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CYP450 Genotyping to Determine Drug Metabolizer Status

» Summary» Procedure Codes
» Description» Selected References
» Prior Approval» Policy History
» Policy
 

Medical Policy: 02.04.48 
Original Effective Date: October 2013 
Reviewed: September 2014 
Revised: September 2014 


Benefit Application
Benefit determinations are based on the applicable contract language in effect at the time the services were rendered. Exclusions, limitations or exceptions may apply. Benefits may vary based on contract, and individual member benefits must be verified. Wellmark determines medical necessity only if the benefit exists and no contract exclusions are applicable. This medical policy may not apply to FEP. Benefits are determined by the Federal Employee Program.

This Medical Policy document describes the status of medical technology at the time the document was developed. Since that time, new technology may have emerged or new medical literature may have been published. This Medical Policy will be reviewed regularly and be updated as scientific and medical literature becomes available.


Description: 

The cytochrome p450 (CYP450) family is involved in the metabolism of a significant proportion of currently administered drugs, and genetic variants in cytochrome p450 are associated with altered metabolism of many drugs. It is proposed that genetic testing for cytochrome p450 variants may assist in selecting and dosing drugs that are impacted by these genetic variants.

 

Drug efficacy and toxicity vary substantially between individuals.  Because drugs and doses are typically adjusted to meet individual requirements as needed by using trial and error, clinical consequences may include a prolonged time to optimal therapy and serious adverse events. 

 

Various factors may influence the variability of drug effects, including age, liver function, concomitant diseases, nutrition, smoking, and drug-drug interactions. Inherited (germline) DNA sequence variation (polymorphisms) in genes coding for drug metabolizing enzymes, drug receptors, drug transporters, and molecules involved signal transduction pathways also may have major effects on the activity of those molecules and also on the efficacy and toxicity of the drug.

 
Pharmacogenomics is the study of how an individual’s genetic inheritance affects the body’s response to drugs. It may be possible to predict therapeutic failures or severe adverse drug reactions in individual patients by testing for important DNA polymorphisms (genotyping) in genes related to the metabolic pathway (pharmacokinetics) or single transduction pathway (pharmacodynamics) of the drug. Potentially, test results could be used to optimize drug choice and/or dose for more effective therapy, avoid serious adverse effects and decrease medical costs.

 

Some CYP450 enzyme genes are highly polymorphic, resulting in some enzyme variants that have variable metabolic capacities among individuals, and some with little to no impact on activity.

 

Individuals with a lack of function activity in these enzymes (CYP2C19, CYP2D6, CYP2C9, etc.) can be classified according to how fast they metabolize medications:

  • Poor metabolizers (PMs): lack active enzyme gene alleles, they will process a certain drug more slowly than normal because of the missing enzyme(s), the medication can build up in their system which can increase the likelihood that it will cause side effects. The individual might still be able to benefit from the medication, but at lower dosages.
  • Intermediate metabolizers (IMs): have one active and one inactive enzyme gene allele, these individuals have a reduced enzyme function in processing drugs, they may not process some medications as well as a normal metabolizer would. This can increase risk of side effects and drug interactions.
  • Normal metabolizers (extensive metabolizers Ems): these individuals have 2 copies (alleles) of the most common (wild type) DNA sequence of a particular CYP450 enzyme gene resulting in an active molecule and are termed extensive metabolizers. Medications are processed normally, these individuals are more likely to benefit from treatment and have fewer side effects than people who don’t process the same medication(s) as well.
  • Ultra-rapid metabolizers (UMs): individuals with more than 2 alleles of an active enzyme gene, which cause the medications to leave the body too quickly and often before they have had a chance to work properly. These individuals will likely need a higher than usual dose of medications.

It is very important to realize that many drugs are metabolized to varying degrees by more than one enzyme, either within or outside of the CYP450 superfamily. In addition, interaction between different metabolizing genes, interaction of genes and environment, and interactions among different non-genetic factors also influence CYP450-specific metabolizing functions. Therefore, identification of a variant in a single gene in the metabolic pathway may be insufficient in all but a small proportion of drugs to explain inter-individual differences in metabolism and consequent efficacy or toxicity.


