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From the Clinical Research Centers |
Burns and Allen Research Institute and Division of Endocrinology, Diabetes, and Metabolism, Cedars-Sinai Medical Center, University of California School of Medicine (V.K., M.A.G., J.S.A.), Los Angeles, California 90048; and Department of Radiological Sciences, Center for the Health Sciences, University of California School of Medicine (L.L.S.), Los Angeles, California 90095
Address all correspondence and requests for reprints to: Dr. John S. Adams, Burns and Allen Research Institute, Division of Endocrinology, Diabetes, and Metabolism, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Room B131, Los Angeles, California 90048. E-mail: adamsj{at}cshs.org
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Abstract |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Both primary hyperparathyroidism and occult vitamin D deficiency are relatively common disorders. Primary hyperparathyroidism has an estimated prevalence of 100 cases/100,000 normal population (5). The prevalence of hypovitaminosis D has been reported to be as high as 32% in healthy, free-living, postmenopausal women during the winter months (6) and up to 54% in the homebound elderly population (7). In a recent retrospective study of 237 patients who attended a specialty osteoporosis practice, 17% of the osteoporotic patients had 25OHD levels below 37.4 nmol/L (15 ng/mL) (6).
Coexistence of vitamin D insufficiency and hyperparathyroidism is not uncommon, even in sun-rich environments that are located at relatively low latitudes (8, 9, 10, 11). Our current report supports this finding and demonstrates that vitamin D repletion is associated with a rapid rebound in BMD even in the face of persistent primary hyperparathyroidism.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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2-h) fasting urine sample for measurement of
calcium and creatinine. The serum 25OHD and
1,25-(OH)2D levels were determined by competitive
protein binding assays (Endocrine Sciences, Inc., Woodland
Hills, CA). The serum iPTH and TSH levels were measured in
immunoradiometric assays (Nichols Institute Diagnostics,
San Juan Capistrano, CA). Calcium, albumin, and creatinine levels were
determined spectrophotometrically. BMD of the lumbar spine and proximal
femur was assessed by dual energy x-ray absorptiometry (Lunar Corp., Madison, WI); the coefficient of variation for
measurement of BMD in spine and femoral neck was 1.0% and 1.2%,
respectively. All patients showed a t score of less than
-1.50 at the hip and/or spine, which was compatible with a diagnosis
of osteopenia or osteoporosis. Fifteen subjects (13 women and 2 men) had low 25OHD levels (10.3 ± 0.6 ng/mL; range, 5–14) and consistently elevated iPTH levels (109.2 ± 13.7 pg/mL; range, 69–252). All patients were supplemented with 1000 mg elemental calcium (Os-Cal 500, SmithKline Beecham, Pittsburgh, PA) and oral vitamin D2 (50,000 IU) was administered twice weekly for a 5-week period. Serum parameters of calcium, albumin, 25OHD, and iPTH were monitored in all subjects until 25OHD and/or iPTH concentrations returned to the normal range.
All data are expressed as the mean ± SE. Statistical comparisons were made using Wilcoxon’s matched pairs test.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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). This finding supported the diagnosis
of primary hyperparathyroidism (i.e. autonomous parathyroid
function), bringing the prevalence of coexistent primary
hyperparathyroidism and vitamin D insufficiency in our cohort of 229
patients with low bone mass to 2.2%. Primary hyperparathyroidism was
confirmed pathologically in patient 1 (Table 1). In this patient
progressive hypercalcemia after vitamin D replacement prompted surgical
removal of a parathyroid adenoma 6 months after initial ascertainment
of her serum chemistry values and 2 months after follow-up measurement
of her BMD by DEXA. In all subjects vitamin D repletion resulted in a
significant increase in 25OHD levels (Table 1) as well as in mean
fasting calcium excretion (calcium/creatinine ratio, 0.06 ± 0.16
to 0.24 ± 0.09; P = 0.03). Although hypercalcemia
did not develop with vitamin D repletion, frank hypercalciuria was
induced in 3 previously normocalciuric individuals (fasting urinary
calcium/creatinine ratio, 0.36, 0.31, and 0.60 in patients 1, 2, and 5,
respectively; normal, <0.16). The other 2 subjects (patients 3 and 4;
Table 1) remained normocalcemic more than 1 yr postcorrection of
vitamin D insufficiency. In these two subjects the diagnosis of
primary, not secondary, hyperparathyroidism was confirmed by a further
rise in iPTH levels after vitamin D replacement; iPTH levels in treated
vitamin D-insufficient patients with secondary hyperparathyroidism
characteristically return to normal within 3 months (12), whereas
persistence of an elevated iPTH concentration for 6 months or more
almost always heralds the presence of pathological parathyroid tissue
at surgery (13). There was no significant change in mean serum
1,25-(OH)2D levels, and the osteocalcin
concentration was not altered by vitamin D repletion in this subset of
patients.
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). Vitamin D repletion resulted in a significant
increase in BMD at both lumbar spine and femoral neck (Table 1) as well
as an improvement in mean t scores from -1.35 ± 0.79
to -0.72 ± 0.86 at the lumbar spine and from -2.96 ± 0.38
to -2.47 ± 0.2 at the femoral neck. The mean interval between
initial and final determinations of BMD was 13 ± 8 months, an
interval long enough to detect a significant change in bone mass for
patients with either primary (3) or secondary (4) hyperparathyroidism.
A monthly rate of increase in 0.005 ± 0.002 and 0.004 ±
0.002 g/cm2 at the spine and hip was measured
with a mean annual increase in BMD of 6.3% and 8.2% at these sites,
respectively. |
Discussion |
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In conclusion, our data confirm that the standard biochemical phenotype for primary hyperparathyroidism can be obscured by coexisting vitamin D insufficiency and can become evident upon adequate vitamin D replacement. Our results also suggest that discovery and treatment of vitamin D insufficiency in patients with low bone mass and primary hyperparathyroidism are worthwhile in advance of definitive treatment of the state of primary hyperparathyroidism.
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Footnotes |
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Received May 4, 2000.
Revised June 13, 2000.
Accepted June 21, 2000.
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This article has been cited by other articles:
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  B Moosgaard, P Vestergaard, L Heickendorff, F Melsen, P Christiansen, and L Mosekilde Plasma 25-hydroxyvitamin D and not 1,25-dihydroxyvitamin D is associated with parathyroid adenoma secretion in primary hyperparathyroidism: a cross-sectional study. Eur. J. Endocrinol., August 1, 2006; 155(2): 237 - 244. [Abstract] [Full Text] [PDF]
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 D. M. Antoniucci, E. Vittinghoff, T. Blackwell, D. M. Black, and D. E. Sellmeyer Vitamin D Insufficiency Does Not Affect Bone Mineral Density Response to Raloxifene J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4566 - 4572. [Abstract] [Full Text] [PDF]
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 M. P. Boyle, M. L. Noschese, S. L. Watts, M. E. Davis, S. E. Stenner, and N. Lechtzin Failure of High-Dose Ergocalciferol to Correct Vitamin D Deficiency in Adults with Cystic Fibrosis Am. J. Respir. Crit. Care Med., July 15, 2005; 172(2): 212 - 217. [Abstract] [Full Text] [PDF]
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A. Grey, J. Lucas, A. Horne, G. Gamble, J. S. Davidson, and I. R. Reid Vitamin D Repletion in Patients with Primary Hyperparathyroidism and Coexistent Vitamin D Insufficiency J. Clin. Endocrinol. Metab., April 1, 2005; 90(4): 2122 - 2126. [Abstract] [Full Text] [PDF]
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