Parathyroid hormone-driven algorithms after thyroid surgery: Not one-size-fits-all.

BACKGROUND: Underreported variation in parathyroid hormone (PTH) assays exists. Using quality improvement methods, we aimed to develop an institution-specific PTH-based protocol to predict hypocalcemia after thyroidectomy. METHODS: We retrospectively reviewed patients who underwent total/completion thyroidectomy. A receiver operating curve (ROC) determined postoperative PTH cut-offs predictive of hypocalcemia. The stakeholders developed PTH-driven calcium management guidelines. Post-implementation outcomes were prospectively measured. RESULTS: Pre-implementation, 95 patients were assessed. PTH ≤1.5 pmol/L (14.1 pg/ml) predicted hypocalcemia (96%sensitivity), and ≥2.8 pmol/L (26.4 pg/ml) predicted normocalcemia (99%specificity) (area under curve = 0.97, SEM = 0.018). PTH on the day of and morning after surgery were identically predictive. Post-implementation, 64 patients were assessed. Hypocalcemia occurred with PTH >2.8 pmol/L in 2 cases (3.1%). Calcium over-prescribing decreased from 13.7% to 3.1% (p = 0.06). Length of stay (LOS) > 2 nights decreased from 13% to 3.1% (p = 0.05). CONCLUSION: A PTH-driven calcium management protocol post-thyroidectomy effectively reduces unnecessary calcium replacement and LOS. Given the variability in PTH assays, each institution may need to use individual cut-offs.

A novel mutation in the Albumin gene (R218S) causing familial dysalbuminemic hyperthyroxinemia in a family of Bangladeshi extraction.

BACKGROUND: Familial dysalbuminemic hyperthyroxinemia (FDH) is a common cause of euthyroid hyperthyroxinemia. Clinical recognition of FDH is crucial for preventing unnecessary therapy in clinically euthyroid patients with abnormal thyroid function tests. Our goal was to identify the cause of abnormal serum tests of thyroid function in a Canadian family of Bangladeshi extraction. PATIENTS: The proposita was found to have elevated free thyroxine (fT4) and free triiodothyronine (fT3) with nonsuppressed thyrotropin (TSH) on screening blood work. After detailed studies excluding hyperthyroidism and resistance to thyroid hormone, blood was obtained from all members of her immediate family for further investigation. METHODS: We conducted laboratory analyses and sequencing of candidate genes. RESULTS: Two members of this family have FDH, caused by a not previously identified mutation in the albumin gene. This mutation, located in exon 7 of the gene (652A>C), produces a single amino acid substitution in the protein molecule (R218S). The mutant albumin is associated with a ninefold increase in serum total T4 and a twofold increase in serum total reverse T3 compared to patients with normal albumin. Modeling data for the R218S variant are compatible with the increased binding affinity of this variant albumin for T4. CONCLUSIONS: The R218S substitution reported here causes FDH that, in terms of the magnitude of serum iodothyronine elevation, is intermediate to the two previously reported mutations at codon 218 FDH: R218H being more mild and R218P more severe.