Leukemia Cutis Medication

  • Author: Jeyanthi Ramanarayanan, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jun 22, 2010
 

Medication Summary

The chemotherapeutic regimen chosen depends on the subtype of leukemia. An extensive discussion of specific chemotherapeutic protocols can be found in eMedicine articles on the individual type of leukemia.

Also see the clinical guideline summary from the American Society of Clinical Oncology, 2006 update of recommendations for the use of white blood cell growth factors: an evidence-based clinical practice guideline.[25]

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Antineoplastic agents

Class Summary

These agents inhibit cell proliferation.

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Daunorubicin hydrochloride (Cerubidine)

 

Inhibits DNA and RNA synthesis by intercalating between DNA base pairs. Daunorubicin is rapidly and widely distributed in the tissues (distribution half-life is 2 min), following IV infusion. Metabolized extensively by the liver.

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Idarubicin hydrochloride (Idamycin)

 

Inhibits cell proliferation by inhibiting DNA and RNA polymerase.

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Cytarabine (Cytosar-U)

 

Converted intracellularly to active compound cytarabine-5'-triphosphate, which inhibits DNA polymerase.

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Tretinoin (Vesanoid)

 

All-trans -retinoic acid derived from naturally occurring all-trans -retinol (vitamin A-1). Oral tretinoin is more than 95% bound to plasma proteins and is metabolized by cytochrome P450 enzymes in liver.

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Arsenic trioxide (Trisenox)

 

Use to treat patients with APL whose conditions have relapsed or are refractory to retinoid or anthracycline chemotherapy. May cause DNA fragmentation and damage or degrade fusion protein PML-RAR alpha in APL.

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Gemtuzumab ozogamicin (Mylotarg)

 

Withdrawn from United States market (June 21, 2010). A confirmatory, postapproval clinical trial was begun in 2004. The trial was designed to determine whether adding gemtuzumab to standard chemotherapy demonstrated an improvement in clinical benefit (survival time) to patients with AML. The trial was stopped early when no improvement in clinical benefit was observed and after a greater number of deaths occurred in the group of patients who received gemtuzumab compared with those receiving chemotherapy alone. At initial approval in 2000, gemtuzumab was associated with a serious liver condition called veno-occlusive disease, which can be fatal. This rate has increased in the postmarket setting.

Monoclonal antibody against CD33 antigen, which is expressed on leukemic blasts in >80% of patients with acute myeloid leukemia and normal myeloid cells. Antibody-antigen complex is then internalized and the calicheamicin derivative is released inside the myeloid cell, where it binds to DNA, resulting in double-strand breaks and cell death. Nonhematopoietic and pluripotent cells not affected. Used for administration to patients >60 y (CD33 positive) in first relapse who are not considered candidates for cytotoxic chemotherapy.

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Etoposide (VePesid, Toposar)

 

Administered as combination salvage chemotherapy in patients with relapsed AML. Inhibits topoisomerase II and causes DNA strand breakage, causing cell proliferation to arrest in the late S or early G2 portion of the cell cycle.

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Methotrexate (Folex PFS, Rheumatrex)

 

Antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction in malignant cells. Administered as combination salvage therapy for relapse.

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Growth factors

Class Summary

These agents are indicated in patients receiving chemotherapy with signs of infection and neutropenia.

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Sargramostim (Leukine)

 

GM-CSF stimulates division and maturation of earlier myeloid and macrophage precursor cells.

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Uricosuric agents

Class Summary

These agents increase the renal clearance of uric acid by inhibiting the renal tubular reabsorption of uric acid.

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Allopurinol (Zyloprim)

 

Inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. Reduces the synthesis of uric acid without disrupting the biosynthesis of vital purines.

