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The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 8 3501-3504
Copyright © 2003 by The Endocrine Society

Special Feature

The Use in Clinical Practice of Parathyroid Hormone Normative Values Established in Vitamin D-Sufficient Subjects

Jean-Claude Souberbielle, Ethel Lawson-Body, Boualem Hammadi, Emile Sarfati, Andrè Kahan and Catherine Cormier

Laboratoire d’Explorations Fonctionnelles (J.-C.S., E.L.-B.) et de Biochimie A (B.H.) Hôpital Necker-Enfants Malades; Service de Rhumatologie (A.K., C.C.) Hôpital Cochin; and Service de Chirurgie (E.S.), Hôpital Saint-Louis, Assistance Publique-Hopitaux de Paris (AP-HP), Paris, France

Address all correspondence and requests for reprints to: J. C. Souberbielle, M.D., Laboratoire d’Explorations Fonctionnelles, Húpital Necker-Enfants Malades, 149 rue de Sëvres, 75015 Paris, France. E-mail: jean-claude.souberbielle{at}nck.ap-hop-paris.fr.


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Discussion
 References
 
We have found recently that excluding subjects with low serum 25OHD has a significant impact on the PTH reference range (10–46 ng/liter instead of 10–65 ng/liter with the same assay). However, before being used routinely, this new range had to be clinically validated. We thus reviewed the chart of 708 consecutive osteopenic patients who were referred to our unit for a biological exploration in search of secondary causes for their low bone mass. They were classified into two groups. Group 1 (n = 360) included the patients for whom no reasons for high PTH were found after examination of their chart. Group 2 (n = 348) included patients with one of the following potential reasons for an increased PTH concentration: hyper- or hypocalcemia, normocalcemic primary hyperparathyroidism (PHPT), renal hypercalciuria, vitamin D insufficiency, chronic renal failure, use of bisphosphonates, and any chronic disease known to potentially alter calcium metabolism. Among the 360 group 1 patients, 15 (4.2%) had a serum PTH level more than 46 ng/liter, which is not different from the theoretical rate of 3% of normal subjects whose serum PTH may be above the 97th centile of the reference ({chi}2 = 2.8; NS). Forty-two group 2 patients had a surgically proven PHPT. Among these, serum PTH was <=65 ng/liter in 17 (40.5%) and <=46 ng/liter in 5 (12%). In conclusion, our proposed PTH reference range allows to identify fewer patients with mild surgically proven PHPT who have a normal serum PTH concentration, without inducing an increase in the rate of falsely high PTH.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Discussion
 References
 
VITAMIN D INSUFFICIENCY IS a very common situation that still remains undetected in many patients. It induces mild secondary hyperparathyroidism with a subsequent increase in bone turnover and, at least in the elderly, an enhanced risk of osteoporotic fracture, mainly at cortical sites (1). It could be defined by the serum concentration of 25OHD below which serum PTH starts to increase in a population (2). We recently proposed to include only normal subjects without low serum 25OHD concentration to establish a reference range for serum PTH (3). By doing this in healthy subjects aged 60–79 yr, we found with a widely used PTH assay that the highest normal concentration at P < 0.05 (46 ng/liter) was consistently lower than what is generally accepted with the same assay (65 ng/liter) (4). However, before being used routinely, this new reference range had to be clinically validated. This is the goal we aimed to achieve in the present study by showing that our proposed PTH reference range induced a decrease in the number of false negative values [i.e. less normal serum PTH levels in surgically proven primary hyperparathyroidism (PHPT)] without an increase in the rate of false positive values (i.e. no more than 3% of high values in normocalcemic patients without any potential reason to have an increased serum PTH concentration).


