Endocrine Abstracts

Hypoparathyridsm and pseudohypoparathyroidsm are the common causes of pathological calcification in the brain though 0.3–1.5% cases are physiological. The clinical presentation of hypoparathyroidsm can vary with the calcium levels and chronicity of hypocalcaemia. We describe a 39-year-old female who had type one diabetes for the last 23 years. She was repeatedly hospitalised with collapse episodes thought to be hypoglycaemic though never proved. She also had primary hypoparathyroidism for the last 10 years and was on calcium and vitamin D supplements. Her adjusted calcium was 2.2–2.5 mmol/l. She had a cataract removed from the right eye and also had an early cataract in the left eye. Her fundal examination did not show any diabetic retinopathy. She also started to have tonic clonic seizures which initially were thought to be due to hypoglycaemic events but the capillary glucose was never documented in these episodes. She had slow speech, serpentine gaze and shuffling gait on examination. Her Chvostek’s and Trousseau’s signs were negative. She was sent for neuropsychological assessment to ascertain the cognitive impairment. There she had CT brain done which showed calcification in basal ganglia, centrum semi ovale bilaterally and also subcortical dense linear calcification bilaterally. She was seen by a neurologist and started on anticonvulsant treatment. Her seizures improved but no improvement in her cognition and gait abnormalities. This case emphasizes the importance of thinking about the whole spectrum of the disease even if the biochemical markers are stable on treatment.