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Medical Policy: 02.04.34
Original Effective Date: November 2011
Reviewed: March 2012
Revised:
Benefit Application
Benefit determinations are based on the applicable contract language in effect at the time the
services were rendered. Exclusions, limitations or exceptions may apply. Benefits may vary
based on contract, and individual member benefits must be verified. Wellmark determines medical
necessity only if the benefit exists and no contract exclusions are applicable. This medical
policy may not apply to FEP. Benefits are determined by the Federal Employee Program.
This Medical Policy document describes the status of medical technology at the time the document
was developed. Since that time, new technology may have emerged or new medical literature may
have been published. This Medical Policy will be reviewed regularly and be updated as scientific
and medical literature becomes available.
Description:
The term, vitamin D, is broad and includes several metabolically interrelated sterol substances that have hormonal activity. Vitamin D has 2 distinctive forms: Vitamin D2 and Vitamin D3. In the skin, 7-dehydrocholesterol is converted by ultraviolet light to vitamin D3. Vitamin D3 is converted in the liver to 25 hydroxyvitamin D [25(OH)D], also known as calcifediol, and the latter is converted in the kidney to 1,25 dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol. 1,25 dihydroxyvitamin D [1,25(OH)2D] is the major biologically active fraction and has a plasma half-life of 4-6 hours. It is increased in sarcoidosis, cat-scratch disease, primary hyperparathyroidism, vitamin D intoxication, and type II vitamin D-dependent rickets. Decreased levels are seen in hypoparathyroidism, pseudohypoparathyroidism, hypercalcemia of malignancy, renal failure, hyperphosphatemia, hypomagnesemia, and type I vitamin D-dependent rickets. 25 hydroxyvitamin D [25(OH)D] has a half-life of 2-3 weeks and is the substance usually measured to assess nutritional adequacy. It is decreased in dietary vitamin D deficiency, liver disease, malabsorption, inadequate sun exposure, and nephrotic syndrome. Increased levels are associated with vitamin D intoxication.
Vitamin D’s chief biologic function is to maintain serum calcium and phosphorus concentrations within normal range by means of enhancing intestinal absorption of calcium and release of calcium and phosphorus from bone. Vitamin D also has non-calciotropic autocrine and paracrine roles such as in the regulation of cell differentiation and proliferation. The enzyme 1-alpha hydroxylase is present in many tissues in addition to the kidney, resulting in extra-renal production of 1,25 dihydroxyvitamin D.
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Prior Approval:
Not applicable
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Policy:
25-hydroxyvitamin D [25(OH)D] serum testing may be considered medically necessary in patients with a clinically documented underlying disease or condition which is specifically associated with vitamin D deficiency or decreased bone density/osteoporosis
25-hydroxyvitamin D [25(OH)D] serum testing is considered not medically necessary for routine or initial screening in the absence of clinical documentation of an underlying disease or condition specifically associated with vitamin D deficiency
1,25 dihydroxyvitamin D [1,25(OH)2D] serum testing may be considered medically necessary in evaluating patients with a clinically documented underlying disease or condition associated with increased or decreased 1,25(OH)2D; examples of such conditions include sarcoidosis, cat-scratch disease, lymphomas, hyper- or hypoparathyroidism, pseudohypoparathyroidism, hypercalcemia of malignancy, renal failure, and granulomatous diseases.
Testing and screening for vitamin D deficiency with 1,25 dihydroxyvitamin D [1,25(OH)2D] serum testing is considered not medically necessary for all indications.
Rationale:
While the serum concentration of 25-hydroxyvitamin D [25(OH)D] is established as the best indicator of vitamin D status, there is significant uncertainty associated with its measurement. Tests that measure serum levels of 25-hydroxyvitamin D [25OH)D] are not standardized. In a between-laboratory assessment, Binkley and colleagues (2010) documented modest variability in agreement on serum results related to methodological differences and lack of standardization. Hollis (2010) noted a disturbing trend in the use by clinical reference labs of “home-brew” diverse liquid chromatography/mass spectrometry (LC/MS) methods that are not subject to U.S. Food and Drug Administration (FDA) oversight.
Serum concentrations that define deficient or insufficient, adequate, and optimal levels of 25-hydroxyvitamin D [25(OH)] are not clearly established. Proposed cutoff points vary widely, leading to inconsistent endorsement among practitioners. In a recent review, (Rosen, 2011) explained that defining a level as low was dependent on the level that is defined as normal. World Health Organization (WHO) standards have defined levels below 10ng/mL as deficient and levels below 20ng/mL as insufficient. But as Rosen (2011) further explained, recent changes in laboratory reference ranges have raised the lower limits of the normal range and when the newer range is used, the prevalence of vitamin D deficiency could be as high as 50 to 80% in the general population. Because serum concentration of 25-hydroxyvitamin D [25(OH)] reflects vitamin D produced in the skin and obtained from food and supplements, confounders such as geographic location, season, exposure to sunlight, African-American ancestry, and dietary intake all impact circulating levels of 25-hydroxyvitamin D [25(OH)]. Thus, it is unclear how vitamin D test results can be used to guide treatment decisions compared to decisions that would be made in the absence of test results, particularly in asymptomatic individuals who are being advised to take vitamin D for their overall wellness, or for those with a condition for which the role of vitamin D has not been clearly defined.
