Melissa K. Thomas, M.D., Ph.D., Donald M. Lloyd-Jones, M.D., Ravi I. Thadhani, M.D., M.P.H., Albert C. Shaw, M.D., Ph.D., Donald J. Deraska, M.D., Barrett T. Kitch, M.D., Eleftherios C. Vamvakas, M.D., Ph.D., Ian M. Dick, M.Sc., Richard L. Prince, M.D., and Joel S. Finkelstein, M.D.
Background Vitamin D deficiency is a major risk factor for boneloss and fracture. Although hypovitaminosis D has been detectedfrequently in elderly and housebound people, the prevalenceof vitamin D deficiency among patients hospitalized on a generalmedical service is unknown.
Methods We assessed vitamin D intake, ultraviolet-light exposure,and risk factors for hypovitaminosis D and measured serum 25-hydroxyvitaminD, parathyroid hormone, and ionized calcium in 290 consecutivepatients on a general medical ward.
Results A total of 164 patients (57 percent) were consideredvitamin D–deficient (serum concentration of 25-hydroxyvitaminD, <15 ng per milliliter), of whom 65 (22 percent) were consideredseverely vitamin D–deficient (serum concentration of 25-hydroxyvitaminD, <8 ng per milliliter). Serum 25-hydroxyvitamin D concentrationswere related inversely to parathyroid hormone concentrations.Lower vitamin D intake, less exposure to ultraviolet light,anticonvulsant-drug therapy, renal dialysis, nephrotic syndrome,hypertension, diabetes mellitus, winter season, higher serumconcentrations of parathyroid hormone and alkaline phosphatase,and lower serum concentrations of ionized calcium and albuminwere significant univariate predictors of hypovitaminosis D.Sixty-six percent of the patients who consumed less than therecommended daily amount of vitamin D and 37 percent of thepatients with intakes above the recommended daily amount werevitamin D–deficient. Inadequate vitamin D intake, winterseason, and housebound status were independent predictors ofhypovitaminosis D in a multivariate model. In a subgroup of77 patients less than 65 years of age without known risk factorsfor hypovitaminosis D, the prevalence of vitamin D deficiencywas 42 percent.
Conclusions Hypovitaminosis D is common in general medical inpatients,including those with vitamin D intakes exceeding the recommendeddaily amount and those without apparent risk factors for vitaminD deficiency.
Vitamin D deficiency is a risk factor for osteopenia and bonefractures.1,2,3,4,5 In ambulatory elderly people whose averageserum concentration of 25-hydroxyvitamin D was slightly low,supplementation with 20 µg (800 IU) of vitamin D and withcalcium substantially reduced the risk of osteoporotic fractures,including hip fractures.6,7 Multiple studies have estimatedthe prevalence of hypovitaminosis D in selected populationsat particular risk for vitamin D deficiency, such as residentsof nursing homes and people over the age of 65, to be between25 and 54 percent.8,9,10,11 However, the prevalence of hypovitaminosisD in more diverse patient populations has not been well characterized.Conditions associated with hypovitaminosis D, such as poor dietaryintake, inadequate sun exposure, and chronic liver and renaldiseases, are common in general medical inpatients, as is therapywith drugs that impair vitamin D activation or accelerate itsclearance, such as phenytoin, carbamazepine, and rifampin. Thus,such inpatients may be at risk for vitamin D deficiency. Becausereplacement therapy is simple and reduces the risk of fractures,an understanding of the prevalence of vitamin D deficiency mayalter routine medical practice and have important public healthimplications.
Methods
Study Subjects
We studied 150 patients admitted consecutively in March 1994and 140 patients admitted consecutively in September 1994 togeneral medical wards at Massachusetts General Hospital. Themonths of March and September were chosen to represent the seasonalnadir and peak, respectively, of serum vitamin D concentrationsin Boston.12 The study was approved by the Subcommittee on HumanStudies of Massachusetts General Hospital, and oral consentwas obtained from the patients (3 of 293 declined to participate).
