ICD-10-CM code Z79.51 or Z79.52 should be reported for an individual on glucocorticoid therapy. ICD-10-CM code Z79.83 should be reported for DXA
Dual-energy X-ray absorptiometry is a means of measuring bone mineral density. Two X-ray beams, with different energy levels, are aimed at the patient's bones. When soft tissue absorption is subtracted out, the bone mineral density can be determined from the absorption of each beam by bone. Dual-energy X-ray absorptiometry is the most widely used and most thoroughly studied bone density me…
ICD-10-CM codes M80.00XA-M80.88XS have been added to the following Group Code lists: Group 2:, Group 3:, Group 5: and Group 8:. The ICD-10-CM codes for intolerance to other available osteoporosis therapy have been moved to Group 4.
Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30-50% of patients receiving chronic glucocorticoid therapy. Vertebral fractures occur early after exposure to glucocorticoids, at a time when …
Glucocorticoid-Induced Osteoporosis. Fracture-risk screening is indicated with initiation of glucocorticoids. If the risk is high because of age, bone mineral density, or the fracture risk assessment tool score, pharmacologic treatment is recommended; bisphosphonates are recommended as first-line treatment. Disclosure forms provided by...
The M80 series of codes is appropriate for either age-related osteoporosis or other osteoporosis, with current pathological fracture. Codes are selected according to the anatomical site of the fracture, not the location of the osteoporosis. 3. Osteoporosis without current pathological fracture
4 Drug-induced osteoporosis.
ICD-10 code M85. 80 for Other specified disorders of bone density and structure, unspecified site is a medical classification as listed by WHO under the range - Osteopathies and chondropathies .
Corticosteroid-induced osteoporosis is the most common form of secondary osteoporosis and the first cause in young people. Bone loss and increased rate of fractures occur early after the initiation of corticosteroid therapy, and are then related to dosage and treatment duration.
T38. 0X5A - Adverse effect of glucocorticoids and synthetic analogues [initial encounter] | ICD-10-CM.
9: Disorder of bone density and structure, unspecified.
M85. 88 - Other specified disorders of bone density and structure, other site | ICD-10-CM.
The first choice for prevention of corticosteroid osteoporosis is a potent oral bisphosphonate—for example, alendronate or risedronate. Intravenous bisphosphonates should be considered for patients intolerant of the oral route.
What can be done to prevent steroid-induced osteoporosis?Stopping smoking.Limiting alcohol intake.Taking more exercise (particularly weight-bearing exercise).Having an adequate calcium and vitamin D intake, and considering supplements if you are not getting enough calcium and/or vitamin D.
Corticosteroids tend to both reduce the body's ability to absorb calcium and increase how fast bone is broken down. The more of these drugs you take and the longer you take them, the greater your risk of developing osteoporosis.
ICD-10 Classifications The ICD-10 section that covers long-term drug therapy is Z79, with many subsections and specific diagnosis codes. Because Plaquenil does not have its own specific category, clinicians should use Z79. 899—Other Long Term (Current) Drug Therapy.
Side EffectsWeight gain.Feeling very hungry.Water retention or swelling.Mood swings.Blurred vision.Feeling nervous or restless.Trouble sleeping.Muscle weakness.More items...•
ICD-10 code Z79. 899 for Other long term (current) drug therapy is a medical classification as listed by WHO under the range - Factors influencing health status and contact with health services .
The accompanying biochemical changes, particularly the marked increase in serum osteocalcin levels, confirm that enhanced bone formation occurred during the recovery phase. These findings suggest that steroid-induced osteoporosis can be reversed at least in young persons.
SymptomsBack pain, caused by a fractured or collapsed vertebra.Loss of height over time.A stooped posture.A bone that breaks much more easily than expected.
The medications most commonly associated with osteoporosis include phenytoin, phenobarbital, carbamazepine, and primidone. These antiepileptic drugs (AEDs) are all potent inducers of CYP-450 isoenzymes.
Bone loss occurs most rapidly in the first 6 months after starting oral steroids. After 12 months of chronic steroid use, there is a slower loss of bone. Inhaled steroids are less likely to cause bone loss than steroids taken by mouth. However, in higher doses, inhaled steroids may also cause bone loss.
Osteoporosis without current pathological fracture. If the patient does not have current pathological fracture, you should select a code from the M81 series (even if the patient had pathological fracture in the past). A sixth digit indicates laterality. For example:
Risk factors for osteoporosis are aging, hypocalcemia, vitamin D deficiency, and osteomalacia. Osteoporosis is an asymptomatic unless complications (e.g., fracture) occur. Loss of bone mass leads to loss of bone strength, such that even a trivial trauma may be severe enough to cause a fracture.
Other osteoporosis with current pathological fracture, which includes: The M80 series of codes is appropriate for either age-related osteoporosis or other osteoporosis, with current pathological frac ture.
