Pædiatric Aspects of Hypoparathyroidism

Me, Macgregor

doi:10.1177/003591576806100618

Cited by 5 publications

(3 citation statements)

References 22 publications

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“…A vigorous and continuing effort has characterized the biochemical defect at this organ (1,23), and our patients satisfy the criteria of renal unresponsiveness. It is, furthermore, undoubted that patients with PsH have a diminished calcemic response to intramuscular PTH (18). Again, our patients satisfy this criterion.…”

Section: Discussionsupporting

confidence: 57%

1,25-Dihydroxycholecalciferol Deficiency: The Probable Cause of Hypocalcemia and Metabolic Bone Disease in Pseudohypoparathyroidism

Drezner

Neelon

Haussler

et al. 1976

The Journal of Clinical Endocrinology & Metabolism

135

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Pseudohypoparathyroidism (PsH) is a genetic disease characterized by hypocalcemia, hyperphosphatemia, and metabolic unresponsiveness to parathyroid hormone (PTH). The administration of PTH elicits neither a significant rise in serum calcium (calcemic response) nor a decrease in the renal tubule reabsorption of phosphorus (phosphaturic response). The diminished phosphaturic response is due to an inability of PTH to generate cyclic AMP in renal tubule cells. We investigated the question of whether hypocalcemia and deficient calcemic response to PTH are due to a similar cyclic AMP defect in bone or to an acquired vitamin D deficiency. Four patients were studied. The active form of vitamin D (1,25-dihydroxycholecalciferol) was measured in 3 and was low. Treatment with vitamin D2 restored the serum calcium and the calcemic response to PTH to normal without changing the impaired renal response. Bone biopsy was performed in 2 patients and showed morphologic evidence of increased osteoclastic activity and osteomalacia. The data indicate that the hypocalcemia and bone disease in PsH are due to active vitamin D deficiency, possibly resulting from the genetic renal lesion.

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Section: Discussionsupporting

confidence: 57%

1,25-Dihydroxycholecalciferol Deficiency: The Probable Cause of Hypocalcemia and Metabolic Bone Disease in Pseudohypoparathyroidism

Drezner

Neelon

Haussler

et al. 1976

The Journal of Clinical Endocrinology & Metabolism

135

View full text Add to dashboard Cite

show abstract

“…In Case 4 hypocalcemia was a significant feature. This appeared too early to be caused by the phosphate load of artificial milk but was compatible with the hypoparathyroidism found in light-for-dates babies (MacGregor 1968, Fanconi & Prader 1968). Breech delivery may have been significant in this infant since complications of pregnancy are known to predispose to neonatal hypocalc2emia (Gittleman et al 1956).…”

Section: Discussionmentioning

confidence: 58%

“…A normal serum calcium estimation in the mother excludes maternal hyperparathyroidism (Wagner et al 1964, MacGregor 1968). Unfortunately plasma proteins were not estimated in Case 4 during the hypocalciemic phase but it may well be that this donor twin was also hypoproteinmmic (Heinrichs 1964, Forfar 1968.…”

Section: Discussionmentioning

confidence: 99%

Preliminary Observations on Two Variations of the Placental Transfusion Syndrome

Dillon

1969

Proceedings of the Royal Society of Medicine

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Transient congenital hypoparathyroidism: Possible association with anomalies of the pulmonary valve

Mallette

Cooper

Kirkland

1982

The Journal of Pediatrics

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Pædiatric Aspects of Hypoparathyroidism

Cited by 5 publications

References 22 publications

1,25-Dihydroxycholecalciferol Deficiency: The Probable Cause of Hypocalcemia and Metabolic Bone Disease in Pseudohypoparathyroidism

1,25-Dihydroxycholecalciferol Deficiency: The Probable Cause of Hypocalcemia and Metabolic Bone Disease in Pseudohypoparathyroidism

Preliminary Observations on Two Variations of the Placental Transfusion Syndrome

Transient congenital hypoparathyroidism: Possible association with anomalies of the pulmonary valve

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