LCD L33996

Coverage Guidance

Language quoted from Centers for Medicare and Medicaid Services (CMS). National Coverage Determinations (NCDs) and coverage provisions in interpretive manuals is italicized throughout the policy. NCDs and coverage provisions in interpretive manuals are not subject to the Local Coverage Determination (LCD) Review Process (42 CFR 405.860[b] and 42 CFR 426 [Subpart D]). In addition, an administrative law judge may not review an NCD. See Section 1869(f)(1)(A)(i) of the Social Security Act.

Unless otherwise specified, italicized text represents quotation from one or more of the following CMS sources:

Title XVIII of the Social Security Act (SSA):

Section 1862(a)(1)(A) excludes expenses incurred for items or services which are not reasonable and necessary for the diagnosis or treatment of illness or injury or to improve the functioning of a malformed body member.

Section 1833(e) prohibits Medicare payment for any claim which lacks the necessary information to process the claim.

Indications and Limitations of Coverage

Abstract:

Vitamin D is a hormone, synthesized by the skin and metabolized by the kidney to an active hormone, calcitriol. An excess of vitamin D may lead to hypercalcemia. Vitamin D deficiency may lead to a variety of disorders. This LCD identifies the indications and limitations of Medicare coverage and reimbursement for these services.

Vitamin D is called a "vitamin" because of its exogenous source, predominately from oily fish in the form of vitamin D2 and vitamin D3. It is really a hormone, synthesized by the skin and metabolized by the kidney to an active hormone, calcitriol, which then acts throughout the body. In the skin, 7-dehydrocholesterol is converted to vitamin D3 in response to sunlight, a process that is inhibited by sunscreen with a skin protection factor (SPF) of 8 or greater. Once in the blood, vitamin D2 and D3 from diet or skin bind with vitamin D binding protein and are carried to the liver where they are hydroxylated to yield calcidiol. Calcidiol then is converted in the kidney to calcitriol by the action of 1a-hydroxylase (CYP27B1). The CYP27B1 in the kidney is regulated by nearly every hormone involved in calcium homeostasis, and its activity is stimulated by PTH, estrogen, calcitonin, prolactin, growth hormone, low calcium levels, and low phosphorus levels. Its activity is inhibited by calcitriol, thus providing the feedback loop that regulates calcitriol synthesis.

An excess of vitamin D is unusual, but may lead to hypercalcemia. Vitamin D deficiency may lead to a variety of disorders, the most infamous of which is rickets. Evaluating patients’ vitamin D levels is accomplished by measuring the level of 25-hydroxyvitamin D. Measurement of other metabolites is generally not medically necessary.

Indications:

Measurement of vitamin D levels is indicated for patients with:

• chronic kidney disease stage III or greater;

• osteoporosis;

• osteomalacia;

• osteopenia;

• hypocalcemia;

• hypercalcemia;

• hypercalciura;

• hypoparathyroidism;

• hyperparathyroidism;

• malabsorption states;

• cirrhosis;

• hypervitaminosis D;

• obstructive jaundice;

• osteosclerosis/petrosis;

• rickets;

• low exposure to sunlight; and

• vitamin D deficiency to monitor the efficacy of replacement therapy

• Obesity

Limitations:

For Medicare beneficiaries, screening tests are governed by statute. Vitamin D testing may not be used for routine screening.

Once a beneficiary has been shown to be vitamin D deficient, further testing is medically necessary only to ensure adequate replacement has been accomplished. Thereafter, annual testing may be appropriate depending upon the indication and other mitigating factors.

Summary of Evidence

Obesity

Obesity has been linked to vitamin D deficiency thought to be due the sequestration of vitamin D in body fat leading to reduced availability of vitamin D and lower dietary intake of vitamin D containing supplements [1, 2]. Early studies found lower serum Vitamin D levels in non-operative morbidly obese patients, with 62% having deficiencies in serum 25-hydroxyvitamin D (25-OHD) levels [3]. A prospective cohort study comparing obese to non-obese subjects found a serum 25-OHD and 1,25-dihydroxy vitamin D was negatively correlated with body mass index (BMI) in Caucasian and African-American adults (p<0.0001 for both groups) [4]. A large Canadian cohort with 5,569 individuals reported that a BMI >30 (obese) was strongly associated with lower levels of serum 25-OHD (<75nmol/L) in both males and females. A multivariate regression analysis that included dietary intake of vitamin D, sunlight exposure, and supplementation showed the impact of BMI was an independent variable (-11.12 (-14.04;-8.21) females and -8.17 (-13.49; -2.85) males [5]. National Health and Nutrition Examination Survey (NHANES) data reported lower concentrations of 25-OHD levels among obese white women compared to leaner counterparts [2]. Obese adults also have been found to have difficulty raising their vitamin D levels by sunlight, ultraviolet light exposure, or supplementation as compared to nonobese adults [6, 7].

Analysis of Evidence

Obesity

The American Association of Clinical Endocrinologists, The Obesity Society and American Society for Metabolic, and Bariatric Surgery Guidelines recommend vitamin D supplements titrated to therapeutic 25-hydroxyvitamin D levels >30ng/ml after bariatric surgery (Grade A recommendation)[8]. Up to Date includes obese patients at a high-risk for vitamin D insufficiency[9]. Obese individual are considered high-risk for vitamin D deficiency. The relationship between obesity and vitamin D deficiency has been clearly reported and supported by societal guidance. Obesity is a reasonably and medically necessary indication for Vitamin D Assay measurement.

Associated Information

N/A

Bibliography

• Holick, M.F., Vitamin D Deficiency. The New England Journal Of Medicine, 2007. 357(3): p. 266-81.

• Yetley, E.A., Assessing the vitamin D status of the US population. 2008. 88(2): p. 558S-564S.

• Buffington, C., et al., Vitamin D deficiency in the morbidly obese. 1993. 3(4): p. 421-424.

• Parikh, S.J., et al., The relationship between obesity and serum 1, 25-dihydroxy vitamin D concentrations in healthy adults. 2004. 89(3): p. 1196-1199.

• Greene-Finestone, L.S., et al., 25-Hydroxyvitamin D in Canadian adults: biological, environmental, and behavioral correlates. Osteoporosis International: A Journal Established As Result Of Cooperation Between The European Foundation For Osteoporosis And The National Osteoporosis Foundation Of The USA, 2011. 22(5): p. 1389-99.

• Holick, M.F., et al., Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. The Journal Of Clinical Endocrinology And Metabolism, 2011. 96(7): p. 1911-30.

• Wortsman, J., et al., Decreased bioavailability of vitamin D in obesity. 2000. 72(3): p. 690-693.

• Mechanick, J.I., et al., Clinical practice guidelines for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient2013 update: cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery. Obesity (Silver Spring, Md ), 2013. 21 Suppl 1: p. S1-27.

• Hughes, B. Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment. UpToDate 9/30/2019 [cited 10/21/2019; Available from: https://www.uptodate.com/contents/vitamin-d-deficiency-in-adults-definition-clinical-manifestations-and-treatment.