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Screen at-risk patients for vitamin D deficiency—now with expanded Medicare coverage

The Endocrine Society recommends regular vitamin D screening for individuals at risk for deficiency.

In accordance with these guidelines, private payers and Medicare offer coverage for patients with conditions that put them at risk for deficiency, including obesity, osteoporosis, and long-term treatment with corticosteroids and anti-seizure medications.

In some jurisdictions (eg, Florida, Pennsylvania, the Southwest region), Medicare coverage includes testing up to 3 times per year.

In most jurisdictions, Medicare has expanded coverage for vitamin D testing for at-risk patients who have a BMI ≥30. When ordering tests for these patients, use the correct ICD-10 codes to support accurate payment and reduce disruptions. For obesity, these are Z68.30–Z68.45. Review our Medicare Coverage and Coding Guide for more information.

Two vitamin D [25-hydroxyvitamin D or 25(OH)D] testing methods from Quest Diagnostics

Quest offers two methods of vitamin D [25(OH)D] testing that can help you regularly assess at-risk patients, identify vitamin D deficiency and disorders, and manage deficiency once diagnosed.

Immunoassay:
  • Provides reliable results suitable for most patients and situations
  • Has fast turnaround times, with results available the day after specimen submission
  • Can be reported at the same time as many other tests
  • Reports total 25(OH)D concentration without differentiating D2 and D3
Liquid chromatography, tandem mass spectrometry (LC/MS/MS):
  • Reliable reference method results
  • Differentiates D2 and D3 and reports their concentrations along with the total 25(OH)D concentration
  • Differentiates the contribution of vitamin D2 and vitamin D3 supplementation


Note: 1,25(OH)2D measurement does not reflect vitamin D status. Measurement of 1,25(OH)2D is useful only in acquired and inherited disorders in the metabolism of 25(OH)D and phosphate, including chronic kidney disease.1
 

Quest vitamin D testing options

Test Name Test Code* Recommended Clinical Use
25-Hydroxyvitamin D,Immunoassay 17306 All patients not on D2 prescription supplementation
QuestAssureD™ 25-Hydroxyvitamin D (D2, D3), LC/MS/MS) 92888 Patients ≥3 years of age on D2 supplementation and those who require separate D2 and D3 measurement
QuestAssureD™ for Infants, 25-Hydroxyvitamin D, LC/MS/MS 91935 Patients <3 years of age
* The diagnosis code information is provided as a convenience to physicians and office staff. Diagnosis codes must be applicable to the patient's symptoms or conditions and must be consistent with documentation in the patient's medical record. Quest Diagnostics does not recommend any diagnosis codes and will only submit diagnosis information provided by the ordering physician, or his/her designated staff.
Forms of vitamin D

Vitamin D is a fat-soluble prohormone with several forms. In humans, the most important forms are vitamin D3 (also known as cholecalciferol) and vitamin D2 (ergocalciferol).

  • Vitamin D3 is the more common form. It is found in food and is also made in sunlight-exposed skin from the conversion of 7-dehydrocholesterol. It is also found in over the counter but not prescription supplement form.
  • Vitamin D2 is derived from fungal and plant sources. It is available in over the counter and prescription supplements used to treat vitamin D deficiency.

Both vitamin D2 and vitamin D3 are converted to 25-hydroxyvitamin D [25(OH)D or calcidiol] in the liver. This is later hydroxylated in the kidneys and other tissues to 1,25-dihydroxyvitamin D [1,25(OH)2D or calcitriol].

  • 25(OH)D is the main form of vitamin D circulating in the blood and the best indicator of vitamin D deficiency or excess in patients not suffering from renal disease.
  • 1,25(OH)2D is the most metabolically active form of vitamin D; however, serum 1,25(OH)2D does not reflect vitamin D reserves, and measurement of 1,25(OH)2D is not useful for monitoring the vitamin D status of patients. Serum 1,25(OH)2D is frequently either normal or even elevated in those with vitamin D deficiency, due to secondary hyperparathyroidism.1
Vitamin D in the body
Screening at-risk patients for vitamin D deficiency