A subgroup of 77 patients with no known risk factors for hypovitaminosisD was defined by excluding patients who were more than 65 yearsof age, housebound or living in a nursing home, or taking anticonvulsantdrugs, or who had a chronic debilitating illness (cancer, acquiredimmunodeficiency syndrome, congestive heart failure, or chronicobstructive pulmonary disease), renal disease (defined as aserum creatinine concentration >1.5 mg per deciliter [133µmol per liter], the presence of the nephrotic syndrome,or the need for dialysis), liver disease (defined as a serumbilirubin concentration >2.0 mg per deciliter [34 µmolper liter] or the presence of hepatitis or cirrhosis), or acondition causing malabsorption of nutrients (inflammatory boweldisease, chronic pancreatitis, or gastric or small-bowel resection).
Evaluation of Clinical Characteristics
Within 24 hours after admission, each patient's record was reviewed.The data collected included age, sex, race, and diagnoses, withemphasis on any history of liver disease, renal disease, gastricor small-bowel surgery, inflammatory bowel disease, pancreatitis,malabsorption, and therapy with anticonvulsant agents (phenytoin,phenobarbital, and carbamazepine), rifampin, or glucocorticoids.Each patient was classified as ambulatory, housebound, livingin a nursing home, or homeless. The patients were not followedduring the hospitalization, except to determine mortality duringthe incident admission.
Dietary and Sun-Exposure Interviews
Study physicians were trained by a research dietitian to obtainstandardized histories of dietary vitamin D intake. A questionnairewas developed that included a list of foods containing vitaminD in amounts of at least 1.25 µg (50 IU) per serving,13and average daily and weekly consumption of these foods wasassessed. Regular use of multivitamins, vitamin D, or calciumsupplements was noted. Exposure to the sun was rated with theuse of a previously validated nine-point scale,14 which measuredthe degree and extent of recent sun exposure, the use of sunscreens,and recent travel to southern locations. Two hundred six patientscompleted both the dietary and sun-exposure interviews. Theremaining 84 patients were unable to provide complete dietaryand sun-exposure information because of impaired mental statusand were excluded from the multivariate analyses.
Laboratory Studies
Morning blood samples were obtained from the patients afteran overnight fast within 24 hours after admission. Serum parathyroidhormone was measured by a two-site immunoradiometric assay.15Serum 25-hydroxyvitamin D was measured by competitive protein-bindingassay (Nichols Institute, San Juan Capistrano, Calif.). Serumvitamin D–binding protein was measured by radioimmunoassay.16Routine chemistries were measured by a Hitachi multichannelanalyzer, and serum ionized calcium was measured by a gas analyzer(Nova Biomedical, Waltham, Mass.). The samples were analyzedin multiple assays; the interassay coefficients of variationwere less than 6 percent for the measurements of parathyroidhormone and 8 to 14 percent for 25-hydroxyvitamin D.
Definition of Hypovitaminosis D
The patients were divided into three diagnostic categories accordingto their serum 25-hydroxyvitamin D concentrations: those withsevere hypovitaminosis D (serum 25-hydroxyvitamin D concentration,less than 8 ng per milliliter [20 nmol per liter]), those withmoderate hypovitaminosis D (serum 25-hydroxyvitamin D concentration,8 to 15 ng per milliliter [20 to 37 nmol per liter]), and thosewith adequate vitamin D stores (serum 25-hydroxyvitamin D concentration,more than 15 ng per milliliter). The definition of severe hypovitaminosisD was based on the lower limit of normal of 9 ng per milliliter(22 nmol per liter) for serum 25-hydroxyvitamin D concentrationsin New England as measured by chromatography in the referencelaboratory (Nichols Institute). The definition of moderate hypovitaminosisD was determined according to the Nichols Institute's normsfor serum 25-hydroxyvitamin D of 16 to 74 ng per milliliter(40 to 185 nmol per liter) in a competitive protein-bindingassay (mean ±2 SD calculated from measurements in 208normal adult subjects in Southern California, Virginia, andNew England in the summer and early fall) and from publisheddata demonstrating that serum parathyroid hormone concentrationsare increased in patients who have serum 25-hydroxyvitamin Dconcentrations that are less than or equal to 15 ng per milliliter.11,17,18
Statistical Analysis
There were no differences between the characteristics of thepatients studied in March and those of the patients studiedin September, and the results were therefore combined. Associationsbetween categorical variables and categories of serum 25-hydroxyvitaminD concentrations were examined by using Pearson's chi-squaretests. Kruskal–Wallis nonparametric analysis of variancewas used to examine associations between continuous variablesand categories of serum 25-hydroxyvitamin D concentrations.For multivariate analyses, vitamin D deficiency was definedas a serum 25-hydroxyvitamin D concentration less than or equalto 15 ng per milliliter. Associations with categorical variableswere examined with the use of two-tailed Fisher's exact tests,and associations with continuous variables were examined withMann–Whitney rank-sum tests.
