Published online Jul 28, 2026. doi: 10.5528/wjtm.118436
Revised: January 30, 2026
Accepted: March 4, 2026
Published online: July 28, 2026
Processing time: 209 Days and 10.4 Hours
Post-thyroidectomy hypocalcemia, usually reflecting temporary or permanent hypoparathyroidism, remains the most frequent metabolic complication after bilateral thyroid surgery and central neck dissection, with reported transient rates of 10%-47.8% and permanent dysfunction in 0.5%-10.7% of patients. This review synthesizes current evidence on the pathophysiology, epidemiology, and clinical impact of post-thyroidectomy hypocalcemia, emphasizing mechanisms such as parathyroid devascularization, mechanical or thermal injury, and inadvertent excision, as well as demographic and surgical risk factors including female sex, younger age, autoimmune thyroid disease, total thyroidectomy, central neck dissection, re-operative surgery, and prior neck irradiation. Preventive strategies are discussed in detail, including preoperative vitamin D and calcium optimi
Core Tip: Post-thyroidectomy hypocalcemia is common but largely preventable when surgeons deliberately integrate parathyroid preservation, preoperative optimization, and hormone-guided risk stratification into routine thyroid practice. A multimodal strategy that combines vitamin D and calcium supplementation in selected patients, meticulous identification and vascular preservation of all parathyroid glands with selective autotransplantation, and early postoperative parathyroid hormone (PTH) measurement to guide targeted supplementation allows safe early discharge for most patients while minimizing symptomatic hypocalcemia, emergency visits, and readmissions. Emerging optical and digital adjuncts, together with evolving PTH replacement therapies, offer additional opportunities for head and neck surgeons to individualize care and further reduce the burden of post-thyroidectomy hypoparathyroidism.
- Citation: Viswanath S, Chisthi MM, Kuttanchettiyar KG. Post-thyroidectomy hypocalcemia: Pathophysiology, prevention, and management strategies for the head and neck surgeon. World J Transl Med 2026; 12(2): 118436
- URL: https://www.wjgnet.com/2220-6132/full/v12/i2/118436.htm
- DOI: https://dx.doi.org/10.5528/wjtm.118436
Thyroidectomy stands as one of the most commonly performed surgical procedures in otolaryngology and general surgery, yet it carries the risk of significant metabolic complications. Among these, post-operative hypocalcemia represents a substantial burden to patients and healthcare systems alike. The condition, stemming from parathyroid gland dysfunction during or after thyroid surgery, has long been recognized as problematic, yet the mechanisms, prevention strategies, and optimal management approaches have evolved considerably over the past two decades.
The parathyroid glands, though diminutive in size-approximately 6 mm × 3 mm × 1 mm and weighing just 20-50 mg each-play an absolutely critical role in maintaining calcium homeostasis. Their strategic location on the posterior surface of the thyroid lobes puts them at direct risk during thyroidectomy procedures. The fragile vascular supply to these glands, comprising up to 30% capillary cells, renders them exquisitely vulnerable to ischemic injury during surgical manipulation and dissection.
The reported incidence of transient hypocalcemia ranges from 10% to 47.8% within the first 24 hours after thyroidectomy, while permanent hypoparathyroidism-defined as dysfunction persisting beyond 6 months-occurs in 0.5%-10.7% of patients[1] (Table 1). This substantial variability reflects differences in surgical technique, surgeon experience, patient demographics, and the heterogeneous definitions employed across published studies. For surgeons performing thyroidectomies, understanding the pathophysiology and implementing evidence-based preventive strategies is essential for optimizing outcomes and patient satisfaction.
| Feature | Transient hypoparathyroidism | Permanent hypoparathyroidism |
| Core definition | Post-operative hypocalcemia due to parathyroid gland stunning or reversible injury, with functional recovery | Irreversible loss of parathyroid function requiring long-term management |
| Duration | Lasts less than 6 months after surgery | Persists for more than 6 months after surgery |
| Biochemical criteria | Low serum calcium with inappropriately low or normal PTH, normalizing within 6 months | Low serum calcium with an undetectable or inappropriately low PTH level persisting beyond 6 months |
| Treatment requirement | Requires calcium ± active vitamin D supplementation, which can be completely discontinued within 6 months | Requires calcium and active vitamin D supplementation to maintain normocalcemia beyond 6 months |
The mechanisms underlying post-thyroidectomy hypocalcemia involve three principal pathways: Devascularization of the parathyroid glands, mechanical trauma from surgical manipulation, and inadvertent removal of parathyroid tissue[4]. Understanding these mechanisms forms the foundation for developing effective prevention strategies.
The arterial blood supply to the parathyroid glands is derived primarily from the inferior thyroid artery, though anatomical variation is common, with contributions from the superior thyroid artery or thymo-thyroid ligament vessels in a significant proportion of cases[5]. The short half-life of parathyroid hormone (PTH)-approximately 3-5 minutes-means that even transient gland ischemia rapidly results in precipitous declines in serum PTH levels[6]. This dramatic drop in hormone production creates an acute biological crisis that reverberates through calcium homeostasis for hours to days.