References

  1. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrin Metab. 2011;96:1911-1930.
  2. Holick MF, 2007 Vitamin D deficiency. N Engl J Med. 357:266-281.
  3. Ginde AA, Liu MC, Camargo CA, et al. Demographic differences and trends of vitamin D insufficiency in the US population, 1988–2004. Arch Intern Med. 2009;169:626-632.
  4. Kumar J, Muntner P, Kaskel FJ, et al. Prevalence and associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001–2004. Pediatrics. 2009;124:e362-e370.
  5. Lai JK, Lucas RM, Clements MS, et al. Assessing vitamin D status: pitfalls for the unwary. Mol Nutr Food Res. 2010;54:1062-1071.
  6. Bringhurst FR, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, eds. Williams Textbook of Endocrinology. 10th ed. Philadelphia, PA: WB Saunders; 2003:1303-1371.
  7. St-Arnaud R, Glorieux FH. Hereditary defects in vitamin D metabolism and action. In: DeGroot LJ, Jameson JL, et al, eds. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders; 2001:1154-1168.
  8. Goldring SR, Krane SM, Avioli LV. Disorders of calcification: osteomalacia and rickets. In: DeGroot LJ, Jameson JL, et al, eds. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders; 2001:1223-1243.
Vitamin D function and deficiency

Vitamin D is critical for maintaining healthy levels of calcium and phosphorus by aiding in their absorption from the gut. This helps the body form and maintain strong bones. Vitamin D also modulates neuromuscular, immune, and other cellular functions.

Vitamin D deficiency can lead to bone diseases such as rickets and osteomalacia. Deficiency has also been associated with a wide range of medical conditions, including heart disease, hypertension, diabetes, and cancer.

Recommendations for 25-hydroxyvitamin D [25(OH)D] levels1,2

Health status ng/mL
Deficiency <20
Insufficiency 21-29
Sufficiency 30-100

Vitamin D deficiency is common. As much as 68%–77% of the population is estimated to have suboptimal (<30 ng/mL) levels of vitamin D.3–5

Low vitamin D concentrations can result from:

  • Inadequate sunlight
  • Dietary deficiency
  • Poor absorption of the vitamin
  • Impaired metabolism of the sterol in the liver


Endocrine Society recommended dietary intake1*

Age IU/day
Infants <1 year 400 - 1000
Children >1 year 600 - 1000
Adults 19 - 70 years 1500 - 2000
Adults > 70 years 1500 - 2000✝

*Whether these levels are enough to provide all the nonskeletal benefits of vitamin D is not known
†Obese adults with BMI >30 require 2-3 times more vitamin D to satisfy their requirement

Screening at-risk patients for vitamin D deficiency

References

1. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrin Metab. 2011;96:1911-1930.

2. Holick MF, 2007 Vitamin D deficiency. N Engl J Med. 357:266-281.

3. Ginde AA, Liu MC, Camargo CA, et al. Demographic differences and trends of vitamin D insufficiency in the US population, 1988–2004. Arch Intern Med. 2009;169:626-632.

4. Kumar J, Muntner P, Kaskel FJ, et al. Prevalence and associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001–2004. Pediatrics. 2009;124:e362-e370.

5. Lai JK, Lucas RM, Clements MS, et al. Assessing vitamin D status: pitfalls for the unwary. Mol Nutr Food Res. 2010;54:1062-1071.

6. Bringhurst FR, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, eds. Williams Textbook of Endocrinology. 10th ed. Philadelphia, PA: WB Saunders; 2003:1303-1371.

7. St-Arnaud R, Glorieux FH. Hereditary defects in vitamin D metabolism and action. In: DeGroot LJ, Jameson JL, et al, eds. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders; 2001:1154-1168.

8. Goldring SR, Krane SM, Avioli LV. Disorders of calcification: osteomalacia and rickets. In: DeGroot LJ, Jameson JL, et al, eds. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders; 2001:1223-1243.

Patients at risk for deficiency should be screened regularly

The Endocrine Society recommends regular screening for individuals at risk for deficiency.

