This Article Abstract Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, Q. Articles by Chihara, K. Search for Related Content PubMed PubMed Citation Articles by Chen, Q. Articles by Chihara, K. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information CT Scans Hazardous Substances DB PARATHYROID HORMONE

Effects of an Excess and a Deficiency of Endogenous Parathyroid Hormone on Volumetric Bone Mineral Density and Bone Geometry Determined by Peripheral Quantitative Computed Tomography in Female Subjects

Division of Endocrinology/Metabolism, Neurology and Hematology/Oncology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan

Address all correspondence and requests for reprints to: Toshitsugu Sugimoto, M.D., Division of Endocrinology/Metabolism, Neurology and Hematology/Oncology, Department of Clinical Molecular Medicine, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. E-mail: sugimot{at}med.kobe-u.ac.jp.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Peripheral quantitative computed tomography (pQCT) is useful for evaluating volumetric bone mineral density (vBMD) as well as bone mineral density (BMD) of cortical and trabecular bones separately. Although PTH affects cortical and trabecular bones differently, the effects of endogenous PTH on vBMD and bone geometry have not previously been examined with pQCT. We, therefore, investigated the effects of an excess and a deficiency of endogenous PTH on bone by employing dual-energy x-ray absorptiometry and pQCT in 36 female patients with primary hyperparathyroidism (hyper), nine female patients with idiopathic or postoperative hypoparathyroidism (hypo), and 100 normal controls matched to age, gender, and body size (cont). Lumbar BMD by dual-energy x-ray absorptiometry was higher in the order: hypo > cont = hyper, and radius-1/3 BMD was significantly higher in the order: hypo > cont > hyper. The area of radius-1/3 was significantly higher in hyper than in cont. As for pQCT, trabecular vBMD was significantly higher in the order: hypo > cont > hyper at the 4% site (hypo, 157.5 ± 36.7 mg/cm³; cont, 123.4 ± 47.5 mg/cm³; hyper, 98.4 ± 41.7 mg/cm³). Cortical vBMD was higher in the order: hypo > cont > hyper at the 20% site (hypo, 1141.1 ± 53.1 mg/cm³; cont, 1090.2 ± 72.9 mg/cm³; hyper, 1038.6 ± 89.1 mg/cm³). Total bone area and endosteal and periosteal circumferences were significantly higher in hyper than in cont and hypo. Cortical area and thickness were higher in the order: hypo > cont > hyper. Bone strength indices were not significantly different among the three groups. In conclusion, vBMD evaluation revealed that an excess of endogenous PTH was catabolic for both cortical and trabecular bones, and that bone mass (especially trabecular bone mass) was preserved under a condition of deficient endogenous PTH. An excess of endogenous PTH stimulated periosteal bone formation, which might partly compensate for a decrease in bone strength induced by low BMD.

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
PTH HAS BEEN shown to be an anabolic agent on bone (1, 2) when administered intermittently. In primary hyperparathyroidism (hyper), there is an excess of endogenous PTH from abnormally functioning parathyroid glands. Silverberg et al. (3) have provided evidence of dual actions of PTH as a bone-anabolic and catabolic hormone by using dual-energy x-ray absorptiometry (DXA). Patients with hyper have reduced bone mineral density (BMD) at the cortical site, whereas bone mass was relatively well preserved in cancellous bone (4, 5, 6, 7). These findings suggested that the effects of endogenous PTH excess were different in trabecular and cortical bones. On the other hand, several studies (8, 9, 10) have demonstrated that patients with hypoparathyroidism (hypo), the state that is deficient of endogenous PTH, have increased BMD at both sites, predominantly rich in trabecular and cortical bone.

