Notification

Lutathera® (Lutetium Lu 177 Dotatate) (Independence Administrators)


Notification Issue Date: 05/31/2019

This version of the policy will become effective 07/01/2019.

The following new policy has been developed to communicate the Company's coverage criteria for Lutathera® (Lutetium Lu 177 Dotatate).



Medical Policy Bulletin


Title:Lutathera® (Lutetium Lu 177 Dotatate) (Independence Administrators)

Policy #:08.01.57

This policy is applicable to the Company’s commercial products only. Policies that are applicable to the Company’s Medicare Advantage products are accessible via a separate Medicare Advantage policy database.


The Company makes decisions on coverage based on Policy Bulletins, benefit plan documents, and the member’s medical history and condition. Benefits may vary based on contract, and individual member benefits must be verified. The Company determines medical necessity only if the benefit exists and no contract exclusions are applicable.

When services can be administered in various settings, the Company reserves the right to reimburse only those services that are furnished in the most appropriate and cost-effective setting that is appropriate to the member’s medical needs and condition. This decision is based on the member’s current medical condition and any required monitoring or additional services that may coincide with the delivery of this service.

This Medical Policy Bulletin 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 Bulletin will be reviewed regularly and be updated as scientific and medical literature becomes available. For more information on how Medical Policy Bulletins are developed, go to the About This Site section of this Medical Policy Web site.



Policy

This policy only applies to members for whom Independence Administrators serves as the claims administrator, as well as those self-funded groups for whom eviCore's Radiation Therapy Services program is not applicable. For all other Independence members, refer to the policy entitled Radiation Therapy Services.

Coverage is subject to the terms, conditions, and limitations of the member's contract.

When services can be administered in various settings, the Company reserves the right to reimburse only those services that are furnished in the most appropriate and cost-effective setting that is appropriate to the member’s medical needs and condition. This decision is based on the member’s current medical condition and any required monitoring or additional services that may coincide with the delivery of this service.

MEDICALLY NECESSARY

Lutathera® (Lutetium Lu 177 Dotatate) is considered medically necessary and, therefore, covered in adult individuals 18 years of age or older for the treatment of inoperable, locally advanced, or metastatic somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumors (GEP-NETs) of the pancreas, foregut, midgut and hindgut, bronchopulmonary tumors, and thymic tumors when ALL of the following criteria are met:
  • The tumor is low-, intermediate-, or well-differentiated high-grade (pathology report documents a Ki-67 index ≤20%)
  • Documented somatostatin receptor expression of a neuroendocrine tumor as detected by somatostatin receptor-based imaging including:
    • 68-Ga-Dotatate Positron Emission Tomography (PET)/Computed Tomography (CT)
    • 68-Ga-Dotatate Positron Emission Tomography (PET)/Magnetic Resonance Imaging (MRI)
    • Somatostatin receptor scintigraphy
  • The individual has documented disease progression while on somatastatin analog therapy (e.g., octreotide, lanreotide)
  • The individual is not receiving long-acting somatostatin analogs (e.g., octreotide, lanreotide) for at least 4 weeks prior to initiating Lutathera® (Lutetium Lu 177 Dotatate)
  • The individual is not receiving short-acting somatostatin analogs (e.g., octreotide) for at least 24 hours prior to initiating Lutathera® (Lutetium Lu 177 Dotatate)
  • The individual does not have severe renal impairment (creatinine clearance, <30 mL/min)
  • The individual has adequate bone marrow function (HgB > 8 g/dl; WBC ≥ 2000/mm3; platelets ≥ 75,000 mm)
  • The individual has adequate hepatic function (total bilirubin ≤ 3 times the upper limit of normal)
  • The individual has a documented Karnofsky Performance Status score ≥ 60
  • The prescribing regimen must be in compliance with the Food and Drug Administration approved dosing, with dosing regimen of 7.4 GBq (200 mCi) every 8 weeks for a total of 4 doses
  • Females of reproductive potential are not pregnant and are using effective contraception