These include patients who have:1

  • Osteoporosis
  • Osteomalacia and rickets
  • Chronic kidney disease
  • Diseases that require certain medications (anti-seizure medications, glucocorticoids, AIDS medications, antifungals, cholestyramine)
  • Malabsorption syndromes, including inflammatory bowel disease, Crohn’s disease, cystic fibrosis, history of bariatric surgery
  • Hyperparathyroidism
  • Hepatic failure

Screening is also recommended for:1

  • African-American and Hispanic children and adults
  • Pregnant and lactating women
  • Older adults with history of falls
  • Older adults with history of nontraumatic fractures
  • Obese children and adults

If a patient is at risk for vitamin D deficiency and has not been tested recently, a test should be ordered to assess levels. Some physicians may wish to monitor people receiving vitamin D therapy to evaluate for compliance and expected change in concentration.

Screening at-risk patients for vitamin D deficiency

References

  1. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrin Metab. 2011;96:1911-1930.
  2. Holick MF, 2007 Vitamin D deficiency. N Engl J Med. 357:266-281.
  3. Ginde AA, Liu MC, Camargo CA, et al. Demographic differences and trends of vitamin D insufficiency in the US population, 1988–2004. Arch Intern Med. 2009;169:626-632.
  4. Kumar J, Muntner P, Kaskel FJ, et al. Prevalence and associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001–2004. Pediatrics. 2009;124:e362-e370.
  5. Lai JK, Lucas RM, Clements MS, et al. Assessing vitamin D status: pitfalls for the unwary. Mol Nutr Food Res. 2010;54:1062-1071.
  6. Bringhurst FR, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, eds. Williams Textbook of Endocrinology. 10th ed. Philadelphia, PA: WB Saunders; 2003:1303-1371.
  7. St-Arnaud R, Glorieux FH. Hereditary defects in vitamin D metabolism and action. In: DeGroot LJ, Jameson JL, et al, eds. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders; 2001:1154-1168.
  8. Goldring SR, Krane SM, Avioli LV. Disorders of calcification: osteomalacia and rickets. In: DeGroot LJ, Jameson JL, et al, eds. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders; 2001:1223-1243.
Test results

All of our vitamin D tests provide the concentration of total 25(OH)D in a patient’s serum, the total 25(OH)D reference range, and suggested cut points to define optimal, insufficiency, and deficiency vitamin D status.

The reference range for 25(OH)D for all 3 tests is 30–100 ng/mL. Tests using the LC/MS/MS method (test code 92888) provide the concentration of 25(OH)D2 and 25(OH)D3. However, neither reference nor interpretative ranges have been established for these components of 25(OH)D.

25(OH)D concentration in various disorders 6-8

Disorder 25(OH) D Concentration
Vitamin D intoxication
Nutritional rickets
Osteomalacia
Secondary hyperparathyroidism
Fat malabsorption disorders, short bowel syndrome
Intestinal diseases causing excessive loss of Vitamin D2 and D3
Anti-convulsant or anti-tuberculosis medications (increased metabolism)
Severe parenchymal liver disease (impaired 25-hydroxylation of vitamin D)
Severe renal disease (impaired 1a-hydroxylation of 25(OH)D) N or ↓
Vitamin D-depent rickets, type I N or ↑
Vitamin D-depent rickets, type II N

↑= Increased levels
N= Normal levels
↓= Decreased levels

Screening at-risk patients for vitamin D deficiency

References

  1. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrin Metab. 2011;96:1911-1930.
  2. Holick MF, 2007 Vitamin D deficiency. N Engl J Med. 357:266-281.
  3. Ginde AA, Liu MC, Camargo CA, et al. Demographic differences and trends of vitamin D insufficiency in the US population, 1988–2004. Arch Intern Med. 2009;169:626-632.
  4. Kumar J, Muntner P, Kaskel FJ, et al. Prevalence and associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001–2004. Pediatrics. 2009;124:e362-e370.
  5. Lai JK, Lucas RM, Clements MS, et al. Assessing vitamin D status: pitfalls for the unwary. Mol Nutr Food Res. 2010;54:1062-1071.
  6. Bringhurst FR, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, eds. Williams Textbook of Endocrinology. 10th ed. Philadelphia, PA: WB Saunders; 2003:1303-1371.
  7. St-Arnaud R, Glorieux FH. Hereditary defects in vitamin D metabolism and action. In: DeGroot LJ, Jameson JL, et al, eds. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders; 2001:1154-1168.
  8. Goldring SR, Krane SM, Avioli LV. Disorders of calcification: osteomalacia and rickets. In: DeGroot LJ, Jameson JL, et al, eds. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders; 2001:1223-1243.

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