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MP 8.01.30 Hematopoietic Stem-cell Transplantation for Chronic Myelogenous Leukemia

Medical Policy    
Section
Therapy
 
Original Policy Date
12/1/99
Last Review Status/Date
Reviewed with literature search/12:2012
Issue
12:2012
  Return to Medical Policy Index

Disclaimer

Our medical policies are designed for informational purposes only and are not an authorization, or an explanation of benefits, or a contract.  Receipt of benefits is subject to satisfaction of all terms and conditions of the coverage.  Medical technology is constantly changing, and we reserve the right to review and update our policies periodically. 


Description

Hematopoietic Stem-Cell Transplantation

Hematopoietic stem-cell transplantation (HSCT) refers to a procedure in which hematopoietic stem cells are infused to restore bone marrow function in cancer patients who receive bone-marrow-toxic doses of cytotoxic drugs with or without whole body radiation therapy. Hematopoietic stem cells may be obtained from the transplant recipient (autologous HSCT) or from a donor (allogeneic HSCT). They can be harvested from bone marrow, peripheral blood, or umbilical cord blood shortly after delivery of neonates. Although cord blood is an allogeneic source, the stem cells in it are antigenically “naïve” and thus are associated with a lower incidence of rejection or graft-versus-host disease (GVHD). Cord blood is discussed in greater detail in policy No. 7.01.50.

Immunologic compatibility between infused hematopoietic stem cells and the recipient is not an issue in autologous HSCT. However, immunologic compatibility between donor and patient is a critical factor for achieving a good outcome of allogeneic HSCT. Compatibility is established by typing of human leukocyte antigens (HLAs) using cellular, serologic, or molecular techniques. HLA refers to the tissue type expressed at the HLA A, B, and DR loci on each arm of chromosome 6. Depending on the disease being treated, an acceptable donor will match the patient at all or most of the HLA loci.

Conventional Preparative Conditioning for HSCT

The conventional (“classical”) practice of allogeneic HSCT involves administration of cytotoxic agents (e.g., cyclophosphamide, busulfan) with or without total body irradiation at doses sufficient to destroy endogenous hematopoietic capability in the recipient. The beneficial treatment effect in this procedure is due to a combination of initial eradication of malignant cells and subsequent graft-versus-malignancy (GVM) effect that develops after engraftment of allogeneic stem cells within the patient’s bone marrow space. While the slower GVM effect is considered to be the potentially curative component, it may be overwhelmed by extant disease without the use of pretransplant conditioning. However, intense conditioning regimens are limited to patients who are sufficiently fit medically to tolerate substantial adverse effects that include pre-engraftment opportunistic infections secondary to loss of endogenous bone marrow function and organ damage and failure caused by the cytotoxic drugs. Furthermore, in any allogeneic HSCT, immune suppressant drugs are required to minimize graft rejection and GVHD, which also increases susceptibility of the patient to opportunistic infections.

The success of autologous HSCT is predicated on the ability of cytotoxic chemotherapy with or without radiation to eradicate cancerous cells from the blood and bone marrow. This permits subsequent engraftment and repopulation of bone marrow space with presumably normal hematopoietic stem cells obtained from the patient prior to undergoing bone marrow ablation. As a consequence, autologous HSCT is typically performed as consolidation therapy when the patient’s disease is in complete remission. Patients who undergo autologous HSCT are susceptible to chemotherapy-related toxicities and opportunistic infections prior to engraftment, but not GVHD.

