Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

In 1942, the Norwegian psychiatrist Eitinger drew attention to the fact that acute psychosis may be the presenting and major symptom of primary hyperparathyroidism. A case of this variety is reported. In the course of two months a 77-year old woman developed an acute psychosis characterized by apathy, amnesia, somatic delusions and hallucinations. Initially, the case was misinterpreted as senile dementia. The serum calcium level was 4.3 mmol/l. After parathyroidectomy her mental symptoms were completely relieved.
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PMID:[Acute psychosis--an unusual clinical manifestation of primary hyperparathyroidism]. 863 74

The case of a 76-year-old female patient is presented with a two-year history of progressive dementia, apathy and gait impairment. Initially, Alzheimer's disease was diagnosed and she was given donepezil for one year with no significant improvement. An extensive blood and biochemical control revealed high serum calcium and parathormone levels, and normal thyroid hormones and anti-thyroid antibodies. Ultrasound of thyroid and parathyroid glands revealed an adenoma of the right parathyroid. The detailed investigation for causes of secondary hyperparathyroidism was negative. Due to the absence of clinical hyperparathyroidism she was initially treated conservatively. At referral, the neurological picture consisted of: mild signs of parkinsonism, moderate dementia (MMSE=15) and severe behavioural disturbances. Because of the continuous aggravation of the cognitive deficit, parathyroidectomy was decided although there were no clinical or laboratory signs of involvement from other organs. Three weeks after the operation the neurological picture showed dramatical improvement. Parkinsonism and behavioural disorders were remarkably reduced and the MMSE score raised to 25. In summary we report an exceptional case of primary hyperparathyroidism (PHPT) presenting as dementia and treated successfully by parathyroidectomy.
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PMID:Dementia as presenting symptom of primary hyperparathyroidism: favourable outcome after surgery. 1865 51