To assess the impact of parathyroid gland (PG) classification on hypoparathyroidism incidence following total thyroidectomy (TT) with central neck dissection (CND) in patients with differentiated thyroid carcinoma (DTC).

In this prospective cohort study, adult patients with DTC who underwent TT with CND between 2021 and 2023 were enrolled, with a maximum follow-up duration of 32 months. A simplified PG classification system was employed, categorizing glands into four distinct types: tightly connected, loosely connected, non-connected, and thymic. The intraoperative frequency of each PG type was recorded based on this classification. Parathyroid hormone (PTH) levels were routinely tested 1 day, 1 month, 6 months and 1 year after surgery. The association between PG classification and the incidence of postoperative hypoparathyroidism was then systematically analysed.

Among 135 patients with DTC (mean age: 48.50 ± 10.52 years; 101 women), 62 patients (45.93%) developed hypoparathyroidism on postoperative day 1 (POD1), while 14 patients (10.37%) experienced hypoparathyroidism on postoperative month 1 (POM1). All patients exhibited PTH normalization within six months, with no permanent hypoparathyroidism cases. A total of 532 PGs were identified: 264 (49.62%) were tightly connected, 150 (28.20%) loosely connected, 95 (17.86%) non-connected, and 23 (4.32%) thymic. The highest prevalence of hypoparathyroidism on POD1 was observed in patients with four tightly connected PGs (p < 0.001). Patients with four tightly connected PGs had a significantly greater incidence of hypoparathyroidism than those with none (p = 0.024). Regression analysis revealed that each additional tightly connected PG increased the risk of hypoparathyroidism by 1.38 times (p = 0.019). Tightly connected PGs demonstrated predictive value for POD1 hypoparathyroidism (AUC = 0.604, cut-off: two tightly connected glands). In contrast, thymic PGs did not provide a protective effect.

PG classification may serve as a valuable tool for surgeons in intraoperative parathyroid preservation and the prediction of postoperative hypoparathyroidism in patients with DTC. Notably, DTC patients with more than two tightly connected PGs are at an elevated risk of developing temporary hypoparathyroidism, emphasizing the importance of meticulous parathyroid preservation during surgical procedures.

Autosomal Dominant Hypocalcemia type 1 (ADH1), caused by gain-of-function variants in the calcium-sensing receptor (CASR), is characterized by a variable degree of hypocalcemia and hypercalciuria with inappropriately low PTH. The clinical spectrum is broad, ranging from being asymptomatic to presenting with severe clinical features of hypocalcemia and end-organ damage such as nephrolithiasis and intracerebral calcifications. Although the underlying pathophysiology is different, ADH1 patients are often managed as patients with 'classical' primary hypoparathyroidism, possibly leading to (exacerbation of) hypercalciuria. New treatments such as PTH analogues and calcilytics directly targeting the CASR are in the pipeline. Specific clinical guidance for treatment and monitoring of ADH1 patients is lacking. The purpose of this study is to provide a literature review on management of ADH1, including new therapies, and to formulate practice recommendations.

We searched for articles and ongoing clinical trials regarding management of ADH1.

Forty articles were included. First we review the conventional treatment of ADH1, focusing on active vitamin D, calcium supplements, thiazide diuretics, phosphorus binders and dietary recommendations. In a second part we give an overview of studies with emerging treatments in ADH1: PTH analogues (PTH1-34, rhPTH1-84, TransCon PTH and others) and calcilytics (preclinical studies and clinical trials). In a third part we discuss literature findings regarding monitoring of ADH1 patients. Finally, we formulate clinical practice recommendations.

We provide an overview of conventional and new treatments for ADH1 patients. Based on these data, we propose practical recommendations to assist clinicians in the management of ADH1 patients.

Hypoparathyroidism denotes parathyroid hormone (PTH) deficiency and impaired mineral metabolism. MBX 2109, a novel prodrug yielding a biologically active PTH peptide agonist (PTH[1-32], extended by a fatty acylated Lys33), is being developed as a long-acting, once-weekly PTH replacement therapy.

Here, we report the safety, pharmacokinetics (PK), and pharmacodynamics (PD) of MBX 2109 in healthy volunteers.

This phase 1, randomized, double-blind, placebo-controlled, multiple ascending-dose study (NCT05158335) enrolled healthy adults, who were randomly assigned 4:1 to receive MBX 2109 (200, 400, 600, and 900 μg; n = 8) or placebo (n = 2) by subcutaneous administration once weekly for 4 doses (days 1, 8, 15, and 22). The primary end point was safety and tolerability. Key secondary end points were PK and PD.

Overall, 40 participants (MBX 2109 n = 32, placebo n = 8) were randomly assigned (mean age, 43.3 years; 22.5% female). Treatment-emergent adverse events (TEAEs) occurred in 50% to 88% of MBX 2109 groups and in 25% of placebo participants. In the MBX 2109 groups, no severe or serious TEAEs were observed. Injection-site reaction was the most common treatment-related TEAE. The half-lives were 79 to 95 hours for MBX 2109 and 184 to 213 hours for the fatty-acylated biologically active PTH peptide, which showed dose- and time-dependent exposure increases.

The sustained-action PTH prodrug MBX 2109 was well tolerated with no unexpected, off-target safety issues. The long half-life and flat exposure profile of MBX 2109's biologically active PTH agonist supports once-weekly administration. MBX 2109 doses were identified for future studies.

Hypoparathyroidism is the inability of parathyroid hormone (PTH) to maintain calcium homeostasis. Patients with post-surgical hypoparathyroidism may have an increased risk of mortality; there is clinical and molecular evidence of the effects of this condition on the cardiovascular system. The aim of this study was to evaluate arterial stiffness by measuring the carotid-femoral pulse wave velocity (PWV) in post-surgical hypoparathyroidism patients. A cross-sectional study was conducted with 30 post-surgical hypoparathyroidism patients and 25 volunteers from the Endocrinology Outpatient Clinic of the Medical School. The SphygmoCor system was used to evaluate arterial stiffness by analyzing the PWV. The mean ages of the hypoparathyroidism (50.4 years) and control individuals (49.6 years) were similar. The mean PWVs were 8.7 and 7.5 m/s in the Hypoparathyroidism and Control groups, respectively (p-value = 0.084). Considering only normotensive patients, PWV was statistically higher in the Hypoparathyroidism Group (7.6 versus 6.5 m/s; p-value = 0.039). For this group, serum ionized calcium, phosphorus, and the calcium x phosphorus product levels were positively associated to PWV. Hypoparathyroidism increases arterial stiffness as assessed by PWV. Serum ionized calcium, phosphorus, and the calcium x phosphorus product are affected. A more effective investigative and therapeutic approach for patients with hypoparathyroidism can help control cardiovascular risk.