Reduced-Intensity Conditioning for Allogeneic HSCT

Reduced-intensity conditioning (RIC) refers to the pretransplant use of lower doses or less intense regimens of cytotoxic drugs or radiation than are used in conventional full-dose myeloablative conditioning treatments. The goal of RIC is to reduce disease burden but also to minimize as much as possible associated treatment-related morbidity and non-relapse mortality (NRM) in the period during which the beneficial GVM effect of allogeneic transplantation develops. Although the definition of RIC remains arbitrary, with numerous versions employed, all seek to balance the competing effects of NRM and relapse due to residual disease. RIC regimens can be viewed as a continuum in effects, from nearly totally myeloablative, to minimally myeloablative with lymphoablation, with intensity tailored to specific diseases and patient condition. Patients who undergo RIC with allogeneic HSCT initially demonstrate donor cell engraftment and bone marrow mixed chimerism. Most will subsequently convert to full-donor chimerism, which may be supplemented with donor lymphocyte infusions to eradicate residual malignant cells. For the purposes of this Policy, the term “reduced-intensity conditioning” will refer to all conditioning regimens intended to be non-myeloablative, as opposed to fully myeloablative (conventional) regimens.

Chronic Myelogenous Leukemia

Chronic myelogenous leukemia (CML) is a hematopoietic stem-cell disorder that is characterized by the presence of a chromosomal abnormality called the Philadelphia chromosome, which results from reciprocal translocation between the long arms of chromosomes 9 and 22. This cytogenetic change results in constitutive activation of BCR-ABL, a tyrosine kinase (TK) that stimulates unregulated cell proliferation, inhibition of apoptosis, genetic instability, and perturbation of the interactions between CML cells and the bone marrow stroma only in malignant cells.

The natural history of the disease consists of an initial (indolent) chronic phase, lasting a median of 3 years, which typically transforms into an accelerated phase, followed by a "blast crisis," which is usually the terminal event. Conventional-dose regimens used for chronic-phase disease can induce multiple remissions and delay the onset of blast crisis to a median of 4–6 years. However, successive remissions are invariably shorter and more difficult to achieve than their predecessors.

Imatinib mesylate (Gleevec®), a selective inhibitor of the abnormal BCR-ABL TK protein, is considered the treatment of choice for newly diagnosed CML. While imatinib can be highly effective in suppressing CML in most patients, it is not curative and is ineffective in 20% to 30%, initially or due to development of BCR-ABL mutations that cause resistance to the drug. Two other TK inhibitors (TKIs, dasatinib, nilotinib) have received marketing approval from the U.S. Food and Drug Administration (FDA) to treat CML following failure or patient intolerance of imatinib. In any case, allogeneic HSCT remains the only treatment capable of inducing durable remissions or cure in CML patients.


Policy

Allogeneic hematopoietic stem-cell transplantation using a myeloablative conditioning regimen may be considered medically necessary as a treatment of chronic myelogenous leukemia.

Allogeneic hematopoietic stem-cell transplantation using a reduced-intensity conditioning (RIC) regimen may be considered medically necessary as a treatment of chronic myelogenous leukemia in patients who meet clinical criteria for an allogeneic HSCT but who are not considered candidates for a myeloablative conditioning allogeneic HSCT.

Autologous hematopoietic stem-cell transplantation is investigational as a treatment of chronic myelogenous leukemia.


Policy Guidelines

Some patients for whom a conventional myeloablative allotransplant could be curative may be considered candidates for RIC allogeneic HSCT. These include those patients whose age (typically older than 60 years) or comorbidities (e.g., liver or kidney dysfunction, generalized debilitation, prior intensive chemotherapy, low Karnofsky Performance Status) preclude use of a standard myeloablative conditioning regimen.

For patients who qualify for a myeloablative allogeneic HSCT on the basis of clinical status, either a myeloablative or reduced-intensity conditioning regimen may be considered medically necessary.


Benefit Application
BlueCard/National Account Issues

The following considerations may supersede this policy:

  • State mandates requiring coverage for autologous bone marrow transplantation offered as part of clinical trials of autologous bone marrow transplantation approved by the National Institutes of Health (NIH)
  • Some plans may participate in voluntary programs offering coverage for patients participating in NIH-approved clinical trials of cancer chemotherapies, including autologous bone marrow transplantation.
  • Some contracts or certificates of coverage (e.g., FEP) may include specific conditions in which autologous bone marrow transplantation would be considered eligible for coverage. 


