Endocrine Abstracts

Introduction: Primary hyperparathyroidism is the most common manifestation of multiple endocrine neoplasia (MEN) type 1, with a frequent involvement of all the parathyroids. In cases where the four glands weren’t resected, a close monitoring should be performed for an early diagnosis of recurrence. Elevated calcium levels with elevated parathormone (PTH) levels in this context makes the physician suspect an adenoma or a hyperplasia of the remaining parathyroid. We herein describe the case of a suspected recurrent hyperparathyroidism which revealed a Munchhausen syndrome.

Observation: We report the case of a 34-year-old man carrying a heterozygous missense mutation of the third exon of the MEN1 gene. He didn’t have gastric nor intestinal tumors. He had two infracentimetric nodules in the tail of the pancreas, with a negative hormonal screening. He had a two millimeters pituitary nodule with normal prolactin and IGF1 levels. For the adrenal tumors, there was a non-functional micronodular hyperplasia. There was no thymic nor bronchopulmonary tumor. The patient presented four years ago a hypercalcemia at 3 mmol/l with elevated PTH levels at 400 pg/ml, and he was operated on with resection of three parathyroid gland containing each an adenoma; the fourth parathyroid gland wasn’t found during surgery. During four years, calcium and PTH levels were normal, with the last normal control respectively at 2,5 mmol/l and 84,5 pg/ml (26,5-96,5), all in favor of a remission. During follow-up, he presented an asthenia and tachycardia with elevated calcium levels at 3,26 mmol/l and PTH at 68,5. In this context, a recurrent hyperparathyroidism was suspected, but cervical ultrasound, computed tomography and parathyroid scintigraphy didn’t find any abnormal or functional gland. The lability of the calcemia and the excessive concern for his disease made us suspected a facticious hypercalcemia, confirmed when he presented a severe hypercalcemia at 4,28 mmol/l, low PTH at 3 pg/ml and elevated vitamin D at 267 ng/ml (>60ng/ml) with the presence in his belongings of calcium-containing pills and ampoules and activated vitamin D. After treatment with intravenous saline and glucocorticoids, his calcemia reached 2,64 mmol/l. He was referred for psychiatric management, confirming the Munchhausen syndrome, with a calcemia level controlled at 2,62 mmol/l.

Conclusion: Hypercalcemia was rarely reported in association of Munchhausen syndrome. In our patient, the calcium and active vitamin D used to treat a member of his family for post-operative hypoparathyroidism and his knowledge of his disease allowed him to use hypercalcemia as a self-inflicted symptom.