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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 4 1646-1649
Copyright © 2004 by The Endocrine Society

The Effects of Age and Other Variables on Serum Parathyroid Hormone in Postmenopausal Women Attending an Osteoporosis Center

Allan G. Need, Peter D. O’Loughlin, Howard A. Morris, Michael Horowitz and B. E. Christopher Nordin

Division of Clinical Biochemistry (A.G.N., P.D.O., B.E.C.N.) and Hanson Centre (A.G.N., P.D.O., H.A.M., M.H., B.E.C.N.), Institute of Medical and Veterinary Science and Department of Medicine (A.G.N., H.A.M., M.H., B.E.C.N.), Royal Adelaide Hospital, Adelaide, South Australia 5000

Address all correspondence and requests for reprints to: A/Pr Allan G. Need, Division of Clinical Biochemistry, Institute of Medical and Veterinary Science, Frome Road, Adelaide, South Australia, SA 5000. E-mail: allan.need{at}imvs.sa.gov.au.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
It has been known for many years that serum PTH rises with age, and it has been suggested that this rise may contribute to bone loss in postmenopausal women. It has been variously attributed to declining renal function, declining calcium absorption efficiency, and declining serum 25-hydroxyvitamin D [25(OH)D] levels.

We studied the effects of age, weight, renal function, radiocalcium absorption, serum ionized calcium, and serum 25(OH)D on serum PTH levels in 918 postmenopausal women attending an osteoporosis center. On simple linear regression, serum PTH was a positive function of age (P = 0.003) and weight (P < 0.001) and an inverse function of serum 25(OH)D (P < 0.001) and serum ionized calcium (P = 0.002). On stepwise regression, serum 25(OH)D was the most significant (negative) determinant of serum PTH, followed in decreasing order of significance by serum ionized calcium (negative) and body weight and age (positive). Serum PTH was not related to radiocalcium absorption. The reciprocal relation between serum PTH and serum 25(OH)D could not be explained by the serum concentration of 1,25-dihydroxyvitamin D, which did not change with age. After adjustment for serum ionized calcium, body weight, and age, the rise in serum PTH appeared to start when serum 25(OH)D fell less than 80 nmol/liter.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
SERUM PARATHYROID HORMONE (PTH) rises with age in both men and women (1, 2, 3, 4, 5, 6, 7, 8, 9, 10), and this has generally been attributed to an age-related decline in renal function (1, 5). The glomerular filtration rate (GFR) is known to decline with age, and serum PTH is elevated in patients with renal insufficiency (11). In one study, the age-related rise in PTH was directly related to the fall in creatinine clearance (1). However, it has also been suggested that an age-related decrease in calcium absorption, perhaps related to falling vitamin D levels (8) and/or reduced serum estrogens (12), could increase serum PTH levels in postmenopausal women. It is well established that the low serum 25-hydroxyvitamin D [25(OH)D] frequently seen in the elderly is associated with a high serum PTH (13, 14), and it has been suggested that serum 25(OH)D levels should be taken into account when defining the normal range of serum PTH (14). It has also recently been suggested that the elderly require a higher serum 25(OH)D to maintain the same serum PTH as younger subjects (13).

Previous studies have not examined all these factors simultaneously or estimated the relative importance of each. To define more clearly the effects of age, weight, renal function, calcium absorption, serum ionized calcium, and serum 25(OH)D on serum PTH, we have examined the data from 918 postmenopausal women attending our osteoporosis clinics and now present the results.


   Subjects and Methods
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 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
We routinely collect fasting blood and urine samples and measure radiocalcium absorption in patients attending our osteoporosis clinics. For the purposes of this study, we included only postmenopausal women, defined by cessation of menstrual periods for at least 12 months or, in those who had undergone hysterectomy, by a serum FSH level above 20 U/liter (premenopausal reference range, 0–10 U/liter). We excluded those who were on treatment for osteoporosis or on relevant medication or with a history of disease liable to affect calcium metabolism.

All subjects attended for blood and urine collection between 0800 and 1000 h, after an overnight fast, and were then given 5 µCi of 45Ca with 20 mg calcium carrier to drink in 250 ml water. A second blood sample was taken exactly 1 h later to measure plasma radioactivity (15). Verbal informed consent was obtained from each patient because the procedure requires a small dose of radiocalcium, but written informed consent was not obtained because the tests were performed for diagnostic reasons.

Serum PTH was measured by an intact assay (Magiclite, Ciba-Corning, Fernwald, Germany), serum 25(OH)D by RIA (Incstar, Stillwater, MN), serum 1,25-dihydroxyvitamin D [1,25(OH)2D] by RIA after HPLC (16), and phosphate and creatinine on the Technicon (Tarrytown, NY) DAX analyzer. Radiocalcium absorption was expressed as an hourly fractional rate (15), and the serum ionized calcium and renal tubular maximum for phosphate reabsorption (TmP) were calculated as previously described (17, 18).

Results are expressed as means (SD). Differences between groups were tested with Student’s t test for unpaired samples, and relations between the variables were tested by Pearson’s correlation coefficients and stepwise linear regression. Results were adjusted for age, weight, and other factors by multiple linear regression. All calculations were performed in Minitab release 12 (State College, PA).


