Parathyroid hormone levels 1 hour after thyroidectomy: an early predictor of postoperative hypocalcemia.

Parathyroid dysfunction leading to hypocalcemia is not uncommon after total or completion thyroidectomy and, if symptomatic, is often associated with significant patient morbidity and a prolonged hospital stay.1 Often, parathyroid tissue is deliberately or inadvertently resected with the surgical specimen. When recognized intraoperatively, normal, devitalized glands should be autotransplanted into the surrounding skeletal muscle. More often though, the observed fall in parathormone (PTH) levels is a result of traumatic injury to the parathyroids during thyroidectomy leading to either transient ischemia or even frank infarction of the glands. Thus, the hyposecretion of PTH may be relatively transient (1.6%–68%) or may be permanent (0.4%–33%).2,3 Intact PTH is secreted by the parathyroid glands in response to serum ionized calcium levels. Intact PTH in an 84-amino acid protein and control of its release is under direct feedback from extracellular calcium ions, as mediated through the cell surface calcium receptor of the parathyrocyte.4 The half-life of intact PTH is measured in minutes and can be reliably assayed.5,6 It is degraded into several smaller proteins with variable half-lives and biologic activity.6 The appearance of postoperative hypocalcemia may be delayed up to 48 hours depending on the levels of such biologically active peptides as well as the patient’s vitamin D and electrolyte status and the presence or absence of “hungry” bone, among other factors.4,5 Because of the lag between the hyposecretion of PTH and the development of symptomatic hypocalcemia, early pharmacologic support with calcium, magnesium and calcitriol can potentially keep high-risk patients eucalcemic and asymptomatic, thereby avoiding morbidity. Early prophylactic administration of calcitriol is important in maintaining eucalcemia in high-risk patients because, as a fat-soluble vitamin, its pharmacokinetics are such that an increase in serum calcium may take 24–48 hours. Thus, the early identification of post-thyroidectomy patients at risk of hypoparathyroidism and hypocalcemia would allow for the early introduction of calcitriol.7 Conversely, patients at low risk of post-thyroidectomy hypocalcemia can be spared the discomfort of excessive blood tests and can reliably be discharged without fear of symptomatic hypcocalcemia. The present study correlates preoperative serum PTH and ionized calcium (Ca2+) levels with those obtained at 1, 6 and 24 hours after total thyroidectomy with an emphasis on the 1-hour PTH (PTH-1) and the subsequent development of hypocalcemia.