PARATHYROID SUPPRESSIBILITY IN HYPERPARATHYROIDISM DUE TO CHRONIC RENAL FAILURE: STUDIES WITH AUTOTRANSPLANTED PARATHYROID TISSUE

Authors

  • WALTER BORN,

    1. Research Laboratory for Calcium Metabolism, Departments of Orthopaedic Surgery (Balgrist) and Medicine, University of Zurich, 8008 Zurich, Switzerland and INSERM Research Unit 64, Tenon Hospital, 35970 Paris, France
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  • MAXIMILIAN A. DAMBACHER,

    1. Research Laboratory for Calcium Metabolism, Departments of Orthopaedic Surgery (Balgrist) and Medicine, University of Zurich, 8008 Zurich, Switzerland and INSERM Research Unit 64, Tenon Hospital, 35970 Paris, France
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  • ALAIN MEYRIER,

    1. Research Laboratory for Calcium Metabolism, Departments of Orthopaedic Surgery (Balgrist) and Medicine, University of Zurich, 8008 Zurich, Switzerland and INSERM Research Unit 64, Tenon Hospital, 35970 Paris, France
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  • RAYMOND ARDAILLOU,

    1. Research Laboratory for Calcium Metabolism, Departments of Orthopaedic Surgery (Balgrist) and Medicine, University of Zurich, 8008 Zurich, Switzerland and INSERM Research Unit 64, Tenon Hospital, 35970 Paris, France
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  • JAN A. FISCHER

    Corresponding author
    1. Research Laboratory for Calcium Metabolism, Departments of Orthopaedic Surgery (Balgrist) and Medicine, University of Zurich, 8008 Zurich, Switzerland and INSERM Research Unit 64, Tenon Hospital, 35970 Paris, France
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Professor J. A. Fischer, Klinik Balgrist, Forchstrasse 340, 8008 Zurich, Switzerland.

SUMMARY

Suppressibility of parathyroid hormone (PTH) secretion by calcium was evaluated in six patients with chronic renal failure and parathyroid tissue autotransplanted into the forearm. One patient was reinvestigated after renal transplantation. Plasma PTH levels were measured in the venous effluent of transplanted parathyroid tissue (VE) and in peripheral blood (PB) with two radioimmunoassays (RIA). One of these detected predominantly the intact human parathyroid hormone-(1–84) [PTH-(1–84)] (N-assay) and another in addition carboxyl (COOH)-terminal fragments (C-assay). At 5 min after the start of 12-min calcium infusions, resulting in a mean increase of plasma calcium levels of 0±6 mmol/l (P < 0±01), PTH was lowered to 44±10% (mean ± SE) (P < 0±01) of preinfusion levels in the VE and to 88±4% (P < 0±05) in PB, when measured in the N-assay; subsequently the plasma calcium level remained raised and PTH level lowered. When estimated in the C-assay, PTH was significantly lowered to 82± 6% (P < 0–05) in the VE at 120 min, and to between 91 ± 2% and 96 ± 2% (P < 0±01- < 0±05) in the PB at 20 to 120 min after the start of the calcium infusions. The results were extended with gel permeation chromatography of representative plasma samples. After renal transplantation and restoration of renal function gel filtration analysis indicated that the levels of intact PTH-(1–84) were 49±6 and of its COOH-terminal fragments 3±5 higher in the VE than in PB. In response to i.v. calcium administration intact PTH and its COOH-terminal fragments were lowered to 25% and 62% in the VE, and to 29% and 86% in PB, respectively. These findings demonstrate that the secretion of intact PTH-(1–84) is suppressed within minutes in response to i.v. calcium administration; a slower fall of the secretion of COOH-terminal PTH fragments was demonstrated only after restoration of near-normal renal function.

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