Chronic hypoparathyroidism is a rare disease associated with an impaired quality of life. Recommendations suggest frequent monitoring of quality of life, but for French-speaking people, only generic scales are available despite the fact that chronic hypoparathyroidism has specific symptoms and impact. The aim of this study was to adapt and validate the French version of Hypoparathyroid Patient Questionnaire 28 (HPQ28), an already validated tool in patients living with chronic hypoparathyroidism, available in English and German. HPQ28 was translated and back-translated from English into French. Translations were harmonized with the original author. Assessment of psychometric properties of the French version of HPQ28 was performed in the ComPaRe-Epi-Hypo e-cohort, a nationwide cohort of adult patients living with chronic hypoparathyroidism in France. Internal consistency was evaluated using Cronbach's alpha. Dimensional validity was studied using confirmatory factor analysis (CFA). Construct validity compared the answers from the French version of HPQ28 with those from the EQ-5D-5L, EQ-5D-VAS, and MYMPO2 instruments. Reliability was evaluated by the intra-class correlation coefficient (ICC) of a test-retest within a 2-wk interval. Between August 2023 and August 2024, 183 patients completed HPQ28, EQ-5D, and MYMOP2 scales. The majority (92%) of the participants were women, with a median[IQR] age of 52[44;60]. Etiology of the disease was neck surgery and genetic abnormalities in 82% and 8% of cases, respectively. Internal consistency was good (Cronbach's alpha 0.93, 95% CI 0.91 to 0.94). CFA found a unidimensional structure of the questionnaire. Construct validity showed positive correlation with MYMOP2 (r = 0.64) and negative correlations with EQ-5D VAS (r = -0.49) and EQ-5D-5L (r = -0.64) scores, as hypothesized. Reliability was adequate, with an ICC of 0.88 (95% CI 0.84 to 0.91). In conclusion, we adapted and validated HPQ28 for French-speaking patients suffering from chronic hypoparathyroidism. It can therefore now be used for both research and clinical follow-up.

Hypoparathyroidism (HPO) is characterized by deficient secretion of parathyroid hormone (PTH), leading to hypocalcemia and disrupted calcium homeostasis. Current treatments rely on calcium and vitamin D supplementation, which do not adequately mimic physiological PTH function. Cell-based therapies offer a potential solution, but optimal culture conditions to preserve the functional properties of primary parathyroid cells remain unclear. This study aims to develop primary rat parathyroid cell cultures that maintain hormone secretion and calcium-sensing abilities and to evaluate their therapeutic potential in a rat model of HPO.

An HPO model was established in rats through surgical excision of the parathyroid glands. Primary parathyroid cells were isolated from these rats and sorted by flow cytometry using epithelial cell adhesion molecule (EpCAM) and calcium-sensing receptor (CaSR) markers. Four different culture media (CM) were tested to determine optimal conditions for sustaining cell functionality. The most effective CM was supplemented with Sonic Hedgehog (Shh), Activin A, and inhibitors of epithelial-mesenchymal transition (EMT). The cultured cells were then transplanted into HPO rats, and serum calcium and PTH levels were monitored to assess therapeutic efficacy.

The optimized CM successfully preserved the hormone-secreting and calcium-sensing functions of primary parathyroid cells over multiple passages. Transplanted cells in HPO rats led to a significant increase in serum calcium and PTH levels compared to untreated controls. The restoration of these levels correlated with the alleviation of hypocalcemic symptoms, indicating effective functional integration of the transplanted cells.

Primary rat parathyroid cells cultured under optimized conditions retained essential functional properties and, upon transplantation, effectively restored calcium homeostasis in an HPO rat model. These results highlight the potential of using cultured primary parathyroid cells as a viable cell-based therapy for HPO, offering a promising alternative to conventional treatments.

to describe and compare the efficacy and safety of the main PTH treatments, namely PTH(1-84) and palopegteriparatide, for the management of hypoparathyroidism.

neither PTH (1-84) nor PTH(1-34) have been shown a clear and consistent favorable impact on the 24 h urinary calcium excretion normalization, while the positive effect on quality of life is still debated. Recently, the Food & Drug Administration and the European Medicines Agency approved palopegteriparatide as the first true replacement therapy for hypoPT management. Palopegteriparatide is a prodrug of PTH(1-34), administered once daily, and designed to provide continuous exposure to released PTH over a 24-h dosing period. According to phase II and phase III studies, palopegteriparatide seems to fill the gaps identified in existing therapies for hypoPT. Palopegteriparatide is the first real replacement therapy for the management of hypoparathyroidism and seems to fill the gaps identified in existing therapies for hypoPT.

In the CNHR study, 35% of postmenopausal women had osteoporosis by BMD or fragility fracture, and 4% had both. Three men ≥ 50 had osteoporosis by BMD or fragility fracture (33.3%; n = 3/9). This suggests that close follow-up of skeletal health is necessary in postmenopausal women, and men ≥ 50 with chronic HypoPT.

Chronic hypoparathyroidism (HypoPT) has been associated with decreased bone turnover and abnormalities in bone mineral density (BMD), microarchitecture, and strength. Current guidelines do not recommend systematic evaluation of skeletal health in patients with chronic HypoPT. Our study assessed skeletal health in pre- and postmenopausal women with chronic HypoPT and adult men.

This prospective study enrolled adults with chronic HypoPT from the Canadian National Hypoparathyroidism Registry. Clinical characteristics, bone fractures, biochemistry, and serum bone biomarkers were assessed at baseline. Skeletal health evaluation included assessments of fragility fractures, BMD at lumbar spine (LS), femoral neck (FN), total hip (TH), 1/3 radial sites, trabecular bone score (TBS), and bone biomarkers.

We present the baseline data of the patients enrolled in the registry. We analyzed a total of 101 patients: 18 men, 35 premenopausal, and 48 postmenopausal women. The mean (SD) age at the onset of HypoPT was 40.7 (16.8) years, and the average disease duration was 11.2 (8.6) years. The most common etiology was postsurgical (74.3% vs. 25.7% non-surgical). Most patients received calcium supplements (89%) and active vitamin D (80%) at baseline. No fragility fractures or low BMD were reported in premenopausal women. However, BMD at LS, FN, TH, and TBS were significantly lower in postmenopausal compared to premenopausal women.