DXA is used to estimate areal BMD of individual bones. However, the areal BMD measured by DXA is different from true volumetric bone mineral density (vBMD), and PTH affects bone geometry as well as BMD (11), suggesting the possibility that DXA is not appropriate for evaluating the effects of PTH on BMD. However, no reports have examined the effects of an excess or a deficiency of endogenous PTH on vBMD and bone geometry by using peripheral quantitative computed tomography (pQCT) in humans. In the present study, we therefore investigated the effects of an excess and a deficiency of endogenous PTH on bone by employing pQCT in 36 female patients with hyper, nine female patients with idiopathic or postoperative hypo, and 100 normal controls matched to age, gender, and body size (cont).

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Subjects

Thirty-six female patients who were diagnosed as hyper, nine female patients with hypo (six idiopathic and three postoperative), and 100 cont participated in this study. Postmenopausal subjects were 34, seven, and 81 in hyper, hypo, and cont groups, respectively. Years after menopause were 13.0 ± 9.0, 14.6 ± 9.3, and 17.2 ± 8.7 yr in hyper, hypo, and cont groups, respectively. In all hyper patients enrolled in the present study, abnormal parathyroid gland swelling was successfully identified by at least one imaging technique among echography, computed tomography, magnetic resonance imaging, or technetium sestamibi scintigraphy; and the biochemical data were compatible with hyper. The diagnosis of hypo was based on clinical symptoms, hypocalcemia, hyperphosphatemia, low serum concentrations of intact PTH, and increases in tubular reabsorption of phosphate. These patients with postoperative hypo were totally thyroparathyroidectomized for papillary thyroid cancers. The data were taken 6–16 yr after the operations, and the patients took active vitamin D₃ for 6–16 yr. Idiopathic hypo patients had been receiving active vitamin D₃ treatment for more than 3 yr to maintain normal serum concentrations of calcium and phosphorus. Baseline indices are shown in Table 1 in hyper and hypo patients and in cont. Serum levels of intact PTH were significantly elevated in hyper patients. In patients with hypo, serum levels of intact PTH were markedly decreased. Height, body weight, body mass index, and length of radius were not different among the three groups. The study was approved by the ethical review board of Kobe University Hospital. All subjects agreed to participate in the study and gave informed consent.

Serum concentrations of intact PTH were measured by immunoradiometric assay (Allegro Intact PTH IRMA kit; Nichols Institute Diagnostics, San Juan Capistrano, CA; normal range, 10–65 ng/liter) (12, 13). The intact PTH RIA kit reacts with human PTH (hPTH)-(1–84), whereas hPTH-(1–34), hPTH-(39–84), and hPTH-(39–68) were nonreactive (14).

BMD measurements by DXA

BMD values were measured by DXA using QDR-2000 (Hologic Inc., Waltham, MA) at lumbar spine and distal one third of radius. BMD was automatically calculated from the bone area (cm²) and bone mineral content (BMC) (g) and expressed absolutely in g/cm². The z-score is the number of SD a given measurement differs from the mean for a sex-, age-, and race-matched reference population. The t-score is the number of SD a given measurement differs from the mean for a normal young adult reference population. The coefficients of variation (precision) of measurements of the lumbar spine and radius were 0.9 and 1.9%, respectively.

BMD measurements by pQCT

pQCT analysis was performed at the nondominant forearm using an XCT-960 device (Stratec, Pforzheim, Germany) with a single energy x-ray source, as previously described (15). All computed tomography scans had a slice thickness of 2.5 mm and a vortex size of 0.59 mm. The scanner was positioned at the site of the forearm whose distance from the ulnar styloid process corresponded to 4% and 20% of forearm length, for distal radius and midradius, respectively. To calculate the structural properties of the cortical shell, trabecular and cortical bone had to be separated. To separate the cortical bone, all voxels (0.295 mm x 0.295 mm x 1 mm) of the scanned image with a BMD lower than the threshold (267 mg/cm³) were eliminated. The BMD was calculated for the cortical bone and the trabecular bone separately. Total area (Tt Ar) is the cross-sectional area of the bone after the soft tissue has been peeled off, and cortical area (Ct Ar) is the region with linear attenuation. Cortical thickness (Ct Th) was defined as the mean distance between inner and outer edge of the cortical shell. Polar strength strain index (SSIp) lies within the theory of stability of mechanical structures against bending or torsion. SSIp was calculated by: (r² x A x CD/1200)/r_max, where A is the area of a voxel (mm²), r is its distance from the center of gravity, CD is the cortical density (mg/mm³) and is divided by the normal physiological density of cortical bone (1,200 mg/mm³), and r_max is the maximum distance of a voxel from the center of gravity (16). The coefficient of variation was under 1%.