Stepwise discriminant analyses were used to identify the variablesthat best predicted vitamin D deficiency and to calculate theaccuracy of those predictors.19 The accuracy of the computeddiscriminant function was estimated by a jackknifed classificationmatrix.20 Variables associated with serum 25-hydroxyvitaminD concentrations in univariate analyses (P<0.10) were eligiblefor inclusion in the multivariate models.
Results
Clinical Characteristics
The characteristics of the patients are shown in Table 1. Fewpatients had conditions often associated with hypovitaminosisD or were taking medications known to alter vitamin D metabolism(Table 2). Three patients with serum 25-hydroxyvitamin D concentrationsof less than 8 ng per milliliter, two patients with concentrationsbetween 8 and 15 ng per milliliter, and three patients withvalues greater than 15 ng per milliliter died while in the hospital.
Table 2. Prevalence of Conditions Often Associated with Hypovitaminosis D in the 290 Patients.
Prevalence of Hypovitaminosis D
The prevalence of hypovitaminosis D in the 290 patients was57 percent (164 patients) (Figure 1). Sixty-five patients (22percent) had severe hypovitaminosis D, and an additional 99patients (34 percent) had moderate hypovitaminosis D. Sixty-threepercent of the patients studied in March and 49 percent of thosestudied in September had serum 25-hydroxyvitamin D concentrationsof 15 ng per milliliter or less. The mean (±SD) serum25-hydroxyvitamin D concentration for all 290 patients was 15±9ng per milliliter. Serum parathyroid hormone concentrationsrose steeply as serum 25-hydroxyvitamin D concentrations declinedbelow 15 ng per milliliter (Figure 2), indicating a physiologicresponse, presumably through hypocalcemia, to the low serum25-hydroxyvitamin D concentrations.
Figure 1. Prevalence of Hypovitaminosis D among 290 Medical Inpatients.
The percentages of patients with serum 25-hydroxyvitamin D concentrations of less than 8 ng per milliliter, 8 to 15 ng per milliliter, or greater than 15 ng per milliliter in the entire study population are shown by the solid bars, and the percentages among the subgroup of 77 patients with no known risk factors for hypovitaminosis D are shown by the open bars. To convert values for 25-hydroxyvitamin D to nanomoles per liter, multiply by 2.50.
Figure 2. Relation between Serum 25-Hydroxyvitamin D Concentrations and Mean (±SE) Serum Concentrations of Parathyroid Hormone in the Study Patients.
The patients were categorized according to their serum 25-hydroxyvitamin D concentrations in increments of 5 ng per milliliter. The slope of the relation between serum 25-hydroxyvitamin D and parathyroid hormone concentrations was not significantly different (P = 0.13) from zero for patients with serum 25-hydroxyvitamin D concentrations greater than 15 ng per milliliter. To convert values for 25-hydroxyvitamin D to nanomoles per liter, multiply by 2.50. To convert values for parathyroid hormone to picomoles per liter, multiply by 0.11.
Variables Associated with Hypovitaminosis D
Anticonvulsant-drug therapy (P = 0.04), renal dialysis (P =0.007), nephrotic syndrome (P = 0.04), and winter season (P= 0.04) were significantly associated with hypovitaminosis D.There were trends toward associations with housebound status(P = 0.07) and female sex (P = 0.08). Of the 60 housebound patients,42 (70 percent) had serum 25-hydroxyvitamin D concentrationsof 15 ng per milliliter or less. Of the 18 most frequently noteddiagnoses (each affecting at least 20 patients), only hypertension(P = 0.009) and diabetes mellitus (P = 0.04) were significantlyassociated with hypovitaminosis D.
