Bones, groans, moans... and salivary stones?

A 46 year old man was referred to hospital by his general practitioner with abnormal bone biochemistry. He had presented with poor appetite, fatigue, myalgia, and backache. Serum calcium, corrected for albumin, was 2.63 mmol/litre (reference range, 2.12–2.62), serum phosphate was 0.85 mmol/litre (normal range, 0.7–1.4), and alkaline phos-phatase was 367 IU/litre (normal range, 80–280). There was no history of previous fractures or of renal calculi. The parathor-mone concentration was raised at 19 pmol/ litre (normal range, 1.3–7.5) and the urinary calcium to creatinine ratio was 0.375 (normal range, 0.085–0.65). Bone densitometry provided evidence of osteoporosis (T score, −3.05). Ultrasound of his neck revealed a solid lesion of low echodensity at the lower pole of the right lobe of the thyroid gland, typical of a parathyroid adenoma. At surgery the lower right parathyroid gland was excised, and confirmed by histology to be an ad-enoma. At outpatients one week before elective parathyroidectomy, the patient reported that he had passed a stone from a salivary gland. He had attended hospital as an emergency two months previously and had been diagnosed as having sialadenitis of the left submandibular gland with a small calculus present in the duct. Subsequently, he became exasperated with the pain and manually forced the calculus out of the duct. There was no history of chronic infection or of other pathology to explain the presence of the calculus. The calculus weighed 2 mg and consisted of calcium phosphate (59%) and calcium oxalate (41%). Sialolithiasis has been reported in hyper-parathyroidism secondary to chronic renal failure, 1 but not previously in primary hyper-parathyroidism. Salivary stone formation may be promoted by the combined eVects of hypercalcaemia and secretory stimulation 2 ; the mechanism involves excessive calcium release into the acinar lumina resulting in calcium phosphate aggregates. Such calcium phosphate intermediates may transform into more stable hard deposits. Their saturation in solution varies widely, partly because of the variation in pH that occurs in saliva. As a result, some of these calcium phosphate aggregates may precipitate. Why do salivary stones occur so much less frequently than urinary stones in hyperpara-thyroidism? Some ions in saliva and urine, such as citrate, inhibit the growth of precipitated crystals, whereas others, like calcium and phosphate, accelerate growth. The balance of these and other molecules might favour stone formation in urine but not in saliva. Certainly, mechanisms invoked to explain urolithiasis in hyperparathyroidism include hypercalciuria, hyperphosphaturia, and hypocitraturia. However, …