UNLABELLED: Primary infantile hypomagnesaemia is an infrequent cause of neonatal hypocalcaemic seizures but one that responds well to magnesium supplementation. We describe a 22-year-old male, first reported at 4 months of age, who is currently free of neurological deficit but has suffered from intermittent hypomagnesaemic tetany and chronic diarrhoea due to large oral magnesium supplements. Hypothesizing that modest hypercalcaemia might prevent the tetany, we conducted a trial of 5 microg/day 1,25(OH)2D3 over 5 days. Despite the resultant increase in calcium, he developed tetany with the reduction of magnesium intake and decline of serum magnesium from 0.63 to 0.39 mmol/l (normal >0.65 mmol/l). After 1,25(OH)2D3 was stopped and the parenteral magnesium injections suspended, 33% of his usual oral supplement was given instead by continuous nasogastric infusion and serum magnesium rose to 0.60 mmol/l. This regimen was better tolerated because of decreased gastrointestinal side-effects and freedom from parenteral injections. We observed that 1,25(OH)2D3 supplements do not promote magnesium retention nor does the resultant hypercalcaemia prevent hypomagnesaemic tetany. CONCLUSION: Continuous nocturnal nasogastric infusion may be considered in lieu of parenteral therapy in primary infantile hypomagnesaemia.

Administration, Oral↗

PubMedDate not supplied

Bone mass in children with congenital hypothyroidism treated with thyroxine since birth.

To determine whether the large doses of thyroxine treatment early in life adversely affect bone mass, we measured bone mass of 20 congenital hypothyroid (CH) patients (8.4 +/- 2.2 years) who were diagnosed and treated since birth. Starting thyroxine dose and current dose were 8.5 +/- 1.9 micrograms/kg/day and 3.1 + 1.2 micrograms/kg/day respectively. Thyroid function and serum biochemical tests for calcium homeostasis were normal at the time of study. Bone mass was measured by dual energy X-ray absorptiometry. Nine siblings served as controls. The patients' bone mineral density was within the normal range of population controls, and was not different from the sibling controls. The patients also had height-adjusted bone mineral content equal to the expected height-adjusted values in the siblings. Our studies indicate that the large doses of thyroxine therapy for CH do not cause osteopenia in childhood.

Absorptiometry, Photon↗

PubMedDate not supplied

Renal osteodystrophy in children on CAPD: a prospective trial of 1-alpha-hydroxycholecalciferol therapy.

The efficacy of 1 alpha-hydroxycholecalciferol in the prevention of renal osteodystrophy in children commencing continuous ambulatory peritoneal dialysis was studied in 12 patients, 0.8-17 years of age, who were randomly assigned to either group I receiving standard therapy or to group II receiving in addition 10-20 ng/kg body weight/day of 1 alpha-hydroxycholecalciferol. Calcium carbonate compounds were used to control hyperphosphataemia. Mean plasma calcium (total and ionised) and phosphate levels were not significantly different between the two groups. All group I patients continued to have elevated plasma immunoreactive parathyroid hormone levels at 6 months compared to only 1 patient in group II (p less than 0.05). Four patients in group I developed subperiosteal erosions on radiography compared to the healing of mild lesions in 2 patients in group II. Bone histomorphometry on iliac crest needle biopsy specimens revealed a significant reduction in osteoid index and seam width in group II. Serum aluminum levels decreased during the course of continuous ambulatory peritoneal dialysis, and the significant staining for bone aluminum in 6 patients at the beginning of the study was no longer present in 5 patients at 6 months. Our data demonstrate that 1 alpha-hydroxycholecalciferol is beneficial in the prevention and treatment of bone disease in children on continuous ambulatory peritoneal dialysis.

Adolescent↗

PubMedDate not supplied

Persistence of Vitamin D-deficiency rickets in Toronto in the 1990s.

To assess the current picture of vitamin D deficiency, we reviewed all 17 cases of vitamin D-deficiency rikets seen in the referral clinic of a children's hospital in Toronto between 1988 and 1993. The diagnosis was made at 7 to 33 months of age. All the children were symptomatic all had biochemical and radiographic abnormalities, two suffered hypocalcemic seizures, and all had bowing of the extremities. Twelve of the children were born to parents who were recent immigrants to Canada. All were of Asian or African origin with dark skin. All the children had been exclusively breastfed with no vitamin D supplementation, and had had little or no sunlight exposure. All the patients responded to vitamin D therapy. We conclude that vitamin D-deficiency rickets remains an environmental/nutritional deficiency disease in this city and that efforts at prevention should target children with pigmented skin from families who are recent immigrants.

Africa↗