A 60-year-old woman, who had been taking lithium for 36 years for bipolar affective disorder, was referred to an endocrinologist by her psychiatrist for investigation of polydipsia and polyuria. Water deprivation did not concentrate her urine, nor did desmopressin, indicating the diagnosis of nephrogenic diabetes insipidus (NDI). She was started on chlorthalidone, a treatment for NDI, and her symptoms improved dramatically. Her polyuria was well controlled on chlorthalidone for 4 years, until she started feel tired and weak and her polyuria worsened. Initially these symptoms were attributed to her depression and lithium therapy. However, routine blood testing revealed a random blood glucose of 18.5 mmol/litre, thereby confirming the diagnosis of type 2 diabetes, and a corrected calcium of 3.02 mmol/litre (normal range 2.1–2.6 mmol/litre). She was started on a diabetic diet, resulting in good diabetes control (confirmed by haemoglobin A1c) and her symptoms improved. The patient's chlorthalidone was stopped as thiazide diuretics can cause hypercalcaemia and her calcium was repeated. The repeat value was higher at 3.07 mmol/litre and her parathormone was alsoelevated at 11.24 pmol/litre, confirming hyperparathyroidism. A parathyroid adenoma was sought but a nuclear medicine scan (Tc99m ssesta-MIBI; technetium 99m-sesta 2-methoxy isobutyl isonitrille) and ultrasound examination of the neck failed to localize an adenoma. It was felt that she had developed parathyroid hyperplasia secondary to chronic lithium therapy (Mallette and Eichhorn, 1986), so her lithium was withdrawn and replaced with sodium valproate. Her NDI and hyperparathyroidism resolved on withdrawal of lithium.
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