Causes may include senility (old age), inadequate intake of calcium and vitamin D, and protein deficiency.
Osteoporosis also may be related to endocrinal conditions, such as Cushing syndrome, hyperthyroid state, thyrotoxicosis, and diabetes mellitus. Finally, osteoporosis may be drug induced, for instance as a result of long-term steroid therapy.
The primary effects are on osteoblasts and osteocytes. Glucocorticoids impair the replication, differentiation and function of osteoblasts and induce the apoptosis of mature osteoblasts and osteocytes. These effects lead to a suppression of bone formation, a central feature in the pathogenesis of GIO.
Glucocorticoid-induced osteoporosis: pathophysiology and therapy. Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30-50% of patients receiving chronic glucocorticoid therapy.
Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30-50% of patients receiving chronic glucocorticoid therapy. Vertebral fractures occur early after exposure to glucocorticoids, at a time when bone mineral density (BMD) declines rapidly. Fractures tend to occur at higher BMD levels than in women with postmenopausal osteoporosis. In human subjects, the early rapid decline in BMD is followed by a slower progressive decline in BMD. Glucocorticoids have direct and indirect effects on the skeleton. The primary effects are on osteoblasts and osteocytes. Glucocorticoids impair the replication, differentiation and function of osteoblasts and induce the apoptosis of mature osteoblasts and osteocytes. These effects lead to a suppression of bone formation, a central feature in the pathogenesis of GIO. Glucocorticoids also favor osteoclastogenesis and as a consequence increase bone resorption. Bisphosphonates are effective in the prevention and treatment of GIO. Anabolic therapeutic strategies are under investigation.
Vertebral fractures occur early after exposure to glucocorticoids, at a time when …. Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30-50% of patients receiving chronic glucocorticoid therapy. Vertebral fractures occur early ...
Glucocorticoids also favor osteoclastogenesis and as a consequence increase bone resorption. Bisphosphonates are effective in the prevention and treatment of GIO. Anabolic therapeutic strategies are under investigation.
Excessive amounts of systemic glucocorticoids lead to clinically significant adverse effects on the musculoskeletal system by inducing inappropriate bone remodeling through direct and indirect mechanisms and muscle atrophy that contributes to osteoporosis and fractures. Early bone loss is driven by changes in levels of estrogen and parathyroid hormone that stimulate receptor activator of nuclear factor-κB ligand (RANKL)–induced osteoclastogenesis. Osteocyte and osteoblast apoptosis prevents effective mechanosensing and new bone formation.
Vertebral fractures are the most common fractures associated with glucocorticoids; the risk of vertebral fracture increases within 3 months after initiation of treatment and peaks at 12 months. 7,8 The relative risk of clinically diagnosed vertebral fracture doubles and the risk of hip fracture increases by approximately 50% among patients who receive 2.5 to 7.5 mg of prednisolone daily. 8 In a study with a follow-up of 6 months to 10 years, glucocorticoids taken at very high doses significantly increased the risk of vertebral fractures; among adults who received 30 mg of prednisolone per day with cumulative doses of at least 5 g, the risk of vertebral fracture increased by a factor of 14 and the risk of hip fracture increased by a factor of 3. The intermittent use of high-dose glucocorticoids with cumulative doses of 1 g or less had less effect on the risk of fracture, 8 whereas the use of high-dose inhaled glucocorticoids (≥1000-μg fluticasone dose equivalents) for more than 4 years increased the risk of fracture slightly (relative risk, 1.10; 95% confidence interval [CI], 1.02 to 1.19). 9
Approximately 1% of all adults and 3% of adults older than 50 years of age receive glucocorticoids for allergies, inflammatory conditions, or cancer. 1 Long-term use of glucocorticoids is associated with clinically significant toxic effects. Fracture is the most common serious and preventable adverse event associated with these agents. 2-4 The risk of fracture increases with age and with the dose and duration of glucocorticoid use 5-7 ( Table 1 ).
Bisphosphonates are recommended as first-line treatment of osteoporosis because of their low cost and safety.
The underlying condition (e.g., rheumatoid arthritis), as well as clinically evident glucocorticoid-associated adverse effects (e.g., muscle weakness and decreased skin integrity), are typically the focus of treating clinicians. Moreover, patients are frequently resistant to the addition of medications to prevent osteoporosis, a condition that does not currently affect their quality of life, and many are concerned about rare potential adverse effects of antiosteoporosis medications. Thus, assessment and treatment of osteoporosis are frequently postponed or missed.
