Deficient understanding of this essential vitamin could wreak havoc on your coding for related testing and diagnoses.
Vitamin D testing is a current Center for Medicare & Medicaid Services (CMS) Comparative Billing Report (CBR) topic. CBRs are educational tools that provide data on Medicare billing trends. They are intended to educate providers about Medicare coverage criteria and coding and billing rules, provide an educational resource, and act as a self-audit tool. Metrics associated with vitamin D testing, as prescribed by the CBR, are:
- Ratio of vitamin D testing to office visits;
- Percent of beneficiaries receiving vitamin D testing for other diagnoses; and
- Average number of vitamin D tests per beneficiary.
Depending on the type of practice/specialty, these numbers may be high, but expected.
Vitamin D Deficiency Causes Disease
Vitamin D is a family of compounds that are essential for growth and formation of teeth and bones. Severely low levels of vitamin D hinder the body’s ability to maintain adequate levels of calcium for bone growth. Vitamin D deficiency is manifested clinically as rickets in children (E64.3 Sequelae of rickets) and osteomalacia in adults (M83.x Adult osteomalacia). Vitamin D is part of an intricate feedback mechanism that helps regulate calcium and phosphate levels in the blood.
A drop in calcium blood levels (E83.51 Hypocalcemia) causes the parathyroid gland to produce parathyroid hormone (PTH). PTH increases the activity of the enzymes that produce the active form of vitamin D. This increase in the concentration of calcium together with vitamin D feeds back to the parathyroid gland to stop PTH release. The production of vitamin D is directly regulated by calcium, phosphate, and calcitriol levels.
Deficiency of vitamin D (E55.9 Vitamin D deficiency, unspecified) is a common problem in many populations, including older adults. Vitamin D deficiency is a nutritional condition developing from:
- Deficiency of vitamin D in the diet;
- Insufficient production of vitamin D in the skin;
- Inadequate absorption of vitamin D from the diet; and/or
- Abnormal conversion of vitamin D to its bioactive metabolites.
Common manifestations of vitamin D deficiency are symmetric low back pain (M54.5 Low back pain), proximal muscle weakness (M62.81 Muscle weakness (generalized)), muscle aches (M79.1 Myalgia), throbbing bone pain elicited with pressure of the sternum (R07.2 Precordial pain), or tibial bone pain (M79.669 Pain in unspecified lower leg).
Two forms of vitamin D can be measured in the blood:
- 25-hydroxyvitamin D, the precursor to the active form made in the liver. Report the measurement procedure with CPT® 82306 Vitamin D; 25 hydroxy, includes fraction(s), if performed.
- 1, 25-dihydroxyvitamin D, the active hormonal form, made in the kidneys. Use 82652 Vitamin D; 1, 25 dihydroxy, include fraction(s), if performed to report this measurement.
Picturing the metabolic pathway of vitamin D helps to understand where this testing fits into the process.
Measurement of Vitamin D
The most accurate way to measure how much vitamin D is in the body is by the 25-hydroxyvitamin D blood test. A level of less than 12 nanograms/milliliter (12 ng/mL) is considered inadequate for bone health; sufficiency is defined as a level greater than 20 ng/mL.
Vitamin D deficiency is not only a matter of decreased exposure to sunlight or dietary intake; three gene variants have been identified that may contribute to the condition. Researchers have found gene variants involved with cholesterol synthesis, vitamin D metabolism, and vitamin D transport are associated with vitamin D levels. The genes subject to testing are associated with the production of the enzymes that transform vitamin D into its various metabolites.
Vitamin D is biologically inactive and requires conversion to its active metabolites. As shown in Figure 1, vitamin D is enzymatically converted in the liver to 25-hydroxyvitamin D (25[OH]D), the major circulating form, and then in the kidney to 1, 25-dihydroxyvitamin D, the active form.
Measurements of 25-hydroxyvitamin D measure the circulating form after conversion in the liver and prior to conversion to the active form in the kidney. Measurement of 1, 25-dihydroxyvitamin D levels determines the amount of circulating active hormonal form made by the kidneys. Analysis of the CYP27B1 gene (CPT® 81479 Unlisted molecular pathology procedure) can determine if the cause is with the enzyme involved in the conversion of 25-hydroxyvitamin D3 into the active form in the kidney. Analysis of the CYP2R1 and CYP27A1 (CPT® 81479) can determine if the cause is with the enzymes involved in converting vitamin D3 into 25-hydroxyvitamin D3 in the liver.
Treatment of Vitamin D Deficiency
The goal of treatment is to normalize vitamin D levels to relieve symptoms and decrease risk of adverse injury-related outcomes. In patients with vitamin D deficiency, treatment may include oral vitamin D2 at 50,000 IU per week for eight weeks. After vitamin D levels normalize, maintenance dosages of vitamin D3 are recommended. Vitamin D3 supplements enter the system between the enzymatic skin and liver conversions.
Frank Mesaros, MPA, MT(ASCP), CPC, CPCO, is CEO of Trusent Solutions, LLC, a management consulting firm specializing in the clinical laboratory industry. Trusent provides revenue stream integrity services to regional laboratories, hospital-based laboratories, and physician office-based laboratories. Mesaros is a member of the Harrisburg, Pa., local chapter.