Statistical analysis

All data were expressed as the mean ± SD for each index. Comparisons among the three groups were made with ANOVA. P values < 0.05 were considered significant.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Comparison of BMD among hyper, hypo, and cont by DXA

We first examined the effects of endogenous PTH on lumbar and radial BMD by DXA. As shown in Table 1, lumbar BMD was higher in the order: hypo > cont = hyper, and radius-1/3 BMD was significantly higher in the order: hypo > cont > hyper. Lumbar BMC was also higher in the order: hypo > cont = hyper, and radius-1/3 BMC was higher in the order: hypo > cont = hyper. Among postmenopausal females, the z-score of lumbar BMD was in the order: hypo (1.43 ± 0.60 mg/cm²) > cont (-0.37 ± 0.77 mg/cm²) = hyper (-0.68 ± 1.04 mg/cm²), and that of radial BMD was significantly higher in the order: hypo (1.47 ± 0.80 mg/cm²) > cont (0.30 ± 1.33 mg/cm²) > hyper (-1.10 ± 1.67 mg/cm²). The area of radius-1/3 was significantly higher in hyper than in the cont, although the areas of lumbar vertebrae 2–4 were not different among the three groups (Table 1).

Comparison of vBMD among hyper, hypo, and cont by pQCT

We next examined the effects of an excess and a deficiency of endogenous PTH on radial vBMD by pQCT. The radius is considered to be rich in trabecular bone at the 4% site and rich in cortical bone at the 20% site. Trabecular vBMD was significantly higher in the order: hypo > cont > hyper at the 4% site. Cortical vBMD was higher in the order: hypo > cont > hyper at 20% site (Table 2). The state of estrogen affects BMD in females. In postmenopausal females, trabecular vBMD was significantly higher in the order: hypo (151.4 ± 28.3 mg/cm³ in seven) > cont (111.8 ± 39.5 mg/cm³ in 81) > hyper (92.3 ± 33.6 mg/cm³ in 34) at the 4% site. Cortical vBMD in postmenopausal females was significantly higher in the order: hypo (1096.5 ± 27.6 mg/cm³ in seven) > cont (1076.0 ± 70.2 mg/cm³ in 81) > hyper (1029.9 ± 83.8 mg/cm³ in 34) at the 20% site.

We examined the effects of endogenous PTH excess or deficiency on bone geometry by pQCT. Table 1 shows bone geometry indices among hyper, hypo, and cont by pQCT. Total bone area and endosteal and periosteal circumferences were significantly higher in hyper than in the cont and hypo groups at both the 4 and 20% sites. Ct Ar and Ct Th were higher in the order: hypo > cont > hyper at both the 4 and 20% sites. These results were consistent in the analysis of postmenopausal females (data not shown). On the other hand, SSIp, a bone strength index, was not significantly different among the three groups (Table 1).

