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  • Title: Histopathology and pathophysiology of secondary hyperparathyroidism due to chronic renal failure.
    Author: Tominaga Y, Sato K, Tanaka Y, Numano M, Uchida K, Takagi H.
    Journal: Clin Nephrol; 1995 Nov; 44 Suppl 1():S42-7. PubMed ID: 8608662.
    Abstract:
    Between 1973 and 1992, 300 patients underwent parathyroidectomy for secondary hyperparathyroidism due to chronic renal failure in our departments. Using parathyroid glands obtained at operation, histopathological studies were performed, and to estimate pathophysiology DNA analysis of parathyroid cell nuclei and calcium-regulated parathyroid hormone (PTH) secretion in vitro were estimated. PTH mRNA expression was evaluated by in situ hybridization. The typical histopathological findings were asymmetric enlargement, nodularities and increased number of oxyphil cells. Secondary hyperplasia was divided into 2 types: diffuse and nodular type hyperplasia. In the histopathological study nodular hyperplasia indicated more aggressive proliferation. In DNA analysis the relative number of scattered cells in the DNA synthesis phase was significantly greater in nodular than in diffuse hyperplasia. The half of the maximal inhibition of PTH secretion for calcium (the set-point) in the cells from nodular hyperplasia was higher than in the cells obtained from diffuse hyperplasia. However, there was no difference in expression of PTH mRNA in nodular and diffuse hyperplasia. These data suggested that nodular hyperplasia was more progressively hyperplastic, had more aggressive proliferative activities and showed more abnormal regulation of PTH secretion. These results imply that to prevent graft-dependent recurrent hyperparathyroidism after parathyroidectomy, the nodular hyperplastic tissue should not be autografted.
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