Test Code 25HDN 25-Hydroxyvitamin D2 and D3, Serum
Additional Codes
Vitamin D Profile (Rainbow Pediatrics)
Vitamin D Metabolites
Vitamin D+Metabolites
Reporting Name
25-Hydroxyvitamin D2 and D3, SUseful For
Diagnosis of vitamin D deficiency
Differential diagnosis of causes of rickets and osteomalacia
Monitoring vitamin D replacement therapy
Diagnosis of hypervitaminosis D
Performing Laboratory
Mayo Clinic Laboratories in RochesterSpecimen Type
SerumSpecimen Required
Collection Container/Tube:
Preferred: Red top
Acceptable: Serum gel
Submission Container/Tube: Plastic vial
Specimen Volume: 0.5 mL
Collection Instructions: Centrifuge and aliquot serum into a plastic vial within 2 hours of specimen collection.
Specimen Minimum Volume
0.25 mL
Specimen Stability Information
Specimen Type | Temperature | Time | Special Container |
---|---|---|---|
Serum | Refrigerated (preferred) | 28 days | |
Frozen | 30 days | ||
Ambient | 7 days |
Reference Values
TOTAL 25-HYDROXYVITAMIN D2 AND D3 (25-OH-VitD)
<10 ng/mL (severe deficiency)*
10-19 ng/mL (mild to moderate deficiency)**
20-50 ng/mL (optimum levels)***
51-80 ng/mL (increased risk of hypercalciuria)****
>80 ng/mL (toxicity possible)*****
*Could be associated with osteomalacia or rickets
**Might be associated with increased risk of osteoporosis or secondary hyperparathyroidism
***Optimum levels in the healthy population
****Sustained levels >50 ng/mL 25OH-VitD along with prolonged calcium supplementation may lead to hypercalciuria and decreased kidney function
*****80 ng/mL is the lowest reported level associated with toxicity in patients without primary hyperparathyroidism who have normal kidney function. Most patients with toxicity have levels >150 ng/mL. Patients with kidney failure can have very high 25-OH-VitD levels without any signs of toxicity, as renal conversion to the active hormone 1,25-OH-VitD is impaired or absent.
These reference ranges represent clinical decision values, based on the 2011 Institute of Medicine report, that apply to males and females of all ages, rather than population-based reference values. Population reference ranges for 25-OH-VitD vary widely depending on ethnic background, age, geographic location of the studied populations, and the sampling season. Population-based ranges correlate poorly with serum 25-OH-VitD concentrations that are associated with biologically and clinically relevant vitamin D effects and are therefore of limited clinical value.
For International System of Units (SI) conversion for Reference Values, see www.mayocliniclabs.com/order-tests/si-unit-conversion.html.
Day(s) Performed
Monday through Friday
Test Classification
This test was developed and its performance characteristics determined by Mayo Clinic in a manner consistent with CLIA requirements. It has not been cleared or approved by the US Food and Drug Administration.CPT Code Information
82306
LOINC Code Information
Test ID | Test Order Name | Order LOINC Value |
---|---|---|
25HDN | 25-Hydroxyvitamin D2 and D3, S | 49590-3 |
Result ID | Test Result Name | Result LOINC Value |
---|---|---|
2897 | 25-Hydroxy D2 | 49054-0 |
2898 | 25-Hydroxy D3 | 1989-3 |
83670 | 25-Hydroxy D Total | 62292-8 |
Interpretation
Based on animal studies and large human epidemiological studies, 25-hydroxyvitamin D2 and D3 (25-OH-VitD) levels below 25 ng/mL are associated with an increased risk of secondary hyperparathyroidism, reduced bone mineral density, and fractures, particularly in the elderly. Intervention studies support this clinical cutoff, showing a reduction of fracture risk with 25-OH-VitD replacement.
Levels less than 10 ng/mL may be associated with more severe abnormalities and can lead to inadequate mineralization of newly formed osteoid, resulting in rickets in children and osteomalacia in adults. In these individuals, serum calcium levels may be marginally low, and parathyroid hormone (PTH) and serum alkaline phosphatase are usually elevated. Definitive diagnosis rests on the typical radiographic findings or bone biopsy/histomorphometry.
Baseline biochemical work-up of suspected cases of rickets and osteomalacia should include measurement of serum calcium, phosphorus, PTH, and 25-OH-VitD. In patients where testing is not completely consistent with the suspected diagnosis, particularly if serum 25-OH-VitD levels are greater than 10 ng/mL, an alternative cause for impaired mineralization should be considered. Possible differential diagnosis includes partly treated vitamin D deficiency, extremely poor calcium intake, vitamin D resistant rickets, renal failure, renal tubular mineral loss with or without renal tubular acidosis, hypophosphatemic disorders (eg, X-linked or autosomal dominant hypophosphatemic rickets), congenital hypoparathyroidism, activating calcium sensing receptor mutations, and osteopetrosis. Measurement of serum urea, creatinine, magnesium, and 1,25-dihydroxyvitamin D (DHVD) is recommended as a minimal additional workup for these patients.
25-OH-VitD replacement in the United States typically consists of vitamin D2. Lack of clinical improvement and no reduction in PTH or alkaline phosphatase may indicate patient noncompliance, malabsorption, resistance to 25-OH-VitD, or additional factors contributing to the clinical disease. Measurement of serum 25-OH-VitD levels can assist in further evaluation, particularly as the liquid chromatography tandem mass spectrometry methodology allows separate measurement of 25-OH-VitD3 and of 25-OH-VitD2, which is derived entirely from dietary sources or supplements.
Patients who present with hypercalcemia, hyperphosphatemia, and low PTH may suffer either from ectopic, unregulated conversion of 25-OH-VitD to 1,25-OH-VitD, as can occur in granulomatous diseases, particular sarcoid, or from nutritionally-induced hypervitaminosis D. Serum 1,25-OH-VitD levels will be high in both groups, but only patients with hypervitaminosis D will have serum 25-OH-VitD concentrations of greater than 80 ng/mL, typically greater than 150 ng/mL.
Clinical Reference
1. Jones G, Strugnell SA, DeLuca HF. Current understanding of the molecular actions of vitamin D. Physiol Rev. 1998;78(4):1193-1231
2. Miller WL, Portale AA. Genetic causes of rickets. Curr Opin Pediatr. 1999;11(4):333-339
3. Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr. 1999;69(5):842-856
4. Vieth R, Ladak Y, Walfish PG. Age-related changes in the 25-hydroxyvitamin D versus parathyroid hormone relationship suggest a different reason why older adults require more vitamin D. J Clin Endocrinol Metab. 2003;88(1):185-191
5. Wharton B, Bishop N. Rickets. Lancet. 2003;362(9393):1389-1400
6. Institute of Medicine (US) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium. In: Ross AC, Taylor CL, Yaktine AL, Del Valle HB, eds. Dietary Reference Intakes for Calcium and Vitamin D. National Academies Press: 2011. Available at www.ncbi.nlm.nih.gov/books/NBK56070
7. Su Z, Narla SN, Zhu Y. 25-Hydroxyvitamin D: Analysis and clinical application. Clinica Chimica Acta. 2014;433:200-205
8. LeFevre ML. US Preventative Services Task Force: Screening for vitamin D deficiency in adults: US Preventative Services Task Force recommendation statement. Ann Intern Med. 2015;162(2):133-140
Report Available
2 to 5 daysMethod Name
Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS)
Portions of this test are covered by patents held by Quest Diagnostics
Forms
If not ordering electronically, complete, print, and send 1 of the following forms with the specimen:
-General Request (T239)
-Renal Diagnostics Test Request (T830)