# Association of Intraoperative Parathyroid Hormone Decline with Early Postoperative Hypocalcemia: A Single-Center Retrospective Study

**Authors:** Suat Evirgen, Elif Menekse, Ecem Avci, Burak Yasin Avci, Çiğdem Tura Bahadır, Cafer Polat

PMC · DOI: 10.3390/diagnostics16040636 · 2026-02-22

## TL;DR

This study explores how a rapid drop in parathyroid hormone during surgery can predict low blood calcium levels afterward.

## Contribution

The study identifies a potential intraoperative rule-out marker for early postoperative hypocalcemia using PTH decline.

## Key findings

- A 15-minute intraoperative PTH decline of less than 75% may rule out early postoperative hypocalcemia.
- Preoperative alkaline phosphatase and parathyroid tumor weight are strong predictors of hypocalcemia.
- The PTH decline's predictive value diminishes when combined with other factors like ALP and tumor weight.

## Abstract

Background/Objectives: Postoperative early hypocalcemia (PEH) is a key postoperative issue after parathyroidectomy in primary hyperparathyroidism. It often leads to long-lasting hypocalcemia, requiring more calcium and active vitamin D supplements. This study aimed to determine whether the extent of intraoperative parathyroid hormone (PTH) decline, measured 15 min after parathyroid tumor excision, could serve as a reliable intraoperative rule-out marker for PEH. Methods: We conducted a retrospective review of 88 adult patients who underwent surgical intervention for a solitary parathyroid tumor at a single institution. Postoperative early hypocalcemia (PEH) was defined as a total serum calcium level <8.5 mg/dL within the postoperative 6th hour or on postoperative day 1, requiring clinical calcium supplementation (oral and/or intravenous), with active vitamin D when appropriate. The percentage decrease in PTH at 15 min post-excision was calculated using morning-of-surgery preoperative PTH values alongside the 15-min post-excision levels. Additional variables assessed included preoperative alkaline phosphatase (ALP), parathyroid tumor weight, and serum concentrations of calcium, phosphate, magnesium, and 25-hydroxyvitamin D. Predictive factors were identified by logistic regression, and the diagnostic accuracy of the 15-min PTH decline was evaluated using receiver operating characteristic (ROC) curve analysis, optimizing cutoff selection with Youden’s index. Odds ratios were standardized per 10-unit increments for ALP and parathyroid tumor weight for interpretability. Results: Of the studied cohort, 10 patients (11.4%) developed PEH. The intraoperative 15-min PTH decline was notably greater in those who developed PEH compared to those who did not (81.2 ± 4.4% vs. 69.9 ± 8.3%; p < 0.001). Univariate logistic regression showed a significant association between the 15-min PTH decline and PEH (OR 1.22 per 1% increment; 95% CI 1.08–1.38). That said, when we added ALP and parathyroid tumor weight to the multivariate models, PTH decline no longer predicted independently. In contrast, ALP (OR 3.11 per 10 U/L; 95% CI 1.34–7.93; p = 0.011) and parathyroid tumor weight (OR 1.22 per 10 mg; 95% CI 1.10–1.48; p = 0.004) stayed significant. Thus, the incremental prognostic contribution of the 15-min PTH decline beyond ALP and parathyroid tumor weight appears limited. The ROC curve for the 15-min PTH decline produced an AUC of 0.883, with an optimal cutoff of 75% providing 100% sensitivity and 74.4% specificity. No patients with a PTH decline below 75% developed PEH. Conclusions: Preoperative ALP and parathyroid tumor weight showed the strongest independent associations with PEH following parathyroid tumor surgery. An intraoperative PTH decline of less than 75% at 15 min may serve as a practical rule-out tool for PEH, although further validation in larger patient populations is warranted.

## Linked entities

- **Chemicals:** calcium (PubChem CID 5460341), phosphate (PubChem CID 1061), magnesium (PubChem CID 5462224), 25-hydroxyvitamin D (PubChem CID 5353325)
- **Diseases:** primary hyperparathyroidism (MONDO:0010837), hypocalcemia (MONDO:0018543)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, CYP27A1 (cytochrome P450 family 27 subfamily A member 1) [NCBI Gene 1593] {aka CP27, CTX, CYP27}, BGLAP (bone gamma-carboxyglutamate protein) [NCBI Gene 632] {aka BGP, OC, OCN}, ALPP (alkaline phosphatase, placental) [NCBI Gene 250] {aka ALP, PALP, PLAP, PLAP-1}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}
- **Diseases:** hungry bone syndrome (MESH:D001847), insulin resistance (MESH:D007333), endocrine diseases (MESH:D004700), muscle cramps (MESH:D009120), MEN (MESH:D018813), Hypocalcemia (MESH:D006996), tetany (MESH:D013746), Parathyroid tumor (MESH:D010282), paresthesia (MESH:D010292), multiple endocrine neoplasia syndromes (MESH:D009377), renal impairment (MESH:D007674), chronic kidney disease (MESH:D051436), secondary or tertiary hyperparathyroidism (MESH:D006962), malignancy (MESH:D009369), parathyroid disorders (MESH:D010279), familial hyperparathyroidism (MESH:D006961), hereditary hyperparathyroidism (MESH:D009386), injury to (MESH:D014947), multigland disease (MESH:D004194), metabolic syndrome (MESH:D024821), PHPT (MESH:D049950), hypoparathyroidism (MESH:D007011), vitamin D deficiency (MESH:D014808)
- **Chemicals:** 25-hydroxyvitamin D (MESH:C104450), 25(OH) vitamin D (-), magnesium (MESH:D008274), calcium (MESH:D002118), calcitriol (MESH:D002117), phosphate (MESH:D010710), vitamin D (MESH:D014807)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12939720/full.md

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Source: https://tomesphere.com/paper/PMC12939720