Overall, 35% of postmenopausal women had osteoporosis by BMD or prior fragility fracture, and 4% had both. Three men ≥ 50 years had osteoporosis by BMD or fragility fracture (33.3%; n = 3/9). This study suggests that close follow-up of skeletal health is necessary in postmenopausal women with chronic HypoPT and men ≥ 50 years.

Hypoparathyroidism is characterized by inadequate parathyroid hormone (PTH) secretion or action and results in hypocalcaemia, and can lead to hyperphosphataemia and hypercalciuria. Most cases of hypoparathyroidism occur as a complication of surgery, with the remainder due to causes including autoimmune disease, genetic causes, infiltrative diseases, mineral deposition or due to abnormalities in serum levels of magnesium. Hypoparathyroidism can cause multisystem disease, with long-term complications resulting from ectopic calcification as well as renal complications with nephrocalcinosis, nephrolithiasis and renal impairment in addition to respiratory, cardiac or neurological manifestations. Conventional therapy consists of oral calcium salts and active vitamin D but it has limitations, including fluctuations in serum levels of calcium and a high pill burden, and can increase the risk of long-term complications. By contrast, PTH replacement therapy can effectively achieve normal serum levels of calcium, and lower serum levels of phosphate. The long-acting PTH analogue, palopegteriparatide, has been shown to normalize urine levels of calcium. In addition, PTH replacement therapy reduces the pill burden. Palopegteriparatide is also associated with improved quality of life in comparison to conventional therapy. This Review summarizes current recommendations regarding the pathophysiology, evaluation and management of hypoparathyroidism and also references the 2022 international hypoparathyroidism guidelines. Palopegteriparatide has now been approved as PTH replacement therapy for hypoparathyroidism. Emerging therapies will also be presented in this Review.

Hypoparathyroidism is a rare endocrine disease characterized by insufficient parathyroid hormone (PTH) secretion by the parathyroid glands, leading to hypocalcemia. In contrast to most hormone deficiencies for which hormone replacement is currently the mainstay of therapy, hypoparathyroidism has conventionally been treated with calcium supplements and active analogs of vitamin D. Although the advent of a replacement therapy with 1-34 and 1-84 PTH represented a major step in the therapeutic history of hypoparathyroidism, several new molecules and different management strategies have recently been developed.

This review investigates the therapeutic approaches currently under investigation for the treatment of hypoparathyroidism. Clinical trials results have been considered and discussed.

This study was aimed to analyze the clinical and genetic characteristics of hypoparathyroidism in children.

We performed a retrospective analysis of 74 patients diagnosed with pediatric hypoparathyroidism from 2014 to 2023, recruited in five medical centers across China. Data of basic information and clinical tests were extracted from patients' records. Whole-exome sequencing (WES), multiplex ligation-dependent probe amplification (MLPA), and chromosomal microarray analysis (CMA) were utilized to identify the genetic causes.

The results indicated a median onset age of 6.07 ± 4.82 years and a median diagnosis age of 6.91 ± 4.88 years. Of the 46 patients who underwent genetic tests, 35 were found to carry pathogenic variants related to hypoparathyroidism. Specifically, 19 cases (19/46, 41.30%) had 22q11.2 microdeletion, while other variations included AIRE (8/46, 17.39%), GATA3 (3/46, 6.52%), CaSR (2/46, 4.34%), and the rest 3 patients with mutations of TBCE, PTH and mitochondrial gene deletion respectively. Convulsions were the most common initial presentation, observed in 43 cases. The non-DGS group exhibited the lowest serum PTH levels compared to DiGeorge syndrome and gene-negative group. Among the 66 patients who underwent cranial CT or MR, 26 (26/66, 39.99%) presented with intracranial calcification.

We reported the largest cohort of childhood hypoparathyroidism with genetic diagnoses, reinforcing the view that genetic disorders account for the majority of pediatric hypoparathyroidism, with the 22q11.2 microdeletion being the most prevalent. Identifying the genetic causes of hypoparathyroidism is crucial for predicting patient outcomes, managing comorbidities, and, importantly, informing decisions regarding the potential use of emerging recombinant human PTH therapy.

This study aimed to assess the styloid process (TBSP) phenotype and to identify suggestive images of calcified atheromatous plaques (CAP) in panoramic radiographs of patients with primary hyperparathyroidism (PHPT) and post-surgical hypoparathyroidism (hypoPT). Additionally, it aimed to analyze the association between the bone mineral status of patients with parathyroid diseases and the radiographic findings.

A cross-sectional case-control study was conducted with individuals diagnosed with PHPT (n = 25) and post-surgical hypoPT (n = 25). A control group (n = 50) comprised individuals without parathyroid gland disorders. Panoramic radiographs were utilized for both quantitative (length) and qualitative (mineralization patterns) evaluation of the TBSP, as well as for assessing the prevalence of CAP.

The frequency of TBSP exceeding 30 mm was significantly higher in the PHPT and post-surgical hypoPT groups compared to the control group. CAP occurred more frequently in the PHPT group. Cases of low bone mineral density (BMD) were associated with PHPT. In the PHPT group, low BMD was linked to an increased average TBSP length (p = 0.025) and a higher frequency of elongated TBSP (p = 0.022). Multivariate analysis revealed an inverse relationship between the T-score of the femoral neck and TBSP length in the PHPT group (p = 0.028).

Compared to the control group, individuals with PHPT and post-surgical hypoPT showed distinct imaging findings related to TBSP and CAP. Individuals with PHPT and low BMD showed a higher frequency of elongated TBSP.

Medullary thyroid cancer (MTC) is a rare subtype of thyroid cancer originating from parafollicular C-cells of the thyroid. Tyrosine kinase inhibitors are used to treat patients with advanced MTC. Selpercatinib is a highly selective RET inhibitor used in the treatment of advanced RET-mutated MTC, having shown higher potency and fewer side effects compared to multikinase inhibitors in clinical trials. As a relatively new drug, its toxicity profile continues to be characterised. This report describes a case of severe acute hypocalcaemia in a 64-year-old male with advanced MTC treated with selpercatinib. The patient, who had stable hypoparathyroidism, experienced acute hypocalcaemia (corrected calcium 1.4 mmol/L) 2 weeks after initiating selpercatinib, requiring hospitalisation for calcium supplementation and monitoring. Selpercatinib was temporarily withheld and later reintroduced at a lower dose, successfully preventing recurrence of hypocalcaemia. Investigations excluded other common or important causes of hypocalcaemia, which led us to conclude that this could be a drug-related adverse event. This case highlights the need for careful monitoring of electrolyte disturbances in patients on selpercatinib, particularly those with pre-existing hypoparathyroidism. Although rare, the development of hypocalcaemia with RET inhibitors may necessitate dose interruptions and adjustments. Our experience has also illustrated that re-challenge with selpercatinib is feasible with appropriate management strategies.

