A 45‐year‐old man presented to the emergency room with an acute episode of laryngeal spasm. He underwent emergency tracheotomy. He had recurrent episodes of generalised tonic–clonic seizures of 4 years' duration and was on phenytoin sodium 400 mg/day. The frequency of seizures had increased, requiring increasing doses of phenytoin. He had pallor, coarse facial features, gum hyperplasia (fig 1), nuclear cataracts, bilateral extrapyramidal rigidity and carpopedal spasm. Investigations showed macrocytic anaemia; hypocalcaemia, serum calcium 0.5 mmol/l (1.1–1.4 mmol/l); hyperphosphataemia 2.0 mmol/l (1.0–1.4 mmol/l); parathyroid hormone 5 ng/l (10–60 ng/l), 25‐hydroxy vitamin D3 30 nmol/l (37.4–200 nmol/l), normal electrocardiogram and phenytoin 22 μg/ml (10–20 μg/ml). A plain cranial computed tomography scan showed bilateral basal ganglia and cortical calcifications (fig 2). In patients with hypoparathyroidism, phenytoin and other microsomal enzyme inducers can accelerate the hepatic inactivation of vitamin D and worsen the hypocalcaemia and its clinical manifestations, including life‐threatening manifestations such as acute laryngeal spasm.
Figure 1 Gum hyperplasia in the 45‐year‐old man presenting with an acute episode of laryngeal spasm. Written patient consent has been obtained to reproduce his images in this paper.
Figure 2 Plain cranial computed tomography scan showing bilateral basal ganglia and cortical calcifications.