Abstract and Introduction
Abstract
Introduction Primary hypoparathyroidism is a rare condition caused by parathyroid hormone deficiency and characterized by hypocalcemia. The clinical manifestations of primary hypoparathyroidism include tetany, seizures, paresthesias, dementia, and parkinsonism. Psychiatric manifestations such as mood disorders are unusual and may constitute a major diagnostic challenge, especially if the typical manifestations caused by hypocalcemia are absent.
Case presentation The patient was a 22-year-old Caucasian man with a history of chronic omeprazole use and periodic seizures, who presented to the emergency department of a secondary hospital in Southern Brazil with symptoms of major depression (sadness, anhedonia, loss of appetite, insomnia, and fatigue) associated with paresthesias affecting his toes. The initial electrocardiogram revealed a prolonged QTc interval. A computed tomography scan of his brain revealed bilateral, nonenhancing hyperdense calcifications involving the putamen and caudate nucleus. An electroencephalogram showed generalized bursts of slow spikes. Blood laboratory study results indicated serum hypocalcemia, hypomagnesemia, and hyperphosphatemia associated with a low parathyroid hormone level. His serum levels of albumin, 25-hydroxyvitamin D, thyroid-stimulating hormone, T3 and T4 thyroid hormones, as well as the results of kidney function tests, were normal. The definitive diagnosis was primary hypoparathyroidism with psychiatric manifestations due to chronic hypomagnesemia induced by proton pump inhibitor use.
Conclusions In some cases, to differentiate between a primary psychiatric disorder and primary hypoparathyroidism with neuropsychiatric symptoms may represent a challenge given that the classical manifestations of hypocalcemia, especially tetany, may be absent in the setting of chronic hypoparathyroidism. Clinicians and psychiatrists should consider primary hypoparathyroidism part of the differential diagnosis during the evaluation of patients with mood symptoms, especially in the context of atypical presentations associated with hypocalcemia.
Introduction
Parathyroid hormone (PTH) plays an important role in the metabolism of calcium and phosphate. In response to a decrease in the serum calcium level, parathyroid cells increase PTH secretion physiologically. Through direct action on the kidney and bone cells, and indirect effects on the bowels, PTH increases serum calcium levels and decreases serum phosphate levels. In addition, PTH promotes bone resorption, decreases urinary calcium excretion, enhances the conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, and increases intestinal calcium absorption, and renal phosphate excretion.[1–3]
Primary hypoparathyroidism is characterized by the absence or decreased secretion of PTH. As a consequence, patients with primary hypoparathyroidism often present clinical manifestations related to hypocalcemia such as tetany, seizures, muscle cramps, paresthesias (affecting the fingertips, toes, and perioral area), and carpopedal spasms. In cases of chronic hypocalcemia, symptoms become less specific, ranging from asymptomatic states to atypical clinical presentations, such as neuropsychiatric manifestations. In this sense, mood disorders, such as depression have been reported rarely as the main manifestation of hypoparathyroidism. The typical laboratory findings of primary hypoparathyroidism include hypocalcemia and hyperphosphatemia in the presence of undetectable or abnormally low levels of PTH. Skull radiographs or computed tomography scans of the brain may reveal symmetrical bilateral basal ganglia calcification. The typical electroencephalogram pattern includes bursts of high-voltage paroxysmal slow waves. Electrocardiography may reveal a prolonged QTc interval and T wave abnormalities owing to hypocalcemia.[4–6]
The etiology of primary hypoparathyroidism includes surgical destruction of parathyroid glands (the most common cause), neck irradiation, autoimmune hypoparathyroidism (isolated or combined with other endocrine deficiencies, for example, polyglandular autoimmunity), idiopathic hypoparathyroidism, hypomagnesemia, Wilson's disease, hemochromatosis, and congenital syndromes (for example, DiGeorge syndrome).[7,8]
Here we describe an unusual case of primary hypoparathyroidism with an atypical predominant manifestation of major depression secondary to hypomagnesemia induced by chronic proton pump inhibitor use. Following the case presentation, we provide a brief discussion and review of previously published data regarding psychiatric manifestations of primary hypoparathyroidism.
J Med Case Reports. 2014;8(326) © 2014 BioMed Central, Ltd.
