Sample Letter of Medical Necessity for Fulgent Early-Onset Epileptic Encephalopathypanel

Sample letter of medical necessity for Fulgent Early-Onset Epileptic EncephalopathyPanel

<Date>

ATTN:<Medical Director/ Physician Name>, MD

<Institution/Insurance Company>

<Street Address>

<City>, <State> <Zip>

Re: <Patient Full Name>DOB: <MM/DD/YYYY>

Member ID: <Enter Member ID>Group ID: <Enter Group ID>

Dear <Medical Director/Physician Name>:

I am writing on behalf <Patient Name>, my patient and your subscriber, to request coverage for the Early-Onset Epileptic EncephalopathyNGS Panel offered through Fulgent Diagnostics, a CLIA certified and CAP accredited laboratory located in Temple City, CA. This letter documents the medical necessity of utilizing this test to confirm the genetic cause of <Patient Full Name>’s epilepsy and includes pertinent information relevant to this patient’s medical history and family history.

Medical History

Patient is a <Age> -year-old <Gender > with a suspected genetic form of epilepsy based on the following symptoms:

____Symptom 1 with ICD code

____Symptom 2 with ICD code

____Symptom 3 with ICD code

Family History

The family history is as follows:

Maternal:

Paternal:

Rationale for Testing

Epilepsy is a neurological condition characterized by sudden and recurrent episodes of seizures. Most epilepsy conditions have a genetic component, and emerging evidence indicates that genetics may have an even greater contribution to epilepsy than previously thought7. It is often difficult to diagnose an epileptic condition clinically due to the overlapping symptoms that exist between specific diagnoses and the number of patients that may present atypically. However, it is important to be able to specify which epileptic condition a patient has due to the potential alteration of medical management. It is important to discover the underlying genetic cause of epilepsy to guide treatment selections and counselling, resulting in positive outcomes for patients7.

Three main underlying types of cause have been described in epilepsy: 1. Genetic, 2. Structural/metabolic, and 3. Unknown1. Even so, those with structural/metabolic conditions may also have a genetic component to their condition1. Recent discoveries have highlighted two important patterns: 1. One gene can be associated with multiple epilepsy syndromes, and 2. One epilepsy syndrome can be associated with multiple genes7. The importance of a genetic diagnosis combined with the complexity of genetic etiology supports the use of a broad multi-gene panel when testing for the genetic cause of epilepsy. This is particularly true in patients that present atypically.Infantile spasms, one of theearly-onset epilepsies, can be a diagnostic challenge since the clinical manifestations may be subtle and may mimic benign conditions3.Spasms can disappear by age three to four years, but may be replaced by other seizure types later on. Infantile spasms are often seen in West syndrome and Ohtahara syndrome, two early-onset epileptic encephalopathies. However, it is difficult to make clinical diagnoses of early-onset epilepsies due to phenotypic overlap an there is evidence that early diagnosis and treatment may improve outcome in patients3.

Establishing a diagnosis for patients is imperative because it can alter medical management for patients with epilepsy. It is well known that patients with uncontrolled epilepsy have more physician office visits, more hospital stays, and longer hospital stays than those with controlled epilepsy2. Patients with uncontrolled epilepsy are twice as likely to be hospitalized or have emergency department visits and accrued twice as high of annual healthcare costs compared to those with uncontrolled epilepsy2.

While there are many options for genetic testing, a multi-gene panel for epilepsy is the most cost efficient test for <Patient Name>. A multiple gene panel possesses the ability to analyze many genes that are known to cause epilepsy simultaneously and has a high probability of identifying a diagnosis for <Patient Name>since <He/She>has a currently unexplained epilepsy. I have determined that this test is medically necessary based off <Patient Name>’s personal and family history.

This genetic test will help clarify <Patient Name>’s diagnosis and, more importantly, guide my recommendations for medical care. This genetic test will impact medical management, screening, and prevention of potential complications of this disease. For epilepsy, a genetic diagnosis can guide specific care for the patient. Some examples of currently established or investigated precision medicine treatments include sodium channel blockers in patients with KCNQ2, SCN2A and SCN8A mutations as well as mTOR-inhibitors in mTORopathies6. However, while sodium channel blockers may work well in patients with these genetic mutations, they are contraindicated in patients with channelopathy genes- such as SCN1A pathogenic mutations- and can cause aggravation of seizures4-5Therefore, it is extremely important to establish a genetic diagnosis for epilepsy patients.