Genetically determined variability in drug response has been traditionally addressed using a trial and error approach to prescribing and dosing, along with therapeutic drug monitoring (TDM) for drugs with a very narrow therapeutic range and/or potential serious adverse effects outside that range. However, TDM is not available for all drugs of interest, and a cautious trial and error approach can lengthen the time to achieving an effective dose.

 

CYP450 enzyme phenotyping (identifying metabolizer status) can be accomplished by administering a test enzyme substrate to a patient and monitoring parent substrate and metabolite concentrations over time. However, testing and interpretation are time-consuming and inconvenient; as a result, phenotyping is seldom performed.

 

Practice Guidelines and Position Statements


 

American College of Cardiology Foundation (ACCF) and American Heart Assocation (AHA) 
A consensus statement by the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) on genetic testing for selection and dosing of clopidogrel was published in 2010.
The recommendations for practice included the following statements:

  • Adherence to existing ACCF/AHA guidelines for the use of antiplatelet therapy should remain the foundation for therapy. Careful clinical judgment is required to assess the importance of the variability in response to clopidogrel for an individual patient and its associated risk to the patient.
  • Clinicians must be aware that genetic variability in CYP enzymes alter clopidogrel metabolism, which in turn can affect its inhibition of platelet function. Diminished responsiveness to clopidogrel has been associated with adverse patient outcomes in registry experiences and clinical trials.
  • The specific impact of the individual genetic polymorphisms on clinical outcome remains to be determined.
  • Information regarding the predictive value of pharmacogenomic testing is very limited at this time; resolution of this issue is the focus of multiple ongoing studies. The selection of the specific test, as well as the issue of reimbursement, is both important additional considerations.
  • The evidence base is insufficient to recommend either routine genetic or platelet function testing at the present time.
  • There are several possible therapeutic options for patients who experience an adverse event while taking clopidogrel in the absence of any concern about medication compliance.

2012 ACCF/AHA Focused Updated of the Guideline for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction

 

Since the FDA announced a “Boxed Warning” on March 12, 2010, about the diminished effectiveness of clopidogrel in patients with an impaired ability to convert the drug into its active form, there has been interest in whether clinicians should perform routine testing in patients being treated with clopidogrel. The routine testing could be for genetic variants fo the CYP2C19 allele and/or for overall effectiveness for inhibition of platelet activity.


The FDA label revision does not mandate testing for CYP2C19 genotypes or overall platelet function. The revision serves to warn clinicians that certain patient subgroups may exhibit reduced clopidogrel-mediated platelet inhibition and emphasizes that clinicians should be aware of alternative treatment strategies to tailor alternative therapies when appropriate.

 
There are no prospective studies that demonstrate that the routine use of these tests couples with modification of antiplatelet therapy improves clinical outcomes or reduces subsequent clinical events. A recent meta-analysis demonstrated an association between the CYP2C19 genotype and clopidogrel responsiveness but no significant association of genotype and cardiovascular events. Several ongoing studies are examining whether genotype assessment with attendant alteration in antiplatelet therapy for those with loss-of-function alleles can improve clinical outcomes.

     
On the basis of current evidence, it is difficult to strongly recommend genotype testing routinely in patients with acute coronary syndrome (ACS), but it might be considered on a case by case basis, especially in patients who experience recurrent ACS events despite ongoing therapy with clopidogrel.

 
Some argue that clinicians should consider routine testing of platelet function, especially in patients undergoing high-risk PCI (percutaneous coronary interventions) to maximize efficacy while maintaining safety. Again, no completed prospective studies have examined such an approach to guide such a sweeping change in clinical management.

 
Our recommendations for the use of genotype testing and platelet function testing seek to strike a balance between not imposing undue burden on clinicians, insurers, and society to implement these strategies in patients with unstable angina (UA) or non-ST-elevation myocardial infarction (NSTEMI) and that of acknowledging the importance of these issues to patients with UA/NSTEMI. Our recommendation that the use of either strategy may have some benefit should be taken in the context of the remarks in this update, as well as the more comprehensive analysis in the ACCF/AHA Clopidogrel Clinical Alert. The Class IIb recommendation of these strategies suggests that a selective, limited approach to platelet genotype assessment and platelet function testing is the more prudent course until better clinical evidence exists for us to provide a more scientific derived recommendation. 

