Endocrine Abstracts

Background: Permanent hypoparathyroidism can result from immune-mediated destruction of the parathyroid glands. Alternatively it may result from activating antibodies to the calcium sensing receptor that decrease parathyroid hormone (PTH) secretion. Autoimmune hypoparathyroidism is a common feature of poliglandular autoimmune syndrome type I. Other causes, all very rare, include irradiation and storage of infiltrative diseases of the parathyroid glands. Neurological signs of hypoparathyroidism include symptomatic or latent tetany, seizures, hemiparesis, difficulty in speaking, ischemic attacks, in case of basal ganglia and cerebral calcifications also choreatetosis, parkinsonism and cerebellar syndrome.

Case report: The authors present the case of a 22-year-old man that was referred to the endocrinology consultation because of undertreated hypoparathyroidism. He also had a personal history of epilepsy, depression, anxiety, agoraphobia, and panic attacks. Partial complex crises started when he was 13 years old (2000). Hypoparathyroidism was diagnosed in 2003 and he developed anxiety disorders 1 year ago. He was medicated with calcium carbonate + calcium lactogluconate (3500 mg/day), calcitriol 0.5 μg/day, valproic acid (1200 mg/day), paroxetine (20 mg/day) and alprazolam (1 mg/day). Laboratory results revealed severe hypocalcemia and hyperphosphatemia, and serum low levels of parathyroid hormone. Medication was adjusted accordingly. We also performed cerebral and parathyroid glands’ imagiologic study. This patient did not have other features of poliglandular autoimmune syndrome type I. Other aetiologies were also excluded.

Conclusion: The authors wish to draw attention to this unusual manifestation of idiopathic hypoparathyroidism and the need to assess serum calcium levels in patients with seizures and other neuropsyquiatric symptoms.