For <Patient Name>, the results of the genetic test are necessary and will lead to changes in my medical management strategies and lead to changes in diagnostic procedures. These diagnostic procedures may be more invasive compared to genetic testing and could be avoided with the results from this test. This would reduce unnecessary cost and risk to the patient. Genetic testing can also have implications for other family members who have similar conditions or may be at risk for a similar condition.

Fulgent’s Early-Onset Epileptic EncephalopathyPanel includes <full sequencing/ full sequencing and delection/duplication analysis/ deletion/duplication analysis only>for all 89 genes included on the panel. Due to the medical risks associated with these mutations and the availability of interventions, this genetic test is medically warranted. Therefore, I am ordering this test because it is medically necessary for my patient.<Patient Name>has provided informed consent for this genetic testing.

A positive result in any of the genes included on this panel would confirm a genetic diagnosis and my patient would thus be managed appropriately for that condition. I request that <Patient Name>be approved for the Early-Onset Epileptic EncephalopathyPanel through Fulgent Diagnostics with the following CPT codes:

In summary, I am requesting that <Patient Name> be approved for the Early-Onset Epileptic EncephalopathyPanel offered by Fulgent Diagnostics. The CPT codes are as follow:

Seq / 81302x1, 81403x1, 81404x6, 81405x6, 81406x13, 81407x4, 81479x102
Del/Dup / 81304x1, 81401x2, 81403x2, 81404x5, 81405x8, 81406x11, 81407x2, 81479x102
Seq & Del/Dup / 81302x1, 81304x1, 81401x2, 81403x2, 81404x7, 81405x9, 81406x14, 81407x4, 81479x204

CPTs listed under CLAB2016 can be found on CMS.gov Fee Schedule released in January 2016. (Reference: Alternative:

* CPTs are based on the genes listed. Adding or removing genes will change the CPTs. In some cases, a CPT may require a specific list of genes while performing both sequencing and deldup to qualify. Fulgent bases the CPT for each Gene on multiple sources: CLAB2016v1, AMA Molecular Pathology Tier 2 Gene Designation Chart, and AMA CPT 2016. Call for more details.

Laboratory:
Fulgent Diagnostics
4978 Santa Anita Ave
Temple City, CA, 91780
I thank you for your review and I hope you will support my recommendation of Fulgent Diagnostics’ Early-Onset Epileptic EncephalopathyPanel for <Patient's full name>. Coordinating and completing complex testing of this nature can take up to several months; we are requesting that the authorization be valid for at least 6 months. If you have any questions, please do not hesitate to contact me using the contact information below.

Sincerely,
<Physician Name>, MD

NPI #: <Physician NPI#>

Contact information:

< Address>

<City>, <State> <Zip>

Contact Phone No.: <phone number>

References

1.Baxendale, S., & Thompson, P. (2016). The new approach to epilepsy classification: Cognition and behavior in adult epilepsy syndromes.Epilepsy & Behavior : E&B,64(Pt A), 253-256. doi:S1525-5050(16)30442-5 [pii]

2.Cramer, J., Wang, Z., Chang, E., Powers, A., Copher, R., Cherepanov, D., & Broder, M. (2014). Healthcare utilization and costs in adults with stable and uncontrolled epilepsy. Epilepsy & Behavior : E&B 31. 356-62. Doi: 10.1016/j.yebej.2013.09.046

3.Krag, A., & Holmes, G. L. (2016). Diagnosing infantile spasms: Accuracy of the internet.Epilepsy & Behavior : E&B,64(Pt A), 239-241. doi:S1525-5050(16)30406-1 [pii]

4.McDonald, C. L., Saneto, R. P., Carmant, L., & Sotero de Menezes, M. A. (2016). Focal seizures in patients with SCN1A mutations: Response to treatment.Journal of Child Neurology,doi:0883073816672379 [pii]

5.Miller, I. O., & de Menezes, M. A. S. (2014). SCN1A-related seizure disorders. In: Pagon RA, et al., editors. GeneReviews. Seattle (WA): University of Washington, Seattle; 1993-2014

6.Reif, P. S., Tsai, M. H., Helbig, I., Rosenow, F., & Klein, K. M. (2016). Precision medicine in genetic epilepsies: Break of dawn?Expert Review of Neurotherapeutics,, 1-12. doi:10.1080/14737175.2017.1253476 [doi]

7.Thomas, R. H., & Berkovic, S. F. (2014). The hidden genetics of epilepsy-a clinically important new paradigm.Nature Reviews.Neurology,10(5), 283-292. doi:10.1038/nrneurol.2014.62 [doi]