 


American Society of Clinical Oncology (ASCO)

2013 Clinical Practice Guideline for the Use of Pharmacologic Interventions for Breast Cancer Risk Reduction

 

 


Testing for CYP2D6 Allelic Variants in the Prevention Setting

 

  
Since the last guideline, additional data have been generated on the relationship between functional allele variants in cytochrome P450 2D6 gene (CYP2D6), use of CYP2D6 inhibitors including selective serotonin reuptake inhibitors, and breast cancer incidence. Data from the NSABP-P1 and STAR trials do not support the use of CYP2D6 testing to identify women not likely to benefit from tamoxifen therapy for breast cancer prevention. 

 

 

 

 
Summary


Clopidogrel and CYP2C19 Variants: The adverse effect of reduced function CYP2C19 alleles on the benefit from the anti-platelet agent clopidogrel have been demonstrated in a number of studies and a meta-analysis. In March 2010, a new black box warning from the U.S. Food and Drug Administration was issued to alert clinicians that genetic testing is available to identify individuals with poor metabolizer variants of CYP2C19 who may not receive the full benefits of clopidogrel and require dose adjustment or use of a different drug. Two subsequent meta-analyses, however, which included more recently published reports and had more stringent definitions of adverse events in patients treated with clopidogrel. This data has not led to a change in the U.S. Food and Drug Administration recommendation. Many experts do not recommend routine testing of patients for clopidogrel resistance by genetic testing for CYP2C19 poor metabolizers.

 
However, the 2012 ACCF/AHA Focused Updated of the Guideline for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction recommends the use of genotype testing and platelet function testing in patients with unstable angina (UA) or non-ST-elevation myocardial infarction (NSTEMI). Also, patients who experience recurrent ACS (acute coronary syndrome) events despite ongoing therapy with clopidogrel.

 
Tetrabenzine (Xenazine): is a monoamine depletory for oral administration, and is indicated for the treatment of chorea (abnormal involuntary movement disorder) associated with Huntington’s disease. The labeling for tetrabenzine states that, although the pharmacokinetics of tetrabenazine and its metabolites in subjects who do not express the drug metabolizing enzyme CYP2D6 (poor metabolizers) have not been systematically evaluated, it is likely that the exposure to beta-HTBZ would be increased compared to subjects to express the enzyme (extensive metabolizers/normal metabolizers), with an increase similar to that observed in patients taking strong CYP2D6 inhibitors. The labeling for tetrabenzine states that “patients should be genotyped for CYP2D6 prior to treatment with daily doses of tetrabenzine over 50mg”, and patients who are poor metabolizers should not be given daily doses greater than 50 mg.

 
For all other medications: most published CYP450 pharmacogenomic studies are retrospective evaluations of CYP450 genotype association with intermediate (e.g., circulating drug concentrations) or, less often, final outcomes (e.g., adverse events or efficacy) and are largely small and underpowered or not designed to examine the clinical effects of homozygous variant poor metabolizers and of ultra-rapid metabolizers, where the strongest effects, if any, would be seen. The hazards associated with poor metabolizers are consequently difficult to interpret and decision making about how to use genotyping information is poorly defined with uncertain outcomes. As a result CYP450 genotyping is investigational. This includes, but is not limited to, CYP450 genotyping for the following indications:

  • selection or dose of selective serotonin reuptake inhibitor (SSRI)
  • selection and dosing of serotonin norepinephrine reuptake inhibitors (SNRIs)
  • selection and dosing of tricyclic antidepressant medications
  • selection or dose of antipsychotic medications
  • selection or dosing of opioid analgesics
  • dose of efavirenz (common component of highly active antiretroviral therapy for HIV infection)
  • dose of immunosuppressant for organ transplantation
  • selection or dose of beta blockers
  •  dosing and management of antituberculosis medications
  • selection or dosing of Tamoxifen 

Current evidence regarding the use of genotyping tests for the determination of drug metabolizer status indicates that while available testing methods may accurately identify genetic variations in an individual, there is insufficient data to demonstrate that such testing, and the clinical decisions made based on the testing, results in a significant impact on health outcomes.  Specifically, clinical trials have not yet adequately demonstrated that such testing results in either enhanced clinical effectiveness, or in decreased short-term or long-term serious adverse events.