The continuation of Lutathera® (Lutetium Lu 177 Dotatate) is considered medically necessary and, therefore, covered when ALL of the following criteria are met:
  • No recurrent grade 2, 3, or 4 thrombocytopenia (see Guidelines)
  • No recurrent grade 3 or 4 anemia and neutropenia (see Guidelines)
  • No recurrent hepatotoxicity (see definition of hepatotoxicity in the Guidelines)
  • No recurrent grade 3 or 4 nonhematologic toxicity (see Guidelines)
  • No renal toxicity requiring a treatment delay of 16 weeks or longer (see definition of renal toxicity in the Guidelines section)

EXPERIMENTAL/INVESTIGATIONAL

Lutathera® (Lutetium Lu 177 Dotatate) is considered experimental/investigational and, therefore, not covered in all other situations in which the above criteria are not met because the safety and/or effectiveness of this service cannot be established by review of the available published peer-reviewed literature.

Lutathera® (Lutetium Lu 177 Dotatate) greater than a total of 4 doses as per the Food and Drug Administration approved regimen is considered experimental/investigational and, therefore, not covered.

REQUIRED DOCUMENTATION

The individual's medical record must reflect the medical necessity for the care provided. These medical records may include, but are not limited to: records from the health care professional's office, hospital, nursing home, home health agencies, therapies, and test reports.

The Company may conduct reviews and audits of services to our members, regardless of the participation status of the provider. All documentation is to be available to the Company upon request. Failure to produce the requested information may result in a denial for the service.
Guidelines

The recommended dose of Lutathera® (Lutetium Lu 177 Dotatate) is 7.4 GBq (200 mCi) every 8 weeks for a total of 4 doses.

There are concerns regarding the competition between somatostatin analogs and Lutathera® (Lutetium Lu 177 Dotatate) for somatostatin receptor binding. Therefore, the following is recommended:
  • Do not administer long-acting somatostatin analogs for 4 to 6 weeks prior to each Lutathera® (Lutetium Lu 177 Dotatate) dose.
  • Discontinue short-acting somatostatin analogs at least 24 hours before each Lutathera® (Lutetium Lu 177 Dotatate) dose.
  • Both long-acting and short-acting somatostatin analogs can be resumed 4 to 24 hours after each Lutathera® (Lutetium Lu 177 Dotatate) dose.

Lutathera® (Lutetium Lu 177 Dotatate) should be discontinued permanently if the individual develops hepatotoxicity defined as bilirubinemia greater than 3 times the upper limit of normal (grade 3 or 4), or hypoalbuminemia less than 30 g/L with a decreased prothrombin ratio less than 70%.

Lutathera® (Lutetium Lu 177 Dotatate) should be discontinued permanently if the individual develops renal toxicity defined as a creatinine clearance of less than 40 mL/min calculated using Cockcroft-Gault equation with actual body weight, or 40% increase in baseline serum creatinine, or 40% decrease in baseline creatinine clearance calculated using Cockcroft-Gault equation with actual body weight.

Common Toxicity Criteria for Adverse Events
Grade
Description
1
Mild; asymptomatic or mild symptoms; clinical or diagnostic observations only; intervention not indicated.
2
Moderate; minimal, local or noninvasive intervention indicated; limiting age-appropriate instrumental activities of daily living and refer to preparing meals, shopping for groceries or clothes, using the telephone, managing money, etc.
3
Severe or medically significant but not immediately life-threatening; hospitalization or prolongation of hospitalization indicated; disabling; limiting self-care activities of daily living and refer to refer to bathing, dressing and undressing, feeding self, using the toilet, taking medications, and not bedridden.
4
Life-threatening consequences; urgent intervention indicated.
5
Death related to adverse event.


KARNOFSKY PERFORMANCE STATUS (KPS)

A scale measuring the ability of individuals to perform ordinary tasks. KPS scores range from 0 to 100; a higher score means a person is better able to carry out daily activities.