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Discussion
 References
 
Patients

We reviewed the medical chart of 708 consecutive osteopenic/porotic patients (74 premenopausal women, 552 menopausal women and 82 men) aged 59.2 ± 13.4 yr. They were referred to our bone/calcium metabolism unit over a 1-yr period (from July 17, 2000, to July 16, 2001) by their primary care physician in search of secondary causes for their low bone mass. The patients came on a single morning to our unit after an overnight fast with a 24-h urine collection obtained at home and had a blood and urine sample for an extensive biological evaluation (EBE) as described in the following Laboratory methods. They also answered a questionnaire aiming to quantify their daily calcium diet (5). Finally, a chart was constituted that included the following data: age, years since menopause for women, weight, actual height and height at the age of 25 yr, the results of previous densitometric and laboratory explorations (if any), history of smoking and alcohol consumption, level of exercise and sunshine exposure, present or previous use of drugs known to affect bone/calcium metabolism (glucocorticoids, anticonvulsants, thiazide diuretics, furosemide, lithium, hormone replacement therapy, bisphosphonates or other antiresorptive treatments, calcium and/or vitamin D supplementation), and medical history (fractures, nephrolithiasis, endocrinopathies, and any situation that induced a more than 2-month period of immobilization). In some of these patients, a second evaluation including an oral calcium load test (6) was performed approximately 2 months later when doubt concerning the diagnosis remained after the EBE, especially in case of unexplained hypercalciuria or suspicion of normocalcemic primary hyperparathyroidism. Our analysis was carried out in two phases.

At first we aimed to evaluate the rate of PTH concentrations greater than 46 ng/liter in patients with an apparently normal calcium metabolism. We considered the data from the complete medical chart that allowed us to classify our patients into two groups. Group 1 included all the patients for whom no reasons for high PTH (see below) were found after examination of their chart. Use of calcium or vitamin D supplementation, adequately treated hypothyroidism (normal TSH), a history of nephrolithiasis without disorder of calcium metabolism, or previous successful surgery for PHPT were not an a priori cause of exclusion from group 1. Group 2 included patients with a documented potential reason for an increased PTH concentration. Our inclusion criteria for group 2 were hyper- or hypocalcemia, normocalcemic PHPT, renal hypercalciuria (these two last conditions were documented by the results of an oral calcium load test), vitamin D deficiency/insufficiency (defined by a serum 25OHD concentration of 30 nmol/liter with our in-house assay) (3), chronic renal failure defined by a glomerular filtration rate (GFR) assessed with the creatinine clearance, 30 ml/min, use of bisphosphonates (present or in the previous 6 months), and any other chronic disease known to potentially alter calcium metabolism including sarcoidosis, untreated or insufficiently treated hypothyroidism documented by a clearly increased TSH concentration, and chronic diseases associated with malabsorption such as celiac disease or cystic fibrosis. When a patient had more than one inclusion criterion for group 2, he or she was classified according to the ranking described above (e.g. a hypercalcemic patient with a low vitamin D store is classified as hypercalcemic). We then considered the serum PTH concentration from the EBE and compared the percentage of group 1 patients with a serum PTH greater than 46 ng/liter (group 1b) to 3%, which corresponds to the theoretical rate of normal subjects that should present a concentration above the 97th percentile of the reference range. In case of a significant difference, it was decided to increase our upper limit of normal PTH by steps of 1 ng/liter until the percentage of high values is not different from 3%.

In the second phase, we aimed to evaluate the rate of falsely normal PTH concentrations in PHPT. We, therefore, constituted a subgroup by considering only the group 2 patients who had surgically proven PHPT. Among these patients we counted those with PTH concentrations of <=65 ng/liter and <=46 ng/liter, respectively.

All patients were informed that their biological data were going to be reviewed in this study, and they gave their consent for that.

Laboratory methods

As stated above, for every patient the EBE was performed on a 24-h urine collection obtained at home and basal fasting blood and urine (second morning void) samples collected between 0830 and 1000 h in our laboratory. A serum aliquot was stored at -20 C to measure 1,25 dihydroxy vitamin D (1,25(OH)2D) when necessary. Serum ionized calcium (Ca2+) was measured by electrometry within a few minutes after sampling (ICa2, Radiometer, Copenhagen, Denmark). Serum and urinary total calcium, phosphate, sodium, and creatinine were measured by means of an automated chemistry analyser (Synchron CX4, Beckman Instruments, Brea, CA). Serum albumin and total alkaline phosphatase activity were measured by colorimetry. Serum TSH was measured with a semiautomated chemiluminescent assay (Behring Diagnostics, Rueil Malmaison, France). Serum PTH was measured by an immunoradiometric assay kit (Allegro Intact PTH, Nichols Institute, San Juan Capistrano, CA). Serum 25OHD (7) and 1,25(OH)2D (8) were measured by radiocompetition after extraction and column purification.