 

Regulatory Status

Diagnostic genotyping tests for certain CYP450 enzymes are now available. Some tests are offered as in-house laboratory developed test services, which do not require U.S. Food and Drug Administration (FDA) approval but which must meet Clinical Laboratory Improvement (CLIA) quality standards.

 
The AmpliChip® (Roche Molecular Systems, Inc.) is an FDA-cleared test for CYP450 genotyping. The AmpliChip® is a microarray consisting of many DNA sequences complementary to 2 CYP450 genes and applied in microscopic quantities at ordered locations on a solid surface (chip). The AmpliChip® tests the DNA from a patient’s white blood cells collected in a standard anticoagulated blood sample for 29 polymorphisms and mutations for the CYP2D6 gene and 2 polymorphisms for the CYP2C19 gene. CYP2D6 metabolizes approximately 25% of all clinically used medications (e.g., dextromethorphan, beta-blockers, antiarrhythmics, antidepressants, and morphine derivatives), including many of the most prescribed drugs. CYP2C19 metabolizes several important types of drugs, including proton-pump inhibitors, diazepam, propranolol, imipramine, and amitriptyline. FDA cleared the test “based on results of a study conducted by the manufacturers of hundreds of DNA samples as well as on a broad range of supporting peer-reviewed literature.” According to FDA labeling, “Information about CYP2D6 genotype may be used as an aid to clinicians in determining therapeutic strategy and treatment doses for therapeutics that are metabolized by the CYP2D6 product.”


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Prior Approval: 

 

Not applicable.


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Policy: 

 

See also medical policy for Genetic Testing for Warfarin Sensitivity  02.01.33

 

CYP450 genotyping (CYP2C19) for the purpose of aiding in the choice of clopidogrel versus alternative antiplatelet agents or in decisions on the optimal dosing for clopidogrel, may be considered medically necessary for any one of the following indications:

  • Patient with unstable angina; or
  • Patient with non-ST-elevation myocardial infarction; or
  • Patient who experiences recurrent acute coronary syndromes (unstable angina/myocardial infarction) despite ongoing therapy with clopidogrel. 

Per American Heart Association: Acute Coronary Syndrome is defined as those situations where the blood supplied to the heart muscle is suddenly blocked.

 
CYP450 genotyping for the purpose of aiding in the choice of clopidogrel versus alternative antiplatelet agents or in decisions on the optimal dosing for clopidogrel for all other indications is considered investigational.

  
Current evidence regarding the use of genotyping tests for the determination of drug metabolizer status indicates that while available testing methods may accurately identify genetic variations in an individual, there is insufficient data to demonstrate that such testing, and the clinical decisions made based on the testing, results in a significant impact on health outcomes.  Specifically, clinical trials have not yet adequately demonstrated that such testing results in either enhanced clinical effectiveness, or in decreased short-term or long-term serious adverse events. Therefore, this testing is considered investigational.


CYP450 genotyping (CYP2D6) may be considered medically necessary for persons who have been prescribed doses of tetrabenazine (Xenazine) greater than 50mg/day. 

 
Repeat Testing for CYP2C19 & CYP2D6

  
Repeat CYP450 genotype testing (CYP2C19, CYP2D6) for the above medically necessary indication has no proven value and is considered investigational. 
 

Genotyping to determine cytochrome P450 (CYP2C19, CYP2D6, CYP2C9, etc.) for the purpose of aiding in the choice of drug or dose to increase efficacy an/or avoid toxicity for all other drugs is considered investigational.  This includes, but is not limited to the following:

  • Selection or dosing of selective serotonin reuptake inhibitors (SSRI)
  • Selection or dosing of antipsychotic drugs
  • Selection or dosing of opioid analgesics
  • Selection and dosing of selective norepinephrine reuptake inhibitors (SNRIs)
  • Selection and dosing of tricyclic antidepressants
  • Dosing of efavirenz (common component of highly active antiretroviral therapy for HIV)
  • Dosing of immunosuppressants for organ transplantation
  • Selection or dose of beta blockers
  • Dosing and management of antituberculosis medications
  • Selection or dosing of Tamoxifen
  • Selection or dosing of Clopidogrel except as indicated above
  • Dosing of Tetrabenzine (Xenazine) except as indicated above