Lower vitamin D intake, exposure to ultraviolet light, and serumconcentrations of ionized calcium and albumin, and higher serumconcentrations of parathyroid hormone and alkaline phosphatasewere associated with lower 25-hydroxyvitamin D concentrations.There was no association between serum concentrations of vitaminD–binding protein and 25-hydroxyvitamin D (Table 3).
Table 3. Association of Continuous Variables with Vitamin D Deficiency.
Vitamin D Intake and Sun Exposure
Serum 25-hydroxyvitamin D concentrations were higher in thepatients with higher vitamin D intakes (Figure 3A and Figure 3B).The mean (±SD) daily vitamin D intake reported was7.5±7.3 µg (300±292 IU). Sixty-seven percentof the patients reported vitamin D intakes less than the recommendeddaily amount for their age (5 µg for adults 19 to 50 yearsold, 10 µg for adults 51 to 70 years old, and 15 µgfor adults 71 or older21). Moderate or severe hypovitaminosisD was present in 66 percent of the patients reporting dailyvitamin D intakes less than the recommended amount for theirage and in 37 percent of the patients reporting daily vitaminD intakes in excess of the recommended amount for their age.Forty-six percent of the patients who reported taking multivitaminsand 60 percent of those who reported not taking multivitaminshad hypovitaminosis D. Increasing exposure to ultraviolet lightwas also associated with higher serum 25-hydroxyvitamin D concentrations(Figure 3A and Figure 3B).
Figure 3. Relation between Daily Vitamin D Intake (Panel A) and Ultraviolet-Light Exposure (Panel B) and Mean (±SE) Serum 25-Hydroxyvitamin D Concentrations in the Study Patients.
The patients were categorized according to vitamin D intake or ultraviolet-light exposure. To convert values for 25-hydroxyvitamin D to nanomoles per liter, multiply by 2.50. To convert values for vitamin D intake to international units, multiply by 40.
Predictors of Hypovitaminosis D
Independent predictors of hypovitaminosis D were identifiedby stepwise multivariate discriminant analysis in which riskfactors for vitamin D deficiency that had a univariate association(P<0.10) with vitamin D deficiency were included in the model.These factors were inadequate vitamin D intake, insufficientsun exposure, winter season, older age, female sex, anticonvulsant-drugtherapy, dialysis, nephrotic syndrome, and being housebound.Inadequate vitamin D intake, winter season, and being houseboundwere significant independent predictors of hypovitaminosis Dand could correctly classify 59 percent of the patients (P<0.001).The addition of the other six variables to the model increasedthe accuracy of the classification to 68 percent.
Prevalence of Hypovitaminosis D in the Patients with No Known Risk Factors
The mean age of the 77 patients in the subgroup with no knownrisk factors for vitamin D deficiency was 44±14 years.Forty-eight (62 percent) were men and 29 (38 percent) were women.The most common diagnoses in this subgroup were coronary arterydisease (39 percent), hypertension (29 percent), diabetes mellitus(17 percent), hypercholesterolemia (16 percent), substance abuse(16 percent), asthma (16 percent), atrial fibrillation (8 percent),and syncope (8 percent). Among these patients, 32 (42 percent)were vitamin D–deficient, of whom 11 had serum 25-hydroxyvitaminD concentrations of less than 8 ng per milliliter and 21 hadvalues between 8 and 15 ng per milliliter (Figure 1).
Discussion
We found a high prevalence (57 percent) of hypovitaminosis Din unselected general medical inpatients. In previous studiesof elderly housebound people and nursing home residents, onequarter to one half were vitamin D–deficient.8,9,10,11The patients we studied were younger than those in many previousstudies, and only a minority were housebound or residents ofa nursing home. Thus, our patients may have been more representativeof the general population than those reported on previously.
