Lithium-induced hyperparathyroidism was first described in 1973 by Garfinkel et. al.
The two cases aim to illustrate Lithium-induced hyperparathyroidism which was previously thought to be a rare occurrence and outline characteristic features of this disorder.
A 51 year old male presented with polydipsia and polyuria. He was known to suffer from bipolar affective disorder with lithium treatment was admitted for a water deprivation test. Further current biochemical profiles revealed:
Corrected Calcium 2.84
(millimoles per litre)
His parathyroid hormone level was extremely high at 151 (NR 1.1-7.1). Sodium 146, potassium 5.3, urea 16.8, creatinine 278 micromoles per litre.
Other biochemistry revealed a low 25 hydroxy-Vitamin D level of 8 (NR 15-100nanomol per litre) and a low daily urinary Calcium excretion of 4.2millimoles per litre (NR 2.5-7.5)
Renal ultrasound showed no evidence of nephrocalcinosis. A neck ultrasound suggested a possible parathyroid mass. Thyroid stimulating hormone 1.02 (NR 0.32-5.0milliU per litre), free thyroxine 8 (NR 9-15 picamol per litre). He was referred to a Parathyroid surgeon and underwent a parathyroidectomy. Histology revealed a grossly enlarged right lower gland (1.67grams) consistent with hyperplasia
His biochemistry showed great improvement Parathyroid 3.20, corrected calcium 2.45.
A 75 year old lady was admitted this July with symptomatic bradycardia. Her past significant history included bipolar affective disorder, a subtotal thyroidectomy for euthyroid multinodular goitre.
Her biochemistry revealed hypercalcaemia corrected 2.62, phosphate 1.31, potassium 4.4, magnesium 0.76, urea 8.5, creatinine 127, alkaline phosphatase 61 (NR 40-135 IU per litre). Thyroid stimulating hormone 1.95
Urinanalysis showed a low 24hour excretion of calcium 0.26
with a parathyroid level of 8.2, Vitamin-D 65
Cardiac telemetry revealed sinus bradycardia with significant pauses
She therefore received a permanent pacemaker and was discharged thereafter.
The mechanism for Lithium induced parathyroid dysfunction seems to be related to inhibition of Parathyroid hormone sensitive adenyl cyclase system
Characteristics of this disorder are:
Low urinary calcium excretion
Histology of parathyroid hyperplasia,
In conclusion calcium should be measured in patients on long term lithium therapy as well as thyroid and electrolyte measurements.
04 - 06 Nov 2002
Society for Endocrinology