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Published on: November 11, 2013
Characterization of Calcium Homeostasis in Lithium-Treated Patients Reveals Both Hypercalcaemia and Hypocalcaemia
Adrian D Meehan1, Göran Wallin2, Johannes Järhult3
1Department of Geriatrics, Faculty of Medicine and Health, Örebro University, 701 85, Örebro, Sweden. adrian.meehan@regionorebrolan.se.
Insights
Lithium treatment frequently causes hypercalcaemia and complex parathyroid dysfunction, impacting calcium homeostasis. Surgical outcomes for lithium-associated hyperparathyroidism (LHPT) are poor, suggesting unique biochemical profiles.
Area of Science:
- Endocrinology
- Pharmacology
- Nephrology
Background:
- Lithium is widely used for psychiatric disorders.
- Hypercalcaemia affects a significant portion of lithium-treated patients (3-30%).
- Lithium-associated hyperparathyroidism (LHPT) pathophysiology is not fully understood.
Purpose of the Study:
- To investigate calcium homeostasis in lithium-treated patients.
- To analyze the impact of lithium treatment duration on calcium metabolism.
- To characterize the biochemical profile of LHPT.
Main Methods:
- Retrospective analysis of medical records from 297 lithium-treated patients.
- Evaluation of serum calcium levels and 24-hour urine calcium.
- Assessment of parathyroidectomy outcomes in suspected LHPT cases.
Main Results:
- 60% of patients remained normocalcaemic; 34% developed hypercalcaemia or suspected LHPT.
- 41% of LHPT patients had low 24-hour urine calcium.
- Parathyroidectomy success rate was 35% for hyperplasia.
Conclusions:
- Hypercalcaemia is highly prevalent during lithium treatment.
- Hypocalcaemic episodes suggest complex parathyroid dysfunction.
- LHPT exhibits distinct biochemical features compared to primary hyperparathyroidism.
Introduction:
Prevalence studies demonstrate that a significant proportion of lithium-treated patients develop hypercalcaemia (3-30%). Lithium-associated hyperparathyroidism (LHPT) is poorly defined, and calcium homeostasis may be affected in a more complicated fashion than purely by elevated PTH secretion. The current study aims to examine in detail calcium homeostasis principally with regard to lithium duration.
Methods:
Medical records of 297 lithium-treated patients (193 women, 104 men; median age 58 years) were examined, and information on gender, age, lithium treatment duration and calcium homeostasis was obtained. The median treatment duration with lithium was 16 (1.5-45) years.
Results:
A total of 8504 calcium values were retrieved. Before initiation of lithium treatment, serum calcium was on average 2.33 mmol/l (2.02-2.60). During the treatment period, 178 patients (60%) remained normocalcaemic, 102 (34%) developed hypercalcaemia or were strongly suspected of LHPT, 17 (6%) had 3 or more intermittent episodes of hypocalcaemia. Forty-one per cent of patients with suspected or confirmed LHPT had low (<4 mmol) 24-h urine calcium levels. The success rate after 33 parathyroidectomies was 35%, hyperplasia being diagnosed in 75% of extirpated glands.
Conclusions:
The prevalence of hypercalcaemia during lithium treatment is very high. In addition, hypocalcaemic episodes appear to occur frequently, possibly reflecting a more complicated parathyroid dysfunction than previously known. Long-term surgical results are unsatisfactory. LHPT biochemical profile is different from that of primary hyperparathyroidism and is in some ways similar to familial hypocalciuric hypercalcaemia.
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