ABSTRACT
Patients with chronic spinal cord injury (SCI), a condition associated with reduced physical function, have been reported to have lower plasma insulin-like growth factor-I (IGF-I) levels than able-bodied persons. We evaluated the potential for daily low-dose baclofen administered over several weeks to increase plasma IGF-I levels. Ten healthy male outpatients with chronic SCI were studied prospectively. Patients received escalating doses of baclofen for 4 weeks at each dose level (5, 10, and 20 mg/d). At each dose of baclofen, an increase in the plasma IGF-I was noted; significant increases in plasma IGF-I occurred at 2 weeks after administration of drug at doses of 10 and 20 mg/d, with a subsequent rise to peak levels on baclofen 20 mg/d [baseline, 205+/-74; peak, 218+/-76 (not significant), 239+/-83 (P<.05), 263+/-87 microg/L (P<.05), at baclofen 5, 10, and 20 mg/d, respectively]. In conclusion, low-dose baclofen administration for 4 weeks stimulated the growth hormone-IGF-I axis in persons with SCI, with the potential for beneficial effects on body composition.
Subject(s)
Baclofen/administration & dosage , Baclofen/pharmacology , Insulin-Like Growth Factor I/metabolism , Muscle Relaxants, Central/administration & dosage , Muscle Relaxants, Central/pharmacology , Spinal Cord Injuries/drug therapy , Adult , Baclofen/therapeutic use , Chronic Disease , Dose-Response Relationship, Drug , Humans , Male , Middle Aged , Muscle Relaxants, Central/therapeutic use , Paraplegia/drug therapy , Quadriplegia/drug therapyABSTRACT
BACKGROUND/OBJECTIVE: An increased prevalence of vitamin D deficiency has been reported in persons with chronic spinal cord injury (SCI), but treatment guidelines for replacement are not available. The purpose of this study was to evaluate two types of vitamin D therapy on calcium metabolism and vitamin D status in persons with SCI. METHODS: Ten subjects with chronic SCI who were vitamin D deficient received 25 hydroxyvitamin D3 [25(OH)D], 50 microg twice a week, for 14 days (Study 1). Regardless of vitamin D status, 40 subjects received vitamin D3 800 IU (20 microg) daily for 12 months (Study 2). Supplemental calcium was administered. The response to therapy was determined by the effect upon serum 25(OH)D levels. Results are expressed as mean +/- standard deviation. RESULTS: In Study 1, serum 25(OH)D levels increased by day 14 (8.7 +/- 2.1 vs 14.7 +/- 3.6 ng/mL; P < 0.0005). However, in 8 of 10 subjects, 25(OH)D levels were still below the absolute lower limit of normal. Serum calcium levels were not significantly different, but urinary calcium excretion increased (103 +/- 81 vs 184 +/- 145 mg/d; P < 0.01). Serum parathyroid hormone (PTH) levels decreased (35 +/- 26 vs 1 7 +/- 12 pg/ mL; P < 0.01). In Study 2, after 12 months of vitamin D supplementation, 9 subjects had an absolute and 23 had a relative vitamin D deficiency, compared with 33 and 6 subjects, respectively, at baseline. By 12 months, the 25(OH)D level increased (10.7 +/- 7.1 to 22.5 +/- 7.5 ng/mL; P < 0.0001) and the serum PTH level decreased (37 +/- 16 vs 25 +/- 11 pg/mL; P < 0.0001). CONCLUSIONS: Although 25(OH)D levels significantly increased in both studies, the replacement therapies employed were not sufficient to recommend for adoption for clinical use, indicating the need for higher doses and/or for longer periods of administration.
