treatment, the mean dynamic GH, IGF-1 index, CTX, P1NP, and N-MID in drug treatment group were significantly higher than those in surgical group (all P<0.001). CTX and N-MID decreased significantly after treatment in drug sensitive group compared with drug insensitive group (35.3% vs 7.2%, P<0.001; 24.1% vs 11.8%, P<0.05), and ΔGH was positively correlated with ΔCTX ( r=0.328, P=0.004). Conclusion:SRLs treatment can reduce bone formation marker N-MID and bone resorption marker CTX, improving the high turnover state of bone metabolism in patients with acromegaly, which may attribute to the reduction of GH and IGF-1 levels.
RESUMO
Objective To investigate the effects of Propofol in blood spinal cord barrier (BSCB) disruption induced by spinal cord ischemia reperfusion injury (SCIRI). Methods 72 Japanese white rabbits were randomly assigned into 3 groups: sham-operation group (S); ischemia/reperfusion group (I/R) and Propofol treatment group (I/R + P). The Group S was separated the aorta without cross-clamping. SCIRI was induced in rabbits by infrarenal aortic occlusion for 30 minutes. Propofol was intravenously infused at 10 minutes before aortic clamping and at onset of reperfusion in the Group I/R + P. The Group S and Group I/R were intravenously infused 0.9%sodium chloride. Hind-limb motor function was assessed using Tarlov criteria, and histological observation by histological examination. The permeability of the BSCB was examined using EB as vascular tracers. The expression of MMP-9, claudin-5 and NF-κB were assessed by Western blot, RT-PCR. Results Propofol minimized the neuromotor dysfunction and histopathological deficits and attenuated EB extravasation. In addition, Propofol suppressed SCIRI-induced increase of MMP-9 and NF-κB. Finally, Propofol reduced the loss of claudin-5. Conclusion Propofol stabilizes the BSCB integrity after SCIRI. This beneficial effect is partly mediated by inhibition of MMP-9 and preservation claudin-5 and relates to inhibiting the NF-κB signal pathway.