Fatigue is a common symptom encountered in clinical practice, often posing a diagnostic challenge due to its myriad underlying causes. A comprehensive clinical history can serve as a valuable guide in such diagnostic dilemmas. A man in his 30s presented with a history of intermittent fatigue. The history of premature cataract surgery prompted an investigation for hypocalcaemia. Subsequent evaluation revealed hypocalcaemia, hyperphosphatemia and low serum parathyroid hormone. Additionally, elevated creatine kinase and lactate dehydrogenase levels were noted. Treatment with calcium and alfacalcidol yielded a favourable response. This case underscores the significance of revisiting clinical history and considering hypocalcaemia as a potential aetiology in cases of unexplained fatigue. It also emphasises the potential for overlooking the diagnosis due to the inconspicuous nature of hypocalcaemic myopathy in idiopathic hypoparathyroidism.

This study presents the cases of two women who developed severe permanent hypoparathyroidism after neck surgery for papillary thyroid cancer and underwent parathyroid allotransplantation. Despite taking high doses of calcium and calcitriol supplements, the patients experienced persistent hypocalcemic symptoms. Fresh parathyroid tissue was removed and prepared from two patients with hyperparathyroidism secondary to end-stage kidney disease and was implanted in the non-dominant forearm of the recipients. Donors and recipients were ABO-compatible, and immunological screening was performed only in Case 2 (HLA typing, panel reactive antibody, and crossmatch tests). A short-term immunosuppressive regimen was adopted, consisting of 3 days of methylprednisolone followed by 7 days of prednisone. In Case 1, oral supplementation decreased to half of the initial dose 1 month after transplantation and to one-fifth at the end of a 12-month follow-up period. In Case 2, intravenous calcium was discontinued 1-week post-transplantation, with no need for its use during the 12-month follow-up period. Serum parathyroid hormone levels did not increase and remained undetectable in both cases. In contrast, serum calcium levels increased significantly, and both patients experienced relief from hypocalcemic symptoms. Parathyroid allotransplantation can be an effective and safe treatment for PH and should be considered in severe cases. Nevertheless, formal recommendations depend on additional studies and validated protocols.

HDR syndrome is an autosomal dominant disorder characterized by hypoparathyroidism (H), deafness (D), and renal dysplasia (R) caused by genetic variants of the GATA3 gene. We present the case of a 38-year-old Japanese man with HDR syndrome who exhibited hypoparathyroidism, sensorineural deafness, renal dysfunction, severe symptomatic hypocalcemia with Chvostek's and Trousseau's signs, and QT prolongation on electrocardiography. He had a family history of deafness and hypocalcemia. Genetic testing revealed a novel GATA3 gene variant at exon 2 (c.48delC), which induces a frameshift resulting in termination at codon 178, causing HDR syndrome. We summarized 45 Japanese cases of HDR syndrome with regard to the mode of onset (familial or sporadic) and the age at diagnosis. In addition, we summarized all previous cases of HDR syndrome with GATA3 gene variants. Mapping of previously reported genetic variants in HDR syndrome revealed that most missense variants were observed at exons 4 and 5 regions in the GATA3 gene. These two regions contain zinc finger domains, demonstrating their functional importance in GATA3 transcription. This review of literature provides a useful reference for diagnosing HDR syndrome and predicting the related future manifestations.

HDR syndrome is a rare disease characterized by hypoparathyroidism, deafness, and renal dysplasia. An autosomal dominant disease caused by heterozygous pathogenic GATA3 variants, the penetrance of each associated condition is variable. Literature reviews have provided some answers, but many questions remain, in particular what the relationship is between genotype and phenotype. The current study examines 28 patients with HDR syndrome combined with an exhaustive review of the literature. Some conditions such as hearing loss are almost always present, while others described as rare initially, do not seem to be so rare after all (genital malformations and basal ganglia calcifications). By modeling pathogenic GATA3 variants found in HDR syndrome, we found that missense variations appear to always be located in the same area (close to the two Zinc Finger domain). We describe new pathogenic GATA3 variants, of which some seem to always be associated with certain conditions. Many audiograms were studied to establish a typical audiometric profile associated with a phenotype in HDR. As mentioned in the literature, hearing function should always be assessed as early as possible and follow up of patients with HDR syndrome should include monitoring of parathyroid function and vesicoureteral reflux in order to prevent complications.

Recently, endoscope has been widely used in thyroid surgery and gasless insufflation transaxillary endoscopic thyroidectomy (GTET) has been the mainstay of thyroid surgery. Parathyroid gland (PG) damage is a common complication of thyroid surgery. Therefore, the aim of this study was to investigate the effect of GTET on hypoparathyroidism (HPT) in patients with thyroid cancer.

According to the surgical approach, the patients were divided into a GTET group and a conventional open thyroidectomy (COT) group. Univariate analysis and logistic regression were used to identify factors associated with PG injury. The odds ratio (OR) and 95% confidence interval (CI) for each independent variable were calculated.

A retrospective analysis was conducted on 405 patients diagnosed with papillary thyroid cancer (PTC). A total of 51 patients experienced PG injury, including 7 cases (5%) of GTET group and 44 cases (16.5%) of COT group (P<0.001). Among them, the incidence of GTET group injury with one PG was 50.4%, two were 2.9%, and COT group were 59.8% and 7.9%, respectively (P=0.006). Univariate and multivariate analysis revealed that GTET was a protective factor for PG injury (OR, 0.251; 95% CI, 0.110-0.576; P=0.001), while Hashimoto's thyroiditis (HT) was identified as a risk factor for PG injury (OR, 2.722; 95% CI, 1.114-6.654; P=0.02).

GTET reduces the incidence of PG injury and nerve injury, when PTC is combined with HT, it increases the risk of PG injury.

