Endocrine Abstracts

As it is known, hypomagnesemia leads to decreased synthesis of Parathyroid hormone (PTH) and can cause PTH resistance. Chronic hypoparathyroidism itself may lead to basal ganglia calcification. We report a 58 years old male, who has suffered from convulsions for over 10 years, with a history of alcohol abuse (more than 25 units of alcohol/week). During this period there have been frequent aware convulsions, resembling to tetany, typical for hypocalcemia. Hypocalcemia and hypomagnesemia had been detected several times. Symptoms usually resolved by administration of Calcium and Magnesium. Patient used to stop taking supplements and continued alcohol abuse as soon as symptoms ameliorated.At the age of 58 patient had 3 tonic-clonic seizures with loss of consciousness, different from previous convulsions. The laboratory investigations showed severe hypocalcemia, hypomagnesemia, very low level of PTH and hyperphosphatemia (ionized Ca_0,60 mmol/l (1.15–1.29), Mg_0.56 mmol/l (0.66–1.07), PTH_2.5 pkg/ml (15–65), Phos_1.54 mmol/l (0.81–1.45), 25(OH)D_24.0 ng/ml. Electroencephalogram showed epileptiform activity (less common to hypocalcemia) and brain CT showed basal ganglia calcification, which may be manifestation of longstanding hypoparathyroidism. According to those findings, patient was diagnosed with structural generalized epilepsy. We believe it is a complication of longstanding hypomagnesemia with secondary hypoparathyroidism. Anticonvulsant (CBZ 200 mg TID) was added to prescription. Main cause of hypomagnesemia seems to be alcohol abuse, but other factors may also exist.

I/v correction of hypocalcemia and hypomagnesemia was followed by oral Magnesium orotate (Mg _ 32.8 mg) two times a day, Calcium Carbonate (Ca _ 500 mg.) three times a day, and Calcitriol 0.5 mcg/daily. Calcitriol was discontinued in several days after Calcium correction. On follow up visit (6–7 weeks later) elevation of PTH level was found _ PTH 10.49 ng/l (12–50), Ca _1.12 mmol/l (1.12–1.32), Mg_ 1.66 mg/dl (1.6–2.6). No more seizures were noted. Non managed chronic hypomagnesemia with secondary longstanding hypoparathyroidism might lead to basal ganglia calcification, followed by development of epilepsy. In our case, it is not till clear, if hypomagnesemia is the only cause of hypoparathyroidism or not, because PTH level still stays below of reference range. However, it is clear, that administration of magnesium increased PTH secretion and decreased severity of hypoparathyroidism. We keep on observing.

Conclusion Serum Magnesium level (as well as Calcium level) should be measured in all patients with seizures. Early diagnosis and management of hypomagnesemia with secondary hypoparathyroidism may prevent long-term irreversible neurologic complications.