منابع مشابه
Evidence for Secondary Hyperparathyroidism
This work was presented in part at the Annual Meeting of the Association of American Physicians, Atlantic City, N. J., May 1971. The present address of Dr. Canterbury and Dr. Reiss is Department of Medicine, University of Miami School of Medicine, Miami, Fla. Received for publication 1 August 1972 and in revised formn 19 September 1972. of hypercalciuria. Primary renal loss of calcium could exp...
متن کاملPathogenesis of secondary hyperparathyroidism.
Chronic renal failure is the primary cause of secondary hyperparathyroidism (SHPT). Patients with mineral metabolism disorders commonly present with low serum calcium levels, hyperphosphatemia, and calcitriol deficiency. In normal renal function subjects, parathyroid cells have a low turnover and rarely undergo mitoses. In uremic conditions, however, parathyroid glands become hyperplasic and le...
متن کاملSecondary and tertiary hyperparathyroidism.
We reviewed the etiology and management of secondary and tertiary hyperparathyroidism. Secondary hyperparathyroidism is characterized by an increase in parathyroid hormone (PTH) that is appropriate and in response to a stimulus, most commonly low serum calcium. In secondary hyperparathyroidism, the serum calcium is normal and the PTH level is elevated. Tertiary hyperparathyroidism is characteri...
متن کاملPathogenesis of secondary hyperparathyroidism.
Hyperplasia of the parathyroid glands and increased concentrations of immunoreactive parathyroid hormone are among the earlier alterations of mineral metabolism in patients with chronic renal failure. In the past five years several investigators have demonstrated that phosphorus retention plays a key role in the development of secondary hyperparathyroidism and chief cell hyperplasia of the para...
متن کاملMechanisms of secondary hyperparathyroidism.
Small decreases in serum Ca(2+) and more prolonged increases in serum phosphate (P(i)) stimulate the parathyroid (PT) to secrete parathyroid hormone (PTH), and 1,25(OH)(2)D(3) decreases PTH synthesis and secretion. A prolonged decrease in serum Ca(2+) and 1,25(OH)(2)D(3), or increase in serum P(i), such as in patients with chronic renal failure, leads to the appropriate secondary increase in se...
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ژورنال
عنوان ژورنال: Annals of Clinical Biochemistry: International Journal of Laboratory Medicine
سال: 1993
ISSN: 0004-5632,1758-1001
DOI: 10.1177/000456329303000524