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
In the present study, the z-score of the radius-1/3 BMD by DXA in patients with hyper was significantly lower than that in cont. These findings are compatible with the previous findings (4, 5, 6, 7, 8, 9, 10). However, the areas of total radius as well as radius-1/3 were significantly larger in hyper patients in the present study. Because bone size affects areal BMD, radial BMD as determined by DXA may not be accurate in hyper patients. Indeed, cortical vBMD by pQCT in hyper patients was significantly lower, compared with those in cont. However, the decrease in cortical vBMD by pQCT was less potent than the decrease in areal BMD by DXA. Because radial area measured by DXA was increased in hyper, the decrease in radial BMD might be overestimated. In our study by pQCT, the trabecular vBMD in patients with hyper was significantly lower than that in cont. The previous study (4) and the present study revealed that lumbar BMD by DXA was relatively preserved, compared with radial BMD, in hyper patients. Following methods reported by Carter et al. (17), we calculated bone mineral apparent density (BMAD) from DXA data. BMAD (BMC/area^3/2) values were 0.162 ± 0.028, 0.123 ± 0.023, and 0.113 ± 0.025 for hypo, cont, and hyper, respectively (hyper vs. cont, P < 0.05; hypo vs. cont, P < 0.001) (17). In a modified method by Tabensky et al. (18), BMAD (BMC/area^4/3) values were 0.303 ± 0.048, 0.229 ± 0.044, and 0.211 ± 0.048 for hypo, cont, and hyper, respectively (hyper vs. cont, P < 0.05; hypo vs. cont, P < 0.001). BMAD data suggested that vBMD at the sites rich in trabecular bone was significantly lower in hyper patients, compared with cont, although the differences of trabecular vBMD in pQCT were greater. The anabolic action of PTH is considered to be more potent in weight-bearing bone (19), and several studies suggested that PTH synergistically stimulates bone formation with mechanical stress (20). The present findings, therefore, suggest that an excess of endogenous PTH is more catabolic in non-weight-bearing trabecular bone than in weight-bearing trabecular bone such as lumbar spine. The findings from the histomorphometry of iliac crest bones suggested that trabecular bone was relatively preserved in hyper patients (21, 22, 23). Therefore, the further analysis of trabecular bone in weight-bearing bone, such as spine QCT, is necessary to clarify trabecular osteopenia in hyper patients more precisely.

Previous studies revealed that BMD of patients with postoperative hypo was increased in both trabecular and cortical bones. In our data by pQCT, trabecular vBMD, but not cortical vBMD, was significantly higher in patients with hypo than in cont. The t-score values (division from the young adult means) of trabecular vBMD in pQCT were -1.100 ± 0.678 in postmenopausal hypo patients. Because postmenopausal high bone turnover rate and bone loss were reported to be attenuated in patients with hypo (8, 9), higher trabecular BMD in hypo would be mainly attributable to the prevention of postmenopausal bone loss, presumably through a reduction in bone turnover rate.

pQCT is useful for quantifying geometric properties of long bone because it can be used to estimate area and circumferences of total bone as well as Ct Ar and Ct Th (24). In the present study, the total bone area and endosteal and periosteal circumferences of the total bone in patients with hyper were significantly higher than those in the cont. Moreover, the area of the distal radius in hyper patients was significantly higher than that in cont. These data, therefore, indicated that an excess of endogenous PTH was anabolic for periosteal bone formation. As for cortical bone, the Ct Ar and Ct Th in patients with hyper were significantly lower than those in the cont. These data indicated that an excess of endogenous PTH leads to thin cortical bone. A continuous excess of PTH increases the activation frequency of bone remodeling on both periosteal and endocortical surfaces. The activation magnitude of bone remodeling is increased during the sustained bone balance between periosteal and endocortical surfaces, resulting in increased periosteal bone formation and endosteal bone resorption.

pQCT helps to estimate bone strength by calculating SSIp, which has recently been elaborated to predict bone strength noninvasively (25). In the present study, SSIp of patients with hyper was similar to the SSIp of the cont and hypo groups. These data suggest that the effects of endogenous PTH on bone strength are less significant than its effects on BMD and bone geometry. Bigger bone size is a logical adaptation to enhance the mechanical competence of bone. Consequently, SSIp of patients with hyper was not significantly different from the SSIp values of the cont and patients with hypo. Periosteal bone formation stimulated by an excess of endogenous PTH might partly compensate for a decrease in bone strength induced by decreased BMD. Recent studies have shown that, in hyper patients, the fracture risk of BMD-preserved vertebrae is relatively higher than that of the forearm (26, 27). This might be partly because an increase in bone size enhanced by PTH preserves bone strength.

