ICD10 code for Vitamin D deficiency
E20.0 Idiopathic hypoparathyroidism
E20.8 Other hypoparathyroidism
E20.9 Hypoparathyroidism, unspecified
E21.0 -E21.3 Hyperparathyroidism and other disorders of parathyroid gland (code range)
E55.0 Rickets, active
E55.9 Vitamin D deficiency, unspecified
E83.3-83.9 Disorders of phosphorus metabolism (code range)
E83.51 Hypocalcemia
E83.52 Hypercalcemia
M81.0 Age-related osteoporosis without current pathological fracture
M81.6 Localized osteoporosis
M81.8 Other osteoporosis without current pathological fracture
M83.0-M83.9 Adult osteomalacia (code range)
M85.9 Disorder of bone density and structure, unspecified
N18.3-N18.5 Chronic kidney disease, Stage III to End stage renal disease (code range)
N25.81 Secondary hyperparathyroidism of renal origin
D51 Vitamin B12 deficiency anemia
Excludes1: vitamin B12 deficiency (E53.8)
D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency
Addison anemia
Biermer anemia
Pernicious (congenital) anemia
Congenital intrinsic factor deficiency
D51.1 Vitamin B12 deficiency anemia due to selective vitamin B12
malabsorption with proteinuria
Imerslund (-Gr?sbeck) syndrome
Megaloblastic hereditary anemia
D51.2 Transcobalamin II deficiency
D51.3 Other dietary vitamin B12 deficiency anemia Vegan anemia
D51.8 Other vitamin B12 deficiency anemias
D51.9 Vitamin B12 deficiency anemia, unspecified
Vitamin d deficiency Indications:
Measurement of vitamin D levels is indicated for patients with:
• chronic kidney disease stage III or greater;
• osteoporosis;
• osteomalacia;
• osteopenia;
• hypocalcemia;
• hypercalcemia;
• hypoparathyroidism;
• hyperparathyroidism;
• hypervitaminosis D;
• rickets; and
• vitamin D deficiency to monitor the efficacy of replacement therapy.
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.
Vitamin D has been described as an immunomodulator targeting various immune cells, including monocytes, macrophages, T-lymphocytes, and B-lymphocytes.5 Studies have suggested that vitamin D plays an important role in maintenance of the immune system. Vitamin D may have a central role in infectious and autoimmune diseases, in particular tuberculosis and type 1 diabetes.
Vitamin D influences the immune response to tuberculosis, and vitamin D deficiency has been associated with increased tuberculosis risk in different populations.6 A meta-analysis explored the association between low serum vitamin D and risk of active tuberculosis in humans.7 After review of studies published between 1980 and 2006, low serum vitamin D levels are associated with higher risk of active tuberculosis.
Low levels of vitamin D have been associated with a higher risk of cardiovascular disease and myocardial infarction.9, 10 A study of over 18,000 men, free from cardiovascular disease ages 40 to 75 years, was conducted with 10 years follow-up.11 Men with 25(OH)D levels less than 16 ng/mL were at 2.42 times higher risk of developing infarction than those with levels >29 ng/mL. Similarly, Wang et al. (2008) reported on 1739 participants without prior cardiovascular disease and those with 25(OH)D levels less than 10 ng/mL had cardiovascular hazard ratio of 1.80 comparing with the ones with higher concentrations.12 Likewise, there have been reports of clinical and epidemiological studies that suggest there may be an association between hypertension and vitamin D status as well as calcium metabolism
In 2010, the Mayo Foundation published a review for clinicians “Vitamin D Deficiency in Adults: When to Test and How to Treat”. The review point on the clinical risk factors for vitamin D severe deficiency such as
** Inadequate oral intake of vitamin D
** Malnutrition
** Limited sun exposure
** Malabsorption including
** Short bowel syndrome
** Pancreatitis
** Inflammatory Bowel Disease
** Amyloidosis
** Celiac Sprue
** Malabsorptive bariatric surgery procedures
** Some antiepileptic medications
** Severe liver disease or failure
** Aging
** Renal insufficiency, glomerular filtration rate <60 p="">
** Nephrotic syndrome
POLICY STATEMENT:
I. Based upon our criteria and assessment of the peer-reviewed literature, screening for Vitamin D deficiency in individuals considered high risk for vitamin D deficiency (See Policy Guideline I) is considered medically appropriate.
II. Based upon our criteria and assessment of the peer-reviewed literature, routine screening for Vitamin D deficiency in healthy adults or children is considered not medically necessary.
