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The mechanism of transient hypocalcaemia following thyroidectomy was studied in 29 consecutive patients undergoing thyroid surgery. Eight of 27 (30%) patients who had a partial thyroidectomy developed transient hypocalcaemia. Hypocalcaemia was attributable to a reduction in renal tubular reabsorption of calcium (P < 0.05), but was not associated with changes in serum values of immunoassayable parathyroid hormone or calcitonin.Thyrotoxicosis is commonly associated with abnor¬ mal calcium and skeletal homeostasis. Abnormali¬ ties include increased bone turnover, particularly bone résorption which gives rise to osteoporosis, hypercalciuria and occasionally hypercalcaemia (Adams et al. 1967;Baxter & Bondy 1967).Hypocalcaemia is a well-recognised phenomenon following thyroidectomy. Permanent and transient forms are recognised. Permanent hypocalcaemia may occur after radical thyroid surgery, which damages the parathyroid glands. The cause of transient hypocalcaemia is less clear. It has been thought to be due to functional hypoparathyroidism (Davis et al. 1961; Riddell 1962), the reversal of thyrotoxic osteodystrophy (Michie et al. 1971; Laitinen 1976), or the release of calcitonin during thyroid manipulation (Wilkin et al. 1977; Watson et al. 1981; Rasmusson et al. 1980) causing decreased efflux of calcium from the skeleton to the extra¬ cellular fluid. The aims of this study were to identify factors of importance in the causation of transient hypo¬ calcaemia and to evaluate the mechanisms whereby it arose. Patients and MethodsThe effect of thyroidectomy was studied in 29 consecu¬ tive patients referred for thyroid surgery. Twenty-seven patients had partial thyroidectomy for thyrotoxicosis (n = 9) or for a non-toxic nodular goitre (n = 18). The 2 remaining patients underwent total thyroidectomy for carcinoma of the thyroid. An additional 11 patients undergoing minor abdominal surgery were assessed and served as controls. All the thyroidectomies were per¬ formed by one surgeon (A.W. H.) using techniques de¬ scribed by Wade (1960). In each case the parathyroid glands were identified at operation and not excised. The thyrotoxic patients had been previously treated with carbimazole. Their pre-operative preparation included bed rest, oral potassium iodide and sedation (oral phenobarbitone 30 mg t.d.s. with amylobarbitone 200 mg at night) for 1 week. They were considered adequately prepared if the pulse rate awake and during sleep was consistently less than 80/min. This criterion was met in 8 of the thyrotoxic patients and the remaining patient required additional treatment with propranolol. Iv fluids including blood transfusions were not administered preor post-operatively.

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