Dear Editor:

Primary hyperparathyroidism (PHPT) presents in several different forms and its clinical presentation varies with age. Young patients with PHPT typically present with the classic bone and kidney disease, whereas older patients tend to have neurocognitive and psychiatric disturbances. We hereby report a unique case of chronic dementia secondary to untreated PHPT in a patient who was admitted with superimposed delirium. His delirium and dementia were treated successfully by medical management of PHPT. To the best of our knowledge, only two prior cases of PHPT presenting as dementia treated by parathyroidectomy have been reported.[1,2]
Case report. Mr. A, a 76-year-old Caucasian man with a past psychiatric history of depression and Alzheimer’s disease (AD), was admitted to the trauma unit after a motor vehicle accident. He had driven on the wrong side of the highway and collided with the incoming traffic. He did not sustain any major head injuries or physical injuries in the accident. On admission, he was confused, agitated, and aggressive with nursing staff. He also responded to auditory and visual hallucinations. He did not recollect the accident. His physical examination was unremarkable with no focal neurologic deficits.

Case presentation. Mr. A was an accountant by profession who filed taxes for his clients. However, he was forgetful and required assistance from his family members for activities of daily living (ADL) for over a year. He was admitted the previous year for episodes of disorientation and forgetfulness, which were increasing in frequency. Due to his cognitive impairment, he was asked to discontinue his job. His cognitive impairment was considered to be a part of AD. Lab results then were significant for moderately high calcium levels of 10.8 and 11.5, each done one month apart, and elevated PTH of 109. He was experiencing depressive symptoms with prominent insomnia, and mirtazapine 15mg at bedtime was initiated.

During the current admission, he was on amlodipine, lisinopril, omeprazole, simvastatin, flunizolide, and mirtazapine 15mg at bedtime. The lab results were unremarkable except for calcium of 11mg/dL, ionized calcium 1.24, phosphate of 1.7mg/dL, PTH 129.3, and magnesium 1.8. Blood ethanol and urine drug screen were negative. Imaging studies revealed no acute pathology, and no surgical interventions were recommended. Results of the scan, however, revealed chronic global cortical atrophy. Neurocognitive testing indicated an extremely low visual-spatial processing, low average immediate memory, and notable difficulty in sustained attention tasks.

During the course of hospitalization, it was noted that his fluctuating sensorium correlated with his serum phosphate and calcium levels. On the days when he refused to take the phosphate, his mental status deteriorated. After the phosphate and calcium levels were corrected, he was more alert and oriented. Interestingly, not only did his acute delirium resolve but the patient’s baseline cognition and ADL improved in the next few weeks.

A temporal relationship between initiation of treatment and resolution of his cognitive symptoms and delirium supports our inference of hypophosphatemia and hypercalcemia secondary to his undiagnosed hyperparathyroidism, being the cause for his delirium and dementia.

Discussion. In our patient, both the neuropsychiatric testing and imaging suggested a diagnosis of dementia, but the cause was found with careful correlation of the lab testing and with clinical presentation. This case highlights that dementia associated with cognitive decline and acutely presenting with superimposed delirium in a medical setting, possibly caused by underlying undiagnosed hyperparathyroidism.

Apathy, depression, and cognitive impairment are common presentations in several geriatric conditions. Primary hyperparathyroidism, though common among geriatric population, may be missed, and the symptoms may be prematurely diagnosed as AD. Since hyperparathyroidism has a good potential for reversal of symptoms by medical and in few cases surgical1,2 interventions, a meticulous workup of all possible differential diagnoses for dementia is crucial.3,4

1. Papageorgiou SG, Christou Y, Kontaxis T, et al. Dementia as presenting symptom of primary hyperparathyroidism: favourable outcome after surgery. Clin Neurol Neurosurg. 2008;110(10):1038–1040. Epub 2008.
2. Molaschi M, Ponzetto M, Romin R, et al. [Neuropsychologic symptoms of primary hyperparathyroidism in the elderly. Report of a clinical case]. Minerva Endocrinol. 1994;19(4):169–174.
3. Watson LC, Marx CE. New onset of neuropsychiatric symptoms in the elderly: possible primary hyperparathyroidism. Psychosomatics. 2002;43(5):413–417.
4. Flicker L, Ames D. Metabolic and endocrinological causes of dementia. Int Psychogeriatr. 2005;17 Suppl 1:S79–S92. Review.

With regards,
Harmit Singh MD
Vithyalakshmi Selvaraj, MD
Prasad R. Padala, MD, MS

Dr. Singh is PGY -1 Resident and Dr. Selvaraj is PGY-4 Resident from the Department of Psychiatry, Creighton-Nebraska Psychiatry Residency Program, Omaha, Nebraska. Dr. Padala is Associate Professor of Psychiatry, University of Medical Center, Omaha, Nebraska.