Persistent elevated serum parathyroid hormone levels with normocalcaemia after parathyroidectomy: Secondary hyperparathyroidism or pseudo- hyperparathyroidism?

Abstract

Introduction: This study aimed to determine the time to normalisation of postoperative parathyroid hormone levels after successful parathyroid surgery and to analyse the pathophysiology of postoperative normocalcaemic hyperparathyroidism.

Method: An observational retrospective study was conducted on a cohort of 186 patients who had undergone parathyroidectomy for primary hyperparathyroidism over a 5-year period. Demographic characteristics, surgical and histopathological data, bone densitometry (pre-and postoperative pharmacological treatment), creatinine plasma levels, and pre-and postoperative parathyroid hormone, calcium and vitamin D levels were recorded as predictive variables. The time to normalisation of the postoperative parathyroid hormone levels was recorded as the output variable. A univariate analysis was performed to investigate the factors related to the time to normalisation of parathyroid hormone levels.

Results: The final study sample was comprised of 176 patients, 46 of which (26.1%) had elevated postoperative parathyroid hormone levels and normocalcaemia. The median time to normalisation of the postoperative parathyroid hormone levels was 6 months. The cumulative probability of having normal parathyroid hormone levels 30 months after surgery was 89%. The time to normalisation was associated only with preoperative parathyroid hormone levels (P =.007; HR: 0.998). Vitamin D and creatinine levels were not associated with time to normalisation of parathyroid hormone levels (P =.744).

Conclusions: Persistently elevated postoperative parathyroid hormone levels with normocalcaemia may occur in one-quarter of patients after parathyroidectomy. Parathyroid hormone levels normalise in up to 90% of cases by 30 months. A high preoperative parathyroid hormone level is predictive of postoperative normocalcaemic hyperparathyroidism, and vitamin D deficiency does not seem to influence the pathogenic mechanism.