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Parathyroid function during acute pancreatitis

M J McMahon, P J Heyburn, M J Playforth

    The British Journal of Surgery
    |February 1, 1982
    PubMed
    Summary
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    Acute pancreatitis can cause hypocalcaemia, characterized by low plasma calcium and altered phosphate handling. Renal function suggests parathyroid hormone (PTH) activity, but measured PTH levels can be variable and potentially inadequate.

    Area of Science:

    • Nephrology
    • Endocrinology
    • Gastroenterology

    Background:

    • Acute pancreatitis frequently disrupts calcium and phosphate homeostasis.
    • Parathyroid hormone (PTH) is a key regulator of calcium and phosphate balance.
    • Renal handling of calcium and phosphate typically reflects PTH activity.

    Purpose of the Study:

    • To investigate the renal handling of calcium and phosphate in acute pancreatitis.
    • To correlate renal changes with parathyroid hormone (PTH) levels and plasma calcium.
    • To explore potential causes of hypocalcaemia in acute pancreatitis.

    Main Methods:

    • Studied 18 patients with acute pancreatitis during the first 5 days post-admission.
    • Calculated ionized calcium from plasma total calcium, albumin, total protein, and pH.

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  • Assessed urine calcium, plasma phosphate, renal tubular reabsorption of phosphate, and PTH levels.

    • Main Results:

    • Six patients presented with hypocalcaemia (Ca < 1.08).
    • Hypocalcaemic patients showed low urine calcium, hypophosphataemia, and reduced renal phosphate reabsorption.
    • Measured PTH levels were variable, and in one case, calcium infusion did not significantly alter PTH.

    Conclusions:

    • Renal changes suggest PTH activity, but measured PTH levels may be misleading.
    • Hypocalcaemia in acute pancreatitis might stem from an inadequate parathyroid response.
    • Caution is advised when interpreting isolated radioimmunoassay PTH data in this clinical context.