Rationale

Allogeneic HSCT

Allogeneic hematopoietic stem-cell transplantation (HSCT) is the only known potentially curative therapy for chronic myelogenous leukemia (CML). It became a standard of treatment for CML in the 1980s when the graft-versus-leukemia (GVL) effect was shown to be the critical factor for long-term disease control. (1) Studies in patients with chronic phase disease who received an human leukocyte antigen (HLA)-matched sibling donor transplant had a 45–75% probability of long-term disease-free survival, while those transplanted with more advanced disease had a 15–40% long-term survival. (2) Young, good-risk patients transplanted early in the chronic phase from HLA-matched but unrelated donors had a 40–60% probability of long-term survival, although it is lower than that of similar patients transplanted from matched sibling donors. (3,4)

CML was once the most common malignancy for which allogeneic HSCT was performed, but by 2005, it was in eighth place among hematologic transplantation indications. A retrospective analysis of data from the Center for International Blood and Marrow Transplant Research Center (CIBMTR) showed that transplantation for CML was in decline prior to U.S. Food and Drug Administraton (FDA) approval of imatinib in 2001. (5) Subsequently, long-term follow-up results from the International Randomized Study of Interferon and STI 571 (IRIS) of imatinib mesylate, plus the availability of 2 additional approved TKI agents (nilotinib and dasatinib), have caused modification of the timing of application of allogeneic HSCT. (6-8) This procedure now is typically delayed in patients with newly diagnosed CML, who will receive imatinib mesylate as front-line treatment. It also may only be used early when a complete molecular response to the drug fails or is not achieved soon after starting imatinib administration.

Allogeneic HSCT has continued to develop, with important advancements in the use of nonmyeloablative or reduced-intensity conditioning (RIC) preparative regimens. RIC regimens were initially conceptualized as a means to extend the use of allogeneic HSCT to the estimated 70% of CML patients who were ineligible for myeloablative conditioning regimens because of advanced age or comorbidities. The use of RIC and allogeneic HSCT is of particular interest for treatment of CML given the relatively pronounced susceptibility of this malignancy to the GVL effect of allogeneic hematopoietic progenitor cells following their engraftment in the host. Overall, among 9 studies compiled in a recent review, outcomes achieved with RIC allogeneic transplants have been similar to those with conventional allotransplants, with overall survival (OS) rates ranging from 35% at 2.5 years to 85% at 5 years among patients in chronic phase 1 at transplant. (9) Among the studies included in this review, treatment-related mortality or nonrelapse mortality (NRM) ranged from 0% to 29% at 1 year. In the largest experience, a retrospective European Group for Blood and Marrow Transplantation (EMBT) study of 186 patients, OS was 54% at 3 years using a variety of RIC regimens in patients in chronic phase 1 (n=118), chronic phase 2 (n=26), acute phase (n=30), and blast crisis (n=12). (10) Among patients transplanted in the first chronic phase (CP1), OS was 69% at 3 years.

RIC regimens have many of the same limitations as standard-intensity conditioning: relapse, graft-versus-host disease (GVHD) (particularly chronic GVHD), and mortality from treatment-related causes other than myelotoxicity. However, in the absence of prospective, comparative, randomized trials, only indirect comparisons can be made between the relative clinical benefits and harms associated with myeloablative and RIC regimens with allogeneic HSCT. Comparison of study results is further compromised by heterogeneity among patients, treatments, and outcome measures. Nonetheless, clinical evidence suggests outcomes in CML are similar with myeloablative and RIC allogeneic HSCT. (6, 9, 10) Thus, RIC allogeneic HSCT should be considered medically necessary for CML patients who would otherwise be expected to benefit from an allogeneic HSCT.

The advent of tyrosine kinase inhibitor (TKI) therapy has altered the treatment paradigm for CML such that the majority of patients are treated initially with a TKI until disease progresses. While progression may occur within months of starting a TKI, this may be delayed for years, as shown by the results of the IRIS trial (8) and other studies. (6, 7) With the addition of two other TKIs (nilotinib and dasatinib) plus the possibility of effective dose escalation with imatinib to override resistance, it is possible to maintain a typical CML patient past the upper age limit (usually 50-55 years) at which a myeloablative allogeneic HSCT is considered an option. (8, 11, 12) These patients would be eligible for an RIC allogeneic HSCT.