Aggressive dissection around the parathyroid glands or thermal injury from energy-sealing devices creates zones of collateral tissue damage that extend beyond the intended surgical field. Maintaining a minimum distance of 3-5 mm from parathyroid tissue has become the standard recommendation for minimizing thermal injury during thyroidectomy[7]. Current energy-sealing devices, while providing excellent hemostasis, can cause unintended thermal spread that damages the delicate vascular supply and parenchyma of the parathyroid glands.
Removal of parathyroid tissue represents a definitive mechanism for hypoparathyroidism. This risk is particularly elevated during central neck dissection for thyroid malignancy, where the proximity of lymph nodes to the inferior parathyroid glands increases the likelihood of inadvertent removal. Each parathyroid gland removed substantially increases the risk of significant hypocalcemia[8].
Certain patient characteristics substantially influence susceptibility to post-operative hypocalcemia. Female patients experience higher rates of both transient and permanent hypoparathyroidism, while male sex has been associated with reduced risk of both transient and permanent hypoparathyroidism[9]. Younger patients, particularly those under 40 years of age, face a substantially elevated risk of transient hypocalcemia, though this age-related risk may reflect biological rather than surgical factors.
Autoimmune thyroid disease, including Graves’ disease and chronic lymphocytic thyroiditis, substantially increases hypocalcemia risk, possibly through chronic inflammatory changes within the parathyroid glands themselves[10]. Preoperative vitamin D deficiency represents a modifiable risk factor that independently predicts postoperative hypocalcemia, highlighting the importance of preoperative biochemical optimization.
The surgical extent-particularly total vs subtotal thyroidectomy-along with surgeon experience, operative technique, and the presence of central neck dissection, remains the strongest surgical predictor of hypoparathyroidism[11]. Prolonged operative time exceeding 120-240 minutes correlates with increased ischemic risk to parathyroid tissue, with hypoparathyroidism rates reaching 62% for procedures lasting beyond 240 minutes[12]. Re-operative thyroidectomy carries the highest risk of permanent hypoparathyroidism due to anatomical distortion from prior surgery, which complicates gland identification and vascular preservation. Prior neck radiation substantially elevates permanent hypoparathyroidism risk through radiation-induced fibrosis and vascular damage[13].
Effective prevention of post-thyroidectomy hypocalcemia requires a comprehensive, multimodal approach beginning well before the patient enters the operating room and extending into the postoperative period.
Vitamin D deficiency has become recognized as an independent and modifiable predictor of postoperative hypocalcemia. A meta-analyses of randomized controlled trials involving over 1000 patients demonstrate convincingly that preoperative calcium and vitamin D supplementation reduces symptomatic hypocalcemia by approximately 46%, with incidence declining by approximately 10%-11% in supplemented patients[14]. Vitamin D exerts its therapeutic benefit by enhancing intestinal calcium absorption through increased expression of calcium-binding proteins, though vitamin D requires up to two weeks to achieve peak effect on serum calcium levels.
For this reason, initiating supplementation at least one to two weeks before thyroidectomy is essential for maximum benefit. Recommended regimens include vitamin D supplementation (alfacalcidol or calcitriol 0.25-2 μg daily) combined with oral calcium (500-1500 mg daily), administered for seven days to six weeks preoperatively, depending on baseline vitamin D status. Patients with severe vitamin D deficiency or those undergoing high-risk procedures such as central neck dissection for thyroid malignancy warrant more aggressive preoperative optimization strategies.
The cornerstone of parathyroid prevention remains meticulous surgical technique, a principle firmly established since Theodor Kocher’s era, which emphasized anatomical precision and hemostasis to reduce mortality. Careful identification of all four parathyroid glands is mandatory, with particular attention given to ectopic glands, which occur in approximately 35% of individuals and may be located in the mediastinum, thymus, or tracheoesophageal groove[15]. While the classical gold-standard approach involves careful in situ identification and preservation of all glands with their vascular supply, modern surgical evolution has introduced nuanced differences between methods. The traditional open transcervical technique provides direct visualization, facilitating the preservation of the delicate branches from the inferior thyroid artery. In contrast, minimally invasive and remote-access approaches (e.g., endoscopic or robotic transaxillary/retroauricular) offer cosmetic advantages but present a distinct anatomical learning curve and may alter the tactile feedback crucial for judging parathyroid viability[16]. A significant historical contribution to this field was the detailed description of parathyroid anatomy and vascular supply by Halsted and Evans[17], which laid the groundwork for all subsequent preservation strategies. Regardless of the approach, the principle of maintaining a critical 3-5 mm distance from parathyroid tissue to minimize thermal injury from advanced energy devices is universally paramount. Systematic identification is mandatory, with particular attention to ectopic glands (occurring in about 35% of individuals), which are at higher risk of inadvertent removal if not actively sought[15]. When a gland appears devascularized or is unavoidably resected, the strategy shifts from preservation to immediate autotransplantation, a technique refined by surgeons like Olson and Wells. Intraoperative tools, such as near-infrared autofluorescence imaging, are emerging as valuable adjuncts to visual assessment for confirming parathyroid identity and predicting vascularity, though their impact on long-term hypocalcemia rates is still being defined[18]. Therefore, the modern execution of the prevention cornerstone adapts timeless principles of gentle handling and vascular preservation to the specific demands and visualization paradigms of contemporary surgical approaches.
