Severe metabolic bone disease in pregnancy mimicking malignancy

Four months after the delivery, the patient was admitted to hospital following a motor vehicle collision. A minimally displaced pelvic fracture was suspected on pelvic radiography. However, the trauma of the collision was minor, and it was unclear whether the lesion seen radiographically was a fracture or a manifestation of the previously suspected metabolic bone disease. Serum calcium was elevated, at 3.43 (normal 2.10-2.60) mmol/L, as were alkaline phosphatase (1046 [normal 30- 130] U/L), parathyroid hormone (244.4 [normal 1.1-6.8] pmol/L [1 pmol/L = 9.49 ng/L]) and urine calcium (29.4 [normal 2.0-7.5] mmol/day). Serum 25-hydroxyvitamin D was reduced, at 9 (normal 80-200) nmol/L. Serum albumin was within normal limits. Although the patient was not pregnant, the level of human chorionic gonadotropin was 92 (normal < 5) U/L, which raised concerns about parathyroid carcinoma. However, subsequent single-photon emission computed tomography and parathyroid scan confirmed parathyroid adenoma (Figure 4). The bone lesions seen on imaging were thought to be secondary to osteitis fibrosa cystica, a complication of primary hyperparathyroidism. The patient had no family history of hyperpara - thyroidism or endocrine diseases. The cure for symptomatic primary hyperparathyroidism is parathyroidectomy, but there are no formal guidelines for the specific treatment of osteitis fibrosa cystica. A recent review of primary hyperparathyroidism suggested maintaining 25- hydroxyvitamin D levels above 50 nmol/L and ensuring adequate calcium intake in patients with asymptomatic hyperparathyroidism, given that parathyroid overactivity may be exacerbated by low levels of 25-hydroxyvitamin D and low calcium intake.2 As for people without hyperparathyroidism, it seems reasonable to aim for vitamin D sufficiency, normocalcemia and adequate calcium intake after parathyroidectomy to achieve maximal regression of bone lesions in osteitis fibrosa cystica. The patient described here had severe vitamin D deficiency (initial 25-hydroxyvitamin D 9 nmol/L) in addition to her primary hyperparathyroidism. It has been proposed that superimposition of vitamin D deficiency on primary hyperparathyroidism may contribute to the de - velopment of skeletal lesions,1 as was seen in this patient. Primary hyperparathyroidism has been associated with 25-hydroxyvitamin D deficiency. In the setting of concomitant 25-hydroxyvitamin D deficiency, higher levels of parathyroid hormone and calcium, more severe dis