ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2012) 29 P448 
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Primary hypoparathyroidism presenting as recurrent TIAs with intracranial calcification

M. Reddy, R. Tanday, R. Agha-Jaffar, J. Valabhji & J. Cox

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Intracranial calcification seen on CT may be an incidental finding or it can be a direct cause of neurological symptoms depending on which areas of the brain are affected. The differential cause for the formation of intracranial calcium deposits include hypoparathyroidism, congenital infections i.e. toxoplasmosis and Fahr’s syndrome.

A 50–year–old woman was referred to the transient ischaemic attack (TIA) clinic in December 2011, with recurrent episodes of dysphasia and right-sided jaw tightening and weakness, each episode lasting 10–20 min. She developed similar symptoms with no other focal neurology during the consultation in the TIA clinic and it was noted that her baseline adjusted calcium done the same morning was very low at 1.13 mmol/l (2.15–2.60). She was immediately admitted to hospital and was treated with 10 ml of i.v. 10% calcium gluconate, followed by infusions of 40 ml of 10% calcium gluconate in 1l of 5% dextrose daily over 3 days. Alphacalcidol 1 microgram twice daily and Adcal D3 two tablets twice daily were started.

The CT findings and blood results (Table 1) were consistent with intracranial calcification caused by primary hypoparathyroidism. Since discharge from hospital she has remained asymptomatic on oral calcium and vitamin D. Addison’s, pernicious anaemia and hypothyroidism have been excluded to rule out type 1 polyglandular autoimmune syndrome.

Our case highlights the importance of always checking the calcium when patients present with ‘neurological’ symptoms as symptomatic hypocalcaemia can mimic various conditions. Secondly, it also brings to attention that hypoparathyroidism, with or without significant hypocalcaemia, must be considered as a cause of intracranial calfication found on imaging of the brain.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

Table 1 Baseline investigations and results obtained
InvestigationResultReference range
Adjusted calcium1.13 mmol/l2.15–2.60
Parathyroid hormone<0.5 pmol/l <0.5 pmol/l(2nd sample)1.1–6.8
Phosphate2.47 mmol/l0.80–1.40
Magnesium0.79 mmol/l0.70–1.00
25–OH Vitamin D<10 nmol/l70–150
TSH0.38 mu/l0.30–4.20
ECGProlonged QT interval
CT HeadExtensive symmetrical intracerebral calcifications are seen in the basal ganglia, centrum semi ovale, subcortical regions in both occipitallobes and cerebellum. There is some effacement of the cerebral sulci and temporal horns are mildly dilated
Creatinine85 umol/l60–125

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