Clinical guidelines and recommendations for management of patients with CML in the context of TKI therapy and allogeneic HSCT have been published. (13-17) They are in concordance with this policy.

Autologous HSCT

A major limitation in the use of autologous HSCT in patients with CML is a high probability that leukemic cells will be infused back into the patient. However, it is recognized that many CML patients still have normal marrow stem cells. Techniques used to isolate and expand this normal clone of cells have included ex vivo purging, long-term culture, and immunophenotype selection. (18) Even without such techniques, there have been isolated case reports of partial cytogenetic remissions after autologous HSCT, and one study has suggested that patients undergoing such therapy may have improved survival compared with historical controls. (2)

Another article summarized the results of 200 consecutive autologous transplants using purged or unpurged marrow from 8 different transplant centers. (19) Of the 200 patients studied, 125 were alive at a median follow-up of 42 months. Of the 142 transplanted in chronic phase, the median survival had not been reached at the time of publication, while the median survival was 35.9 months for those transplanted during an accelerated phase. Other data consist of small, single institution case series using a variety of techniques to enrich the population of normal stem cells among the harvested cells. (2) Additional reports of small, uncontrolled studies with a total of 182 patients (range: 15–41 patients) given autotransplants for CML included patient populations that varied across the studies. Some focused on newly diagnosed patients or those in the first year since diagnosis. (20, 21) Others focused on patients who did not respond to or relapsed after initial treatment using interferon alfa. (22, 23) Finally, some focused on patients transplanted in the late chronic phase (24) or after transformation to accelerated phase or blast crisis. (25) Although some patients achieved complete or partial molecular remissions and long-term disease-free survival, these studies do not permit conclusions free from the influence of patient selection bias. All autotransplanted patients included in these reports were treated before imatinib mesylate or newer TKIs became available. Since these agents have been shown to induce major hematologic and, less often, cytogenetic remissions, even among patients in accelerated phase and blast crisis, future studies of autotransplants for CML may focus on patients who fail or become resistant to imatinib mesylate. Alternatively, it may be incorporated into combination regimens used for high-dose therapy. (26)

Summary

There has been a significant change in clinical transplantation practice for chronic myelogenous leukemia (CML) patients, particularly over the past decade subsequent to the commercial introduction of imatinib, and subsequently dasatinib and nilotinib. (17) The TK inhibitors (TKIs) have replaced allogeneic hematopoietic stem-cell transplantation (HSCT) as initial therapy in patients with chronic phase CML. (15) However a significant proportion of cases fail to respond to TKIs, develop resistance to them, or become unable to tolerate all TKIs and go on to allogeneic HSCT. Allogeneic HSCT represents the only potentially curative option for those patients in accelerated or blast phase. (16) Given the successes seen with TKIs in chronic phase CML, and the risks associated with myeloablative autologous HSCT, the latter has declined in use to the extent that few anecdotal reports have been published since the TKI era began.(16)

Practice Guidelines and Position Statements

National Comprehensive Cancer Network (NCCN) Guidelines

The 2012 NCCN guidelines (v2.2013) recommend allogeneic bone marrow transplant as an alternative treatment option only for high-risk settings (Available online at: http://www.nccn.org/professionals/physician_gls/pdf/cml.pdf):

  • patients who do not achieve hematologic remission after 3 months of TKI (imatinib, dasatinib, nilotinib) therapy
  • patients with no cytogenetic response or those in cytogenetic relapse at 6, 12, or 18 months, after achieving initial hematologic remission after 3 months of imatinib therapy
  • patients progressing on a TKI to accelerated phase or blast crisis
  • patients unable to tolerate any TKI inhibitor

Nonmyeloablative allogeneic HSCT is recommended only within a clinical trial.

Autologous bone marrow transplant for CML is not addressed in the NCCN guidelines.

