Philip G. Rose

Bone mineral status in growth hormone deficiency

Bone mineral status was monitored by photon absorptiometry in 18 children with growth hormone deficiency. Before exogenous growth hormone therapy, bone mineral content, bone width, and BMC/BW were below predicted values. Delayed maturation, as assessed by skeletal age, accounted for approximately 35% of the deficit for these values. Height velocity doubled during therapy, and BMC, BW, and BMC/BW increased commensurate with height and weight increases so that the relative deficit was unchanged. The pathogenesis of relative osteopenia in growth hormone deficiency was not determined.

Osteopenia in juvenile diabetes.

SummaryThe bone mineral status of fifty-one children with diabetes mellitus was studied by single photon absorptiometry. The mean bone mineral content was 13% below values predicted by age, sex, height, and weight. Those children whose diabetes was one year or less in duration were as osteopenic as those whose diabetes was of longer duration. The demineralized children received a higher daily insulin dose than the others. No association was noted between the degree of skeletal demineralization and sex, statural growth, renal function, and serum calcium and phosphorus. No significant changes in bone mineral content were noted longitudinally.

Skeletal demineralization in Turner's syndrome.

SummaryThe bone mineral status of 17 girls with Turners syndrome was evaluated by single photon absorptiometry. Bone mineral content (BMC) was 25.4% below that predicted by normalization for age, sex, height, weight, and bone width. Only 25% of this demineralization could be attributed to delayed skeletal maturation. Bones of girls who received estrogen replacement therapy were less demineralized than those of the others. The bone mineral deficit became less pronounced with advancing age. It could not be determined if the apparent effect of estrogens was related to age or if the apparent improvement with age was really due to an effect of estrogen treatment. For 8 subjects followed longitudinally there was no significant change in the BMC deficit.

Bone status of children receiving anticonvulsant therapy

Bone mineral status was assessed by direct photon absorptiometry on 140 children and adolescent hospital outpatients receiving long-term anticonvulsant drug therapy and on 132 institutionalized mentally retarded subjects, 74 of whom were receiving anticonvulsant drugs. Serum calcium, phosphorus and alkaline phosphatase concentrations were determined for the hospital outpatients. Average deviations of bone mineral content (%BMC) ranged from 8.4-16.2% of normal values predicted from regression analysis. A trend toward increased demineralization was associated with length of anticonvulsant drug therapy. Mentally retarded subjects and hospital subjects with seizures accompanied by other serious disorders showed significantly greater osteopenia than hospital subjects with seizures alone. A lack of association of BMC with presence of anticonvulsant drug therapy in the mentally retarded population suggested that their low %BMC values were due to other factors related to the nature of the sample and the condition of institutionalization. Biochemical values showed a lack of association with osteopenia. A comparison of the present results on compact bone with results of others involving osteoid of trabecular bone suggests that anticonvulsant drug therapy affects these tissues differently and that the chemistry of the blood more closely reflects the osteoid proliferation of the trabecular bone rather than the changes related to the osteopenia of compact bone.

Bone mineral status measured by direct photon absorptiometry in institutionalized adults receiving long-term anticonvulsant therapy and multivitamin supplementation

SummaryThe effects of long-term anticonvulsant drug therapy and multivitamin supplementation on bone mineral status were evaluated by direct photon absorptiometry in 53 adult residents of an institution for the mentally disturbed. Results demonstrated a similar amount of osteopenia for control subjects and those on anticonvulsant drugs. Average osteopenia was 8% for control subjects and 6% for subjects taking anticonvulsant drugs. Significant osteopenia was found in 25% of subjects taking anticonvulsant drugs and 20% of control subjects. Multivitamin supplementation had a beneficial effect on bone status in both subject groups. The use of anticonvulsant drugs had a significant effect on levels of alkaline phosphatase. Elevated alkaline phosphatase was found in 37% of subjects taking anticonvulsant drugs and 22% of control subjects. Hypocalcemia was found only in subjects taking anticonvulsant drugs (19%). Average calcium values were similar for both subject groups. Multivitamins were shown to have no significant effect on alkaline phosphatase or calcium values. Because both control subjects and those taking anticonvulsant drugs showed similar levels of osteopenia, factors other than anticonvulsant drug therapy appeared to adversely affect bone mineral status in this population. Conversely, multivitamin supplementation and the dietary control present in the institutionalized setting appear to have ameliorated the osteopenia commonly seen in anticonvulsant-treated populations without greatly modifying elevated alkaline phosphatase and hypocalcemia.

Long term follow-up of bone mineral status in children with renal disease.

Bone mineral content (BMC) was measured by photon absorptiometry in the non-dominant forearm of children with chronic renal failure followed for a total of 2472 months. From 48 children, 302 measurements were made, and changes which occurred in BMC over time were correlated with several factors. Patients were divided into those who had received glucocorticoids (group 1) and those who had not (group 2). Group 1 patients had a lower mean serum creatinine (Cr) (p<0.05), a lower growth velocity (p>0.02) and were more demineralized than group 2 patients. There was no correlation between BMC and height velocity or estimated creatinine clearance. BMC and height Z-score (SDS) were highly correlated. Over the period of study, group 1 patients remained shorter, had a lower height velocity, a lower BMC Z-score and a lower BMC for each serum creatinine level. Long-term therapeutic intervention with oral 1,25(OH)2D improved bone mineral status in three children in the nonsteroid group, but none of those in the steroid group. This study demonstrates that steroid administration is probably the most important factor causing bone demineralization, possibly even more important than renal failure.