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Contributor Information and Disclosures
Author

Jeyanthi Ramanarayanan, MD  Assistant Professor, Department of Medicine, Division of Medical Oncology, Roswell Park Cancer Institute

Jeyanthi Ramanarayanan, MD is a member of the following medical societies: American Association of Physicians of Indian Origin and American Society of Hematology

Disclosure: Nothing to disclose.

Coauthor(s)

Shweta Singhal, MD  Resident Physician, Department of Internal Medicine, Rochester General Hospital

Shweta Singhal, MD is a member of the following medical societies: American College of Physicians

Disclosure: Hematology-Oncology None None

Specialty Editor Board

Noah S Scheinfeld, MD, JD, FAAD  Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Private Practice

Noah S Scheinfeld, MD, JD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Optigenex Consulting fee Independent contractor

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD  Associate Professor of Dermatology, Penn State University College of Medicine; Staff Dermatologist, Penn State Milton S Hershey Medical Center

Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Association of Professors of Dermatology, North American Hair Research Society, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Department of Dermatology, Geisinger Medical Center

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References

  1. Cho-Vega JH, Medeiros LJ, Prieto VG, Vega F. Leukemia cutis. Am J Clin Pathol. Jan 2008;129(1):130-42. [Medline].

  2. Agis H, Weltermann A, Fonatsch C, et al. A comparative study on demographic, hematological, and cytogenetic findings and prognosis in acute myeloid leukemia with and without leukemia cutis. Ann Hematol. Feb 2002;81(2):90-5. [Medline].

  3. Kaddu S, Smolle J, Cerroni L, Kerl H. Prognostic evaluation of specific cutaneous infiltrates in B-chronic lymphocytic leukemia. J Cutan Pathol. Dec 1996;23(6):487-94. [Medline].

  4. Baer MR, Barcos M, Farrell H, Raza A, Preisler HD. Acute myelogenous leukemia with leukemia cutis. Eighteen cases seen between 1969 and 1986. Cancer. Jun 1 1989;63(11):2192-200. [Medline].

  5. Shaikh BS, Frantz E, Lookingbill DP. Histologically proven leukemia cutis carries a poor prognosis in acute nonlymphocytic leukemia. Cutis. Jan 1987;39(1):57-60. [Medline].

  6. Cerroni L, Hofler G, Bck B, Wolf P, Maier G, Kerl H. Specific cutaneous infiltrates of B-cell chronic lymphocytic leukemia (B-CLL) at sites typical for Borrelia burgdorferi infection. J Cutan Pathol. Mar 2002;29(3):142-7. [Medline].

  7. Su WP, Buechner SA, Li CY. Clinicopathologic correlations in leukemia cutis. J Am Acad Dermatol. Jul 1984;11(1):121-8. [Medline].

  8. Jones D, Dorfman DM, Barnhill RL, Granter SR. Leukemic vasculitis: a feature of leukemia cutis in some patients. Am J Clin Pathol. Jun 1997;107(6):637-42. [Medline].

  9. Pranteda G, Gueli N, Innocenzi D. Skin vasculitis with direct vessel infiltration by leukaemic cells: a case report. Acta Derm Venereol. Jun-Jul 2001;81(3):215-6. [Medline].

  10. Smoller BR. Leukemic vasculitis: a newly described pattern of cutaneous involvement. Am J Clin Pathol. Jun 1997;107(6):627-9. [Medline].

  11. Fadilah SA, Alawiyah AA, Amir MA, Cheong SK. Leukaemia cutis presenting as leonine facies. Med J Malaysia. Mar 2003;58(1):102-4. [Medline].

  12. Heskel NS, White CR, Fryberger S, Neerhout RC, Spraker M, Hanifin JM. Aleukemic leukemia cutis: juvenile chronic granulocytic leukemia presenting with figurate cutaneous lesions. J Am Acad Dermatol. Sep 1983;9(3):423-7. [Medline].

  13. Chang HY, Wong KM, Bosenberg M, McKee PH, Haynes HA. Myelogenous leukemia cutis resembling stasis dermatitis. J Am Acad Dermatol. Jul 2003;49(1):128-9. [Medline].