In conclusion, evaluation of vBMD and bone geometry by pQCT revealed that an excess of endogenous PTH was catabolic for both cortical and trabecular bone, and that bone mass (especially trabecular bone mass) was preserved under conditions of deficient endogenous PTH. An excess of endogenous PTH stimulated periosteal bone formation, which might partly compensate for a decrease in bone strength induced by low BMD.

	Acknowledgments

 
We thank Mr. Takeshi Sugishita for his expert assistance and advice.

	Footnotes

 
Abbreviations: BMAD, Bone mineral apparent density; BMC, bone mineral content; BMD, bone mineral density; cont, normal controls matched to age, gender, and body size; Ct Ar, cortical area; DXA, dual-energy x-ray absorptiometry; hPTH, human PTH; hypo, hypoparathyroidism; hyper, primary hyperparathyroidism; pQCT, peripheral quantitative computed tomography; SSIp, polar strength strain index; Tt Ar, total area; vBMD, volumetric BMD.

Received March 26, 2003.

Accepted June 24, 2003.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Cosman F, Lindsay R 1998 Is parathyroid hormone a therapeutic option for osteoporosis? A review of the clinical evidence. Calcif Tissue Int 62:475–480[CrossRef][Medline]
2. Neer RM, Arnaud CD, Zanchetta JR, Prince R, Gaich GA, Reginster JY, Hodsman AB, Eriksen EF, Ish-Shalom S, Genant HK, Wang O, Mitlak BH 2001 Effect of parathyroid hormone-(1–34) on fracture and bone mineral density in postmenopausal women with osteoporosis. N Engl J Med 344:1434–1441[Abstract/Free Full Text]
3. Silverberg SJ, Shane E, de la Cruz L, Dempster DW, Feldman F, Seldin D, Jacobs TP, Siris ES, Cafferty M, Parisien MV, Lindsay R, Clemens TL, Bilezikian JP 1989 Skeletal disease in primary hyperparathyroidism. J Bone Miner Res 4:283–291[Medline]
4. Dempster DW, Cosman F, Parisien M, Shen V, Lindsay R 1993 Anabolic actions of parathyroid hormone on bone. Endocr Rev 14:690–709[Abstract/Free Full Text]
5. Bilezikian JP, Silverberg SJ, Shane E, Parisien M, Dempster DW 1991 Characterization and evaluation of asymptomatic primary hyperparathyroidism. J Bone Miner Res 6(Suppl 2):S85–S89
6. Wishart J, Horowitz M, Need A, Nordin BE 1990 Relationship between forearm and vertebral mineral density in postmenopausal women with primary hyperparathyroidism. Arch Intern Med 150:1329–1331[Abstract/Free Full Text]
7. Minisola S, Rosso R, Romagnoli E, Pacitti MT, Scarnecchia L, Carnevale V, Mazzuoli G 1993 Trabecular bone mineral density in primary hyperparathyroidism: relationship to clinical presentation and biomarkers of skeletal turnover. Bone Miner 20:113–123[Medline]
8. Abugassa S, Nordenstrom J, Eriksson S, Sjoden G 1993 Bone mineral density in patients with chronic hypoparathyroidism. J Clin Endocrinol Metab 76:1617–1621[Abstract]
9. Fujiyama K, Kiriyama T, Ito M, Nakata K, Yamashita S, Yokoyama N, Nagataki S 1995 Attenuation of postmenopausal high turnover bone loss in patients with hypoparathyroidism. J Clin Endocrinol Metab 80:2135–2138[Abstract]
10. Duan Y, De Luca V, Seeman E 1999 Parathyroid hormone deficiency and excess: similar effects on trabecular bone but differing effects on cortical bone. J Clin Endocrinol Metab 84:718–722[Abstract/Free Full Text]
11. Miller PD, Bilezikian JP 2002 Bone densitometry in asymptomatic primary hyperparathyroidism. J Bone Miner Res 17(Suppl 2):N98–N102