KPS
Definition
100
Normal; no complaint; no evidence of disease
90
Able to carry on normal activity; minor signs of symptoms of disease
80
Normal activity with effort; some sign or symptoms of disease
70
Cares for self; unable to carry on normal activity of do active work
60
Requires occasional assistance, but is able to care for most personal needs
50
Requires considerable assistance and frequent medical care
40
Disabled; requires special care and assistance
30
Severely disabled; hospitalization is indicated, although death not imminent
20
Very sick; hospitalization necessary; active support treatment is necessary
10
Moribund; fatal processes progressing rapidly
0
Dead


BENEFIT APPLICATION

Subject to the terms and conditions of the applicable benefit contract, Lutathera® (Lutetium Lu 177 Dotatate) is covered under the medical benefits of the Company’s products when the medical necessity criteria and Dosing and Frequency Requirements listed in this medical policy are met.

Services that are experimental/investigational are a benefit contract exclusion for all products of the Company. Therefore, they are not eligible for reimbursement consideration.

US FOOD AND DRUG ADMINISTRATION (FDA) STATUS

Lutathera® (lutetium Lu 177 dotatate) was approved by FDA on January 26, 2018, for the treatment of somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumors, including foregut, midgut, and hindgut neuroendocrine tumors in adults.

PEDIATRIC USE

Lutathera® (Lutetium Lu 177 Dotatate) is not indicated for use in pediatric individuals less than 18 years of age.
Description

NEUROENDOCRINE TUMORS

Neuroendocrine tumors are a heterogeneous group of tumors that originate from the neuroendocrine cells in the diffuse neuroendocrine system anywhere in the body but more commonly in the gastrointestinal tract and the respiratory system. Approximately 61% of all neuroendocrine tumors originate from gastrointestinal system or pancreas and are referred to as gastroenteropancreatic neuroendocrine tumors. Lung neuroendocrine tumors may also be referred to as pulmonary neuroendocrine tumors, pulmonary carcinoids, or bronchopulmonary neuroendocrine tumors. Gastroenteropancreatic neuroendocrine tumors may further be characterized as functional or nonfunctional based on whether they secrete hormones that result in clinical symptoms particularly serotonin, which results in “carcinoid syndrome” that is characterized by flushing and diarrhea.

Neuroendocrine tumors are classified as orphan diseases by the Food and Drug Administration (FDA). Based on an analysis of Surveillance, Epidemiology, and End Results Program registry data from 1973 to 2012 (Dasari A, 2017), the overall incidence of neuroendocrine tumors has been reported to be in the range of 6.98 per 100,000 people per year.

DIAGNOSIS

Neuroendocrine tumors are not easy to diagnose because of the rarity of the condition. Symptoms are often nonspecific or mimic other disorders such as irritable bowel syndrome (in the case of gastroenteropancreatic neuroendocrine tumors) or asthma (in the case of a lung neuroendocrine tumors) resulting in an average diagnosis delay of 5 to 7 years after symptom onset (Frilling A, 2012). In many cases, diagnosis is incidental to imaging for other unrelated cause. Most gastroenteropancreatic neuroendocrine tumors express somatostatin receptors that can be imaged using a radiolabeled form of the somatostatin analogue octreotide (e.g., 111In pentetreotide).

TREATMENT APPROACH

There is a general lack of prospective data to guide the treatment of neuroendocrine tumors. Gastroenteropancreatic neuroendocrine tumors are chemotherapy-responsive neoplasms, and platinum-based chemotherapy represents the backbone of treatment for both early and advanced-stage tumors (Sorbye H, 2014). Surgery alone or followed by chemotherapy along with treatment of hormone-related symptoms may be the initial approach for localized disease. For asymptomatic individuals with slow progression, observation with routine surveillance imaging is an option. The prognosis for individuals with metastatic well-differentiated gastroenteropancreatic neuroendocrine tumors is highly variable. Based on retrospective analyses of large databases, the prognosis for individuals with metastatic gastroenteropancreatic neuroendocrine tumors is variable. The median overall survival (from diagnosis) for individuals with metastatic pancreatic neuroendocrine tumors has been reported to range from 2 to 5.8 years (Yao JC, 2008; Strosberg J, 2009), while the median overall survival for small bowel neuroendocrine tumors has been reported as 7.9 years (Ter-Minassian M, 2013).