It is unclear why the prevalence of vitamin D deficiency wasso high. Low levels of ultraviolet-light exposure and vitaminD intake are probably important factors. The definition of vitaminD deficiency may also affect estimates of its prevalence. Wedefined categories of severe and moderate hypovitaminosis Don the basis of a series of observations in the literature.11,17,18,22Serum parathyroid hormone concentrations have been found toincrease when serum 25-hydroxyvitamin D concentrations fallbelow 15 ng per milliliter in elderly housebound people,11 andwe found a similar relation in the patients we studied. In postmenopausalwomen, bone density is lower in those who have serum 25-hydroxyvitaminD concentrations of 15 ng per milliliter or less.23 Thus, thereis strong physiologic evidence that serum 25-hydroxyvitaminD concentrations of 15 ng per milliliter or less are insufficientto maintain adequate skeletal integrity.
In fact, other investigators have reported that serum 25-hydroxyvitaminD concentrations above 15 ng per milliliter may not be sufficientto exclude hypovitaminosis D. There are seasonal changes inboth serum parathyroid hormone concentrations and bone densityin patients with serum 25-hydroxyvitamin D concentrations of37 ng per milliliter (92 nmol per liter) or less.24,25 Increasingpatients' serum 25-hydroxyvitamin D concentrations to 20 ngper milliliter (50 nmol per liter) through supplementation withvitamin D increases serum 1,25-dihydroxyvitamin D concentrations,26and some experts have suggested that serum 25-hydroxyvitaminD concentrations should exceed 30 ng per milliliter (75 nmolper liter). Had we used such a definition of vitamin D deficiencyto categorize our patients, 93 percent of them would have beenconsidered vitamin D–deficient.
Previous estimates of the prevalence of hypovitaminosis D inoutpatients were substantially lower than in our study.9,27The higher prevalence of vitamin D deficiency in this studymay be related in part to the relatively low solar intensityin New England12 or to the nature of our patients. Medical inpatientsare more likely than outpatients to have conditions associatedwith vitamin D deficiency. However, 42 percent of our healthysubgroup were vitamin D–deficient, providing evidencethat these results are not attributable to severity of illness.
A large number of patients with vitamin D intakes above therecommended daily amount were vitamin D–deficient. Becausemilk products contain variable amounts of vitamin D,28 vitaminD intake may have been overestimated. Multivitamin therapy wasnot protective. This finding might reflect inaccurate self-reporting,because the majority of multivitamin supplements contain 10µg of vitamin D. Our data support the conclusion thatthe current recommended daily intakes of vitamin D, which wererecently revised upward,21 may be insufficient. For example,a daily intake of 5 µg of vitamin D was less effectivein preventing bone loss than a daily intake of 20 µg inpostmenopausal women.29 Moreover, daily administration of 10µg of vitamin D in patients with high dietary calciumintakes did not protect against fractures,30 whereas 20 µgof vitamin D per day plus calcium decreased the risk of fracturesin elderly women with lower dietary calcium intakes.6,7
Our multivariate models could predict vitamin D deficiency withan accuracy of 59 to 68 percent, making them only slightly moreaccurate than predictions that would have occurred by chance.Because the assessment of common clinical risk factors failedto identify many patients with hypovitaminosis D, screeningby using serum 25-hydroxyvitamin D concentrations may be requiredto identify patients with vitamin D deficiency.