The role of vitamin D has been investigated and recently received considerable media attention for a number of indications other than bone health, including cardiovascular disease and hypertension, diabetes and metabolic syndrome, colon, prostate, and breast cancer, reproductive health, immune function, and neuropsychological function. The studies of these conditions are diverse and inconclusive. Accordingly, it has not been reliably determined whether or how vitamin D impacts the risk of developing any of these conditions, or whether altering exposure to vitamin D provides a protective effect. Large, randomized, controlled trials will be required to identify the role of vitamin D in these and other conditions.
A comprehensive systematic review published in 2010 by the Institute of Medicine of the National Academies (IOM) evaluated the current evidence and concluded that there is strong evidence from rigorous testing to support the importance of vitamin D in promoting bone growth and maintenance, but did not identify any specific conditions for which testing of serum levels of 25-hydroxyvitamin D [25(OH)] may be indicated.
Presently, no evidence-based clinical practice guideline recommends vitamin D screening of persons without a clinically documented underlying disease or condition which is specifically associated with the risk of decreased bone density or osteoporosis.
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Procedure Codes and Billing Guidelines:
- To report provider services, use appropriate CPT* codes, Modifiers, Alpha Numeric (HCPCS level 2) codes, Revenue codes, and/or ICD-9-CM diagnostic codes.
- 82306 Vitamin D; 25 hydroxy, includes fraction(s), if performed
- 82652 Vitamin D; 1,25 dihydroxy, includes fraction(s), if performed
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Selected References:
- Agency for Healthcare Research and Quality. Effectiveness and Safety of Vitamin D in Relation to Bone Health. Evaluation report. 2007. Available from: http://www.ahrq.gov/downloads/pub/evidence/pdf/vitamind/vitad.pdf
- Institute of Medicine of the National Academies. Dietary Reference Intakes for Calcium and Vitamin D. November 2010. Available from: http:/www.iom.edu/Reports/2010/Dietary-Reference-in takes-for-Calcium-and-Vitamin-D.aspx.
- Rosen CJ. Vitamin D Insufficiency. N Engl J Med 2011; 364(3):248-54.
- Binkley N, Krueger DC, Morgan S et al. Current Status of Clinical 25-hydroxyvitamin D Measurement: An Assessment of Between-Laboratory Agreement. Clin Chim Acta. 2010 December 14;411(23-24):1976-82. doi: 10.1016/j.cca.2010.08.018.
- Norman AW, Bouillon R, Whiting SJ et al. 13th Workshop Consensus for Vitamin D Nutritional Guidelines. J Steroid Biochem Mol Biol. 2007 March; 103(3-5):204-5.
- National Institutes of Health Office of Dietary Supplements. Dietary Supplement fact Sheet: Vitamin D. Updated 2/25/2011. Available from: http://ods.od.nih.gov/factsheets/vitamind
- Motiwala SR, Wang TJ. Vitamin D and cardiovascular disease. Curr Opin Nephrol Hypertens 2011 Apr 23. [Epub ahead of print].
- Fang F, Kasperzyk JL, Shui I et al. Prediagnostic plasma vitamin D metabolites and mortality among patients with prostate cancer. PLoS ONE 6(4):e18625. doi: 10.1371/journal.pone.0018625
- Rajakamur K, de Las Heras J, Chen TC et al. Vitamin d status, adiposity, and lipids in black american and caucasian children. J Clin Endocrinol Metab. 2011 May;96(5):1560-7. Epub 2011 Mar 2.
- Patel R, Rizvi A. Vitamin D deficiency in patients with congestive heart failure: mechanisms, manifestations, and management. May 2011;104(5):325-30. doi: 10.1097/SMJ.obo13e318213cf6b.
- Melamed ML, Michos ED, Post W et al. 25-hydroxyvitamin D levels and the risk of mortality in the general population. Arch Intern Med 2008 Aug 11;168(15):1629-37.
- Hollis BW. Assessment and Interpretation of Circulating 25-Hydroxyvitamin D and 1,25-Dihydroxyvitamin D in the clinical environment. Endocrinol Metab Clin N Am.2010 June;39(2):271-86. doi:10.1016/j.ecl.2010.02.012.
- Hanley DA, Cranney A, Jones G et al. Vitamin D in adult health and disease: a review and guideline statement from Osteoporosis Canada (summary). CMAJ Sep 7 2010;182(12):1315-19. doi: 10.1503/cmaj.091062.
- Holick MF, Binkley NC, Bischoff-Ferrari, et al. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2011 July;96(7):1911-1930.
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Policy History:
Date Reason Action
May 2011 Literature review New policy
March 2012 Annual review Policy renewed
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of technology assessment of new and emerging treatments, devices,
drugs, etc. They are developed to
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advice and treatment of members. Our medical policies may be updated
and therefore are subject to change without notice.
*Current Procedural Terminology © 2012 American Medical Association. All Rights Reserved.
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