Serum hsCRP and visfatin are elevated and correlate to carotid arterial stiffness in spinal cord-injured subjects.

STUDY DESIGN: Cross-sectional comparison, control group. OBJECTIVES: To investigate the relationship between carotid arterial stiffness and circulating markers for cardiovascular disease (CVD) in spinal cord-injured (SCI) subjects compared with able-bodied (AB) individuals. SETTING: University Research Laboratory, University of Louisville. METHODS: SCI (n=14) and AB (n=13) subjects between 20-52 years of age were recruited to participate in the study. B-mode Doppler ultrasound was used to obtain carotid artery diameter measurements. Arterial stiffness was assessed via the stiffness index and distensibility coefficient. Markers of CVD risk were obtained by fasting blood draw. RESULTS: Carotid arterial stiffness index (P=0.061) and distensibility coefficient (P=0.370) were not different between the SCI and AB groups. The SCI group had higher high-sensitivity C-reactive protein (hsCRP) (P=0.046), triglycerides (P=0.017), leptin (P=0.040) and visfatin (P<0.001) compared with the control group. Visfatin (r=0.559, P=0.047), hsCRP (r=0.633, P=0.037), insulin (r=0.637, P=0.019) and HOMA (r=0.614, P=0.026) significantly correlated with carotid arterial stiffness index in the SCI group. CONCLUSION: This study demonstrated that SCI subjects are at a high cardiovascular risk as indicated by elevated hsCRP levels. Elevations in hsCRP and visfatin may contribute to accelerated atherogenic processes in the SCI population.

Does concurrent acute ethanol ingestion during omeprazole therapy affect pituitary gonadal axis in male subjects?

OBJECTIVE: Literature suggests that both ethanol and omeprazole may affect the endocrine system. We studied the effect of concurrent use of ethanol and omeprazole on the pituitary gonadal axis in healthy males. METHODS: Serum testosterone, luteinizing hormone, and follicle stimulating hormone levels were assessed in a fasting state before and after ingestion of 0.5 g/kg bodyweight of ethanol. Subjects then received omeprazole therapy (20 mg 2x/d for one week) followed by assessment of hormone levels before and after ethanol ingestion as done previously. RESULTS: Total testosterone levels before and after ethanol at baseline declined an average of 46.6 ng/dL (n = 8; p = NS). The testosterone levels before and after ethanol following omeprazole therapy rose an average of 55.4 ng/dL (n = 8; p = NS). There was no significant difference in the change of ethanol induced testosterone concentrations as a result of omeprazole therapy. Similarly the free testosterone, follicle stimulating hormone, and luteinizing hormone were also not affected by ethanol or omeprazole alone or in combination. CONCLUSIONS: We conclude that omeprazole and/or acute ingestion of ethanol do not affect the pituitary gonadal axis in healthy male subjects.