Hypoparathyroidism is a rare disease that markedly reduces bone remodeling, leading to increased bone mineral density and changes in bone microarchitecture. However, it is currently unclear how these changes affect fracture risk. In this study, we investigated bone mass by dual-energy x-ray absorptiometry, the occurrence of morphometric vertebral fractures, and bone microarchitecture by assessing trabecular bone score in women with postsurgical hypoparathyroidism. We included 67 women with hypoparathyroidism aged 52.9 ± 12.3 years and 63 age- and body mass index-matched controls, which were assessed for femoral and lumbar spine bone mineral density, trabecular bone score, and vertebral fractures by dual-energy x-ray absorptiometry. Women with hypoparathyroidism had significantly higher bone mineral density at the lumbar spine, femoral neck, and total hip compared with controls despite similar trabecular bone score values. Vertebral fracture assessment indicated that two women with hypoparathyroidism presented vertebral fractures, both aged over 65 years. Conversely, no vertebral fractures were detected in control women. In a multivariate linear regression model, we found that older age, diabetes, and lower lumbar spine mineral density were significant predictors of lower trabecular bone score values. Our findings indicate that vertebral fractures are not common among women with postsurgical hypoparathyroidism aged under 65 years. Moreover, trabecular bone score values were similar in women with hypoparathyroidism and age-matched controls and were associated with traditional risk factors for fractures, such as older age, type 2 diabetes, and lower spine bone mineral density. LAY SUMMARY: Chronic parathyroid hormone deficiency decreases bone turnover and modifies skeletal properties, although the impact of these changes on fracture risk remains unclear. We studied 67 women with postsurgical hypoparathyroidism and 63 age and body mass index-matched healthy controls and found that bone mineral density is increased in women with hypoparathyroidism despite similar trabecular bone score values and a low occurrence of morphometric vertebral fractures. This suggests that the low bone turnover in hypoparathyroidism increases bone mass, but this is not accompanied by improved bone microarchitecture, indicating that trabecular bone score may be a valuable tool to complement the assessment of skeletal health and the risk of fractures in this condition.

Anorexia nervosa (AN) is life-threatening because of many physical complications, hence a quantitative indicator for early therapeutic intervention through hospitalization is needed. Here, we compared the demographics of 21 patients with AN who required intensive treatment in the internal medicine ward and those of 61 patients with AN who directly admitted to the psychiatric ward. We developed a risk score for severe physical complications in patients with AN, by using six items with significant differences between two groups; body mass index, blood urea nitrogen, corrected calcium, albumin, aspartate transaminase, and C-reactive protein (area under the curve = 0.824).

Endocrine regulation of bone metabolisms is the focus of the "Skeletal Endocrinology" series of meetings.

To report on the outcome of the discussion on the role of vitamin D/PTH axis in endocrine osteopathies held during the 10th Skeletal Endocrinology Meeting which took place in Stresa (Italy) in March 2023.

Vitamin D/PTH axis has relevant influence on several outcomes in the general population and in patients affected by endocrinopathies such as hypoparathyroidism and secreting pituitary adenomas.

Assessing the status of the vitamin D/PTH axis and using vitamin D and PTH as therapeutic agents is mandatory in several endocrine-related bone metabolic conditions.

Hypoparathyroidism is a rare disorder characterized by a deficiency in PTH resulting in hypocalcemia, hyperphosphatemia, and hypercalciuria. Eneboparatide is an investigational peptide agonist of the PTH1 receptor for the treatment of chronic hypoparathyroidism (HP).

To evaluate the efficacy, safety, and tolerability of eneboparatide in HP patients.

Open-label, phase 2 study.

Twenty-eight patients (21 women, 7 men), mean age (range): 58 years (28-72), with HP were enrolled into 2 consecutive cohorts (C1, n = 12 and C2, n = 16).

Following an optimization period, daily subcutaneous injections of eneboparatide were administered for 3 months at a 20 µg/day (C1) or 10 µg/day (C2) starting dose. Conventional therapy was progressively removed, and eneboparatide could be titrated up to 60 µg (C1) or 80 µg (C2).

Proportion of patients achieving independence from conventional therapy, albumin-adjusted serum calcium (ADsCa), 24-h urine calcium (uCa), serum bone turnover markers (serum carboxy-terminal telopeptide of type I collagen and procollagen 1 intact N-terminal propeptide), bone mineral density (BMD), and adverse events (AEs).

After 3 months, ≥ 88% of patients achieved independence from conventional therapy while mean ADsCa was maintained within target range (7.8-9 mg/dL). Eneboparatide induced a rapid and sustained reduction of mean 24-hour uCa, even among patients with hypercalciuria. Bone turnover markers slightly increased, and BMD remained unchanged, consistent with progressive resumption of physiologic bone turnover. Eneboparatide was well tolerated with no serious AEs.

Eneboparatide allowed independence from conventional therapy and maintenance of serum calcium within a target range while normalizing uCa excretion and producing a balanced resumption of bone turnover.

Differentiation of human embryonic stem cells (hESCs) into human embryonic stem cells-derived parathyroid-like cells (hESC-PT) has clinical significance in providing new therapies for congenital and acquired parathyroid insufficiency conditions. However, a highly reproducible, well-documented method for parathyroid differentiation remains unavailable. By imitating the natural process of parathyroid embryonic development, we proposed a new hypothesis about the in vitro differentiation of parathyroid-like cells. Transcriptome, differentiation marker protein detection and parathyroid hormone (PTH) secretion assays were performed after the completion of differentiation. To optimize the differentiation protocol and further improve the differentiation rate, we designed glial cells missing transcription factor 2 (GCM2) overexpression lentivirus transfection assays and constructed hESCs-derived parathyroid organoids. The new protocol enabled hESCs to differentiate into hESC-PT. HESC-PT cells expressed PTH, GCM2 and CaSR proteins, low extracellular calcium culture could stimulate hESC-PT cells to secrete PTH. hESC-PT cells overexpressing GCM2 protein secreted PTH earlier than their counterpart hESC-PT cells. Compared with the two-dimensional cell culture environment, hESCs-derived parathyroid organoids secreted more PTH. Both GCM2 lentiviral transfection and three-dimensional cultures could make hESC-PT cells functionally close to human parathyroid cells. Our study demonstrated that hESCs could differentiate into hESC-PT in vitro, which paves the road for applying the technology to treat hypoparathyroidism and introduces new approaches in the field of regenerative medicine.

Patients with the 22q11.2 deletion syndrome (22q11DS) frequently display cardiological and psychiatric diseases, but are also at increased risk for endocrine manifestations. The aim of this study was to evaluate the screening, prevalence, and management of hypoparathyroidism and thyroid disease in patients with 22q11DS, to evaluate the metabolic profile, and to compare these results with current literature and guidelines.

We performed a retrospective study of patients with genetically confirmed 22q11DS, followed at the center for human genetics of the University Hospitals Leuven, resulting in a cohort of 75 patients. Medical history, medication, and laboratory results concerning hypoparathyroidism, thyroid dysfunction, and the metabolic profile were collected.