III. Based upon our criteria and assessment of the peer-reviewed literature, screening for Vitamin D deficiency for nonskeletal diseases (e.g., cardiovascular disease, cancer, and autoimmune disease) is considered not medically necessary.
POLICY GUIDELINES:
I. Individuals that are high risk for vitamin D deficiency include, but are not limited to:
A. Osteomalacia;
B. Osteoporosis;
C. Chronic kidney disease;
D. Hepatic failure;
E. Malabsorption syndromes (e.g., cystic fibrosis, inflammatory bowel disease, Crohn’s disease, bariatric surgery, radiation enteritis);
F. Hyperparathyroidism
G. Medications (e.g., antiseizure, glucocorticoids, AIDS medications, antifungals, cholestyramine);
H. African-American and Hispanic children and adults
I. Pregnant and lactating women;
J. Older adults (age greater than 65 years) with history of falls or nontraumatic fractures;
K. Obese children and adults (BMI greater than 30 kg/m2 );
L. Granuloma-forming disorders (e.g., sarcoidosis, tuberculosis, histoplamosis, coccidiomycosis, berylliosis);
M. Some lymphomas.
II. Serum concentration of 25 hydroxyvitamin D (25OHD) is the optimal clinical indicator of vitamin D metabolism due to the rapid conversion of vitamin D to 25 OHD with only a small fraction converted to 1,25 hydroxyvitamin D (1, 25 OHD).
III. The Federal Employee Health Benefit Program (FEHBP/FEP) requires that procedures, devices or laboratory tests approved by the U.S. Food and Drug Administration (FDA) may not be considered investigational and thus these procedures, devices or laboratory tests may be assessed only on the basis of their medical necessity.
DESCRIPTION:
A major source of vitamin D for most humans comes from exposure of the skin to sunlight typically between 1000 hours and 1500 hours in the spring, summer, and fall. Vitamin D produced in the skin may last at least twice as long in the blood compared with ingested vitamin D. A variety of factors reduce the skin’s production of vitamin D3, including increased skin pigmentation, aging, and the topical application of a sunscreen. An alteration in the zenith angle of the sun caused by a change in latitude, season of the year, or time of day dramatically influences the skin’s production of vitamin D3. Few foods naturally contain vitamin D2 or vitamin D3 however some foods have been fortified with Vitamin D.
Vitamin D deficiency results in abnormalities in calcium, phosphorus, and bone metabolism. Specifically, vitamin D deficiency causes a decrease in the efficiency of intestinal calcium and phosphorus absorption of dietary calcium and phosphorus, resulting in an increase in parathyroid hormone (PTH) levels. Secondary hyperparathyroidism maintains serum calcium in the normal range at the expense of mobilizing calcium from the skeleton and increasing phosphorus wasting in the kidneys. As a result there may be bone weakness and a generalized decrease in bone mineral density (BMD), resulting in osteopenia and osteoporosis. Vitamin D deficiency may also cause muscle weakness making standing and walking difficult for affected children. In the elderly, more frequent falls may occur, which increases their risk of fracture.
<60 p="">
D50 Iron deficiency anaemia
D500 Iron deficiency anaemia secondary to blood loss (chronic)
D501 Sideropenic dysphagia
D508 Other iron deficiency anaemias
D509 Iron deficiency anaemia, unspecified
D51 Vitamin B12 deficiency anaemia
D510 Vitamin B12 deficiency anaemia due to intrinsic factor deficiency
D511 Vitamin B12 deficiency anaemia due to selective vitamin B12 malabsorption with proteinuria
D512 Transcobalamin II deficiency
<60 p="">
D513 Other dietary vitamin B12 deficiency anaemia
<60 p="">
RATIONALE:
The Endocrine Society Task Force for Evaluation, Treatment and Prevention of Vitamin D deficiency (2011) recommended screening for vitamin D deficiency in individuals at risk for deficiency. The Task Force did not recommend population screening for vitamin D deficiency in individuals who are not at risk (high quality evidence).
High risk for vitamin D deficiency include those individuals with osteoporosis, chronic kidney failure, malabsoprtion syndromes, hyperparathyroidism, African-American and Hispanic children and adults, pregnant or lactating women, older adults with history of falls or non-traumatic fractures, obese children or adults (BMI greater than 30 kg/m2 ), granuloma-forming disorders, and some lymphomas.