Intraoperative PTH assay has emerged as a valuable tool providing real-time assessment of parathyroid function and identifying patients at the highest risk for postoperative hypocalcemia. An intact PTH (IPTH) level below 10 pg/mL obtained 10 to 20 minutes after total thyroidectomy correlates with a significantly increased risk of transient or permanent hypoparathyroidism[19]. The superiority of this approach lies in its ability to identify high-risk patients while the surgeon remains in the operating room, enabling interventions such as selective parathyroid autotransplantation to substantially reduce permanent hypoparathyroidism risk.
Selective IPTH-guided parathyroid autotransplantation in patients with very low IPTH levels abolishes the risk of permanent hypoparathyroidism while reducing transient hypocalcemia rates and the overall calcium supplementation burden compared to routine autotransplantation of all parathyroids[20]. This strategy allows surgeons to reserve autotransplantation for those patients who truly need it, avoiding unnecessary grafting when parathyroid function is preserved.
Near-infrared autofluorescence imaging and indocyanine green fluorescence angiography represent emerging technologies that enhance parathyroid identification and real-time assessment of vascular perfusion. NIRAF has been shown to achieve detection rates ranging from 78%-100% in published series[21]. Indocyanine green (ICG)-enhanced imaging permits real-time evaluation of parathyroid blood supply, guiding autotransplantation decisions when devascularization is detected[22]. These technologies prove particularly valuable in complex cases-central neck dissection, re-operative thyroidectomy, and minimally invasive approaches-where anatomical distortion increases inadvertent gland injury risk.
When a parathyroid gland is inadvertently removed or demonstrates compromised blood supply during surgery, selective autotransplantation represents the definitive strategy for preventing permanent hypoparathyroidism. Fresh autotransplantation into the sternocleidomastoid muscle, using either sliced or minced parathyroid fragments (1 mm3 pieces) placed in separate muscle pockets, results in graft functionality rates exceeding 90%[23]. The long-term success of this procedure is not guaranteed, with reported failure rates necessitating permanent supplementation ranging from 10% to 30%; outcomes are more favorable in the context of secondary hyperparathyroidism compared to autotransplantation following thyroidectomy for cancer[24,25]. This approach markedly reduces the risk of permanent hypoparathyroidism compared to leaving devitalized tissue in situ, making it an essential component of comprehensive surgical management. Consequently, diligent long-term follow-up is paramount, focusing on serial measurements of serum calcium and IPTH levels, where a detectable PTH in a normocalcemic patient signifies graft function, which may take weeks to months to fully manifest[26]. The absolute contraindication for parathyroid auto-transplantation is known or suspected parathyroid carcinoma, due to the risk of disseminating malignant cells. Relative contraindications that require careful surgical judgment include transplantation of tissue of uncertain viability or identity, active local infection at the recipient site, severe medical frailty, and significant intra-operative instability that precludes prolonging the procedure[27].
The early detection of patients at risk for post-thyroidectomy hypocalcemia is critical for guiding perioperative management and preventing unnecessary hospitalization.
Postoperative IPTH measurement 4 to 6 hours after thyroidectomy is the most reliable early predictor of hypocalcemia, as levels drop precipitously following gland devascularization[28,29]. Evidence robustly supports IPTH-based risk stratification. An IPTH level below 10 pg/mL identifies the highest-risk group, while levels of 10-19 pg/mL and 20-29 pg/mL represent intermediate risk. An IPTH level ≥ 30 pg/mL is associated with a very low (3%-5%) risk of significant hypocalcemia[30,31]. Importantly, risk exhibits significant sex-based differences, with females at a higher risk for a given IPTH level[8].
While biochemical hypocalcemia is common, occurring in 22%-48% of patients, symptomatic manifestations (e.g., paresthesias, tetany) develop in a smaller subset (24%-30%) and can be biphasic, often worsening on postoperative days 2-3[32-34]. Management depends on severity: Mild, asymptomatic biochemical hypocalcemia may resolve spontaneously, whereas serum calcium < 1.85 mmol/L (< 8.0 mg/dL) necessitates aggressive intervention to prevent serious complications like cardiac arrhythmias or laryngospasm[35].
Contemporary protocols support safe same-day or short-stay discharge using integrated risk assessment. Patients who are normocalcemic with an IPTH ≥ 20-30 pg/mL can typically be discharged within 24 hours with appropriate outpatient follow-up[36]. Comprehensive discharge criteria should include: (1) IPTH ≥ 15–30 pg/mL; (2) Serum calcium ≥ 1.85 mmol/L; (3) Absence of symptoms; (4) A favorable parathyroid gland status score; and (5) Thorough patient education on symptom recognition[37,38].
In clinical practice, postoperative IPTH levels can be efficiently stratified to guide management. High-risk patients (IPTH < 10 pg/mL) require vigilant monitoring and proactive calcium supplementation. Intermediate-risk patients (IPTH 10-29 pg/mL) benefit from selective supplementation based on trend and symptoms. Low-risk patients (IPTH ≥ 30 pg/mL) with normal calcium levels can be managed conservatively, often qualifying for early discharge. This framework, centered on a single timely measurement, standardizes care and optimizes resource utilization (Figure 1).
The management of symptomatic hypocalcemia differs substantially depending on severity and requires a tiered approach balancing aggressive intervention with careful monitoring.