PHARMACOLOGICAL TREATMENT
First-Line Treatment Options

Somatostatin Analogues (Octreotide and Lanreotide)

Somatostatin is a peptide that binds to somatostatin receptors that are expressed in a majority of carcinoid tumors and inhibits the secretion of a broad range of hormones. Somatostatin analogues (e.g., octreotide, lanreotide) were initially developed to manage the hormonal symptoms related to neuroendocrine tumors, they were found to exert antiproliferative activity, and clinical studies have demonstrated prolonged progression-free survival (PFS) in individuals with neuroendocrine tumors treated with somatostatin analogues (Rinke A, 2009; Caplin ME, 2015). However, the role of somatostatin analogues in individuals with nonfunctioning neuroendocrine tumors is unclear (Ramage JK, 2012).

Commercially available long-acting release forms of octreotide and lanreotide (e.g., Sandostatin LAR, Somatuline Depot), which are administered intramuscularly on a monthly basis, have largely eliminated the need for daily self-injection of short-acting subcutaneous formulations (A-berg K, 2015; O'Toole D, 2000).

Second-Line Treatment Options

Currently, there are no data to support a specific sequence of therapies and only streptozocin, everolimus, and sunitinib are FDA approved for the treatment of pancreatic neuroendocrine tumors.

Mechanistic Target of Rapamycin Inhibitors

The mechanistic target of rapamycin is an enzyme that regulates cell metabolism and proliferation in response to environmental stimuli. It is upregulated in a variety of malignancies in response to stimulation by growth factors and cytokines. Whole-exome genomic analysis has shown that approximately 15% of pancreatic neuroendocrine tumors are associated with somatic variants in genes associated with the mechanistic target of rapamycin pathway (Strosberg J, 2013). Everolimus, an oral mechanistic target of rapamycin inhibitor, has been shown to significantly prolonged PFS vs placebo in individuals with pancreatic neuroendocrine tumors (RADIANT-3 trial) (Yao JC, 2011), and lung and gastrointestinal neuroendocrine tumors nonfunctional (RADIANT-4 trial) (Yao JC, 2016). Note that everolimus is approved by FDA for adults with progressive neuroendocrine tumors of pancreatic origin and adults with progressive, well-differentiated, nonfunctional neuroendocrine tumors of gastrointestinal or lung origin that are unresectable, locally advanced or metastatic. The RADIANT-2 trial individuals with progressive advanced neuroendocrine tumors associated with carcinoid syndrome failed to show a statistically significant improvement in the primary end point of PFS (Pavel ME, 2011).

Tyrosine Kinase Receptor Inhibitors

Neuroendocrine tumors frequently overexpress the vascular endothelial growth factor and receptor. Sunitinib, is a multi-targeted tyrosine kinase inhibitor that targets multiple signaling pathways and growth factors and receptors including vascular endothelial growth factor and receptor 1, 2, and 3 (Strosberg J, 2013). It has been shown that daily sunitinib at a dose of 37.5 mg improves PFS, overall survival, and the overall response rate as compared with placebo among individuals with advanced pancreatic neuroendocrine tumors (Raymond E, 2011). Note that sunitinib is FDA approved for the treatment of progressive, well-differentiated pancreatic neuroendocrine tumors in individuals with unresectable locally advanced or metastatic disease.

