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      Bone mineral and hormone status in paraplegics

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      Spinal Cord
      Springer Nature

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          Abstract

          Nineteen men who had suffered permanent paraplegia a median of 4 years previously were studied. Eight also had varying degrees of neurological deficit of the upper extremities. Bone mineral, biochemical and hormonal values were compared to those in an age-matched control group in order to detect evidence of systemic osteopenia. There were very considerable individual variations in bone mineral density (BMD) deficits among patients compared to controls, probably partly due to methodological problems. Significant BMD deficits were found in the metaphysis (45%) and diaphysis (26%) of the tibia, while the deficit of the distal forearm was barely significant for the group as a whole. There was a negative correlation between time since injury and degree of BMD deficit in the lower extremity. Those with neurological affection of the upper extremities had a greater BMD deficit of their arms than those with neurologically intact arms. It was concluded that osteopenia in paraplegics is largely confined to the paralysed extremities, and thus not systemic. Serum alanine aminotransferase, phosphate, follicle stimulating hormone, and free androgen index (testosterone/sex hormone binding globulin) were mainly within normal limits, but significantly higher in paraplegics than in controls. Osteopenia in these patients is thus not due to gonadal dysfunction.

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          Effect of prolonged bed rest on bone mineral.

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            The effect of supplemental oral phosphate on the bone mineral changes during prolonged bed rest.

            Five healthy young men were studied during 24-30 wk of continuous bed rest. During the first 12 wk of bed rest, untreated subjects increased calcium excretion in the urine by 109 mg/day and in the feces by 147 mg/day. The rate of total body calcium loss was 0.5-0.7% per month. Losses of central calcaneus mineral, assessed by gamma ray transmission scanning, occurred at a tenfold higher rate, whereas the mineral content of the radius did not change. Changes in phosphorus balance resembled the calcium pattern, and increased excretion of nitrogen and hydroxyproline also occurred during bed rest. Upon reambulation, the subjects' calcium balance became positive in 1 month and recovery of their calcaneus mineral was complete within 10-20 wk. Treatment with potassium phosphate supplements (1327 mg P/day) entirely prevented the hypercalciuria of bed rest, but fecal calcium tended to increase. During the first 12 wk, calcium balance was slightly less negative (mean - 193 mg/day) than during bed rest without added phosphate (mean - 267 mg/day). This effect was not seen during the second 12 wk of bed rest. The patterns of magnesium excretion were similar to those of calcium. Fecal and urinary phosphorus excretions were doubled, and phosphorus balance became positive (+ 113 mg/day). Mineral loss from the central calcaneus was similar to that of untreated subjects. It is concluded that this form of phosphate supplementation reduces urinary calcium excretion but does not prevent bone loss during bed rest.
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              Osteoporosis and Decline of Gonadal Function in the Elderly Male

              The bone mineral content was evaluated in 30 male subjects aged between 60 and 90 years using the relief of the percent cortical area (PCA) at the level of the second phalanx of the left-hand index finger, by Garn’s method. This was to evaluate the rate of bone loss with increasing age. Testosterone, androstenedione, estrone, 17β-estradiol plasma levels were determined in all subjects by the RIA method. 60% of our patients showed increased bone resorption (PCA < 55%); in these subjects testosterone and androstenedione plasma levels were significantly lower than in subjects not affected by osteoporosis. A positive linear correlation is evident between PCA and testosterone, androstenedione and estrone plasma levels. Thus, like in women, decline of gonadic function determines an increased bone resorption in men too.
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                Author and article information

                Journal
                Spinal Cord
                Spinal Cord
                Springer Nature
                1362-4393
                1476-5624
                May 1992
                May 1 1992
                : 30
                : 5
                : 343-347
                Article
                10.1038/sc.1992.80
                1598175
                6adf4940-6617-4e6d-b4da-5e8ede2373a8
                © 1992

                http://www.springer.com/tdm

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