Symptomatic hypocalcemia requires immediate recognition and intervention. Clinical manifestations include perioral and extremity paresthesias, carpopedal spasm, tetany, laryngospasm, and, in severe cases, seizures and cardiac arrhythmias. The Chvostek sign (twitching of the upper lip with tapping anterior to the earlobe) and Trousseau sign (carpopedal spasm elicited by blood pressure cuff inflation for 3 minutes) serve as useful clinical indicators of latent tetany.
Oral supplementation represents the first-line approach for hypocalcemic patients without life-threatening symptoms. Elemental calcium should be started at 500-1000 mg three times daily and titrated upward based on biochemical response and symptom resolution. Calcium carbonate (containing 40% elemental calcium) and calcium citrate (28% elemental calcium) are the preferred formulations; calcium citrate is advantageous in patients on acid-suppressive medications who have impaired gastric calcium absorption.
Concurrent calcitriol (active vitamin D metabolite) administration is essential, with usual starting doses of 0.25-1.0 μg daily in divided doses. Calcitriol is preferable to ergocalciferol because of its rapid onset of action (hours to days), potent biological effect on intestinal calcium absorption, and short half-life, enabling rapid dose titration. Dose escalation should proceed every 4-7 days until a low-normal serum calcium level is achieved.
Severe symptomatic hypocalcemia with ionized calcium < 0.8 mmol/L (or total corrected calcium < 1.85 mmol/L) in patients with tetany, seizures, or arrhythmias warrants intravenous calcium gluconate administration[39]. Calcium chloride should be avoided peripherally due to tissue necrosis risk; calcium gluconate is safe for peripheral infusion. Standard loading doses consist of 1-2 g (10-20 mL of 10% solution) diluted in 50-100 mL of 5% dextrose, infused slowly over 10-20 minutes with continuous cardiac monitoring[40]. Rapid administration risks cardiac arrhythmias, bradycardia, and hypotension; infusion should proceed cautiously with ECG monitoring, particularly in patients receiving digoxin.
Patients frequently develop recurrent hypocalcemia after the initial IV dose. Repeat IV calcium doses of 1-2 g gluconate over 60 minutes may be necessary every 1-4 hours, depending on symptom severity and serum calcium trajectory.
Hypomagnesemia fundamentally impairs PTH secretion and renal response to PTH, creating a critical bottleneck to successful calcium repletion. Serum magnesium should be checked in all patients with hypocalcemia; if depleted, aggressive magnesium repletion must precede or accompany calcium supplementation, as correction of hypomagnesemia alone can normalize both PTH levels and serum calcium[41]. However, IV magnesium sulfate can transiently chelate calcium; therefore, magnesium supplementation should be delayed until calcium levels show improvement or administered in a staggered fashion relative to IV calcium dosing.
Permanent hypoparathyroidism, persisting beyond 6 months post-thyroidectomy, requires indefinite supplementation with careful monitoring. The primary management goals include maintaining symptomatic control, sustaining serum calcium in the low-normal range (2.00-2.12 mmol/L), preserving normal serum phosphate (0.8-1.5 mmol/L), and maintaining a calcium-phosphate product below 4.4 mmol2/L2 to prevent ectopic calcification[42].
Long-term supplementation regimens typically employ calcium carbonate 1-2 g three times daily combined with calcitriol 0.5-2.0 μg daily in divided doses, with individual requirements varying widely. Thiazide diuretics reduce urinary calcium excretion by increasing distal renal tubular calcium reabsorption and represent important adjunctive therapy. Combined thiazide administration with a low-sodium, low-phosphate diet and oral phosphate binders substantially improves supplementation efficacy and reduces hypercalciuria risk.
Serum calcium, phosphorus, and creatinine should be monitored weekly to monthly during initial dose adjustments, with measurements every 3-6 months once therapy stabilizes. Patients with permanent hypoparathyroidism require ongoing endocrinology co-management with biochemical monitoring every 3-6 months initially, then semi-annually once stable.
Permanent hypoparathyroidism, affecting 1.6% to 10.7% of thyroidectomy patients, results in lifelong supplementation requirements with substantial morbidity[32]. Patients with permanent hypoparathyroidism face significantly elevated risks of serious long-term complications, including nephrolithiasis, nephrocalcinosis, progressive renal insufficiency, posterior subcapsular cataracts, basal ganglia calcifications, and neuropsychiatric complications.
The increased renal complications-affecting approximately 30% of patients with chronic hypoparathyroidism-result from chronic hypercalciuria (> 300 mg/day) induced by vitamin D supplementation combined with impaired renal calcium reabsorption[43]. Neuropsychiatric complications are prevalent: Depression and anxiety are common complications, affecting a substantial proportion of patients with hypoparathyroidism compared to controls[44]. These psychological manifestations persist despite biochemical correction of calcium levels, suggesting direct PTH deficiency effects on central nervous system function.
Despite optimal supplementation regimens achieving normocalcemia, patients demonstrate significantly impaired health-related quality of life compared to healthy controls and patients with hypothyroidism alone. Studies using standardized quality-of-life questionnaires demonstrate worse scores across all domains, with particular deficits in mental health and general health perception. The impairment in quality of life is independent of serum calcium levels, indicating inherent PTH deficiency effects.
