An Algorithm Informed by the Parathyroid Hormone Level Reduces Hypocalcemic Complications of Thyroidectomy

Ó The Author(s) 2010. This article is published with open access at Springerlink.com Background Measurement of the parathyroid hormone (PTH) level following total thyroidectomy (TTx) may allow prediction of postoperative hypocalcemia. We present an algorithmic method of managing hypocalcemia preemptively, based on the PTH level 1 h after operation. Materials and methods We examined 423 consecutive patients undergoing TTx at a single institution. A subset of patients were managed using an algorithm involving routine postoperative oral calcium administration and the early addition of oral calcitriol in patients with a low 1-h postoperative PTH level. Algorithm patients were compared to a concurrent, conventionally managed group. Outcomes measured included serum calcium levels, symptoms of hypocalcemia, postoperative complications, and receipt of intravenous (IV) calcium. Results The algorithm was applied in 135 patients, and 288 patients were managed conventionally. Critically low calcium levels (total calcium \7.5 mg/dl [1.88 mmol/l] or ionized calcium \0.94 mmol/l) were less common in algorithm patients (10.6 % vs. 25.3%; p \ 0.005). Much of this difference was attributable to the protective impact of the algorithm on patients undergoing TTx for cancer, 30% of whom developed critically low calcium levels when managed conventionally. Among patients requiring IV calcium, algorithm patients received fewer doses (1.29 vs

Iodide organification defect in a cold thyroid nodule: Absence of iodide effect on cyclic AMP accumulation

A follicular adenoma of the thyroid was ‘hot’ one hour after 99mTc pertechnetate administration, but ‘cold’24 h after 131I iodide administration. Incubation of the tissue in vitro demonstrated a defect in iodide binding to proteins that was abolished by addition of an H2O2 generating system. In this tissue iodide failed to inhibit TSH-induced cyclic AMP accumulation. The results show that iodide oxidation is required for its inhibitory action on cyclic AMP accumulation in human thyroid.SCOPUS: ar.jFLWNAinfo:eu-repo/semantics/publishe