Numerous randomized trials have shown that bisphosphonates (alendronate, risedronate, zoledronate, and ibandronate) increase bone mineral density in patients who receive glucocorticoids. 24-29 In a 2016 Cochrane review that included 12 randomized trials and involved 1343 participants, participants who received bisphosphonates had a 43% (95% CI, 9 to 65) lower risk of new vertebral fractures than participants who received calcium, vitamin D, or both; the estimated number needed to treat to prevent one glucocorticoid-induced vertebral fracture was 31. 30 In patients who received bisphosphonate treatment for osteoporosis for 3 to 5 years, serious adverse events, including atypical femoral fractures and osteonecrosis of the jaw, have been reported to be rare (<0.01% and <0.001%, respectively). 31,32 Given their low cost and good safety profile, oral bisphosphonates are recommended as first-line agents to prevent glucocorticoid-induced fractures unless there are contraindications or unacceptable side effects. Intravenous bisphosphonates may be preferred in patients who are not adherent to oral bisphosphonates or in those who cannot safely take the oral formulation.
Denos umab inhibits bone resorption by binding to RANKL and interfering with the development of osteoclasts. A noninferiority trial comparing denos umab with risedronate in patients who were beginning to receive glucocorticoids and in those who had received these agents long-term showed superiority of denosumab with respect to increases in bone mineral density at the spine at 12 months and noninferiority with respect to rates of fracture. 36 Some but not all studies have shown a higher risk of infection with denosum ab than with bisphosphonates. 37,38 Given the limited available safety data, denosumab is generally not recommended as the first-line treatment in patients taking multiple immunosuppressive drugs or a biologic treatment.
Prescriptions of oral glucocorticoids, together with date of initiation of oral glucocorticoid use, were identified through the appropriate ATC code (H2A2) . Data were extracted on patient demographics (age and gender) and the medical department accessed. Fractures occurring prior to the index date were identified on the basis of their corresponding ICD-10 codes (Supplementary Table 3). Fractures of the hip, vertebra, femur, proximal humerus, rib and distal radius, as well as osteoporotic pathological fractures were considered. Underlying medical conditions at the index date were identified from ICD-10 codes (Supplementary Table 4). Nine such conditions were considered of particular interest, since they are frequent reasons for prescribing glucocorticoids (Supplementary Table 4). Bone densitometry examinations were identified from the corresponding procedure codes (Supplementary Table 5). Osteoporosis treatments of interest [bisphosphonates, active Vitamin D3 analogues, teriparatide, selective estrogen-receptor modulators, Vitamin K2, anti-receptor activator of nuclear factor-KB ligand (RANKL) antibodies, and anti-sclerostin antibodies] were identified from their ATC or MDV codes (Supplementary Table 6).
Glucocorticoids are used for their anti-inflammatory and immunosuppressive properties in a wide variety of chronic medical conditions, including collagen diseases, respiratory disorders, allergic diseases, renal disease, and post-transplant rejection. However, their long-term use may result in the development of glucocorticoid-induced osteoporosis (GIOP) as an undesirable adverse event [ 1, 2, 3 ]. GIOP is an important health issue due to the widespread long-term use of glucocorticoids in the management of many medical conditions [ 4, 5, 6, 7, 8, 9 ].
Glucocorticoid-induced osteoporosis (GIOP) is associated with a high fracture risk. Practice guidelines by the Japanese Society for Bone and Mineral Research in 2014 recommend bone densitometry and appropriate treatment to reduce this risk. The study objectives were to describe characteristics of GIOP patients in Japan and to evaluate their management in a subgroup of patients without comorbid cancer.
Correct coding requires that a bone metastasis diagnosis (ICD-10-CM code C79.51) be present on the claim as the primary diagnosis and the original cancer or history of cancer be included as the secondary diagnosis. This article does not limit the primary cancer (as long as it is a solid tumor and not a myeloma or other cancer of the blood). Effective for dates of service on or after 01/04/2018, the FDA has approved denosumab (Xgeva®) for the treatment of skeletal-related events in patients with multiple myeloma.
For management of hypercalcemia of malignancy (ICD-10-CM code E83.52)
HCPCS code J0897 should be used to report denosumab (Prolia™, Xgeva™) for claims submitted to the Part A and Part B MAC.
Contractors may specify Revenue Codes to help providers identify those Revenue Codes typically used to report this service. In most instances Revenue Codes are purely advisory. Unless specified in the article, services reported under other Revenue Codes are equally subject to this coverage determination. Complete absence of all Revenue Codes indicates that coverage is not influenced by Revenue Code and the article should be assumed to apply equally to all Revenue Codes.
CPT codes, descriptions and other data only are copyright 2021 American Medical Association. All Rights Reserved. Applicable FARS/HHSARS apply.
This LCD supplements but does not replace, modify or supersede existing Medicare applicable National Coverage Determinations (NCDs) or payment policy rules and regulations for Bisphosphonates (Intravenous [IV]) and Monoclonal Antibodies in the Treatment of Osteoporosis and Their Other Indications.
This LCD addresses “incident to” drugs that are not self-administered for certain patients with osteoporosis. The other indications for these drugs are also addressed.