Post-thyroidectomy hypocalcemia represents the leading cause of emergency department visits and hospital readmissions following outpatient thyroidectomy. Among 17046 patients undergoing outpatient thyroidectomy at 374 United States facilities, 7.5% had emergency department treat-and-release encounters and 2.3% required readmission, with hypocalcemia-related diagnoses accounting for 9.9% of treat-and-release visits and 22.2% of readmissions[45]. These represent preventable healthcare encounters; PTH testing and calcitriol administration to patients at risk have been found to reduce the incidence of hypocalcemia and associated emergency department visits after total thyroidectomy[46].
The significant variability in post-thyroidectomy hypocalcemia outcomes across institutions reflects inconsistent implementation of evidence-based protocols. Institutional adoption of standardized, PTH-guided management algorithms substantially reduces complications, readmissions, and unnecessary interventions while improving patient safety and cost-effectiveness. Contemporary practice supports PTH-guided risk stratification for selective management. Most protocols consistently incorporate three critical elements: (1) Measurement of IPTH within 4-6 hours post-operatively; (2) Explicit risk stratification thresholds; and (3) Selective supplementation based on risk category rather than routine empiric therapy. Educational interventions substantially improve compliance.
Preliminary evidence suggests that computer-assisted deep learning models show feasibility for recognizing parathyroid-specific NIRAF signals on intraoperative images, potentially enabling automated parathyroid detection and reducing operator dependence; however, the clinical translation of such technologies faces barriers, including cost, availability, and a significant learning curve for integration into routine surgical workflow[47]. Similarly, while quantitative assessment of ICG fluorescence intensity using machine learning algorithms may standardize vascular assessment and improve prediction of postoperative parathyroid function, these advanced techniques also contend with similar limitations of accessibility and interpretative expertise.
Recombinant PTH (1-84) has shown promise in some studies, improving biochemical parameters and quality of life in chronic hypoparathyroidism patients, though its high cost remains a substantial barrier to widespread clinical implementation[48]. Long-acting PTH analogs and combination therapies targeting calcium-sensing receptor signaling represent novel approaches currently in clinical development.
Polygenic risk scores incorporating genetic variants associated with hypoparathyroidism risk, combined with preoperative laboratory parameters and intraoperative factors, may enable individualized prediction of permanent hypoparathyroidism risk with sufficient precision to guide selective autotransplantation decisions beyond current IPTH-based approaches; the routine clinical adoption of such genomic tools awaits further validation and the overcoming of practical hurdles related to testing complexity and integration into existing clinical pathways.
Post-thyroidectomy hypocalcemia remains a significant source of morbidity, emergency healthcare utilization, and healthcare costs. A comprehensive, multimodal approach incorporating preoperative optimization, meticulous surgical technique, selective intraoperative parathyroid autotransplantation based on IPTH assessment, and PTH-guided risk stratification substantially reduces both symptomatic hypocalcemia and permanent hypoparathyroidism. Standardized institutional protocols emphasizing postoperative IPTH measurement within 4-6 hours, explicit risk stratification, and selective rather than routine supplementation enable safe early discharge, reduce unnecessary medication burden, and prevent preventable readmissions and emergency department visits. Emerging technologies, including fluorescence angiography and deep learning algorithms, combined with pharmacologic advances in PTH replacement, promise further optimization of surgical outcomes and improved quality of life for patients undergoing thyroidectomy. Head and neck surgeons who embrace these evidence-based approaches will substantially enhance perioperative outcomes while reducing healthcare costs and patient morbidity.
| 1. | Alqahtani SM, Alatawi AS, Alalawi YS. Post-Thyroidectomy Hypocalcemia: A Single-Center Experience. Cureus. 2021;13:e20006. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1] [Cited by in RCA: 9] [Article Influence: 1.8] [Reference Citation Analysis (0)] |
| 2. | Orloff LA, Wiseman SM, Bernet VJ, Fahey TJ 3rd, Shaha AR, Shindo ML, Snyder SK, Stack BC Jr, Sunwoo JB, Wang MB. American Thyroid Association Statement on Postoperative Hypoparathyroidism: Diagnosis, Prevention, and Management in Adults. Thyroid. 2018;28:830-841. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 197] [Cited by in RCA: 336] [Article Influence: 42.0] [Reference Citation Analysis (0)] |
