An 87 year old lady with a background of longstanding cognitive impairment was referred to our service with biochemical evidence of primary hyperparathyroidism. The patient had past medical history of type 2 diabetes mellitus, osteoporosis, hypothyroidism, ischaemic heart disease and primary hyperparathyroidism (under observation in a neighbouring health board). There was no pharmacological cause for cognitive impairment identified. Following acute admission after a fall with increased confusion her calcium was re-checked. Calcium was 3.23 mmol/l with an inappropriately non-suppressed corresponding PTH of 11.4 pmol/l. 25 hydroxy-vitamin D was 55 nmol/l. Renal function and other bloods including thyroid function tests were unremarkable. Hypercalcaemia was initially treated with IV fluids. This lady had previously been diagnosed with cognitive impairment with significant functional impact on her life. She was under the care of the old age psychiatry team. Calcium had been found to be elevated at the time of initial diagnosis with cognitive impairment, however it had consistently been only mildly raised and on account of her co-morbidities, no intervention had been undertaken other than intermittent blood monitoring. The patient was dependent on daily carers, was doubly incontinent and required help with all self-care. This was attributed to cognitive decline secondary to dementia. The patient was commenced on cinacalcet 30 mg twice daily as her calcium had consistently been above 3 mmol/l during her admission. On review at the outpatient clinic 4 months following commencement of cinacalcet, serum calcium had normalised to 2.30 mmol/l. The patient no longer had carers, was no longer incontinent and had become self-caring again. Her daughter reported that her mother was now independently doing her own housework and that her memory impairment had entirely resolved. This interesting case suggests cinacalcet should be considered in patients with cognitive impairment and inoperable primary hyperparathyroidism.