Chemotherapy

Response to chemotherapy for advanced neuroendocrine tumors of the gastrointestinal tract and lung is highly variable and, at best, modest. Tumor response rates are generally low and no PFS benefit has been clearly demonstrated. Therefore, the careful selection of individuals is critical to maximize the chance of response and avoid unnecessary toxicity. In advanced neuroendocrine tumors, platinum-based regimens are generally used. They include cisplatin and etoposide (most widely used), carboplatin and etoposide, 5-fluorouracil, capecitabine, dacarbazine, oxaliplatin, streptozocin, and temozolomide (Garcia-Carbonero R, 2016).

Lutetium 177 Dotatate

Lutetium 177 dotatate is a radiolabeled-somatostatin analogue that binds to somatostatin receptor expressing cells, including malignant somatostatin receptor-positive tumors. It is then internalized and beta particle emission from lutetium 177 induces cellular damage by formation of free radicals in somatostatin receptor-positive and neighboring cells.

Lutathera® (Lutetium Lu 177 dotatate) [Advanced Accelerator Applications (AAA), New York, NY] received FDA approval on January 26, 2018. Lutathera® is approved for the treatment of somatostatin receptor positive gastroenteropancreatic neuroendocrine tumors (GEP-NETs), including foregut, midgut, and hindgut neuroendocrine tumors, in adults. Lutathera® is the first available FDA-approved Peptide Receptor Radionuclide Therapy (PRRT), a form of treatment comprising of a targeting molecule that carries a radioactive component. Currently, there are no other radiolabled somatostatin analog conjugates that are FDA approved specifically for use in PRRT.

FDA approval for Lutathera® was based on the results from two studies, NETTER 1 (Strosberg J, 2017; U.S. Food and Drug Administration, 2018) and ERASMUS (Kwekkeboom DJ, 2008; Brabander T, 2017; U.S. Food and Drug Administration, 2018).

NETTER 1 was an open-label randomized, controlled trial (RCT) that compared treatment with Lutathera® to octreotide in individuals with inoperable, progressive somatostatin receptor-positive midgut carcinoid tumors. Eligibility included a Ki-67 index ≤20%, confirmed presence of somatostatin receptors on all lesions (octreoscan uptake that of the normal liver), Karnofsky Performance Status score ≥ 60, creatinine clearance ≥ 50 mL/min, no prior treatment with Peptide Receptor Radionuclide Therapy (PRRT), and no prior external radiation therapy to more than 25% of the bone marrow. Randomization was stratified by octreoscan tumor uptake score (grade 2, 3 or 4) and the length of time that individuals had been on the most recent constant dose of octreotide prior to randomization (≤ 6 or > 6 months). The primary outcome was progression free survival (PFS). A total of 229 individuals were randomized to either Lutathera® (7.4 GBq [200 mCi]) for four infusions every 8 weeks concurrently with 30 mg of long-acting octreotide (n = 116) or 60 mg of high-dose octreotide alone (n = 113). At the data-cutoff date for the primary analysis, PFS at 20 months was 65.2% (95% confidence interval [CI], 50.0 to 76.8) in the Lutathera® group and 10.8% (95% CI, 3.5 to 23.0) in the control group. The response rate was 18% in the Lutathera® group versus 3% in the control group (P<0.001). In the planned interim analysis of overall survival (OS), 14 deaths occurred in the Lutathera® group and 26 in the control group ([hazard ratio: 0.40] P=0.004). Grade 3 or 4 neutropenia, thrombocytopenia, and lymphopenia occurred in 1%, 2%, and 9%, respectively, of individuals in the Lutathera® group as compared with no individuals in the control group, with no evidence of renal toxic effects during the observed time frame. Adverse events (AEs) that were considered by the investigator to be related to trial treatment occurred in 129 individuals: 95 individuals (86%) in the Lutathera® group and 34 individuals (31%) in the control group. The most common AEs among individuals in the Lutathera® group were nausea (65 individuals [59%]) and vomiting (52 individuals [47%]). Other common AEs in the Lutathera® group included fatigue or asthenia, abdominal pain, and diarrhea.