| 3. | Bollerslev J, Rejnmark L, Marcocci C, Shoback DM, Sitges-Serra A, van Biesen W, Dekkers OM; European Society of Endocrinology. European Society of Endocrinology Clinical Guideline: Treatment of chronic hypoparathyroidism in adults. Eur J Endocrinol. 2015;173:G1-20. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 343] [Cited by in RCA: 297] [Article Influence: 27.0] [Reference Citation Analysis (0)] |
| 4. | Del Rio P, Rossini M, Montana CM, Viani L, Pedrazzi G, Loderer T, Cozzani F. Postoperative hypocalcemia: analysis of factors influencing early hypocalcemia development following thyroid surgery. BMC Surg. 2019;18:25. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 45] [Cited by in RCA: 68] [Article Influence: 9.7] [Reference Citation Analysis (0)] |
| 5. | Zhou L, Zhang M, Xu D, Shi J, Pan G, Zhang Y, Peng Y. The application of subcapsular saline injection to preserve the parathyroid gland during thyroidectomy. Heliyon. 2023;9:e21543. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 2] [Reference Citation Analysis (0)] |
| 6. | Mak NTJJ, Li J, Vasilyeva E, Hiebert J, Guo M, Lustig D, Holmes D, Wiseman SM. Intraoperative parathyroid hormone measurement during parathyroidectomy for treatment of primary hyperparathyroidism: When should you end the operation? Am J Surg. 2020;219:785-789. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 10] [Cited by in RCA: 12] [Article Influence: 2.0] [Reference Citation Analysis (0)] |
| 7. | Alqahtani SM. Post-thyroidectomy hypoparathyroidism: A clinical surgical dilemma. Saudi Med J. 2024;45:1305-1311. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 3] [Reference Citation Analysis (0)] |
| 8. | Noureldine SI, Genther DJ, Lopez M, Agrawal N, Tufano RP. Early predictors of hypocalcemia after total thyroidectomy: an analysis of 304 patients using a short-stay monitoring protocol. JAMA Otolaryngol Head Neck Surg. 2014;140:1006-1013. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 39] [Cited by in RCA: 60] [Article Influence: 5.5] [Reference Citation Analysis (0)] |
| 9. | Villarroya-Marquina I, Lorente-Poch L, Sancho J, Sitges-Serra A. Influence of gender and women’s age on the prevalence of parathyroid failure after total thyroidectomy for multinodular goiter. Gland Surg. 2020;9:245-251. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 4] [Cited by in RCA: 15] [Article Influence: 2.5] [Reference Citation Analysis (0)] |
| 10. | Teisseyre M, Moranne O, Renaud S. Late diagnosis of chronic hypocalcemia due to autoimmune hypoparathyroidism. BMJ Case Rep. 2021;14:e243299. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 3] [Reference Citation Analysis (0)] |
| 11. | Edafe O, Balasubramanian SP. Incidence, prevalence and risk factors for post-surgical hypocalcaemia and hypoparathyroidism. Gland Surg. 2017;6:S59-S68. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 26] [Cited by in RCA: 53] [Article Influence: 5.9] [Reference Citation Analysis (0)] |
| 12. | Maheshwari M, Khan IA. Risk Factors for Transient and Permanent Hypoparathyroidism Following Thyroidectomy: A Comprehensive Review. Cureus. 2024;16:e66551. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 6] [Reference Citation Analysis (0)] |
| 13. | Sitges-Serra A. Etiology and Diagnosis of Permanent Hypoparathyroidism after Total Thyroidectomy. J Clin Med. 2021;10:543. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 10] [Cited by in RCA: 43] [Article Influence: 8.6] [Reference Citation Analysis (0)] |
| 14. | Xing T, Hu Y, Wang B, Zhu J. Role of oral calcium supplementation alone or with vitamin D in preventing post-thyroidectomy hypocalcaemia: A meta-analysis. Medicine (Baltimore). 2019;98:e14455. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 23] [Cited by in RCA: 38] [Article Influence: 5.4] [Reference Citation Analysis (0)] |
| 15. | Maleki Z. Parathyroid Gland. In: Klijanienko J, Cochand-Priollet B, Choussy O, Golusiński W, editors. Diagnostic Procedures in Patients with Neck Masses. Cham: Springer, 2024: 287-300. [DOI] [Full Text] |
| 16. | Zhang D, Wang T, Dionigi G, Zhang J, Zhao Y, Xue G, Liang N, Sun H. Comparison of parathyroid hormone kinetics in endoscopic thyroidectomy via bilateral areola with open thyroidectomy. BMC Surg. 2019;19:190. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 1] [Cited by in RCA: 4] [Article Influence: 0.6] [Reference Citation Analysis (0)] |
| 17. | Halsted WS, Evans HM. I. The Parathyroid Glandules. Their Blood Supply and their Preservation in Operation upon the Thyroid Gland. Ann Surg. 1907;46:489-506. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 120] [Cited by in RCA: 105] [Article Influence: 5.5] [Reference Citation Analysis (0)] |
| 18. | Benmiloud F, Godiris-Petit G, Gras R, Gillot JC, Turrin N, Penaranda G, Noullet S, Chéreau N, Gaudart J, Chiche L, Rebaudet S. Association of Autofluorescence-Based Detection of the Parathyroid Glands During Total Thyroidectomy With Postoperative Hypocalcemia Risk: Results of the PARAFLUO Multicenter Randomized Clinical Trial. JAMA Surg. 2020;155:106-112. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 53] [Cited by in RCA: 157] [Article Influence: 26.2] [Reference Citation Analysis (0)] |