Of the total cohort, 26 patients (35%) had at least one hypocalcaemic episode. During hypocalcaemia, parathyroid hormone (PTH) was measured in only 12 patients with 11 having normal or low PTH, confirming a diagnosis of hypoparathyroidism. Recurrent episodes of hypocalcaemia occurred in seventeen patients (23%). Adherence to the guidelines was low, with 13% of patients having a yearly serum calcium evaluation, 12% receiving daily calcium supplements, and 20% receiving non-active vitamin D. Hypothyroidism was present in 31 patients (44%) and hyperthyroidism in 6 patients (8%). Information on body mass index (BMI) was available in 52 patients (69%), of which 38% were obese (BMI ≥ 30 kg/m2).

Hypoparathyroidism, hypothyroidism, and obesity are common endocrine manifestations in patients with 22q11DS but are probably underdiagnosed and undertreated, indicating the need for multidisciplinary follow-up including an endocrinologist.

Iatrogenic hypoparathyroidism is a common cause of postthyroidectomy hypocalcaemia. It has varying incidence rates after neck surgery in Saudi Arabia, ranging from 0.07% to 65.30%. Hypoparathyroidism can manifest with a spectrum of symptoms, ranging from mild to severe and life-threatening. This study aimed to assess the rate and predictors of iatrogenic hypoparathyroidism after thyroid surgery and its natural course.

This retrospective cohort study used a data collection form to extract patient information from the electronic healthcare system (Best-Care) for patients treated from 2017 to 2022. Patients' demographics, surgical specifics and biochemical profiles were recorded for subsequent analysis.

Among the 343 patients who underwent thyroidectomy, 130 (37.9%) developed hypoparathyroidism, primarily within the first day after surgery. Calcium or vitamin D supplementation before surgery did not significantly influence hypoparathyroidism development. Notably, extensive combined lymph node dissection was significantly associated with postoperative hypoparathyroidism development (p = 0.0004). More patients who underwent central and lateral lymph node dissection (n = 19, 79.17%) developed hypoparathyroidism than patients who underwent central (n = 18, 40.91%) or lateral (n = 8, 38.10%) dissection alone. Permanent hypoparathyroidism was observed in 40 patients (11.66%).

This study revealed a high incidence of iatrogenic hypoparathyroidism and high rates of permanent hypoparathyroidism. Further research is warranted to better comprehend the risk factors and optimise management strategies for iatrogenic hypoparathyroidism. Overall, our findings emphasise the need for vigilant monitoring and effective management of patients undergoing thyroidectomy and the significance of postoperative replacement therapies.

Thyroid surgery often results in ischemia-reperfusion injury (IRI) to the parathyroid glands, yet the mechanisms underlying this and how to ameliorate IRI remain incompletely explored. Our study identifies a polyphenolic herbal extract-gallic acid (GA)-with antioxidative properties against IRI. Through flow cytometry and CCK8 assays, we investigate the protective effects of GA pretreatment on a parathyroid IRI model and decode its potential mechanisms via RNA-seq and bioinformatics analysis. Results reveal increased apoptosis, pronounced G1 phase arrest, and significantly reduced cell proliferation in the hypoxia/reoxygenation group compared to the hypoxia group, which GA pretreatment mitigates. RNA-seq and bioinformatics analysis indicate GA's modulation of various signaling pathways, including IL-17, AMPK, MAPK, transient receptor potential channels, cAMP, and Rap1. In summary, GA pretreatment demonstrates potential in protecting parathyroid cells from IRI by influencing various genes and signaling pathways. These findings offer a promising therapeutic strategy for hypoparathyroidism treatment.

Chronic pancreatitis (CP) is a progressive inflammatory disease with an increasing global prevalence. In recent years, a strong association between CP and metabolic bone diseases (MBDs), especially osteoporosis, has been identified, attracting significant attention in the research field. Epidemiological data suggest a rising trend in the incidence of MBDs among CP patients. Notably, recent studies have highlighted a profound interplay between CP and altered nutritional and immune profiles, offering insights into its linkage with MBDs. At the molecular level, CP introduces a series of biochemical disturbances that compromise bone homeostasis. One critical observation is the disrupted metabolism of vitamin D and vitamin K, both essential micronutrients for maintaining bone integrity, in CP patients. In this review, we provide physio-pathological perspectives on the development and mechanisms of CP-related MBDs. We also outline some of the latest therapeutic strategies for treating patients with CP-associated MBDs, including stem cell transplantation, monoclonal antibodies, and probiotic therapy. In summary, CP-associated MBDs represent a rising medical challenge, involving multiple tissues and organs, complex disease mechanisms, and diverse treatment approaches. More in-depth studies are required to understand the complex interplay between CP and MBDs to facilitate the development of more specific and effective therapeutic approaches.

Syndromic obesity refers to obesity occurring with additional clinical findings, such as intellectual disability/developmental delay, dysmorphic features, and congenital malformations. PURPOSE OF REVIEW: To present a narrative review regarding the genetic etiology, clinical description, and molecular diagnosis of syndromic obesity, which is a rare condition with high phenotypic variability and genetic heterogeneity. The following syndromes are presented in this review: Prader-Willi, Bardet-Biedl, Pseudohypoparathyroidism, Alström, Smith-Magenis, Cohen, Temple, 1p36 deletion, 16p11.2 microdeletion, Kleefstra, SIM1-related, Börjeson-Forssman-Lehmann, WAGRO, Carpenter, MORM, and MYT1L-related syndromes. RECENT FINDINGS: There are three main groups of mechanisms for syndromic obesity: imprinting, transcriptional activity regulation, and cellular cilia function. For molecular diagnostic, methods of genome-wide investigation should be prioritized over sequencing of panels of syndromic obesity genes. In addition, we present novel syndromic conditions that need further delineation, but evidences suggest they have a higher frequency of obesity. The etiology of syndromic obesity tends to be linked to disrupted neurodevelopment (central) and is associated with a diversity of genes and biological pathways. In the genetic investigation of individuals with syndromic obesity, the possibility that the etiology of the syndromic condition is independent of obesity should be considered. The accurate genetic diagnosis impacts medical management, treatment, and prognosis, and allows proper genetic counseling.