National Cancer Institute (NCI) Clinical Trial Database (PDQÒ)

A search of the National Cancer Institute clinical trial database (PDQÒ) identified 10 active Phase II/III trials in the U.S. including allografting, using various conditioning regimens, as well as different stem-cell sources and mobilization protocols. (Available online at: http://www.cancer.gov/clinicaltrials/search/results?protocolsearchid=7038344).

References:

 

  1. Maziarz RT. Who with chronic myelogenous leukemia to transplant in the era of tyrosine kinase inhibitors? Curr Opin Hematol 2008; 15(2):127-33.
  2. Bhatia R, Verfaillie CM, Miller JS et al. Autologous transplantation therapy for chronic myelogenous leukemia. Blood 1997; 89(8):2623-34.
  3. McGlave PB, Shu XO, Wen W et al. Unrelated donor marrow transplantation for chronic myelogenous leukemia: 9 years' experience of the national marrow donor program. Blood 2000; 95(7):2219-25.
  4. Weisdorf DJ, Anasetti C, Antin JH et al. Allogeneic bone marrow transplantation for chronic myelogenous leukemia: comparative analysis of unrelated versus matched sibling donor transplantation. Blood 2002; 99(6):1971-7.
  5. Giralt SA, Arora M, Goldman JM et al. Impact of imatinib therapy on the use of allogeneic haematopoietic progenitor cell transplantation for the treatment of chronic myeloid leukaemia. Br J Haematol 2007; 137(5):461-7.
  6. Apperley JF. Managing the patient with chronic myeloid leukemia through and after allogeneic stem cell transplantation. Hematology Am Soc Hematol Educ Program 2006:226-32.
  7. Druker BJ, Guilhot F, O'Brien SG et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med 2006; 355(23):2408-17.
  8. Fernandez HF, Kharfan-Dabaja MA. Tyrosine kinase inhibitors and allogeneic hematopoietic cell transplantation for chronic myeloid leukemia: targeting both therapeutic modalities. Cancer Control 2009; 16(2):153-7.
  9. Chakrabarti S, Buyck HC. Reduced-intensity transplantation in the treatment of haematological malignancies: current status and future-prospects. Curr Stem Cell Res Ther 2007; 2(2):163-88.
  10. Crawley C, Szydlo R, Lalancette M et al. Outcomes of reduced-intensity transplantation for chronic myeloid leukemia: an analysis of prognostic factors from the Chronic Leukemia Working Party of the EBMT. Blood 2005; 106(9):2969-76.
  11. Kantarjian H, Shah NP, Hochhaus A et al. Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med 2010; 362(24):2260-70.
  12. Saglio G, Kim DW, Issaragrisil S et al. Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med 2010; 362(24):2251-9.
  13. Baccarani M, Cortes J, Pane F et al. Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet. J Clin Oncol 2009; 27(35):6041-51.
  14. von Bubnoff N, Duyster J. Chronic myelogenous leukemia: treatment and monitoring. Dtsch Arztebl Int 2010; 107(7):114-21.
  15. Cervantes F, Mauro M. Practical management of patients with chronic myeloid leukemia. Cancer 2011; 117(19):4343-54.
  16. Jain N, van Besien K. Chronic myelogenous leukemia: role of stem cell transplant in the imatinib era. Hematol Oncol Clin North Am 2011; 25(5):1025-48.
  17. Pavlu J, Szydlo RM, Goldman JM et al. Three decades of transplantation for chronic myeloid leukemia: what have we learned? Blood 2011; 117(3):755-63.
  18. Szatrowski TP. Progenitor cell transplantation for chronic myelogenous leukemia. Semin Oncol 1999; 26(1):62-6.
  19. McGlave PB, De Fabritiis P, Deisseroth A et al. Autologous transplants for chronic myelogenous leukaemia: results from eight transplant groups. Lancet 1994; 343(8911):1486-8.
  20. Meloni G, Capria S, Vignetti M et al. Ten-year follow-up of a single center prospective trial of unmanipulated peripheral blood stem cell autograft and interferon-alpha in early phase chronic myeloyd leukemia. Haematologica 2001; 86(6):596-601.
  21. Podesta M, Piaggio G, Sessarego M et al. Autografting with Ph-negative progenitors in patients at diagnosis of chronic myeloid leukemia induces a prolonged prevalence of Ph-negative hemopoiesis. Exp Hematol 2000; 28(2):210-5.
  22. Boiron JM, Cahn JY, Meloni G et al. Chronic myeloid leukemia in first chronic phase not responding to alpha-interferon: outcome and prognostic factors after autologous transplantation. EBMT Working Party on Chronic Leukemias. Bone Marrow Transplant 1999; 24(3):259-64.
  23. McBride NC, Cavenagh JD, Newland AC et al. Autologous transplantation with Philadelphia-negative progenitor cells for patients with chronic myeloid leukaemia (CML) failing to attain a cytogenetic response to alpha interferon. Bone Marrow Transplant 2000; 26(11):1165-72.
  24. Michallet M, Thiebaut A, Philip I et al. Late autologous transplantation in chronic myelogenous leukemia with peripheral blood progenitor cells mobilized by G-CSF and interferon-alpha. Leukemia 2000; 14(12):2064-9.
  25. Pigneux A, Faberes C, Boiron JM et al. Autologous stem cell transplantation in chronic myeloid leukemia: a single center experience. Bone Marrow Transplant 1999; 24(3):265-70.
  26. Mauro MJ, Deininger MW. Chronic myeloid leukemia in 2006: a perspective. Haematologica 2006; 91(2):152.

