These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Important hypercalcaemia due to hyperparathyroidism induced by lithium].
    Author: Lions C, Precloux P, Burckard E, Soubirou JL, Escarment J.
    Journal: Ann Fr Anesth Reanim; 2005 Mar; 24(3):270-3. PubMed ID: 15792560.
    Abstract:
    Lithium treatment, which is still extensively used in bipolar affective disorders, may give rise to hypercalcaemia induced by hyperparathyroidism. We present a patient of 50-year-old treated with lithium for 19 years for bipolar illness and who developed an important hypercalcaemia. After symptomatic treatment of the hypercalcaemia and extrarenal dialysis the clinical evolution was favorable but measurements of serum calcium and parathormon showed that he had developed hyperparathyroidism. Neck exploration was performed and parathyroid adenomas, which had been detected by scintigraphy was removed. The lithium treatment expose to many side effects. Among other biologically and clinically important effects of lithium the possible induction of hyperparathyroidism was first suggested in 1973. Since, 1973, since about forty case reports have been described. Few cross-sectional studies show a relationship of lithium to hyperparathyroidism. Unusual metabolic features are associated with hyperparathyroidism and long-term lithium treatment: low urinary calcium excretion, normal urinary cyclic AMP excretion. The mechanism probably results from lithium linking with the calcium receptor on the parathyroid and then stimulating PTH secretion. The cessation of lithium therapy does not lead to normocalocaemia and a parathyroidectomy is usually indicated.
    [Abstract] [Full Text] [Related] [New Search]