Expression of results

Continuous variables are expressed as mean ± SD. Between-group comparisons were assessed by ANOVA. Percentages were compared by the {chi}2 test. Correlations were assessed by the Spearman {rho} test. A P value of 0.05 was considered as significant.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Discussion
 References
 
After the first phase of our evaluation, 360 and 348 patients were classified into groups 1 and 2, respectively. This classification is detailed in Table 1Go, according to the inclusion criteria for group 2. Among group 1 patients, 15 (4.2%) had a serum PTH level greater than 46 ng/liter (group 1b), which is not different from the theoretical rate of 3% ({chi}2 = 2.8; NS). We thus considered that there was no need to increase our upper limit of normal PTH above 46 ng/liter. None of the 15 group 1b patients had a serum PTH above 65 ng/liter, and it should be noted that although not having strict criteria of exclusion from group 1 as described in the Patients section, four of these group 1b patients had a low GFR (creatinine clearance of 33, 38, 43, and 48 ml/min), one was treated with high doses of glucocorticoids at the moment of evaluation and two had a very low daily calcium intake (175 and 225 mg per 24 h). Among the 348 group 2 patients, 46 (13.2%) had a serum PTH concentration above 65 ng/liter, whereas 126 (36.2%) had a serum PTH concentration above 46 ng/liter. Details concerning the percentages of serum PTH levels above 46 and 65 ng/liter in the different subgroups of group 2 are shown in Table 2Go.


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  		TABLE 1. Mean (±SD) serum PTH of 703 consecutive osteoporotic patients

 

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  		TABLE 2. Number (%) of patients from the different subgroups of our group 2 (patients with a potential cause for high serum PTH) who had a serum PTH concentration >46 ng/liter and >65 ng/liter, respectively

 
As stated in Table 1Go, 42 patients had a surgically proven PHPT, of whom two (4.8%) were normocalcemic (serum Ca2+, 1.30 mmol/liter). In these 42 patients, 25 had a serum 25OHD of 30 nmol/liter, and serum PTH correlated negatively with serum 25OHD (Fig. 1Go). Serum PTH was <=65 ng/liter in 17 patients (40.5%) and <=46 ng/liter in 5 patients (12%). The PTH concentration of the two patients with normal Ca2+ was 159 and 57 ng/liter, respectively. These two patients had no other reason to have a high serum PTH, and they had an oral calcium load test that showed only a small decrease in serum PTH despite a significant increase in Ca2+.



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  		FIG. 1. Scatterplot of the 25OHD concentration against the PTH concentration of the 42 patients with a surgically proven PHPT. The fine horizontal line represents the upper limit of the usual PTH reference range with the Nichols Allegro assay (65 ng/liter), whereas the thick horizontal line represents the upper limit of our proposed reference range, which takes vitamin D status into account (46 ng/liter). Similarly, a vertical line has been drawn at a 25OHD concentration of 30 nmol/liter (open circles, women; closed circles, men).

 