Current evidence regarding the use of genotyping tests for the determination of drug metabolizer status indicates that while available testing methods may accurately identify genetic variations in an individual, there is insufficient data to demonstrate that such testing, and the clinical decisions made based on the testing, results in a significant impact on health outcomes.  Specifically, clinical trials have not yet adequately demonstrated that such testing results in either enhanced clinical effectiveness, or in decreased short-term or long-term serious adverse events. Therefore, this testing is considered investigational.

 

Definitions

 

Cytochrome P450: Refers to a family of 60 different enzymes involved in drug and toxin metabolism.

 

Genotype testing: Determining the DNA sequence in genes.

 

Polymorphisms: Refers to genetic variation between individuals resulting in differences in gene expression, in this case differing activity of various enzymes.





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Procedure Codes and Billing Guidelines: 

  • To report provider services, use appropriate CPT* codes, Alpha Numeric (HCPCS level 2) codes, Revenue codes, and/or diagnosis codes.
  • 81225 CYP2C19 (cytochrome P450, family 2, subfamily C, polypeptide 19) (eg, drug metabolism), gene analysis common variants (eg *2, *3, *4, *8, *17) 
  • 81226 CYP2D6 (cytochrome P450, family 2, subfamily D, polypeptide 6) (eg. drug metabolism), gene analysis common variants (eg *2, *3, *4, *5, *6, *9, *10, *17, *19, *29, *35, *41, *1XN, *2XN, *4XN)  
  • 81227 CYP2C9 (cytochrome P450, family 2, subfamily C, polypeptide 9) (eg, drug metabolism), gene analysis, common variants (eg, *2, *3, *5, *6)

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Selected References: 