| 19. | Essa MS, Ahmad KS, Fadey MA, El-Shaer MO, Salama AMF, Zayed ME. Role of perioperative parathormone hormone level assay after total thyroidectomy as a predictor of transient and permanent hypocalcemia: Prospective study. Ann Med Surg (Lond). 2021;69:102701. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 4] [Cited by in RCA: 6] [Article Influence: 1.2] [Reference Citation Analysis (0)] |
| 20. | Sun H, Gao L, Xiao G, Xie L, Zhuang Y, Wang J. Selective parathyroid autotransplantation prevent permanent hypoparathyroidism after total thyroidectomy with central neck dissection. Front Surg. 2025;12:1565581. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 1] [Reference Citation Analysis (0)] |
| 21. | Safia A, Abd Elhadi U, Massoud S, Merchavy S. The impact of using near-infrared autofluorescence on parathyroid gland parameters and clinical outcomes during total thyroidectomy: a meta-analytic study of randomized controlled trials. Int J Surg. 2024;110:3827-3838. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 6] [Cited by in RCA: 13] [Article Influence: 6.5] [Reference Citation Analysis (0)] |
| 22. | Moreno-Llorente P, García-Barrasa A, Pascua-Solé M, Videla S, Otero A, Muñoz-de Nova JL. Usefulness of ICG Angiography-Guided Thyroidectomy for Preserving Parathyroid Function. World J Surg. 2023;47:421-428. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 15] [Reference Citation Analysis (0)] |
| 23. | Barczyński M, Gołkowski F, Nawrot I. Parathyroid transplantation in thyroid surgery. Gland Surg. 2017;6:530-536. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 21] [Cited by in RCA: 34] [Article Influence: 3.8] [Reference Citation Analysis (0)] |
| 24. | Yuan Q, Liao Y, Zhou R, Liu J, Tang J, Wu G. Subtotal parathyroidectomy versus total parathyroidectomy with autotransplantation for secondary hyperparathyroidism: an updated systematic review and meta-analysis. Langenbecks Arch Surg. 2019;404:669-679. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 8] [Cited by in RCA: 36] [Article Influence: 5.1] [Reference Citation Analysis (0)] |
| 25. | Sitges-Serra A, Ruiz S, Girvent M, Manjón H, Dueñas JP, Sancho JJ. Outcome of protracted hypoparathyroidism after total thyroidectomy. Br J Surg. 2010;97:1687-1695. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 147] [Cited by in RCA: 185] [Article Influence: 11.6] [Reference Citation Analysis (0)] |
| 26. | Edafe O, Antakia R, Laskar N, Uttley L, Balasubramanian SP. Systematic review and meta-analysis of predictors of post-thyroidectomy hypocalcaemia. Br J Surg. 2014;101:307-320. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 468] [Cited by in RCA: 485] [Article Influence: 40.4] [Reference Citation Analysis (0)] |
| 27. | Wilhelm SM, Wang TS, Ruan DT, Lee JA, Asa SL, Duh QY, Doherty GM, Herrera MF, Pasieka JL, Perrier ND, Silverberg SJ, Solórzano CC, Sturgeon C, Tublin ME, Udelsman R, Carty SE. The American Association of Endocrine Surgeons Guidelines for Definitive Management of Primary Hyperparathyroidism. JAMA Surg. 2016;151:959-968. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 1112] [Cited by in RCA: 878] [Article Influence: 87.8] [Reference Citation Analysis (0)] |
| 28. | Jumaily JS, Noordzij JP, Dukas AG, Lee SL, Bernet VJ, Payne RJ, McLeod IK, Hier MP, Black MJ, Kerr PD, Raffaelli M, Bellantone R, Lombardi CP, Dietrich MS. Prediction of hypocalcemia after using 1- to 6-hour postoperative parathyroid hormone and calcium levels: an analysis of pooled individual patient data from 3 observational studies. Head Neck. 2010;32:427-434. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 9] [Cited by in RCA: 16] [Article Influence: 1.0] [Reference Citation Analysis (0)] |
| 29. | Mazotas IG, Wang TS. The role and timing of parathyroid hormone determination after total thyroidectomy. Gland Surg. 2017;6:S38-S48. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 16] [Cited by in RCA: 27] [Article Influence: 3.0] [Reference Citation Analysis (0)] |
| 30. | Carter Y, Chen H, Sippel RS. An intact parathyroid hormone-based protocol for the prevention and treatment of symptomatic hypocalcemia after thyroidectomy. J Surg Res. 2014;186:23-28. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 34] [Cited by in RCA: 33] [Article Influence: 2.8] [Reference Citation Analysis (0)] |
| 31. | Inversini D, Rausei S, Ferrari CC, Frattini F, Anuwong A, Kim HY, Liu X, Wu CW, Tian W, Liu R, Dionigi G. Early intact PTH (iPTH) is an early predictor of postoperative hypocalcemia for a safer and earlier hospital discharge: an analysis on 260 total thyroidectomies. Gland Surg. 2016;5:522-528. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 17] [Cited by in RCA: 25] [Article Influence: 2.5] [Reference Citation Analysis (0)] |
| 32. | Kuczma P, Triponez F. Hypoparathyroidism after thyroidectomy: a matter of definition, experience and new adjuncts. Gland Surg. 2024;13:1873-1877. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 1] [Reference Citation Analysis (0)] |
