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Effect of age on circulating immunoreactive and bioactive parathyroid hormone levels in women
Author(s) -
Forero Martha Susana,
Klein Robert F.,
Nissenson Robert A.,
Nelson Karen,
Iii Hunter Heath,
Arnaud Claude D.,
Riggs Lawrence B.
Publication year - 1987
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650020502
Subject(s) - medicine , antiserum , endocrinology , parathyroid hormone , adenylate kinase , cyclase , renal function , hormone , urinary system , kidney , chemistry , antibody , calcium , immunology , receptor
Although levels of serum immunoreactive parathyroid hormone (iPTH) increase with age in women, this could be caused by retention of non‐biologically active PTH fragments by the aging kidney. In 102 normal women, aged 30 to 89 yr, serum iPTH increased with age by 58% ( r = 0.33, p < 0.001) with antiserum GP‐1M (which has midmolecule specificity) and 43% ( r = 0.32, p < 0.001) with antiserum CH‐12M (which may have whole molecule specificity); urinary cAMP/GFR excretion increased by 29% ( r = 0.22, p < 0.05). The results of these assays were validated by comparison with serum levels of biologically active PTH (BioPTH) in immunoextracts of serum followed by renal adenylate cyclase assay in a selected subgroup of 25 of the women. Serum BioPTH correlated with serum iPTH assessed by antiserum GP‐1M ( r = 0.48, p < 0.05) and antiserum CH‐12M ( r = 0.48, p < 0.05) but not with urinary cAMP. The data are consistent with an increase of parathyroid function with aging: clearly, we do not find decreased parathyroid function as would be expected if age‐related bone loss was not mediated, in part, by PTH.