The Agency for Healthcare Research and Quality report on Vitamin D and Calcium: a systematic review of health outcomes (2009) found that no qualified systematic reviews have evaluated the association between vitamin D intake or serum 25(OH)D concentrations and incidence of cardiovascular disease, body weight in adults, total cancer incidence and mortality, immune function-related outcomes, and pregnancy. There is fair evidence between low serum 25 (OH)D levels and rickets. However no threshold level has been determined when rickets will not occur. The association between low serum 25 (OH)D levels and the risk of falls, fractures or performance measures among postmenopausal women or elderly men is inconsistent. There is fair evidence to support an association between serum 25(OH)D and BMD or changes in BMD at the femoral neck in postmenopausal women and elderly men. However more recent studies show no significant effects of vitamin D supplementation on BMD in children or adults.
The Institute of Medicine (IOM) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium assessed the health outcomes associated with vitamin D and calcium (2010). The Committee found that the evidence supported a role for these nutrients in bone health but not in other health conditions. In addition, the Committee assigned an upper level to both vitamin D and calcium intake noting that beyond these levels the risk of harm increases. Too much calcium has been associated with kidney stone formation while very high levels of vitamin D are known to cause kidney and tissue damage.
The Institute for Clinical Systems Improvement (ICSI) Health Care Guidelines; Preventative Services for Adults recommendation states there is insufficient evidence to assess the balance of benefits and harms of counseling adults to get an adequate intake of vitamin D and calcium in order to prevent either cancer or bone fractures (Weak Recommendation). The evidence for effectiveness states that adequate calcium intake from food sources and supplements promote bone health; however, the evidence is insufficient to recommend counseling for noninstitutionalized, community-dwelling, asymptomatic adults without previous history of fractures or cancer. However, vitamin D supplementation does appear to be effective in preventing injury from falls in community-dwelling adults aged 65 years and over who are at increased risk for falls.
The U.S. Preventative Task Force (USPSTF) guidelines for Vitamin D and Calcium Supplementation to Prevent Fractures (2013) concluded that the current evidence is insufficient to assess the balance of the benefits and harms of combined vitamin D and calcium supplementation for the primary prevention of fractures in premenopausal women or in men (Grade I statement).
In addition the current evidence is insufficient to assess the balance of the benefits and harms of daily supplementation with greater than 400 IU of vitamin D3 and greater than 1,000 mg of calcium for the primary prevention of fractures in non-institutionalized postmenopausal women (Grade I statement). The USPSTF recommends against daily supplementation with 400 IU or less of vitamin D3 and 1,000 mg or less of calcium for the primary prevention of fractures in non-institutionalized postmenopausal women. (Grade: D Recommendation).
The U.S. Preventative Task Force (USPSTF) guidelines for Screening for Vitamin D deficiency in adults: U.S. Preventive Services Task Force Recommendation Statement (2015) found no studies that evaluated the direct benefit of screening for vitamin D deficiency in adults. The Task Force found adequate evidence that the harms of treatment of vitamin D deficiency are small to none. No studies reported on the harms of treatment of vitamin D deficiency or identified a significant increase in total adverse events, hypercalcemia, kidney stones, or gastrointestinal symptoms.
The Task Force found adequate evidence that treatment of asymptomatic vitamin D deficiency has no benefit on cancer, type 2 diabetes mellitus, risk for death in community-dwelling adults, and risk for fractures in persons not selected on the basis of being at high risk for fractures. The Task Force found inadequate evidence on the benefit of treatment of asymptomatic vitamin D deficiency on other outcomes, including psychosocial and physical functioning. Although the evidence is adequate for a few limited outcomes, the overall evidence on the early treatment of asymptomatic, screendetected vitamin D deficiency in adults to improve overall health outcomes is inadequate.
The USPSTF concluded that the evidence on screening for vitamin D deficiency in community-dwelling, nonpregnant, asymptomatic adults aged 18 years or older to improve health outcomes is insufficient and that the balance of benefits and harms of screening and early intervention cannot be determined.
ICD9: 252.00-252.1 Disorders of the parathyroid gland (code range)
268.0 Rickets, active
268.2 Osteomalacia, unspecified
268.9 Unspecified vitamin D deficiency
275.3 Disorders of phosphorus metabolism
275.41 Hypocalcemia
275.42 Hypercalcemia
585.3-585.6 Chronic kidney disease, Stage III to End stage renal disease (code range)
588.81 Secondary hyperparathyroidism (of renal origin)
733.00 Osteoporosis, unspecified
733.01 Senile osteoporosis
733.02 Idiopathic osteoporosis
733.03 Disuse osteoporosis
733.09 Other, osteoporosis
733.90 Disorder of bone and cartilage, unspecified