12. Nussbaum SR, Zahradnik RJ, Lavigne JR, Brennan GL, Nozawa-Ung K, Kim LY, Keutmann HT, Wang CA, Potts Jr JT, Segre GV 1987 Highly sensitive two-site immunoradiometric assay of parathyrin, and its clinical utility in evaluating patients with hypercalcemia. Clin Chem 33:1364–1367[Abstract/Free Full Text]
13. Frolich M, Walma ST, Paulson C, Papapoulos SE 1990 Immunoradiometric assay for intact human parathyroid hormone: characteristics, clinical application and comparison with a radio-immunoassay. Ann Clin Biochem 27:69–72
14. D’Amour P, Palardy J, Bahsali G, Mallette LE, Delean A, Lepage R 1992 The modulation of circulating parathyroid hormone immunoheterogeneity in man by ionized calcium concentration. J Clin Endocrinol Metab 74:525–532[Abstract]
15. Ruegsegger P, Durand E, Dambacher MA 1991 Localization of regional forearm bone loss from high-resolution computed tomographic images. Osteoporos Int 1:76–80[CrossRef][Medline]
16. Ashizawa N, Nonaka K, Michikami S, Mizuki T, Amagai H, Tokuyama K, Suzuki M 1999 Tomographical description of tennis-loaded radius: reciprocal relation between bone size and volumetric BMD. J Appl Physiol 86:1347–1351.[Abstract/Free Full Text]
17. Carter DR, Bouxsein ML, Marcus R 1992 New approaches for interpreting projected bone densitometry data. J Bone Miner Res 7:137–145[Medline]
18. Tabensky AD, Williams J, Deluca V, Briganti E, Seeman E 1996 Bone mass, areal, and volumetric bone density are equally accurate, sensitive, and specific surrogates of the breaking strength of the vertebral body: an in vitro study. J Bone Miner Res 11:1981–1988[Medline]
19. Iida-Klein A, Zhou H, Lu SS, Levine LR, Ducayen-Knowles M, Dempster DW, Nieves J, Lindsay R 2002 Anabolic action of parathyroid hormone is skeletal site specific at the tissue and cellular levels in mice. J Bone Miner Res 17:808–816[CrossRef][Medline]
20. Ryder KD, Duncan RL 2000 Parathyroid hormone modulates the response of osteoblast-like cells to mechanical stimulation. Calcif Tissue Int 67:241–246[CrossRef][Medline]
21. Parisien M, Silverberg SJ, Shane E, de la Cruz L, Lindsay R, Bilezikian JP, Dempster DW 1990 The histomorphometry of bone in primary hyperparathyroidism: preservation of cancellous bone structure. J Clin Endocrinol Metab 70:930–938[Abstract/Free Full Text]
22. Parisien M, Mellish RW, Silverberg SJ, Shane E, Lindsay R, Bilezikian JP, Dempster DW 1992 Maintenance of cancellous bone connectivity in primary hyperparathyroidism: trabecular strut analysis. J Bone Miner Res 7:913–919[Medline]
23. Parisien M, Cosman F, Mellish RW, Schnitzer M, Nieves J, Silverberg SJ, Shane E, Kimmel D, Recker RR, Bilezikian JP, Lindsay R, Dempster DW 1995 Bone structure in postmenopausal hyperparathyroid, osteoporotic, and normal women. J Bone Miner Res 10:1393–1399[Medline]
24. Lehmann R, Wapniarz M, Kvasnicka HM, Baedeker S, Klein K, Allolio B 1992 Reproducibility of bone density measurements of the distal radius using a high resolution special scanner for peripheral quantitative computed tomography (Single Energy PQCT). Radiology 32:177–181
25. Martin RB 1991 Determinants of the mechanical properties of bones. J Biomech 24(Suppl 1):79–88
26. Khosla S, Melton III LJ, Wermers RA, Crowson CS, O’Fallon WM, Rings BL 1999 Primary hyperparathyroidism and the risk of fracture: a population-based study. J Bone Miner Res 14:1700–1707[CrossRef][Medline]
27. Vestergaard P, Mollerup CL, Frokjear VG, Christiansen P, Blichert-Toft M, Mosekilde L 2000 Cohort study of risk of fracture before and after surgery for primary hyperparathyroidism. BMJ 321:598–602[Abstract/Free Full Text]