The importance of vitamin D deficiency is related primarilyto bone integrity. Because vitamin D is required for calciumhomeostasis, secondary hyperparathyroidism may develop in patientswith vitamin D deficiency. With increasing severity of hypovitaminosisD and secondary hyperparathyroidism, patients progress fromstates of increased bone turnover and decreased bone mass tostates of impaired, and ultimately absent, mineralization withgeneralized osteomalacia.1 Many patients with osteoporotic fractureshave low serum 25-hydroxyvitamin D concentrations.4,5 Becausetreatment with vitamin D and calcium increases bone mass andsubstantially reduces the risk of fractures,3,6,7,31 the diagnosisof vitamin D deficiency warrants attention. In addition to itseffect on the skeleton, hypovitaminosis D may affect other organsystems adversely, resulting in muscle weakness and pain,2 progressionof osteoarthritis,32 or impaired macrophage activation.33
Our study had several limitations. Many patients were acutelyill. Although it is possible that acute illness could have suppressedcutaneous vitamin D synthesis, the half-life of serum 25-hydroxyvitaminD is approximately three weeks,34 so an arrest of synthesisshould not have affected serum 25-hydroxyvitamin D concentrationsrapidly. Substantial reductions in serum concentrations of vitaminD–binding protein are needed to lower serum 25-hydroxyvitaminD concentrations. Such reductions occur in only a few clinicalconditions, such as severe hepatic failure, nephrotic syndrome,and severe malnutrition,2,35 which were rare in our patients.Furthermore, we found no relation between serum concentrationsof 25-hydroxyvitamin D and those of vitamin D–bindingprotein in our patients. Thus, it seems unlikely that changesin concentrations of serum vitamin D–binding protein dueto acute illness can explain our findings. Finally, the higherserum parathyroid hormone concentrations in the patients withlow serum 25-hydroxyvitamin D concentrations attest to the physiologicimportance of the latter. In fact, we may have underestimatedthe prevalence of hypovitaminosis D by not identifying patientswith low serum 1,25-dihydroxyvitamin D concentrations despiteadequate serum 25-hydroxyvitamin D concentrations.
In conclusion, we found a high prevalence of hypovitaminosisD in unselected medical inpatients in the United States. Standardclinical risk factors were poor predictors of vitamin D deficiency.Maintaining vitamin D intake at the level of the current recommendeddaily amount or using multivitamins may not be sufficient toensure adequate vitamin D stores. Because of the potential adverseeffects of vitamin D deficiency on the skeleton and other organsystems, widespread screening for vitamin D deficiency or routinevitamin D supplementation should be considered.
Supported by grants from the National Institutes of Health (RR-1066,R29-DK43341, DK07028, and DK02476) and the American Kidney Fund.
We are indebted to the nursing staff of the Mallinckrodt GeneralClinical Research Center at Massachusetts General Hospital forprocessing patient samples; to the resident physicians and staffof the Bigelow medical services for facilitating patient participation;to Deborah Lentz, R.D., Ellen Anderson, R.D., and Jane Hubbard,R.D., for conducting dietary analyses; to Dr. Gino Segre ofthe endocrine laboratory for assisting with measurements ofserum parathyroid hormone and 25-hydroxyvitamin D; to Dr. RogerBouillon for providing vitamin D–binding protein antiserum;to Dr. John T. Potts, Jr., for encouraging and supporting researchby house staff; and to Dr. Robert Neer for providing scholarlyadvice.
Source Information
From the Endocrine Unit (M.K.T., D.J.D., J.S.F.), Department of Medicine (D.M.L.-J., R.I.T., A.C.S., B.T.K.), and the Department of Pathology (E.C.V.), Massachusetts General Hospital and Harvard Medical School, Boston; and the Department of Medicine, University of Western Australia, Perth (I.M.D.), and the Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands (R.L.P.) — both in Australia.
Address reprint requests to Dr. Finkelstein at the Endocrine Unit, Bulfinch 327, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114.
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Eastell, R., Arnold, A., Brandi, M. L., Brown, E. M., D'Amour, P., Hanley, D. A., Rao, D. S., Rubin, M. R., Goltzman, D., Silverberg, S. J., Marx, S. J., Peacock, M., Mosekilde, L., Bouillon, R., Lewiecki, E. M.
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Hegge, K. A., Fornoff, A. S., Gutierres, S. L., Haack, S. L.
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White, J. H.
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Cauley, J. A., LaCroix, A. Z., Wu, L., Horwitz, M., Danielson, M. E., Bauer, D. C., Lee, J. S., Jackson, R. D., Robbins, J. A., Wu, C., Stanczyk, F. Z., LeBoff, M. S., Wactawski-Wende, J., Sarto, G., Ockene, J., Cummings, S. R.
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Melamed, M. L., Michos, E. D., Post, W., Astor, B.
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Gardner, R. L., Harris, F., Vittinghoff, E., Cummings, S. R.
