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Progression of uremic hyperparathyroidism involves allelic loss on chromosome 11

Journal Article · · Journal of Clinical Endocrinology and Metabolism; (United States)
;  [1]; ; ;  [2];  [3];  [4]
  1. Univ. of Florence (Italy) Yale Univ. School of Medicine, New Haven, CT (United States)
  2. Univ. of Florence (Italy)
  3. Univ. of Parma (Italy)
  4. National Institute of Health, Bethesda, MD (United States)

In occasional cases of secondary hyperparathyroidism, long term stimulation of the parathyroid glands leads from compensatory to autonomous hyperfunction, and thus, hypercalcemia develops. This clinical entity, named tertiary hyperparathyroidism, is possibly due to the formation of an adenoma in one of the hyperplastic glands. Previous studies have shown that parathyroid adenomas may arise with allelic loss on chromosome 11. The authors tested for allelic loss at several loci on chromosome 11 in 12 enlarged parathyroid glands from 6 uremic patients and found loss of heterozygosity in 2 of the glands from 2 different patients with higher serum calcium levels (11.3 [+-] 0.29 vs. 9.8 [+-] 0.28 mg/dL; P < 0.004) and, therefore, ascribable to the so-called tertiary hyperparathyroidism. The 2 glands with allelic loss were significantly greater in mass than those without loss (3.42 [+-] 0.37 vs. 1.60 [+-] 0.54 g; P < 0.001). These data offer new evidence that autonomous parathyroid proliferation in uremic patients can develop through over-growth by a monoclonal tumor, presumably with inactivation of a tumor suppressor gene(s) on chromosome 11. 33 refs., 4 figs., 2 tabs.

OSTI ID:
6827940
Journal Information:
Journal of Clinical Endocrinology and Metabolism; (United States), Journal Name: Journal of Clinical Endocrinology and Metabolism; (United States) Vol. 76:1; ISSN JCEMAZ; ISSN 0021-972X
Country of Publication:
United States
Language:
English