25-hydroxyvitamin-d-2 and Cerebral-Palsy

25-hydroxyvitamin-d-2 has been researched along with Cerebral-Palsy* in 2 studies

Other Studies

2 other study(ies) available for 25-hydroxyvitamin-d-2 and Cerebral-Palsy

ArticleYear
Osteopenia in cerebral palsy.
    Archives of disease in childhood, 1994, Volume: 71, Issue:3

    The bone mineral density of the lumbar spine was assessed in nine non-ambulant children with cerebral palsy combined with measurements of serum 25-hydroxyvitamin D, parathyroid hormone, and urinary calcium excretion. Three children with recurrent fractures received treatment with bisphosphonates for periods ranging from 12-18 months. All the children demonstrated a severe reduction in bone mineral density even when allowance was made for their body weight. There were no consistent abnormalities of vitamin D or parathyroid hormone status. Three children had gross hypercalciuria. Each of the children treated with bisphosphonates demonstrated an increment in bone density ranging from 20-40% with no apparent adverse effects.

    Topics: 25-Hydroxyvitamin D 2; Adolescent; Bone Density; Bone Diseases, Metabolic; Calcifediol; Calcium; Cerebral Palsy; Child; Child, Preschool; Diphosphonates; Female; Fractures, Bone; Humans; Lumbar Vertebrae; Male; Parathyroid Hormone

1994
Factors causing rickets in institutionalised handicapped children on anticonvulsant therapy.
    Archives of disease in childhood, 1981, Volume: 56, Issue:6

    An epidemiological study on vitamin D-dependent rickets was carried out in severely handicapped institutionalised children on long-term anticonvulsant therapy. Nine (10%) of 94 patients had overt rickets on the basis of roentgenological bone changes and biochemical indices, but 46 patients in hospital without medication, and 50 epileptic patients attending an outpatient clinic and taking anticonvulsants had no sign of rickets. Causative factors for the development of rickets were evaluated. Administration of anticonvulsive drugs depressed the serum 25-hydroxyvitamin D (25-OHD) level, but this was not the major factor in the development of rickets. Vitamin D intake seemed to be about average in these patients and its supplementation increased their serum 25-OHD level. This serum 25-OHD level was not maintained by supplemental vitamin D, unless the children were exposed to sunlight. These results indicate that although several factors--such as anticonvulsants, low vitamin D intake, and inactivity--are concerned in the development of rickets, the main cause is lack of sun in institutionalised handicapped children.

    Topics: 25-Hydroxyvitamin D 2; Adolescent; Anticonvulsants; Cerebral Palsy; Child; Child, Institutionalized; Child, Preschool; Diet; Food, Fortified; Humans; Hydroxycholecalciferols; Physical Exertion; Rickets; Sunlight; Vitamin D

1981