Severe hypercalcemia due to teriparatide

Abstract

Osteoporosis that is by far the most common metabolic bone disease, has been defined as a skeletal disorder characterized by compromised bone strength predisposing a person to an increased risk of fracture. Anabolic therapy with teriparatide, recombinant human parathyroid hormone (PTH 1-34), stimulates bone formation and resorption and improves trabecular and cortical microarchitecture. Teriparatide is indicated for the treatment of men and postmenopausal women with osteoporosis who are at high risk for fracture, including those who have failed or are intolerant of previous osteoporosis therapy. In conclusion, although teriparatide seems quite effective in the treatment of osteoporosis, it may cause life-threatening hypercalcemia. Therefore, patients should be closely monitored if symptoms of hypercalcemia are present during teriparatide treatment. Sustained hypercalcemia due to teriparatide treatment can not be seen in literature so we wanted to emphasize that severe hypercalcemia may develop due to teriperatide.

Safety issues and adverse reactions with osteoporosis management

“…Moderate asymptomatic hypercalcemia and hypercalciuria is a relatively common finding after few days of TPD treatment [65,66]. It resolves immediately after cessation of treatment, but also spontaneously without altering TPD treatment [67].…”

The Proteasome Inhibitor Carfilzomib Suppresses Parathyroid Hormone-induced Osteoclastogenesis through a RANKL-mediated Signaling Pathway

“…Although recombinant PTH(1-34) (teriparatide) is currently used as an anabolic agent for the treatment of osteoporosis, the administration of dosing and daily subcutaneous injection is problematic. PTH treatment can cause an increase of serum calcium and hypercalcemia in some osteoporosis patients, which can prompt cessation of PTH treatment (4,5). A better understanding of those mechanisms mediating the anabolic and catabolic effects of PTH could overcome the current limitations of PTH-based treatment of osteoporosis.…”

Modulation of Transient Receptor Potential Channels 3 and 6 Regulates Osteoclast Function with Impact on Trabecular Bone Loss

“…A variety of medications that suppress bone resorption by affecting the activity of osteoclasts have been developed so far [38,39]. Despite their good efficiency in increasing bone mass, these drugs are associated with a number of side effects that limit their therapeutic application in a subgroup of patients that would benefit from an intervention [40,41]. TRPC3 is already in the focus of interest as a target for pharmacological interventions due to the observation that gain of function is associated with pathologies of the cardiovascular system and the brain [42].…”