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
The subjects’ mean age, body weight, and biochemical variables are shown in Table 1Go. Their mean age was 64 yr (range, 35–94) and mean weight 65 kg (range, 31–131). Mean serum 25(OH)D was 61 nmol/liter (range, 5–196), but it was less than 40 nmol/liter in 190 subjects (21%) and less than 60 nmol/liter in 467 subjects (51%). Mean serum creatinine was 0.068 mmol/liter (range, 0.030–0.160), and mean serum PTH was 4.8 pmol/liter (range, 0.2–17.0).


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  		TABLE 1. Demographic and biochemical variables in 918 postmenopausal women (mean, SD)

 
The coefficients of correlation between the variables are shown in Table 2Go. PTH was a positive function of age (P < 0.01) and weight (P < 0.001) and a negative function of serum ionized calcium (P < 0.01) and 25(OH)D (P < 0.001) (Table 2Go). There was no significant correlation between serum PTH and either calcium absorption or serum creatinine. Serum 1,25(OH)2D was a positive function of 25(OH)D (P < 0.001) and PTH (P < 0.001) and a negative function of serum ionized calcium (P < 0.05), phosphate (P < 0.05), and creatinine (P < 0.001). Serum phosphate was a negative function of weight (P < 0.001) and PTH (P < 0.001), and TmP was a negative function of age (P < 0.05), serum creatinine (P < 0.001), and PTH (P < 0.001). The inverse correlation between TmP and serum PTH remained after adjustment for age and body weight (P < 0.001).


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  		TABLE 2. Pearson correlation coefficients between age, weight (kilograms), serum ionized calcium (Ca2+), radiocalcium absorption, fraction per hour (AT), serum 25(OH)D, serum 1,25(OH)2D, serum creatinine (Creat), serum phosphate (Phosphate), TmP, and serum pth (PTH) in 918 postmenopausal women

 
When PTH was regressed simultaneously on age, weight, radiocalcium absorption, serum ionized calcium, 25(OH)D, and creatinine, four variables, viz. age, weight, serum ionized calcium, and 25(OH)D, remained significant, with 25(OH)D being the most significant (Table 3Go). Calcium absorption and serum creatinine remained nonsignificant. All four significant determinants of serum PTH remained significant after exclusion of the subjects with serum 25(OH)D less than 40 nmol/liter. The relationship between serum PTH and serum 25(OH)D, after adjusting for age, weight, and serum ionized calcium, is shown in Fig 1Go. The major rise in serum PTH occurred as serum 25(OH)D levels fell less than 50 nmol/liter (P < 0.00001).


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  		TABLE 3. Stepwise multiple linear regression of serum PTH (picograms per milliliter) on age (years) weight (kilograms), and serum 25(OH)D and ionized calcium (milligrams per deciliter) (Ca2+) in 918 postmenopausal women

 


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  		FIG. 1. Residual serum PTH (picograms per milliliter), after adjustment for age, weight, and serum ionized calcium, plotted against serum 25(OH)D, nanomoles per liter (mean, SD).

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
An increase in serum PTH with age is well recognized. It has been variously attributed to declining renal function, declining residual estrogen levels, declining calcium absorption, diminished response to 25(OH)D, and to aging itself (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13).

Our observations suggest that the most significant factor in the PTH rise with age is the decline in serum 25(OH)D. This is compatible with the lack of correlation between PTH and age described by Gallagher et al. (19) in a population with a low prevalence of vitamin D insufficiency (3.3% in women and 0.4% in men). Our observation that body weight was a significant positive determinant of serum PTH has been previously described in elderly institutionalized subjects (20) and in obese men (21), although weight loss does not appear to reduce serum PTH (22). It has been suggested that the rather small summer rise in serum 25(OH)D in overweight subjects (due to distribution in body fat) (23) might lead to prolonged stimulation of the parathyroid glands (20); but in our data, weight remains a significant determinant of PTH even after adjustment for serum 25(OH)D. The results suggest that more PTH is required to maintain fasting serum calcium in heavier, than in lighter, subjects. Perhaps weight protects the skeleton from the bone-resorbing action of PTH to some extent.

Serum PTH was also inversely related to serum ionized calcium, which we believe demonstrates the way in which extracellular calcium is maintained overnight, because the samples were collected in the fasting state. Our data show a trend for a positive relation between serum ionized calcium and 25(OH)D that is not significant. We conclude that the increase in PTH in response to low serum 25(OH)D maintains ionized calcium at near-normal levels so effectively as to mask a fall in ionized calcium due to a deficiency of 25(OH)D.

The inverse relationship between serum PTH and serum 25(OH)D, which we here confirm, is complex and its full explanation uncertain. It cannot to be due to the negative effect of low 25(OH)D on 1,25(OH)2D production because serum 1,25(OH)2D rises (almost certainly in response to PTH) (23) as serum 25(OH)D falls less than 40 nmol/liter.