  14. Connelly TJ, Kauh YC, Luscombe HA, Becker G. Leukemic macrocheilitis associated with hairy-cell leukemia and the Melkersson-Rosenthal syndrome. J Am Acad Dermatol. Feb 1986;14(2 Pt 2):353-8. [Medline].

  15. Freiman A, Muhn CY, Trudel M, Billick RC. Leukemia cutis presenting with fingertip hypertrophy. J Cutan Med Surg. Jan-Feb 2003;7(1):57-60. [Medline].

  16. Ikeda T, Sakurane M, Uede K, Furukawa F. A case of symmetrical leukemia cutis on the eyelids complicated by B-cell chronic lymphocytic lymphoma. J Dermatol. Jul 2004;31(7):560-3. [Medline].

  17. Ferreira M, Caetano M, Amorim I, Selores M. Leukemia cutis resembling a flare-up of psoriasis. Dermatol Online J. Mar 30 2006;12(3):13. [Medline].

  18. High DA, Luscombe HA, Kauh YC. Leukemia cutis masquerading as chronic paronychia. Int J Dermatol. Nov 1985;24(9):595-7. [Medline].

  19. Simon CA, Su WP, Li CY. Subungual leukemia cutis. Int J Dermatol. Nov 1990;29(9):636-9. [Medline].

  20. Beynet D, Oro AE. Leukemia cutis presenting as a Sister Mary Joseph nodule. Arch Dermatol. Sep 2004;140(9):1170-1. [Medline].

  21. Watanabe H, Okuyama R, Tagami H, Aiba S. Leukaemia cutis developing in a pressure ulcer. Acta Derm Venereol. 2004;84(5):412-3. [Medline].

  22. Burns CA, Scott GA, Miller CC. Leukemia cutis at the site of trauma in a patient with Burkitt leukemia. Cutis. Jan 2005;75(1):54-6. [Medline].

  23. Weinel S, Malone J, Jain D, Callen JP. Therapy-related leukaemia cutis: a review. Australas J Dermatol. Nov 2008;49(4):187-90. [Medline].

  24. Chao SC, Lee JY, Tsao CJ. Leukemia cutis in acute lymphocytic leukemia masquerading as viral exanthem. J Dermatol. Apr 1999;26(4):216-9. [Medline].

  25. Smith TJ, Khatcheressian J, Lyman GH, et al. 2006 update of recommendations for the use of white blood cell growth factors: an evidence-based clinical practice guideline. J Clin Oncol. Jul 1 2006;24(19):3187-205. [Medline].

  26. Poiesz BJ, Papsidero LD, Ehrlich G, et al. Prevalence of HTLV-I-associated T-cell lymphoma. Am J Hematol. Jan 2001;66(1):32-8. [Medline].

  27. Roboz GJ, Knovich MA, Bayer RL, et al. Efficacy and safety of gemtuzumab ozogamicin in patients with poor-prognosis acute myeloid leukemia. Leuk Lymphoma. Oct 2002;43(10):1951-5. [Medline].

  28. Schwonzen M, Kuehn N, Vetten B, Diehl V, Pfreundschuh M. Phenotyping of acute myelomonocytic (AMMOL) and monocytic leukemia (AMOL): association of T-cell-related antigens and skin-infiltration in AMOL. Leuk Res. 1989;13(10):893-8. [Medline].

  29. Sievers EL, Larson RA, Stadtmauer EA, et al. Efficacy and safety of gemtuzumab ozogamicin in patients with CD33-positive acute myeloid leukemia in first relapse. J Clin Oncol. Jul 1 2001;19(13):3244-54. [Medline].

  30. Yoshie O, Fujisawa R, Nakayama T, et al. Frequent expression of CCR4 in adult T-cell leukemia and human T-cell leukemia virus type 1-transformed T cells. Blood. Mar 1 2002;99(5):1505-11. [Medline].

