Abstract
Permanent hypoparathyroidism has become the most common and the most severe complication after thyroid surgery. In our experience, some patients suffer from permanent hypocalcemia and related symptoms despite normal parathyroid hormone (PTH) values after thyroid surgery. The aim of this work was to present a series of such patients with long-term hypocalcemia and normal PTH values to evaluate to what extent parathyroid function was impaired by thyroidectomy, and determine whether irregularities of bone and calcium metabolism were associated with this phenomenon. We present a series of eight patients with normal PTH and subnormal calcium levels at follow-up 2 months after thyroid surgery. Outcome parameters were intra- and postoperative PTH and calcium kinetics, and the following markers of calcium and bone metabolism at long-term follow-up: serum calcium, total serum albumin, ionized calcium, magnesium, PTH, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, urinary calcium, urinary creatinine, osteocalcin, c-terminal telopeptide of type I collagen, and alkaline phosphatase. All patients had normal calcium and PTH levels at the start of the operation. The intraoperative decline in PTH was >90%; the trough (3.3% of preoperative value) was reached 3 hours after surgery. Patients underwent complete determination of bone metabolism parameters during long-term follow-up 13.8 ± 2.4 months after surgery. Hypocalcemia was found in all eight patients, as well as PTH levels within the normal range. In three patients (3/8 = 37.5%), none of the other parameters was altered. In the remaining five patients, only isolated abnormalities in bone and calcium metabolism parameters were found (i.e., alterations in urinary calcium, thyrotropin, 25-hydroxyvitamin D, osteocalcin, and c-terminal telopeptide of type I collagen). An intraoperative injury to the parathyroid glands or their vascularization is the likely contributing factor to the development of permanent hypocalcemia with normal PTH values after thyroid surgery. The remaining parathyroid tissue is subject to a maximum stimulus by hypocalcemia and, therefore, is able to maintain PTH values in the normal range. These are still too low to re-establish normal serum calcium levels. In these patients, the term "hypoparathyroidism" might be replaced with "parathyroid insufficiency."
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