  • UpToDate. Overview of Pharmacogenomics, Kelan Tantisira, M.D., MPH, Scott T. Weiss, M.D., MS. January 28, 2013.
  • UpToDate.  Clopidogrel Resistance and Clopidogrel Treatment Failure, Udaya S. Tantry, PhD, Charles H. Hennekens, M.D., DrPH, James L. Zehnder, M.D., Paul A. Gurbel, M.D. August 6, 2013
  • JAMA, December 28, 2011-Vol 306, No24. Michael V. Holmes, MBBS, Msc, Pablo Perel, PhD, Tina Shah, PhD, Aroon D. Hingorani, PhD, Juan P. Casas, PhD. CYP2C19 Genotype, Clopidogrel Metabolism, Platelet Function, and Cardiovascular Events. A Systemic Review and Meta-Analysis
  • American Heart Association. Circulation Cardiovascular Interventions. Guillaume Pare and John W. Eikelboom. 2011; 4:514-521. CYP2C19 Genetic Testing Should not be Done in all Patients Treated with Clopidogrel who are Undergoing Percutaneous Coronary Intervention
  • Chest. Chest/141/2/February 2012 Supplement. John W. Eikelboom, MBBS; Jack Hirsh, M.D., FCCP; Frederick A. Spencer, M.D.; Trevor P. Baglin, MBChB, PhD; and Jeffrey I. Weitz, M.D., FCCP. Antiplatelet Drugs. Antithrombotic Therapy and Preventions of Thromobosis, 9th ed: Amerincan College of Chest Physicians Evidence-Based Clinical Practice Guidelines.
  • Chest. Chest 2012; 141(2) (Suppl):e120S-151S. Jeffrey I.Weitz, M.D. FCCP; John W. Eikelboom, MBBS; and Meyer Michael Samama, M.D.. New Antithrombotic Drugs. Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence Based Clinical Practice Guidelines.
  •  MedScape Reference Drugs, Diseases and Procedures. December 14, 2011. Clopidogrel Dosing and CYP2C19
  • ECRI. Test Intended as Clopidogrel Companion Diagnostic gets FDA Clearance as Guidance Test. Published 12/11/2012.
  • 2012 ACCF/AHA Focused Update of the Guideline for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction. http://content.onlinejacc.org
  • ACCF/AHA Clopidogrel Clinical Alert: Approaches to the FDA “Boxed Warning”. Journal of the American College of Cardiology Vol. 56, No. 4.2010
  • UpToDate Overview of Pharmacogenomics. Kelan Tantisira, M.D., MPH, Scott T. Weiss, M.D. MS. Topic Last Updated July 29, 2014. www.uptodate.com
  • UpToDate Clopidogrel Resistance and Clopiogrel Treatment Failure. Udaya S. Tantry, PhD, Charles H. Hennekens, M.D., DrPH, James L. Zehnder, M.D., Paul A. Gurbel, M.D.. Topic last updated June 13, 2014
  •   Roche AmpliChip Ctyochrome P450 Genotype Testing and Affymetrix GeneChip Microarray Instrumentation System K042259. www.fda.gov
  • PubMed. The AmpliChip CYP450 Genotyping test: Integrating a New Clinical Tool. www.ncbi.nlm.nih.gov
  • Tom Lynch, PharmD and Amy Price, M.D., The Effect of Cytochrome P450 Metabolism on Drug Response Interactions, and Adverse Effects. 2007 American Academy of Family Physicians. www.aafp.org
  • ECRI. Hotline Response. Pharmacogenomic Testing to Guide Treatment of Behavioral Disorders. March 2014. www.ecri.org
  • EGAPP. Recommendations from the EGAPP Working Group: Testing for Cytochrome P450 Polymorphisms in Adults with Nonpsychotic Depression Treated with Selective Serotonin Reuptake Inhibitors. December 2007.
  •  Martin J. Lee KC. Pharmacogenomics of Antidepressants for Major Depressive Disorder. Ment Health Clin. 2012;1(9):17. Available at http://CPNP.org./resource/mnc/2012/03/pharmacogenomics-antidepressants-major-depressive-disorder. Accessed August 25, 2014
  • KR Crews, et al. Clinical Pharmacogenetics Implementation Consortium Guidelines for Cytochrome P450 2D6 Genotype and Codeine Therapy: 2014. www.nature.com
  • MedScape. Pharmacogenomics of Opioids and Perioperative Pain Management. Pharmacogenomics. 2012;13 (15):1719-1740. www.medscape.com
  • Jaekyu Shin, Pharm.D., Julie A. Johnson, Pharm.D. Pharmacogenetics of Beta Blockers. Phamacotherapy. 2007;27(6):874-887. www.medscape.com
  • Christoph Wyen, et.al. Cytochrome P450 2V6 (CYP2B6) and Constitutive Androstane Receptor (CAR) polymorphisms are Associated with Early Discontinuation of Efavirenz-Containing Regimens. Journal of Antimicrobial Chemotherapy 2011;66:2092-2098.
  • UpToDate. Isoniazid Hepatotoxicity. Anne M. Larson, M.D., FACP, Amy L. Graziani, PharmD. Topic Last Updated April 3, 2014. www.uptodate.com
  • Y-Shin Huang, Recent Progress in Genetic Variation and Risk of Antituberculosis Drug Induced Liver Injury. ScienceDirect October 14, 2013. www.sciencedirect.com
  • UpToDate. Huntington Disease. Management. Oksana Suchowersky, M.D., FRCPC, FCCMG. Topic Last Updated April 22, 2014. www.uptodate.com
  • Tetrabenazine in Huntington’s Disease Chorea. Clinical Medicine: Therapeutics. www.la-press.com
  • American Society of Clinical Oncology: 2013 Use of Pharmacologic Interventions for Breast Cancer Risk  Clinical Practice Guideline. Journal of Clinical Oncology 2013.49.3122    

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Policy History: 

Date                                  Reason                               Action

October 2013                                                               New policy

September 2014                 Annual review                      Policy revised                        


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*Current Procedural Terminology © 2012 American Medical Association. All Rights Reserved.

 
Contact Information
New information or technology that would be relevant for Wellmark to consider when this policy is next reviewed may be submitted to:
  Wellmark Blue Cross and Blue Shield
  Medical Policy Analyst
  P.O. Box 9232
  Des Moines, IA 50306-9232
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