Hypoparathyroidism is characterized by chronic hypocalcemia with low or abnormal parathyroid hormone levels. Thyroid surgery remains a predominant cause of hypoparathyroidism, often preventable by partial thyroidectomy. Although hypoparathyroidism can impair quality of life (QOL), data remain limited for Latin America. We aimed to characterize clinical manifestations and QOL in patients with postsurgical hypoparathyroidism.

This case-control study included patients (>18 years) who underwent total thyroidectomy (TT) for differentiated thyroid cancer (DTC) with postsurgical hypoparathyroidism (Group 1, Cases) and those with DTC who underwent TT without postsurgical hypoparathyroidism (Group 2, Controls). Clinical records were collected, and the SF-36v2 QOL survey and a structured symptom survey were applied. A logistic multivariate regression analysis was performed.

This study included 106 subjects (Group 1, N=41; Group 2, N=65). Group 1 patients were younger, had a higher frequency of lymph node resection, and more frequently received Ι-131 than Group 2 patients (p<0.05). In the SF-36v2 survey, Group 1 had fewer physical-functioning scores (odds ratio, 3.8; 95% confidence interval, 1.2-11.7) and lower scores in mental and physical components than Group 2 and national records. Commonly reported symptoms include paresthesia, daily fatigue, and memory alterations. Treatment adherence rates were 56% and 71% for calcium and calcitriol, respectively. Furthermore, 24% of patients experienced one or more hypoparathyroidism drug-related adverse effects.

Patients with postsurgical hypoparathyroidism had an impaired QOL, a high frequency of disease-associated symptoms, and limited treatment adherence. These results should be considered when deciding the best surgical alternative for DTC.

Hypoparathyroidism (HP) is a rare endocrine disease commonly caused by the removal or damage of parathyroid glands during surgery and resulting in transient (tHP) or chronic (cHP) disease. cHP is associated with multiple complications and comorbid conditions; however, the economic burden has not been well characterized. The objective of this study was to evaluate the healthcare resource utilization (HCRU) and costs associated with post-surgical cHP, using tHP as a reference.

This analysis of a US claims database included patients with both an insurance claim for HP and thyroid/neck surgery between October 2014 and December 2019. cHP was defined as an HP claim ≥ 6 months following surgery and tHP was defined as only one HP claim < 6 months following surgery. The cHP index date was the first HP diagnosis claim following their qualifying surgery claim, whereas the tHP index date was the last HP diagnosis claim following the qualifying surgery claim. Patients were continuously enrolled at least 1 year pre- and post-index. Patients' demographic and clinical characteristics, all-cause HCRU, and costs were descriptively analyzed. Total all-cause costs were calculated as the sum of payments for hospitalizations, emergency department, office/clinic visits, and pharmacy.

A total of 1,406 cHP and 773 tHP patients met inclusion criteria. The average age (52.1 years cHP, 53.5 years tHP) and representation of females (83.2% cHP, 81.2% tHP) were similar for both groups. Neck dissection surgery was more prevalent in cHP patients (23.6%) than tHP patients (5.3%). During the 1-2 year follow-up period, cHP patients had a higher prevalence of inpatient admissions (17.4%), and emergency visits (26.0%) than the reference group -tHP patients (14.4% and 21.4% respectively). Among those with a hospitalization, the average number of hospitalizations was 1.5-fold higher for cHP patients. cHP patients also saw more specialists, including endocrinologists (28.7% cHP, 15.8% tHP), cardiologists (16.7% cHP, 9.7% tHP), and nephrologists (4.6% cHP, 3.3% tHP).

This study demonstrates the increased healthcare burden of cHP on the healthcare system in contrast to patients with tHP. Effective treatment options are needed to minimize the additional resources utilized by patients whose HP becomes chronic.

This study aimed to evaluate the cardiovascular risk of patients with post-surgical hypoparathyroidism through coronary calcium score (CACS) evaluation andcardiovascular risk calculators.

Patients with post-surgical hypoparathyroidism (HG = 29) were compared to a control group (CG = 29), matched by sex and age. Demographic and clinical data were captured by a questionnaire or patient files. Both groups performed a thoracic-computed tomography to evaluate the CACS and the cardiovascular risk was calculated by two risk calculators.

In the HG, the supplementation of calcium varied between 500 to 2,000 mg/day and the mean calcitriol was 0.5 ± 0.29 mcg/day. The mean serum calcium and phosphorus were 8.32 ± 0.68 and 4.92 ± 0.87 mg/dL, respectively, and in the range recommended for hypoparathyroidism. The Brazilian Society of Cardiology's risk calculator showed a difference among groups, with no patient in the HG with low risk, but the CACS was similar. A positive CACS in the HG was associated with obesity and high BMI but not with calcium and/or vitamin D supplementation.

In conclusion, patients with hypoparathyroidism did not show increased CACS, and it was not related to supplementation.

Patients with hypoparathyroidism (hypoPT) have low bone turnover and high bone mineral density (BMD). However, data on fracture risk are conflicting. The objectives of this study were: 1. To describe clinical/biochemical characteristics of hypoPT patients followed at a single medical center. 2. To identify postsurgical hypoPT patients and investigate their fracture rate compared with gender/age-matched post-surgical normocalcemic patients.

Retrospective analysis of patient's medical records treated at the tertiary medical center in 2010-2021 identified by computerized medical database search.

The cohort included 133 patients (91% women, mean age 64 ± 13 years) of whom 105 (79%) had post-thyroidectomy hypoparathyroidism and the remainder had an autoimmune/idiopathic/other etiology. Mean follow-up time was 21 ± 12 and 27 ± 12 years, respectively. The control group included 142 post-thyroidectomy patients without hypoparathyroidism. Patients in the postsurgical hypoparathyroidism group were older and had higher calcium and PTH levels at diagnosis than the non-surgical hypoPT patients. Comparing the postsurgical hypoPT and postsurgical normocalcemic control patients revealed a significantly higher BMD in the hypoPT group. Yet, fracture rates were 31% in the postsurgical hypoparathyroidism group and 21% in the control group (P = 0.1) over a similar median follow-up period (17 and 18.4 years, respectively). In both groups the most common fracture site was the spine (50% and 70%, respectively; p = 0.33), mainly nonclinical morphometric fractures. Higher phosphorus blood level was associated with increased fracture risk.

The relatively high BMD in patients with postsurgical hypoparathyroidism is not associated with lower fracture risk. Silent morphometric fractures are quite common in this group of patients.