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Wagner, D., Sidhom, G., Whiting, S. J., Rousseau, D., Vieth, R.
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Mehrotra, R., Kermah, D., Budoff, M., Salusky, I. B., Mao, S. S., Gao, Y. L., Takasu, J., Adler, S., Norris, K.
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Wolf, M., Betancourt, J., Chang, Y., Shah, A., Teng, M., Tamez, H., Gutierrez, O., Camargo, C. A. Jr., Melamed, M., Norris, K., Stampfer, M. J., Powe, N. R., Thadhani, R.
(2008). Impact of Activated Vitamin D and Race on Survival among Hemodialysis Patients. J. Am. Soc. Nephrol.
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Wang-Gillam, A., Miles, D. A., Hutchins, L. F.
(2008). Evaluation of Vitamin D Deficiency in Breast Cancer Patients on Bisphosphonates. The Oncologist
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Giovannucci, E., Liu, Y., Hollis, B. W., Rimm, E. B.
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Gordon, C. M., Feldman, H. A., Sinclair, L., Williams, A. L., Kleinman, P. K., Perez-Rossello, J., Cox, J. E.
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Bowden, S. A., Robinson, R. F., Carr, R., Mahan, J. D.
(2008). Prevalence of Vitamin D Deficiency and Insufficiency in Children With Osteopenia or Osteoporosis Referred to a Pediatric Metabolic Bone Clinic. Pediatrics
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Holick, M. F, Chen, T. C
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Blum, M., Dallal, G. E., Dawson-Hughes, B.
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(2008). A longitudinal study of serum 25-hydroxyvitamin D and intact parathyroid hormone levels indicate the importance of vitamin D and calcium homeostasis regulation in multiple sclerosis. J. Neurol. Neurosurg. Psychiatry
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Wang, T. J., Pencina, M. J., Booth, S. L., Jacques, P. F., Ingelsson, E., Lanier, K., Benjamin, E. J., D'Agostino, R. B., Wolf, M., Vasan, R. S.
(2008). Vitamin D Deficiency and Risk of Cardiovascular Disease. Circulation
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Dawson-Hughes, B., Chen, P., Krege, J. H.
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Rowling, M. J., Gliniak, C., Welsh, J., Fleet, J. C.
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Bouillon, R., Norman, A. W., Lips, P., Cava, R. C., Javier, A. N. D., Howe, W. R., Dellavalle, R., Baroncelli, G. I., Holick, M. F.
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Tylavsky, F. A., Ryder, K. M., Li, R., Park, V., Womack, C., Norwood, J., Carbone, L. D., Cheng, S.
(2007). Preliminary Findings: 25(OH)D Levels and PTH Are Indicators of Rapid Bone Accrual in Pubertal Children. J. Am. Coll. Nutr.
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Burleigh, E., McColl, J., Potter, J.
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Wallis, D. E., Penckofer, S.
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Weng, F. L, Shults, J., Leonard, M. B, Stallings, V. A, Zemel, B. S
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Martins, D., Wolf, M., Pan, D., Zadshir, A., Tareen, N., Thadhani, R., Felsenfeld, A., Levine, B., Mehrotra, R., Norris, K.
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Shinchuk, L., Holick, M. F.
(2007). Vitamin D and Rehabilitation: Improving Functional Outcomes. Nutr Clin Pract
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Wicherts, I. S., van Schoor, N. M., Boeke, A. J. P., Visser, M., Deeg, D. J. H., Smit, J., Knol, D. L., Lips, P.
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Pittas, A. G., Lau, J., Hu, F. B., Dawson-Hughes, B.
(2007). The Role of Vitamin D and Calcium in Type 2 Diabetes. A Systematic Review and Meta-Analysis. J. Clin. Endocrinol. Metab.
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Forman, J. P., Giovannucci, E., Holmes, M. D., Bischoff-Ferrari, H. A., Tworoger, S. S., Willett, W. C., Curhan, G. C.