Codes

Number

Description

CPT 38204 Management of recipient hematopoietic cell donor search and cell acquisition
  38205 Blood-derived hematopoietic progenitor cell harvesting for transplantation, per collection, allogeneic
  38206 Blood-derived hematopoietic progenitor cell harvesting for transplantation, per collection, autologous
  38208 Thawing of previously frozen harvest
  38209 Washing of harvest
  38210 Specific cell depletion with harvest, T-cell depletion
  38211 Tumor cell depletion
  38212 Red blood cell removal
  38213 Platelet depletion
  38214 Plasma (volume) depletion
  38215 Cell concentration in plasma, mononuclear, or buffy coat layer
  38220 Bone marrow, aspiration only
  38221 Biopsy, needle or trocar
  38230 Bone marrow harvesting for transplantation
  38240 Bone marrow or blood-derived peripheral stem-cell transplantation; allogeneic
  38241 Bone marrow or blood-derived peripheral stem-cell transplantation; autologous
ICD-9 Procedure 41.00 Bone marrow transplant, not otherwise specified
  41.01 Autologous bone marrow transplant without purging
  41.02 Allogeneic bone marrow transplant with purging
  41.03 Allogeneic bone marrow transplant without purging
  41.04 Autologous hematopoietic stem-cell transplant without purging
  41.05 Allogeneic hematopoietic stem-cell transplant without purging
  41.06 Cord blood stem-cell transplant
  41.07 Autologous hematopoietic stem-cell transplant with purging
  41.08 Allogeneic hematopoietic stem-cell transplant with purging
  41.09 Autologous bone marrow transplant with purging
  41.91 Aspiration of bone marrow from donor for transplant
  99.79 Other therapeutic apheresis (includes harvest of stem cells)
ICD-9 Diagnosis 205.10-205.11 Chronic myeloid leukemia code range
HCPCS    
  Q0083-Q0085 Chemotherapy administration code range
  J9000-J9999 Chemotherapy drug code range
  S2140 Cord blood Cord blood harvesting for transplantation, allogeneic
  S2142 Cord blood-derived stem-cell transplantation, allogeneic
  S2150 Bone marrow or blood-derived peripheral stem-cell harvesting and transplantation, allogeneic or autologous, including pheresis, high-dose chemotherapy, and the number of days of post-transplant care in the global definition (including drugs; hospitalization; medical surgical, diagnostic, and emergency services)
ICD-10-CM (effective 10/1/14) C92.10-C92.12 Chronic myeloid leukemia, BCR/ABL-positive code range
  C92.20-C92.22 Atypical chronic myeloid leukemia, BCR/ABL-negative code range
ICD-10-PCS (effective 10/1/14)   ICD-10-PCS codes are only used for inpatient services
  30230G0, 30230X0, 30230Y0 Administration, circulatory, transfusion, peripheral vein, open, autologous, code by substance (bone marrow, cord blood or stem cells, hematopoietic)
  30230G1, 30230X1, 30230Y1 Administration, circulatory, transfusion, peripheral vein, open, nonautologous, code by substance (bone marrow, cord blood or stem cells, hematopoietic)
  30233G0, 30233X0, 30233Y0 Administration, circulatory, transfusion, peripheral vein, percutaneous, autologous, code by substance (bone marrow, cord blood or stem cells, hematopoietic)
  30233G1, 30233X1, 30233Y1 Administration, circulatory, transfusion, peripheral vein, percutaneous, nonautologous, code by substance (bone marrow, cord blood or stem cells, hematopoietic)
  30250G0, 30250X0, 30250Y0 Administration, circulatory, transfusion, peripheral artery, open, autologous, code by substance (bone marrow, cord blood or stem cells, hematopoietic)
  30250G1, 30250X1, 30250Y1 Administration, circulatory, transfusion, peripheral artery, open, nonautologous, code by substance (bone marrow, cord blood or stem cells, hematopoietic)
  30253G0, 30253X0, 30253Y0 Administration, circulatory, transfusion, peripheral artery, percutaneous, autologous, code by substance (bone marrow, cord blood or stem cells, hematopoietic)
  30253G1, 30253X1, 30253Y1 Administration, circulatory, transfusion, peripheral artery, percutaneous, nonautologous, code by substance (bone marrow, cord blood or stem cells, hematopoietic)
  6A550ZT, 6A550ZV Extracorporeal Therapies, pheresis, circulatory, single, code by substance (cord blood, or stem cells, hematopoietic)
  6A551ZT, 6A551ZV Extracorporeal Therapies, pheresis, circulatory, multiple, code by substance (cord blood, or stem cells, hematopoietic)
Type of Service Therapy
Place of Service Inpatient/Outpatient


