A New Transport Solution for Parathyroid Allotransplantation: Effects on Cell Viability and Calcium-Sensing Receptors

Goncu B., YÜCESAN E., Ozdemir B., Basoglu H., Kandas N. O. , AKBAŞ F., ...More

BIOPRESERVATION AND BIOBANKING, vol.16, no.4, pp.278-284, 2018 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 16 Issue: 4
  • Publication Date: 2018
  • Doi Number: 10.1089/bio.2018.0008
  • Journal Indexes: Science Citation Index Expanded, Scopus
  • Page Numbers: pp.278-284


Background: Cold ischemia protects organs and tissues by slowing their metabolism, but it also causes ischemic injury. Minimizing cold ischemia has been an important goal in parathyroid auto- and allotransplantation, as well as the transplantation of other major organs. Parathyroid glands are responsible for calcium homeostasis by releasing parathormone (PTH) into the blood circulation. Functionality of a new parathyroid transport solution (NPTS) and effects on cell viability, PTH secretion, and calcium-sensing receptor (CaSR) levels during cold ischemia were evaluated. Materials and Methods: A NPTS was prepared, and the pH was adjusted to a range of 7.2-7.4 and kept at +4 degrees C until use. Seven patients with parathyroid hyperplasia secondary to chronic renal failure who were scheduled to undergo subtotal parathyroidectomy were enrolled in the study. Glands were cold-preserved in NPTS with different time intervals (0, 6, 12, 18, and 24 hours), and then parathyroid cell viability before and after cryopreservation, PTH secretion, and CaSR levels were determined. Results: The mean cell viability before cryopreservation was 92.7% (range 89.2%-97.2%). There were no significant differences in cell viability rates before and after cryopreservation (p=0.1168 and p=0.4085, respectively), and CaSR levels (p=0.5446) were not significant. Conclusions: NPTS is a solution designed specifically for parathyroid tissue transplantation. This patent pending product can support cellular viability and PTH release, as well as protect CaSR functionality for up to 24 hours of cold ischemia.