Osteoporosis, a metabolic bone disease characterized by low bone mineral density and deterioration of bone microarchitecture, has led to a high risk of fatal osteoporotic fractures worldwide. Accumulating evidence has revealed that sexual dimorphism is a notable feature of osteoporosis, with sex-specific differences in epidemiology and pathogenesis. Specifically, females are more susceptible than males to osteoporosis, while males are more prone to disability or death from the disease. To date, sex chromosome abnormalities and steroid hormones have been proven to contribute greatly to sexual dimorphism in osteoporosis by regulating the functions of bone cells. Understanding the sex-specific differences in osteoporosis and its related complications is essential for improving treatment strategies tailored to women and men. This literature review focuses on the mechanisms underlying sexual dimorphism in osteoporosis, mainly in a population of aging patients, chronic glucocorticoid administration, and diabetes. Moreover, we highlight the implications of sexual dimorphism for developing therapeutics and preventive strategies and screening approaches tailored to women and men. Additionally, the challenges in translating bench research to bedside treatments and future directions to overcome these obstacles will be discussed.

The triad of hypercalcemia, metabolic alkalosis, and acute kidney injury associated with ingesting high doses of calcium and absorbable bases characterizes the calcium-alkali syndrome. Clinical Case. We report the case of a patient with postthyroidectomy hypoparathyroidism 15 years ago due to differentiated thyroid cancer who presented with severe hypercalcemia. He had adequate control of calcemia for many years on treatment with calcitriol and calcium carbonate and hypertension treated with amlodipine, losartan, and hydrochlorothiazide. After a period of loss to follow-up, he suddenly presents with severe hypercalcemia, metabolic alkalosis, and loss of renal function. Upon hydration and withdrawal of calcitriol and calcium replacements, hypercalcemia resolved. The etiological investigation identified no granulomatous or neoplastic diseases, but an aldosterone-producing adrenal incidentaloma was found. The cause of hypercalcemia in this patient was calcium-alkali syndrome due to calcium carbonate replacement potentiated by hydrochlorothiazide and primary aldosteronism. Six months after the hospitalization and suspension of calcium and vitamin D, the patient returned to hypocalcemia, reinforcing the diagnosis.

Although seldom described, the calcium-alkali syndrome is an expected complication for individuals with postoperative hypoparathyroidism, as they require lifelong calcium and vitamin D supplementation. This case also shows the importance of hydrochlorothiazide use and primary aldosteronism as possible triggers of life-threatening hypercalcemia.

A previous nationwide study from Sweden showed that the rate of permanent hypoparathyroidism is high and under-rated in the Swedish Quality Register. This retrospective population-based study aimed to validate the rate and diagnosis of permanent hypoparathyroidism found in the previous study. A secondary aim was to assess the relationship between the rate of low parathyroid hormone (PTH) levels within 24 h after surgery and the rate of permanent hypoparathyroidism.

All patients who underwent total thyroidectomy from 2005 to 2015 in a region of Sweden were included. Data were retrieved from local health records, the National Patient Registry, the Swedish Prescribed Drug Registry, and the Swedish Quality Register. A strict definition of permanent hypoparathyroidism was used, including biochemical data and attempts to stop the treatment.

A total of 1636 patients were included. Altogether, 143 patients (8.7 per cent) developed permanent hypoparathyroidism. Of these, 102 (6.2 per cent) had definitive permanent hypoparathyroidism, whereas 41 (2.5 per cent) had possible permanent hypoparathyroidism, because attempts to stop the treatment were lacking (28) or patients were lost to follow-up (13). The agreement between the Swedish Quality Register and the chart review was 29.3 per cent. A proportion of 23.2 per cent with a PTH level below the reference value corresponded to a 6.7 per cent rate of permanent hypoparathyroidism.

The risk of permanent hypoparathyroidism after total thyroidectomy is high. Some patients are overtreated because attempts to stop the treatment are lacking. Quality registers might underestimate the risk of permanent hypoparathyroidism. Approximately one-quarter of all patients with low PTH levels immediately after surgery developed permanent hypoparathyroidism.

Hypoparathyroidism is a relatively rare endocrine disorder defined as inadequate parathyroid hormone (PTH) secretion leading to a clinical syndrome characterized by hyperphosphatemia and hypocalcemia. This condition has high morbidity; patients present with a heterogeneous range of emotional, mental, and physical symptoms. We present our experience with PTH transplantation, using parathyroid glands surgically removed in the setting of secondary hyperparathyroidism, with a description of the clinical course, immunosuppressive management, and surgical technique.

Between 2017 and 2021, 3 patients underwent parathyroid allotransplantation at the University of Illinois at Chicago. The 2 outcomes of interest were (1) symptomatic relief and improvement in calcium levels and (2) time to graft failure, defined as the presence of undetectable PTH levels.

All 3 patients experienced dramatic improvement in their debilitating symptoms, even though 2 patients required repeated PTH transplantation procedures. One patient had a remarkable course with symptom resolution, normalization of PTH levels, and a great reduction in calcium supplementation.

The use of hyperplastic glands from patients with secondary hyperparathyroidism undergoing 4-gland parathyroidectomy with autotransplantation represents an important source. However, a uniform definition of graft viability and prospective studies with long follow-ups are needed to address how much parathyroid tissue is optimally transplanted and the need for immunosuppression. Most patients affected by hypoparathyroidism are successfully managed by medical treatment; however, some do not respond to therapy and present debilitating symptoms related to hypocalcemia. This subgroup may benefit from parathyroid allotransplantation. Our 3 patients had remarkable improvement in their symptoms with the adoption of hyperplastic glands. Two out of 3 patients required multiple procedures to sustain symptom control.

With a demonstrated association between adiposity and parathyroid hormone (PTH) levels, we hypothesized that patients with a higher body mass index (BMI) would have lower rates of postoperative hypoparathyroidism following total thyroidectomy.

retrospective review of patients undergoing total thyroidectomy from 2015 to 2021. Demographics, BMI, surgical indications, and laboratory data including pre- and postoperative PTH values were examined.

Of the 352 patients with complete clinicopathologic data, most were female (n = 272, 77.3%) with an average age of 42.7 (SD+/-19.4). Obese (BMI 30-39.99) was most common BMI group (n = 108, 30.8%), with 11.7% (n = 41) morbidly obese (BMI > 40). Morbidly obese patients had significantly higher postoperative PTH levels than BMI < 18.5 (46.0 vs 19.3 pg/mL, P = .004). Patient race was significantly associated with pre- and postoperative PTH (P = .03, P = .004.) On multivariable analysis, preoperative PTH, race, and BMI were independent predictors of higher postoperative PTH (P < .05 for all).

Patients with higher BMI and non-white race have relative protection from postoperative hypoparathyroidism.