Development of ‘Primary’ Hyperparathyroidism during Lithium Therapy: Longitudinal Study

Christiansen, Claus; Baastrup, P. C.; Transbøl, Ib

doi:10.1159/000117770

Cited by 61 publications

(21 citation statements)

References 9 publications

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“…McHenry et al have reported that 80% of patients treated with lithium for 6 to 24 months experience a 10% increase in serum calcium levels. Christiansen et al re-ported that both serum calcium and PTH levels increased by 30% in the same population, and several other authors have also reported a 10% -60% increased prevalence of hypercalcemia and hyperparathyroidism in patients taking lithium [11][12][13][14].…”

Section: Discussionmentioning

confidence: 99%

“…↑ Parathyroid volume and parathyroid hyperplasia [2,5,11] LAH is associated with multiglandular hyperplasia in 25% -55% cases (Table 1) compared to 15% in PHPT, which is attributed to direct stimulation of parathyroid gland by lithium. In patients on chronic lithium therapy neck ultrasound demonstrates increased parathyroid gland volume.…”

Section: Mechanism Of Action Explanatationmentioning

confidence: 99%

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Lithium Associated Hyperparathyroidism: An Evidence Based Surgical Approach

Ballehaninna¹,

Nguyen²,

Chamberlain³

2011

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Background: Long-term lithium use in psychiatric patients may lead to lithium associated hyperparathyroidism (LAH). Although anecdotal case reports have appeared, an evidence based algorithm for management of LAH is lacking. Methods: A comprehensive literature search was performed using PubMed with keywords; "lithium" "hypercalcemia" "hyperparathyroidism" "sestamibi" "intra-operative parathyroid hormone (IOPTH) monitoring" "parathyroidectomy" and "medical management". All English language publications addressing etiology and clinical management issues concerning LAH were critically analyzed. Results: Lithium associated hyperparathyroidism occurs in 4.3% -6.3% of chronic lithium users compared to the general population which has an incidence of 0.5% -1%. 194 cases of LAH have been reported which includes 10 patients (5%) treated medically and 170 patients (88%) who underwent parathyroidectomy. No details were available for 14 patients (7%). Among parathyroidectomy patients, 104 (59%) had adenomatous disease and 66 (39%) had multiglandular hyperplasia. Preoperative localization studies were utilized in only 22 patients (13%) and IOPTH monitoring was reported in only 3 studies (32 patients, 19%). Among surgical patients, bilateral neck exploration (BNE) was the most common approach performed in 162 patients (95%); focused neck exploration was utilized in only 8 patients (5%). Parathyroidectomy normalized LAH biochemical changes in nearly all patients (90% -97%) in the early post-operative period, but recurrent hyperparathyroidism occurred in 8% -42% of patients. Conclusion: LAH is an under appreciated and poorly understood endocrine disorder. LAH has a higher incidence of multiglandular disease and bilateral neck exploration is mandatory in majority for disease control. Nonsurgical approaches may be useful in select patients on short-term lithium therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Mechanism Of Action Explanatationmentioning

confidence: 99%

Lithium Associated Hyperparathyroidism: An Evidence Based Surgical Approach

Ballehaninna¹,

Nguyen²,

Chamberlain³

2011

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“…219 The features of lithium-induced hypercalcemia are similar to those of FHH. 220 Serum PTH levels are non-suppressed or moderately raised, and tubular reabsorption of calcium is increased. Both short-term and long-term clinical studies indicate that lithium administration increases the PTH secretory set point, 216,220 a conclusion supported by the in vitro effects of lithium on cultured parathyroid cells, both bovine and human.…”

Section: Increases In Set Point and In Cell Proliferationfurther Exammentioning

confidence: 99%

Parathyroid Growth

2015

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“…Lithium may induce hyperparathyroidism by acting as a calcilytic on the calcium sensing receptor (CaSR) [173]. In early studies, lithium has been associated with a decreased bone mineral content (BMC) in the forearm [174][175][176] and bone mineral density (BMD) of the lumbar spine [177] possibly mediated through induction of hyperparathyroidism [178].…”

Section: Lithiummentioning

confidence: 99%

Adverse Effects of Drugs on Bone and Calcium Metabolism/Physiology

Vestergaard

2007

Clinic Rev Bone Miner Metab

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Drugs may affect bone turnover and density in many ways. However, the disease for which the drugs are administered may also contribute to bone loss. Infection with human immunodeficiency virus leads to a loss of bone mineral, while treatment with highly active antiretroviral therapy does not seem to contribute to further bone loss. Type 1 diabetes is associated with a decrease in bone mineral, while type 2 diabetes is associated with an increase. The new class of thiazolidinediones (glitazones) has been associated with an increased loss of bone mineral. In breast cancer treatment, tamoxifen is associated with an increased bone mineral, while the newer class of aromatase inhibitors through a decrease in serum oestradiol are associated with an increased loss of bone mineral. Strong analgesics (opioids) may decrease bone mineral density through inhibition of gonadotrophins while weak analgesics such as the non-steroidal anti-inflammatory drugs may increase bone mineral through an effect on the prostaglandin system. However, possibly through an increased risk of falls, the weak analgesics are associated with an increased risk of fractures. Proton pump inhibitors may lead to a decreased calcium absorption and thus a decreased bone mineral and an increased risk of fractures.

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Development of ‘Primary’ Hyperparathyroidism during Lithium Therapy: Longitudinal Study

Cited by 61 publications

References 9 publications

Lithium Associated Hyperparathyroidism: An Evidence Based Surgical Approach

Lithium Associated Hyperparathyroidism: An Evidence Based Surgical Approach

Parathyroid Growth

Adverse Effects of Drugs on Bone and Calcium Metabolism/Physiology

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