The ERASMUS study was a retrospective, case series that included 1214 individuals with bronchial and gastroenteropancreatic neuroendocrine tumors (GEP-NETs) who received Lutathera®, 610 of whom were treated with a cumulative dose of at least 100 mCi (3.7 GBq) for safety analysis. Another subgroup of 443 Dutch individuals were treated with a cumulative dose of at least 600 mCi (22.2 GBq). The objective response rate (ORR) of the total group of individuals was 39%. Stable disease (SD) was reached in 43% of individuals. PFS and OS for all neuroendocrine tumor individuals were 29 months [95% confidence interval (CI), 26–33 months] and 63 months (95% CI, 55–72 months). Long-term toxicity included acute leukemia in four individuals (0.7%) and myelodysplastic syndrome in nine individuals (1.5%). No therapy-related long-term renal or hepatic failure occurred.
References


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Kong G, Grozinsky-Glasberg S, Hofman MS, et al. Efficacy of peptide receptor radionuclide therapy for functional metastatic paraganglioma and pheochromocytoma. J Clin Endocrinol Metab. 2017;102(9):3278-3287.

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Pavel ME, Hainsworth JD, Baudin E, et al. Everolimus plus octreotide long-acting repeatable for the treatment of advanced neuroendocrine tumours associated with carcinoid syndrome (RADIANT-2): a randomised, placebo-controlled, phase 3 study. Lancet. 2011;378(9808):2005-2012.

Puranik AD, et al. Peptide receptor radionuclide therapy with (90)Y/(177)Lu-labelled peptides for inoperable head and neck paragangliomas (glomus tumours). Eur J Nucl Med Mol Imaging. 2015;42(8):1223-30.

Ramage JK, Ahmed A, Ardill J, et al. Guidelines for the management of gastroenteropancreatic neuroendocrine (including carcinoid) tumours (NETs). Gut. 2012;61(1):6-32.

Raymond E, Dahan L, Raoul JL, et al. Sunitinib malate for the treatment of pancreatic neuroendocrine tumors. N Engl J Med. 2011;364(6):501-513.

Rinke A, Muller HH, Schade-Brittinger C, et al. Placebo-controlled, double-blind, prospective, randomized study on the effect of octreotide LAR in the control of tumor growth in patients with metastatic neuroendocrine midgut tumors: a report from the PROMID Study Group. J Clin Oncol. 2009;27(28):4656-4663.

Romer A, et al. Somaostatin-based radiopeptide therapy with [177Lu-DOTA]-TOC versus [90Y-DOTA]-TOC in neuroendocrine tumours. Eur J Nucl Med Mol Imaging. 2014;41(2):214-22.

Sabet A, Dautzenberg K, Haslerud T, et al. Specific efficacy of peptide receptor radionuclide therapy with (177)Lu-octreotate in advanced neuroendocrine tumours of the small intestine. Eur J Nucl Med Mol Imaging. 2015;42(8):1238-46.

Sabet A, Ezziddin K, Pape UF, et al. Accurate assessment of long-term nephrotoxicity after peptide receptor radionuclide therapy with (177)Lu-ostreotate. Eur J Nucl Med Mol Imaging. 2014;41(3):505-10.

Sabet A, Haslerud T, Pape UF, et al. Outcome and toxicity of salvage therapy with 177Lu-octreotate in patients with metastatic gastroenteropancreatic neuroendocrine tumours. Eur J Nucl Med Mol Imaging. 2014;41(2):205-10.

Sampaio IL, Luiz HV, Violante LS, et al. Treatment of gastroenteropancreatic neuroendocrine tumors with (177)Lu-DOTA-TATE: Experience of the Portuguese Institute of Oncology in Porto. Acta Medica Portuguesa. 2016;29(11):726-733.

Savelli G, et al. Final results of a phase 2A study for the treatment of metastatic neuroendocrine tumors with a fixed activity of (90) Y-DOTA-D-Phe1-Tyr3 octreotide. Cancer. 2012;118(11):2915-24.