This article has been cited by other articles:

				S. J. Silverberg, E. M. Lewiecki, L. Mosekilde, M. Peacock, and M. R. Rubin Presentation of Asymptomatic Primary Hyperparathyroidism: Proceedings of the Third International Workshop J. Clin. Endocrinol. Metab., February 1, 2009; 94(2): 351 - 365. [Abstract] [Full Text] [PDF]

				H. Kaji, M. Yamauchi, R. Nomura, and T. Sugimoto Improved Peripheral Cortical Bone Geometry after Surgical Treatment of Primary Hyperparathyroidism in Postmenopausal Women J. Clin. Endocrinol. Metab., August 1, 2008; 93(8): 3045 - 3050. [Abstract] [Full Text] [PDF]

				S. De Geronimo, E. Romagnoli, D. Diacinti, E. D'Erasmo, and S. Minisola The risk of fractures in postmenopausal women with primary hyperparathyroidism Eur. J. Endocrinol., September 1, 2006; 155(3): 415 - 420. [Abstract] [Full Text] [PDF]

				I. Charopoulos, S. Tournis, G. Trovas, P. Raptou, P. Kaldrymides, G. Skarandavos, K. Katsalira, and G. P. Lyritis Effect of Primary Hyperparathyroidism on Volumetric Bone Mineral Density and Bone Geometry Assessed by Peripheral Quantitative Computed Tomography in Postmenopausal Women J. Clin. Endocrinol. Metab., May 1, 2006; 91(5): 1748 - 1753. [Abstract] [Full Text] [PDF]

				C. Kristo, R. Jemtland, T. Ueland, K. Godang, and J. Bollerslev Restoration of the coupling process and normalization of bone mass following successful treatment of endogenous Cushing's syndrome: A prospective, long-term study Eur. J. Endocrinol., January 1, 2006; 154(1): 109 - 118. [Abstract] [Full Text] [PDF]

				A Iida-Klein, S S. Lu, R Kapadia, M Burkhart, A Moreno, D W Dempster, and R Lindsay Short-term continuous infusion of human parathyroid hormone 1-34 fragment is catabolic with decreased trabecular connectivity density accompanied by hypercalcemia in C57BL/J6 mice J. Endocrinol., September 1, 2005; 186(3): 549 - 557. [Abstract] [Full Text] [PDF]

				D. Miao, J. Li, Y. Xue, H. Su, A. C. Karaplis, and D. Goltzman Parathyroid Hormone-Related Peptide Is Required for Increased Trabecular Bone Volume in Parathyroid Hormone-Null Mice Endocrinology, August 1, 2004; 145(8): 3554 - 3562. [Abstract] [Full Text] [PDF]

				M. Bastepe, A. Raas-Rothschild, J. Silver, I. Weissman, S. Wientroub, H. Juppner, and D. Gillis A Form of Jansen's Metaphyseal Chondrodysplasia with Limited Metabolic and Skeletal Abnormalities Is Caused by a Novel Activating Parathyroid Hormone (PTH)/PTH-Related Peptide Receptor Mutation J. Clin. Endocrinol. Metab., July 1, 2004; 89(7): 3595 - 3600. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, Q. Articles by Chihara, K. Search for Related Content PubMed PubMed Citation Articles by Chen, Q. Articles by Chihara, K. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information CT Scans Hazardous Substances DB PARATHYROID HORMONE