مقاله انگلیسی رایگان در مورد منجر شدن کم کاری غده پارتیروئید به تشنج – هینداوی 2018

An adult onset seizure is a scenario often encountered by internists. Patients are often labeled as epileptic and in some cases, appropriate investigations to assess for provoking factors and/or treatable causes are overlooked. ,is case report highlights such a scenario when a patient with hypocalcemia-associated seizures due to underlying idiopathic hypoparathyroidism (IH) was treated for idiopathic epilepsy for a decade. We consider the entity of acute symptomatic seizures and a reasonable approach to investigating adults with new onset seizures. Furthermore, we highlight hypocalcemia as a cause for seizures and discuss the occurrence of brain calcinosis in IH and the role of brain calcinosis versus hypocalcemia as the aetiology of seizures in these patients.

2. Case Report

A 24-year-old man presented to the emergency department with recurrent seizures preceded by a history of perioral and fingertip paresthesia. He was diagnosed with epilepsy at the age of 14 and treated with sodium valproate but denied a full diagnostic workup for seizures. On examination, both Chvostek’s and Trousseau’s signs were present. On biochemical investigations, his serum-corrected calcium measured 1.03 mmol/L (2.15–2.5 mmol/L), magnesium 0.72 mmol/L (0.63–1.05 mmol/l), and phosphate 2.57 mmol/L (0.78–1.42 mmol/L), and a total 25-OH vitamin D measured 55.98 nmol/L (deficient <50 nmol/L, insufficient 52.5–72.5 nmol/L, and sufficient >72.5 nmol/L). His serum parathyroid hormone was 0.6 pmol/L (1.6–6.9 pmol/L), despite vitamin D insufficiency, confirming a diagnosis of IH. A computed tomography (CT) brain scan showed calci- fication of the basal ganglia (Figures 1 and 2) and cerebellum (Figure 3). ,is patient was initially treated with an intravenous calcium infusion and subsequently started on chronic oral calcium supplementation along with alfacalcidol to maintain a serum calcium level in the low normal range. Sodium valproate was stopped as it was felt that his seizures were likely secondary to the profound hypocalcemia. At the 4- month follow-up visit, he was seizure free.