Seregni E, Maccauro M, Chiesa C, et al. Treatment with tandom [90y]DOTA-TATE and [177Lu]DOTA-TATE of neuroendocrine tumours refractory to conventional therapy. Eur J Nucl Med Mol Imaging. 2014;41(2):223-30.

Serveri S, et al. Feasibility and utility of re-treatment with (177)Lu-DOCTATE in GEP-NENs relapsed after treatment with (90)Y-DOTATOC. Eur J Nucl Med Mol Imaging. 2015;42(13):1955-63.

Spetz J, Langen B, Rudqvist N, et al. Hedgehog inhibitor sonidegib potentiates (177)Lu-octreotate therapy of GOT1 human small intestine neuroendocrine tumors in nude mice. BMC Cancer. 2017;17:1 Article Number: 528.

Sorbye H, Strosberg J, Baudin E, et al. Gastroenteropancreatic high-grade neuroendocrine carcinoma. Cancer. 2014;120(18):2814-2823.

Sowa-Staszczak A, et al. Peptide receptor radionuclide therapy as a potential tool for neoadjuvant therapy in patients with inoperable neuroendocrine tumours (NETs). Eur J Nucl Med Mol Imaging. 2011;38(9):1669-74.

Soydal Ç, Peker A, Özkan E, et al. The role of baseline Ga-68 DOTATATE positron emission tomography/computed tomography in the prediction of response to fixed-dose peptide receptor radionuclide therapy with lu-177 DOTATATE. Turkish Journal of Medical Sciences. 2016;46(2):409-413.

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Strosberg J, El-Haddad G, Wolin E, et al. Phase 3 trial of (177)Lu-dotatate for midgut neuroendocrine tumors. N Engl J Med. 2017;376(2):125-135.

Strosberg J, Gardner N, Kvols L. Survival and prognostic factor analysis in patients with metastatic pancreatic endocrine carcinomas. Pancreas. 2009;38(3):255-258.

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Coding

Inclusion of a code in this table does not imply reimbursement. Eligibility, benefits, limitations, exclusions, precertification/referral requirements, provider contracts, and Company policies apply.

The codes listed below are updated on a regular basis, in accordance with nationally accepted coding guidelines. Therefore, this policy applies to any and all future applicable coding changes, revisions, or updates.

In order to ensure optimal reimbursement, all health care services, devices, and pharmaceuticals should be reported using the billing codes and modifiers that most accurately represent the services rendered, unless otherwise directed by the Company.

The Coding Table lists any CPT, ICD-9, ICD-10, and HCPCS billing codes related only to the specific policy in which they appear.

CPT Procedure Code Number(s)

N/A


Professional and outpatient claims with a date of service on or before September 30, 2015, must be billed using ICD-9 codes. Professional and outpatient claims with a date of service on or after October 1, 2015, must be billed using ICD-10 codes.

Facility/Institutional inpatient claims with a date of discharge on or before September 30, 2015, must be billed with ICD-9 codes. Facility/Institutional inpatient claims with a date of discharge on or after October 1, 2015, must be billed with ICD-10 codes.


ICD - 10 Procedure Code Number(s)

N/A


Professional and outpatient claims with a date of service on or before September 30, 2015, must be billed using ICD-9 codes. Professional and outpatient claims with a date of service on or after October 1, 2015, must be billed using ICD-10 codes.

Facility/Institutional inpatient claims with a date of discharge on or before September 30, 2015, must be billed with ICD-9 codes. Facility/Institutional inpatient claims with a date of discharge on or after October 1, 2015, must be billed with ICD-10 codes.


