Association of Obesity on Rates of Multiglandular Disease in Primary Hyperparathyroidism: A Cohort Study

Justin Bauzon; Judy Jin; Salem Noureldine; Sarah Ziqi Wang; Tim Beck; Gustavo Romero-Velez

doi:10.1016/j.jss.2024.12.006

Association of Obesity on Rates of Multiglandular Disease in Primary Hyperparathyroidism: A Cohort Study

J Surg Res. 2024 Dec 28:305:349-355. doi: 10.1016/j.jss.2024.12.006. Online ahead of print.

Authors

Justin Bauzon¹, Judy Jin¹, Salem Noureldine², Sarah Ziqi Wang¹, Tim Beck¹, Gustavo Romero-Velez³

Affiliations

¹ Cleveland Clinic Foundation, Department of Endocrine Surgery, Cleveland, Ohio.
² Section of Endocrine Surgery, Department of Surgery, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia.
³ Cleveland Clinic Foundation, Department of Endocrine Surgery, Cleveland, Ohio. Electronic address: [email protected].

PMID: 39733472
DOI: 10.1016/j.jss.2024.12.006

Abstract

Introduction: Primary hyperparathyroidism (PHPT) is more prevalent in populations with obesity. Obesity-related vitamin D deficiency may affect rates of multigland parathyroid disease, but this relationship is less clear. We aimed to assess the relationship between obesity and the rate of multigland disease in patients with PHPT.

Methods: Patients who underwent parathyroidectomy from 2015 to 2021 for sporadic PHPT at a tertiary center were retrospectively analyzed. The primary outcome was rates of single-gland versus four-gland parathyroid hyperplasia in relation to obesity. Secondary outcomes included analysis of serum biochemistries [parathyroid hormone (PTH), calcium, 25(OH) vitamin D (25OHD)] before and 6 mo postoperatively based on obesity classification: no obesity (body mass index [BMI] <30 kg/m²), Class 1 (BMI 30-34.9 kg/m²), Class 2 (BMI 35-39.9 kg/m²), Class 3 (BMI ≥40 kg/m²). Statistical analysis was performed using Chi-square, Mann-Whitney U, and Kruskal-Wallis tests where applicable.

Results: Of 2634 patients who underwent parathyroidectomy, a total of 1173 had obesity. Obesity did not confer any differences in the proportion of four-gland versus single-gland hyperplasia (25 versus 26%, P = 0.79). Compared to patients without obesity, preoperative PTH levels were higher in patients with Class 2 [86 (interquartile range [IQR] 66-118) versus 95 (IQR 70-137) pg/mL, P = 0.001] and Class 3 [86 (IQR 66-118) versus 104 (76-150) pg/mL, P < 0.001] obesity. Conversely, 25OHD before surgery was lower across obesity subclasses [no obesity: 36.0 (25.3-49.3), Class 1: 32.5 (24.0-46.0), Class 2: 32.9 (22.0-44.6), Class 3: 31.7 (20.4-45.0) ng/mL, P < 0.001]. Postoperative PTH and 25OHD improved in all cohorts. No calcium-related differences were found among patients based on obesity classification.

Conclusions: Obesity is not associated with an increased rate of four-gland hyperplasia in patients with PHPT, and therefore should not alter surgical management. The levels of 25OHD in patients with obesity should be monitored for vitamin deficiency preoperatively and postoperatively.

Keywords: Four-gland parathyroid hyperplasia; Hyperparathyroidism; Morbid obesity; Multiglandular disease; Obesity; Parathyroid adenoma; Primary hyperparathyroidism.