Abstract
IntroductionPrevalence 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.MethodsMedical 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.ResultsA 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.ConclusionsThe 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.
Highlights
Introduction Prevalence studies demonstrate that a significant proportion of lithium-treated patients develop hypercalcaemia (3–30%)
The current study aims to examine in detail calcium homeostasis principally with regard to lithium duration
While a plethora of theoretical models exist regarding lithium’s role in the development of hypercalcaemia, the predominant conceptual model suggests that lithium affects the ‘‘set-point’’ of parathyroid glands by way of calcium sensing receptors [8, 9]
Summary
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. Though lithium-associated hyperparathyroidism (LHPT) was first documented by Garfinkel et al [2] in 1973, the endocrinopathy remains ill-defined. While a plethora of theoretical models exist regarding lithium’s role in the development of hypercalcaemia, the predominant conceptual model suggests that lithium affects the ‘‘set-point’’ of parathyroid glands by way of calcium sensing receptors [8, 9]. It is purported that lithium may stimulate the nascent development or ‘‘de-masking’’ of parathyroid adenoma or hyperplasia [10, 11]. Controversy still surrounds the histopathological background of LHPT [12, 13] and the appropriate management of the condition has yet to be fully demonstrated, with the risk of persistent or recurrent disease after routine parathyroidectomy alarming [14]
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