The positive relationship between serum PTH and 1,25(OH)2D confirms that PTH is a significant positive regulator of 1,25(OH)2D production, exerted through control of the renal vitamin D 1{alpha}-hydroxylase. Similar observations were reported by Orwoll et al. (4) who studied a group of 62 normal men, 30–92 yr old, in whom PTH rose and 25(OH)D fell with age but 1,25(OH)2D did not change. Others have reported no change in 1,25(OH)2D with age in men (7). It appears, therefore, that serum 25(OH)D has a modulating effect on serum PTH in its own right and not through its effect on serum 1,25(OH)2D. Perhaps peripheral tissues, including the parathyroids, are able to produce 1,25(OH)2D from 25(OH)D locally, or perhaps 25(OH)D is able to interact with vitamin D receptors in the bone despite its low affinity for them. The gene for 25(OH)D 1 {alpha}-hydroxylase (P450C1) is certainly expressed in bone (24).

The significant inverse correlation between PTH and TmP in our study indicates a biological effect of circulating PTH. The relationship remained after adjusting for age (P < 0.001), so the fall in TmP with age reflects the rise in PTH with age. A fall in TmP has previously been reported to occur in men with age but not in women (9).

The rise in PTH with age was not related to the fall in calcium absorption with age by either simple or multiple linear regression (when other factors such as weight and serum 25(OH)D were taken into account). It has been suggested that the rise in serum PTH with age is due, in whole or in part, to a decrease in calcium absorption (8, 25), but previous studies were unable to show a correlation between calcium absorption and PTH, and nor can we.

We did not measure residual estrogen levels in these postmenopausal women. It is possible, but unlikely, that they could contribute to the age-related rise in PTH. It is controversial whether PTH changes at the menopause, and we think it unlikely that small variations in the comparatively very low estradiol levels found in postmenopausal women would have any effect on PTH. It is interesting that residual serum estrogen levels in postmenopausal women appear to protect against hip fracture (26, 27), but our study suggests that this does not occur through an effect of estrogen on serum PTH. Serum estradiol has been positively related to lumbar spine bone density in one study of postmenopausal women (28); and in a similar vein, serum testosterone was related to lumbar spine, trochanter, and total body bone density in another (29).

The lack of any relationship in our data between renal function and serum PTH is, perhaps, surprising. Renal failure is well known to increase PTH (11), and the GFR certainly falls with age in our cases, as demonstrated by the rise in serum creatinine. Marcus et al. (1) described a significant inverse relation between serum PTH and creatinine clearance in 158 normal subjects of age 23–85 yr. They used a RIA to the midregion of the PTH molecule and probably measured the inactive fragments of PTH, which tend to accumulate as renal function declines. We use an assay that measures the intact PTH molecule and more truly reflects PTH secretion. Imanaka et al. (2) reported that the cAMP and urinary phosphate responses to iv PTH were less in elderly, than in young, men but that this difference became insignificant after correction for renal function. They did not, however, measure serum 25(OH)D in their study. Because PTH does rise in renal failure, we must conclude that renal function in our subjects was above the threshold for this effect.

Although calcium absorption is an important determinant of calcium balance (30), we could find no relationship between radiocalcium absorption and PTH. However, the validity of our radiocalcium absorption test is confirmed yet again by its correlation with serum 1,25(OH)2D (P < 0.001; Table 2Go). We have demonstrated an inverse relationship between bone resorption markers and calcium absorption (31); and one might expect that the signal to increase bone resorption in the presence of calcium malabsorption would be PTH, although our data do not show it. The likely explanation is that the previous day’s calcium absorption has little bearing on serum PTH in the fasting state; it is already switched on to maintain the overnight ionized calcium concentration.

After correcting for serum 25(OH)D, ionized calcium, and body weight, age still appears to have some influence on serum PTH. It has been suggested that more PTH is required to maintain serum 1,25(OH)2D levels in the elderly (14), but our data can shed no light on that concept.

In summary, once age-related changes in body weight and 25(OH)D are allowed for, there is little effect of age on PTH. Instead of laboratories reporting age-adjusted reference ranges for PTH, we believe they would do better to advise their requesting clinicians to take into account body weight and vitamin D status in interpreting the results. Because low levels of serum 25(OH)D are associated with increased bone resorption markers (23), we believe that the assessment of postmenopausal women for increased fracture risk should include measurement of serum 25(OH)D and PTH. Our data also suggest that 25(OH)D levels should be maintained above 50 nmol/liter to avoid levels of PTH which may cause excessive bone resorption.


   Footnotes
 
Abbreviations: GFR, Glomerular filtration rate; 25(OH)D, 25 hydroxyvitamin D; 1,25(OH)2D, 1,25-dihydroxyvitamin D; TmP, renal tubular maximum for phosphate reabsorption.

Received September 3, 2003.

Accepted January 6, 2004.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Marcus R, Madvig P, Young G 1984 Age-related changes in parathyroid hormone and parathyroid hormone action in normal humans. J Clin Endocrinol Metab 58:223–230[Abstract/Free Full Text]
  2. Imanaka S, Onishi T, Morimoto S, Takamoto S, Kohno H, Kumahara Y.1985 Comparison for renal responses to synthetic human PTH (1–24) administration in normal young and elderly male subjects Calcif Tissue Int 37:357–362
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