 
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Involvement of the face in a patient with acute myelogenous leukemia. Courtesy of Grant Anhalt, MD.
Red-brown papules can be seen in leukemia cutis. They are confluent in this patient. Courtesy of Nevena Damjanov, MD, and Elizabeth Prechtel.
Papules and nodules on the face of an African American patient with acute myelogenous leukemia (AML). Courtesy of Mona Mofid, MD.
A patient with typical plum-colored lesions seen in leukemia cutis. This patient had acute myelogenous leukemia. Courtesy of Grant Anhalt, MD.
This photograph shows linear areas, which are more violaceous in color, likely due to trauma to the area, such as excoriation, which results in hemorrhage into the skin. Frequent hemorrhage into the skin can make any inflammatory skin lesion appear more violaceous in patients with leukemia. Courtesy of Nevena Damjanov, MD, and Elizabeth Prechtel.
Low-power view of leukemia cutis acute myeloblastic leukemia (AML-M1). Note the perivascular and periadnexal infiltrate with relative epidermal sparing. Courtesy of Kim Hiatt, MD.
This is a higher power view of leukemia cutis acute myeloblastic leukemia (AML-M1). This photo illustrates a perivascular infiltrate of leukemic cells. The nuclei are round to oval with little cytoplasm. Courtesy of Kim Hiatt, MD.
Leukemia cutis of acute monocytic leukemia. Perivascular and periadnexal infiltration is also present, but the cell morphology is distinct. Many of the nuclei are folded or indented. The cytoplasm of the leukemic cells is gray-blue and more abundant than in the M1 subtype. Courtesy of Kim Hiatt, MD.
Low-power view of acute promyelocytic leukemia cutis with a perivascular and periadnexal but also interstitial infiltrate, with epidermal sparing but significant upper dermal edema, which could be confused with Sweet syndrome at a low-power view. Courtesy of Kim Hiatt, MD.
Acute promyelocytic leukemia cutis at high power. The round-to-indented nuclei with prominent cytoplasmic granules are evident. Courtesy of Kim Hiatt, MD.
Photo illustrates leukocyte esterase staining of the cytoplasm of the leukemic cells in acute promyelocytic leukemia. Courtesy of Kim Hiatt, MD.
Leukemia cutis at low power demonstrating a Grenz zone and intercalation of leukemic cells between collagen bundles. Courtesy of Keliegh Culpepper, MD.
A higher-power view of intercalation of leukemic cells between collagen bundles. Courtesy of Keliegh Culpepper, MD.
Table 1. Incidences of Types of Leukemia
Type of LeukemiaIncidence in the United StatesPercentage of Patients with Leukemia Cutis (%)
AML2.5 cases per 100,000 population13
Acute lymphocytic leukemia1.3 cases per 100,000 population3
Chronic myelogenous leukemia (CML)1-2 cases per 100,000 population2-8
Chronic lymphocytic leukemia (CLL)2.3 cases per 100,000 population8
Hairy cell leukemia0.6-2.9 cases per 1,000,000 population8
Adult T-cell leukemiaExtremely low40-70
Table 2. Recommended Immunohistochemical Stains For Leukemia Cutis
Cell LineageCD Antigen Marker
T cellCD45 (LCA) strongly positive



CD45RO usually strongly positive



CD3 positive but only scattered



B cellCD20 strongly positive but scattered in normal B cells, weakly positive or negative in abnormal small B cells, positive in abnormal large B cells



CD43 usually negative



GranulocytesLysozyme strongly positive in well and poorly differentiated granulocytes



Chloroacetate esterase positive in well-differentiated granulocytes



CD68 usually negative in all granulocytes



MonocytesLysozyme strongly positive in well and poorly differentiated monocytes



Chloroacetate esterase usually negative



CD68 positive in well-differentiated monocytes



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