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C Cornish

Publications and source records attributed to C Cornish.

5 recordsLinked to original sources
PubMed1991

Immunoreactive serum calcitonin and skeletal histology in chronic renal failure.

Serum calcitonin and serum parathyroid hormone (PTH) were measured in 50 patients undergoing regular haemodialysis for end-stage chronic renal failure, and an analysis of osteoclast and osteoblast activities was made in bone biopsies obtained by iliac crest trephine. Osteoclast and osteoblast activities were studied in a multivariate analysis in relation to factors which might reasonably be thought to influence activity, namely serum calcitonin, serum PTH, serum calcium, serum inorganic phosphate, and bone aluminium. Only serum PTH correlated strongly with osteoclast activity (p = 0.0047). Serum PTH correlated also with osteoblast activity (p = 0.0024). Serum inorganic phosphate correlated negatively with osteoblast activity (p = 0.0082). Serum calcitonin did not correlate with osteoclast or osteoblast activities but did correlate strongly with bone aluminium in a multivariate analysis (p = 0.0078). Bone aluminium did not correlate independently with osteoclast or osteoblast activities. This study affirms the implied powerful role of PTH in influencing osteoclast and osteoblast activities in end-stage chronic renal failure.

Adult↗
PubMed1987

A 6-hour human parathyroid hormone (1-34) infusion protocol: studies in normal and hypoparathyroid subjects.

Parathyroid hormone (PTH)-resistant states are usually diagnosed by the failure of an acute PTH injection to elicit a rise in urinary cAMP and phosphate or, less commonly, by the failure of repeated PTH injections to raise serum calcium. We have established a 6 hour infusion of human PTH (1-34) which identifies PTH-resistant hypoparathyroid subjects on the basis of serum 1,25-dihydroxyvitamin D (1,25(OH)2D) and calcium responses. 1,25-Dihydroxyvitamin D levels increased by at least 58 pmol/liter and serum calcium by at least 0.1 mmol/liter in PTH-responsive hypoparathyroid subjects (n = 6), whereas in pseudohypoparathyroid subjects (n = 5) these levels rose by less than 22 pmol/liter and 0.06 mmol/liter respectively. The responsiveness of urinary phosphate excretion, expressed as the renal threshold phosphate concentration (TmPO4/GFR), to PTH also clearly separated the pseudohypoparathyroid patients from the other subjects. Differences in urinary calcium responses were observed though this parameter was less reliable in the identification of individual PTH-resistant or PTH-sensitive hypoparathyroid patients. Nephrogenous cAMP did not discriminate between groups when this protocol was used. This test has the potential to facilitate and extend the classification of PTH-resistant states.

Adult↗