Index

Chronic Myelogenous Leukemia, High-Dose Chemotherapy
High-Dose Chemotherapy, Chronic Myelogenous Leukemia
Stem-Cell Transplant, Chronic Myelogenous Leukemia


Policy History

Date Action Reason
12/01/99 Add to Therapy section New policy. Policy represents revision of 8.01.15 to focus entirely on CML; policy statement unchanged.
10/08/02 Replace policy Policy updated, new references added; no change in policy statement
12/18/02 Replace policy Update CPT codes only
07/15/04 Replace policy Literature review update for the period of May 2002 through May 2004; policy statement unchanged
09/27/05 Replace policy Literature review update for the period of May 2004 through August 2005; policy statement unchanged. Reference number 17 updated
04/17/07 Replace policy Literature review update; policy statement unchanged. Reference numbers 17 and 19 added. Prior reference 17 (NCCN) updated and changed to reference number 18.
06/12/08 Replace policy Policy updated with literature review. References 20-24 added. Prior reference 18 (NCCN) updated and changed to reference number 24. “High-dose chemotherapy” removed from policy title and policy statements, but policy statements remain otherwise unchanged
11/13/08 Replace policy - correction only A sentence in the Rationale section related to the range of “treatment-related mortality or nonrelapse mortality” was revised to indicate it is based on data from reference 21 and moved to that section of the paragraph
12/10/09 Replace policy – change in policy statement Literature review update, policy reorganized and written to reflect new position and material on RIC related to use of allogeneic SCT. Prior reference 24 updated, new references 6-8 were added
12/09/10 Replace policy Policy updated with literature search; no change to policy statements. References 11-14 added; reference 23 updated
06/09/11 Replace policy – code update only CPT code 38242 and HCPCS codes G0265-G0267 deleted from code table
12/08/11 Replace policy Policy updated with literature search; no change to policy statements. References 15-17 added
12/13/12 Repalce Policy
Policy updated with literature search. No new references added. No change to policy statements.