| 33. | AlQahtani A, Parsyan A, Payne R, Tabah R. Parathyroid hormone levels 1 hour after thyroidectomy: an early predictor of postoperative hypocalcemia. Can J Surg. 2014;57:237-240. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 29] [Cited by in RCA: 36] [Article Influence: 3.0] [Reference Citation Analysis (0)] |
| 34. | Fathy A, Eldeeb S, Abd-Elrheem Y. Profile of the causes of symptomatizing hypocalcemia in infants and children. J Curr Med Res Pract. 2023;8:92. [RCA] [DOI] [Full Text] [Cited by in RCA: 1] [Reference Citation Analysis (0)] |
| 35. | Tredici P, Grosso E, Gibelli B, Massaro MA, Arrigoni C, Tradati N. Identification of patients at high risk for hypocalcemia after total thyroidectomy. Acta Otorhinolaryngol Ital. 2011;31:144-148. [PubMed] |
| 36. | Duval M, Bach-Ngohou K, Masson D, Guimard C, Le Conte P, Trewick D. Is severe hypocalcemia immediately life threatening? Endocr Connect. 2018;7:1067-1074. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 24] [Cited by in RCA: 23] [Article Influence: 2.9] [Reference Citation Analysis (0)] |
| 37. | Sekar S, Belavendra A, Jacob PM. Early Discharge and Selective Calcium Supplementation after Thyroidectomy Based on Post-Operative Day 1 Parathormone and Calcium Level: A Prospective Study. Indian J Endocrinol Metab. 2020;24:319-324. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 4] [Cited by in RCA: 7] [Article Influence: 1.2] [Reference Citation Analysis (0)] |
| 38. | Sitges-Serra A. The PGRIS and parathyroid splinting concepts for the analysis and prognosis of protracted hypoparathyroidism. Gland Surg. 2017;6:S86-S93. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 7] [Cited by in RCA: 24] [Article Influence: 2.7] [Reference Citation Analysis (0)] |
| 39. | Riordan F, Brophy C, Murphy MS, Sheahan P. Predictive value of postoperative day 1 parathyroid hormone levels for early and late hypocalcaemia after thyroidectomy. Langenbecks Arch Surg. 2022;407:1653-1658. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 12] [Reference Citation Analysis (0)] |
| 40. | Turner J, Gittoes N, Selby P; Society for Endocrinology Clinical Committee. Endocrine Society - Endocrine Emergencies Guidelines: Emergency management of acute hypocalcaemia in adult patients. Endocr Connect. 2016;5:G7-G8. [RCA] [PubMed] [DOI] [Full Text] [Full Text (PDF)] [Cited by in Crossref: 41] [Cited by in RCA: 40] [Article Influence: 4.0] [Reference Citation Analysis (0)] |
| 41. | Gandhi A, Mortensen M, Alsayed M, Targovnik JH, Vinales KL, Correa RR. Hypomagnesemia-Induced Hypocalcemia Successfully Treated With Sodium-Glucose Cotransport Inhibitor (SGLT-2i), a Case Report. J Endocr Soc. 2021;5:A201-A201. [RCA] [DOI] [Full Text] [Full Text (PDF)] [Cited by in RCA: 1] [Reference Citation Analysis (0)] |
| 42. | Khan AA, Ali DS, Bilezikian JP, Björnsdottir S, Collins MT, Cusano NE, Ebeling PR, Fuleihan GEH, Fukumoto S, Giustina A, Kaiser SM, Koch CA, Khan T, Keating P, Liu JM, Mantzoros CS, Mannstadt M, Mithal A, Perrier ND, Rayes M, Rizzoli R, Rhee Y, Rubin MR, Roszko KL, Shrayyef M, Shoback DM, Sikjær T, Siggelkow H, Sfeir J, Thakker R, Van Uum S, Winer KK, Yavuz DG, Yildiz BO, AbuAlrob H, Brandi ML. Best practice recommendations for the diagnosis and management of hypoparathyroidism. Metabolism. 2025;171:156335. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 10] [Reference Citation Analysis (0)] |
| 43. | Gronemeyer K, Fuss CT, Hermes F, Plass A, Koschker AC, Hannemann A, Völzke H, Hahner S. Renal complications in chronic hypoparathyroidism - a systematic cross-sectional assessment. Front Endocrinol (Lausanne). 2023;14:1244647. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 17] [Reference Citation Analysis (0)] |
| 44. | Riggs JE. Neurologic manifestations of electrolyte disturbances. Neurol Clin. 2002;20:227-239, vii. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 125] [Cited by in RCA: 96] [Article Influence: 4.0] [Reference Citation Analysis (0)] |
| 45. | Visenio MR, Reddy S, Sturgeon C, Elaraj DM, Ritter HE, McDow AD, Merkow RP, Bilimoria KY, Yang AD. Emergency department use after outpatient thyroidectomy across three states. Surgery. 2024;175:41-47. [RCA] [PubMed] [DOI] [Full Text] [Cited by in RCA: 3] [Reference Citation Analysis (0)] |
| 46. | Youngwirth L, Benavidez J, Sippel R, Chen H. Postoperative parathyroid hormone testing decreases symptomatic hypocalcemia and associated emergency room visits after total thyroidectomy. Surgery. 2010;148:841-4; discussion 844. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 47] [Cited by in RCA: 47] [Article Influence: 2.9] [Reference Citation Analysis (0)] |
| 47. | Avci SN, Isiktas G, Berber E. A Visual Deep Learning Model to Localize Parathyroid-Specific Autofluorescence on Near-Infrared Imaging : Localization of Parathyroid Autofluorescence with Deep Learning. Ann Surg Oncol. 2022;. [RCA] [PubMed] [DOI] [Full Text] [Cited by in Crossref: 6] [Cited by in RCA: 8] [Article Influence: 2.0] [Reference Citation Analysis (0)] |
| 48. | Ramacciotti CF, Pereyra MC, Cohen EN. [Hypoparathyroidism treated with recombinant human parathyroid hormone [rhPTH(1-84)]]. Medicina (B Aires). 2020;80:289-291. [PubMed] |