Hyperthyroidism after surgery for primary hyperparathyroidism

• Published in: Langenbeck's archives of surgery Vol. 384; no. 6; pp. 568 - 575
• Main Authors: Lindblom, P, Valdemarsson, S, Westerdahl, J, Tennvall, J, Bergenfelz, A
• Format: Journal Article
• Language: English
• Published: Germany 01.12.1999
• Subjects: Aged; Breast Neoplasms - complications; Female; Humans; Hyperparathyroidism - surgery; Hyperthyroidism - etiology; Male; Parathyroidectomy; Postoperative Complications - etiology; Thyroid Hormones - metabolism
• ISSN: 1435-2443; 1435-2451
• DOI: 10.1007/s004230050245

The coexistence of hyperthyroidism and primary hyperparathyroidism (pHPT) has been reported. We have questioned whether hypercalcemia or surgical trauma contribute to transient hyperthyroidism following parathyroid surgery. Twenty-six pHPT and eleven breast cancer patients were compared regarding pre-, peri- and postoperative thyrotropin (TSH), free thyroxine (T4) and free triiodothyronine (T3) concentrations. Thyroglobulin concentration, occurrence of autonomous thyroid nodules, and variables reflecting surgical trauma were compared in pHPT patients with and without postoperative hyperthyroidism. Postoperatively, eleven pHPT patients demonstrated T4 and T3 concentrations above normal, and nine developed symptoms of mild thyrotoxicosis. A parallel rise in TSH and T4 concentrations was seen during both parathyroid and breast cancer surgery. Compared with patients with no postoperative hyperthyroidism, patients with postoperative hyperthyroidism showed a parallel rise in mean thyroglobulin and T4/T3 concentrations as well as higher thyroglobulin concentrations. However, there was no difference in variables assessing surgical trauma nor in occurrence of autonomous thyroid nodules. The peri-operative rise in TSH was preceded by a decrease in calcium. Transient hyperthyroidism after parathyroid surgery is not infrequent. The condition seems to be self-limiting, since symptoms invariably subsided without treatment. Manipulation of the thyroid gland is most likely the major contributing factor to postoperative hyperthyroidism. However, it may not be the sole explanation, since our data suggest a more multifactorial scenario.