ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 GP16 | DOI: 10.1530/endoabs.63.GP16

The effect of parathyroidectomy on glucose homeostasis and incretin hormone release in patients with primary hyperparathyroidism: a pilot study

Vasiliki Antonopoulou1, Maria Grammatiki1, Theocharis Koufakis1, Spyridon Karras1, Maria Yavropoulou1, Niki Katsiki1, Spyridon Gerou2, Elpida Gavana2, Lemonia Skoura3, Pantelis Zebekakis1, Theodosios Papavramidis4 & Kalliopi Kotsa1

1Division of Endocrinology and Metabolism, First Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, Ahepa Hospital, Thessaloniki, Greece; 2Laboratories ‘Analysis’, Thessaloniki, Greece; 3Department of Microbiology, Aristotle University of Thessaloniki, Ahepa Hospital, Thessaloniki, Greece; 41st Department of Surgery, Aristotle University of Thessaloniki, Ahepa Hospital, Thessaloniki, Greece.

Background: Primary hyperparathyroidism (PHPT) has been linked to glucose homeostasis disorders, leading to insulin resistance and type 2 diabetes mellitus. Previous small studies evaluating the effect of parathyroidectomy (PTX) on various parameters of glucose metabolism have produced conflicting results. The impact of PTX on incretin hormone levels has not been studied yet. The aim of this pilot study was to investigate the effect of PTX on markers of glucose metabolism and insulin resistance, as well as on incretin hormone levels in patients with PHPT.

Methods: Fourteen non-diabetic patients with PHPT were included in this study. All patients were scheduled for a curative PTX. Preoperatively, fasting plasma glucose(FPG), fasting insulin(I), gastric inhibitory polypeptide(GIP), glucagon-like peptide-1(GLP-1), calcium, phosphorus, parathyroid hormone (PTH) and 25-hydroxyvitamin-D [25(OH)D] were measured. Homeostasis Model Assessment (HOMA2) was used for estimating insulin resistance (HOMA2-IR), β-cell function (HOMA2-B) and insulin sensitivity (HOMA2-S). QUICKI index for insulin sensitivity was also calculated. A 75g oral glucose tolerance test (OGTT) was performed to further evaluate glucose, insulin and incretin response as well as insulin sensitivity using the Matsuda Index. All measurements and calculations were repeated 6 weeks post-PTX.

Results: Patients had a mean age of 52.9±10 years (female:male ratio=12:2). Preoperatively, PTH was positively correlated with HOMA2-B (r=0.74, P=0.002) and GLP-1 (r=0.79, P=0.02). After PTX, calcium and PTH levels were normalized and phosphorus was increased. Body mass index also increased slightly (P=0.02). A significant increase was observed in GLP-1 response during OGTT after PTX (in 60 min: 55.2 (79.8) vs 91.5 (74.4) pg/ml, P=0.05 and in 120 minutes: 71.3 (51.3) vs 91.3 (74.0) pg/ml, P=0.03). GIP response was not significantly altered. Postoperatively, the correlation between HOMA2-B and PTH remained significant (r=0.55, P=0.04), whereas PTH was also associated positively with HOMA2-IR (r=0.56, P=0.04) and negatively with Matsuda index (r=−0.58, P=0.03) and QUICKI (r=−0.41, P=0.04).

Conclusion: To our knowledge, this is the first study investigating the effect of PTX on incretin hormone levels in PHPT patients. The increase of the GLP-1 response observed after curative surgery may potentially reflect the partial recovery of glucose homeostasis. Additional findings of this pilot study indicate a correlation between PTH and indices of β-cell function in PHPT patients. Larger studies are needed to clarify the pathophysiology background behind PHPT and glucose metabolism and to evaluate the impact of PTX on this association.