말기 신부전증에 의한 이차성 부갑상선 기능항진증 환자에서 부갑상선 조직의 세포자가사멸 연구 = The Apoptotic Labeling Index of Parathyroid Tissue in Patients with the Secondary Hyperparathyroidism of End Stage Renal Disease

다국어 초록 (Multilingual Abstract)

Purpose: The cause of renal hyperparathyroidism is unclear and the role of hyperphosphatamia is the only well established cause of renal osteodystrophy. The long life span of the parathyroid cells and the absence of a definite tissue marker for nodular parathyroid gland prohibit the timing of surgical intervention. The discrepancy between proliferation and apoptosis has been proposed as one possible cause of nodular development of the parathyroid gland in patients suffering with renal osteodystrophy. In the present study, we investigated the apoptotic labeling index of the parathyroid tissue in patients with renal hyperparathyroidism. Methods: The parathyroid tissues of 76 patients with renal hyperparathyroidism and those of 33 normal glands were used for determining the level of apoptosis by performing a Tdt-mediated dUTP nick end labeling (TUNEL) assay. The patients' information was collected by a review of the clinical charts. Statistical comparison was done via two tailed t-tests. Results: The averages of the TUNEL indices were 0.19 in the normal parathyroid glands and 1.84 in the hyperplastic parathyroid glands (P=0.00). The TUNEL index was higher in the oxyphil type of cells than in the chief cells and the water clear cell types (P=0.01). There was statistically significant correlation of the TUNEL index with the duration of the dialysis and less than 10 years dialysis showed a 2.23 index, which was higher than that of the longer term dialysis patients (P=0.00). The preoperative PTH level, recurrence, the Ki-67 labeling index and the pathologic type didn't show any statistical correlation with the TUNEL index (P＞0.05). Conclusion: Our findings showed that the TUNEL index is useful for separating the cases of advanced renal hyperparathyroidism from the early ones and the TUNEL index is well correlated with hyperplastic types of cells. A decrease of apoptosis could be a probable cause of the progression of parathyroid hyperplasia in renal patients who are on dialysis support. (Korean J Endocrine Surg 2008; 8:250-255)