   Discussion
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
References
 
This study validated over a 1-yr period the use in clinical practice of a serum PTH reference range that takes vitamin D status into account and may improve the diagnosis of PHPT. Although most PHPT patients are asymptomatic, surgery remains the definitive treatment as recently highlighted by an expert panel that revised the guidelines for surgery in PHPT (9). When compared with the recommendations of the previous consensus conference (10), the main change appears to concern osteoporosis. Indeed, it is now recommended to propose surgery to any PHPT patient with osteoporosis, i.e. with a bone mineral density T-score -2.5 at any site, instead of the previous recommendation of a bone mineral density Z-score -2 at the forearm. If the laboratory screening of osteoporotic patients becomes more widely performed and includes the measurement of serum PTH as proposed recently by Tannenbaum et al. (11), it is likely that more and more asymptomatic PHPT patients who meet at least one of the criteria for surgery (osteoporosis in this case) will be identified. The diagnosis of PHPT is based on the biological evaluation that usually shows an inappropriately high PTH in the presence of hypercalcemia, but it should be stressed that normocalcemic PHPT also exists (12). Even if high normal serum PTH in the presence of hypercalcemia strongly argues for the diagnosis of PHPT, this diagnosis is considered easier when serum PTH is clearly above the normal range. We thus believe that the diagnosis of PHPT may be improved by the use of our proposed new PTH reference range because fewer patients will have a normal serum PTH concentration. This is illustrated by our finding that 17 of 42 (40.5%) PHPT patients had normal serum PTH if the traditional normal values were used, whereas only five (12%) of them had a normal value with our new reference range. This rate of normal serum PTH in patients in whom PHPT was surgically proven may appear very high but may be due to the reason for recruiting the patients (the diagnosis of PHPT was made in these patients because they had been tested for secondary causes of osteoporosis).

The use of our proposed PTH reference range could also induce an increase in the detection of high serum PTH in otherwise normocalcemic patients. Before the diagnosis of normocalcemic PHPT can be established, it will be highly important to rule out carefully any other potential causes of high PTH as outlined (9). This includes any chronic disease associated with malabsorption such as cystic fibrosis (13) or celiac disease (14), both conditions often being associated with vitamin D deficiency endocrinopathies such as hypothyroidism (15), renal hypercalciuria (16), chronic renal failure (the definition of which must be more clearly defined in terms of GFR), very low daily calcium intake, use of drugs having an influence on calcium metabolism such as anticonvulsants (17), furosemide (18), lithium (19), or bisphosphonates (20), and vitamin D insufficiency. Concerning this last condition, it is now consensual that serum 25OHD is the correct functional indicator of vitamin D status (21). However, not all the patients with a low serum 25OHD concentration have a high PTH concentration. We found that 26% of our osteoporotic patients who had a serum 25OHD level <=30 nmol/liter had a serum PTH above 46 ng/liter, whereas only 7% had a PTH above 65 ng/liter, a result highly comparable with what we found in healthy elderly subjects (3). One can consider that the cut-off we used for 25OHD (30 nmol/liter) to define vitamin D insufficiency is quite conservative. Indeed higher cut-offs are considered, usually 50 nmol/liter (2, 9, 22, 23), although higher values up to 75 nmol/liter and above are also suggested (24, 25). It should be stressed, however, that discrepancies among 25OHD assays have been published (26, 27, 28), and we have recently reported that our in-house 25OHD assay gives results that are approximately 30% lower than the most currently used assays (29). Our cut-off is thus closer to the more widely accepted value of 50 nmol/liter.

It was recently recommended by Bilezikian et al. (9) that "better-defined normative values for age, gender, menopausal status, and race for both PTH and calcium would be helpful." This is an important point because it has been reported that serum PTH is higher in black than white people (30, 31, 32) and in the elderly than the young (33, 34). However, 25OHD is also known to be usually lower in black than white people (30) and in the elderly than the young (34), and this can explain part of the higher PTH found in blacks and elderly people. We thus propose that the above-mentioned recommendation should be reevaluated after elimination from a reference population of any subject with vitamin D insufficiency. This supposes that, when establishing a PTH reference range, 25OHD must be measured beforehand and the 25OHD cut-off has been clearly defined in the various populations to be tested.

In conclusion, we have shown that excluding subjects with low serum 25OHD has a significant impact on the PTH reference range (3) and allows to identify more patients with mild PHPT and high serum PTH, without inducing an increase in the rate of falsely high PTH. This may be important in light of the recent proposition to measure PTH routinely in osteoporotic women in search of secondary diagnoses and the recent recommendation to consider osteoporosis at any bone site as a criterion for surgery in PHPT patients.


   Footnotes
 
Abbreviations: EBE, Extensive biological evaluation; GFR, glomerular filtration rate; PHPT, primary hyperparathyroidism.

Received January 22, 2003.

Accepted March 24, 2003.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 References
 

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