ICD -10 Diagnosis Code Number(s)

MEDICALLY NECESSARY


C25.4 Malignant neoplasm of endocrine pancreas

C74.10 Malignant neoplasm of medulla of unspecified adrenal gland

C74.11 Malignant neoplasm of medulla of right adrenal gland

C74.12 Malignant neoplasm of medulla of left adrenal gland

C74.90 Malignant neoplasm of unspecified part of unspecified adrenal gland

C74.91 Malignant neoplasm of unspecified part of right adrenal gland

C74.92 Malignant neoplasm of unspecified part of left adrenal gland

C75.5 Malignant neoplasm of aortic body and other paraganglia

C7A.00 Malignant carcinoid tumor of unspecified site

C7A.010 Malignant carcinoid tumor of the duodenum

C7A.011 Malignant carcinoid tumor of the jejunum

C7A.012 Malignant carcinoid tumor of the ileum

C7A.019 Malignant carcinoid tumor of the small intestine, unspecified portion

C7A.020 Malignant carcinoid tumor of the appendix

C7A.021 Malignant carcinoid tumor of the cecum

C7A.022 Malignant carcinoid tumor of the ascending colon

C7A.023 Malignant carcinoid tumor of the transverse colon

C7A.024 Malignant carcinoid tumor of the descending colon

C7A.025 Malignant carcinoid tumor of the sigmoid colon

C7A.026 Malignant carcinoid tumor of the rectum

C7A.029 Malignant carcinoid tumor of the large intestine, unspecified portion

C7A.090 Malignant carcinoid tumor of the bronchus and lung

C7A.091 Malignant carcinoid tumor of the thymus

C7A.092 Malignant carcinoid tumor of the stomach

C7A.093 Malignant carcinoid tumor of the kidney

C7A.094 Malignant carcinoid tumor of the foregut, unspecified

C7A.095 Malignant carcinoid tumor of the midgut, unspecified

C7A.096 Malignant carcinoid tumor of the hindgut, unspecified

C7A.098 Malignant carcinoid tumors of other sites

C7A.1 Malignant poorly differentiated neuroendocrine tumors

C7A.8 Other malignant neuroendocrine tumors

C7B.00 Secondary carcinoid tumors, unspecified site

C7B.01 Secondary carcinoid tumors of distant lymph nodes

C7B.02 Secondary carcinoid tumors of liver

C7B.03 Secondary carcinoid tumors of bone

C7B.04 Secondary carcinoid tumors of peritoneum

C7B.09 Secondary carcinoid tumors of other sites

C7B.8 Other secondary neuroendocrine tumors

D3A.00 Benign carcinoid tumor of unspecified site

D3A.010 Benign carcinoid tumor of the duodenum

D3A.011 Benign carcinoid tumor of the jejunum

D3A.012 Benign carcinoid tumor of the ileum

D3A.019 Benign carcinoid tumor of the small intestine, unspecified portion

D3A.020 Benign carcinoid tumor of the appendix

D3A.021 Benign carcinoid tumor of the cecum

D3A.022 Benign carcinoid tumor of the ascending colon

D3A.023 Benign carcinoid tumor of the transverse colon

D3A.024 Benign carcinoid tumor of the descending colon

D3A.025 Benign carcinoid tumor of the sigmoid colon

D3A.026 Benign carcinoid tumor of the rectum

D3A.029 Benign carcinoid tumor of the large intestine, unspecified portion

D3A.090 Benign carcinoid tumor of the bronchus and lung

D3A.091 Benign carcinoid tumor of the thymus

D3A.092 Benign carcinoid tumor of the stomach

D3A.094 Benign carcinoid tumor of the foregut, unspecified

D3A.095 Benign carcinoid tumor of the midgut, unspecified

D3A.096 Benign carcinoid tumor of the hindgut, unspecified

D3A.098 Benign carcinoid tumors of other sites

D3A.8 Other benign neuroendocrine tumors



HCPCS Level II Code Number(s)

A9513 Lutetium Lu 177, dotatate, therapeutic, 1 mC


Revenue Code Number(s)

N/A

Coding and Billing Requirements



Policy History

08.01.57
07/01/2019The following new policy has been developed to communicate the Company's coverage criteria for Lutathera® (Lutetium Lu 177 Dotatate).

Version Effective Date: 07/01/2019
Version Issued Date: 07/01/2019
Version Reissued Date: N/A

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