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Camargo, C. A Jr, Rifas-Shiman, S. L, Litonjua, A. A, Rich-Edwards, J. W, Weiss, S. T, Gold, D. R, Kleinman, K., Gillman, M. W
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Zhou, W., Heist, R. S., Liu, G., Asomaning, K., Neuberg, D. S., Hollis, B. W., Wain, J. C., Lynch, T. J., Giovannucci, E., Su, L., Christiani, D. C.
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Lappe, J. M., Davies, K. M., Travers-Gustafson, D., Heaney, R. P.
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McMahon, M. M., Sarr, M. G., Clark, M. M., Gall, M. M., Knoetgen, J. III, Service, F. J., Laskowski, E. R., Hurley, D. L.
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Aloia, J. F, Talwar, S. A, Pollack, S., Feuerman, M., Yeh, J. K
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Visser, M., Deeg, D. J., Puts, M. T., Seidell, J. C, Lips, P.
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Felsenfeld, A. J., Levine, B. S.
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Das, G, Crocombe, S, McGrath, M, Berry, J L, Mughal, M Z
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Allain, T. J., Kirthisingha, V., Beresford, P. A., Bell, N. J.
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Wong, T. S. F., Lau, V. M. H., Lim, W., Fung, G.
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Cigolini, M., Iagulli, M. P., Miconi, V., Galiotto, M., Lombardi, S., Targher, G.
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Holick, M. F.
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Poole, K. E. S., Loveridge, N., Barker, P. J., Halsall, D. J., Rose, C., Reeve, J., Warburton, E. A.
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Steingrimsdottir, L., Gunnarsson, O., Indridason, O. S., Franzson, L., Sigurdsson, G.
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Rockell, J. E., Green, T. J., Skeaff, C. M., Whiting, S. J., Taylor, R. W., Williams, S. M., Parnell, W. R., Scragg, R., Wilson, N., Schaaf, D., Fitzgerald, E. D., Wohlers, M. W.
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Holick, M. F.
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Rajakumar, K., Fernstrom, J. D., Janosky, J. E., Greenspan, S. L.
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Zhou, W., Suk, R., Liu, G., Park, S., Neuberg, D. S., Wain, J. C., Lynch, T. J., Giovannucci, E., Christiani, D. C.
(2005). Vitamin D Is Associated with Improved Survival in Early-Stage Non-Small Cell Lung Cancer Patients. Cancer Epidemiol. Biomarkers Prev.
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Moore, C. E., Murphy, M. M., Holick, M. F.
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Broadbent, A., Glare, P., Crawford, B.
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Antoniucci, D. M., Vittinghoff, E., Blackwell, T., Black, D. M., Sellmeyer, D. E.
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Gutierrez, O., Isakova, T., Rhee, E., Shah, A., Holmes, J., Collerone, G., Juppner, H., Wolf, M.
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Rodd, C., Mushcab, S. A.l.
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Holick, M. F., Siris, E. S., Binkley, N., Beard, M. K., Khan, A., Katzer, J. T., Petruschke, R. A., Chen, E., de Papp, A. E.
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Sachan, A., Gupta, R., Das, V., Agarwal, A., Awasthi, P. K, Bhatia, V.
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Teng, M., Wolf, M., Ofsthun, M. N., Lazarus, J. M., Hernan, M. A., Camargo, C. A. Jr, Thadhani, R.
(2005). Activated Injectable Vitamin D and Hemodialysis Survival: A Historical Cohort Study. J. Am. Soc. Nephrol.
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Sato, Y., Iwamoto, J., Kanoko, T., Satoh, K.
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Levis, S., Gomez, A., Jimenez, C., Veras, L., Ma, F., Lai, S., Hollis, B., Roos, B. A.
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Smith, S. M., Zwart, S. R., Block, G., Rice, B. L., Davis-Street, J. E.
(2005). The Nutritional Status of Astronauts Is Altered after Long-Term Space Flight Aboard the International Space Station. J. Nutr.
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Calvo, M. S., Whiting, S. J., Barton, C. N.
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Holick, M. F
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Heaney, R. P
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Calvo, M. S, Whiting, S. J, Barton, C. N
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Fleet, J. C
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Weaver, C. M, Fleet, J. C
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