Hypoparathyroidism, Brain Calcifications and Seizures
Aldo Bertoli *
Department of System’s Medicine, University of Rome “Tor Vergata”, Viale Oxford, 8100133 Rome, Italy.
Alessia Valentini
Department of System’s Medicine, University of Rome “Tor Vergata”, Viale Oxford, 8100133 Rome, Italy.
Alessandro Mauriello
Department of Biomedicine and Prevention, University of Rome “Tor Vergata”, Viale Oxford, 8100133 Rome, Italy.
Umberto Tarantino
Department of Orthopeadics and Traumatology, University of Rome “Tor Vergata”, Viale Oxford, 8100133 Rome, Italy.
*Author to whom correspondence should be addressed.
Abstract
Background: The most common cause of hypoparathyroidism is iatrogenic in the context of surgical procedures to the neck and commonly the thyroid gland. Hypoparathyroidism is characterized by hypocalcaemia, hyperphosphatemia and low or inappropriately normal levels of parathyroid hormone (PTH) and may be associated with multiorgan complications and variable clinical presentation. Seizures may be the only presenting symptom and may result in antiepileptic therapy. Knowledge of all possible consequences of hypoparathyroidism is essential for correct patient management.
Case Description: A 76-year-old woman was admitted due to loss of consciousness, seizures and hypocalcemia. She had had total thyroidectomy over 60 years ago for toxic goiter, complicated by permanent hypoparathyroidism. Her calcium levels were erratic, treated with calcium, colecalciferol and calcitriol. She developed progressive confusion, and had convulsive episode before hospitalization. Clinical investigation revealed widespread cerebral calcifications, EEG abnormalities and diffuse skeletal abnormalities. Later, during hip replacement surgery, bone histopathology showed bone marrow substitution by fibrous tissue undergoing ossification. All clinical problems occurring to the patient can be referred to hypoparathyroidism and consequent hypocalcemia not adequately corrected, including early bilateral cataracts.
In the absence of consolidated hormone replacement therapy, treatment of hypoparathyroidism is represented by vitamin D and calcium supplementation. In our case, the total absence of PTH and its role on vitamin D activation did not allow optimal control of serum calcium, despite normal levels of 25-hydroxyvitamin D being observed. The achievement of target values in serum calcium was obtained only with calcitriol. Treatment with levetiracetam was thus suspended and no more seizures occurred at two year follow-up.
Conclusion: Awareness that convulsions can only be caused by hypocalcemia, even in the presence of organic brain injuries, can help patients avoid using unnecessary medications and their potentially harmful side effects.
Keywords: Hypoparathyroidism, hypocalcemia, seizures, brain calcifications, aging