Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Leukemia Cutis Clinical Presentation

  • Author: Kyle Devins; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Feb 24, 2015
 

History

Patients present complaining of the appearance of single or multiple skin lesions. Lesions may be localized or generalized. Color may range from violaceous or brick-red to skin colored. The appearance of skin lesions in leukemia cutis is further described in the Physical section. A current or past history of leukemia is present in most patients. In patients with no history of leukemia, eliciting symptoms of systemic disease is particularly important to reach the correct diagnosis. Because of the nonspecific appearance of the skin lesions in leukemia cutis, skin biopsy with follow-up bone marrow biopsy is necessary to confirm the diagnosis.

The lesions of leukemia cutis are most often asymptomatic. In chronic lymphocytic leukemia (CLL) and human T-lymphotropic virus type I (HTLV-1)–induced ATLL, significant pruritus may be present. A typical presentation of acute adult T-cell leukemia/lymphoma (ATLL) includes a history of fever, chills, and lethargy. Many cases of associated dermatitis, which may be extremely pruritic, have been described. Other symptoms that may be reported include abdominal pain, cough, and diarrhea. Patients may report abdominal fullness due to the hepatosplenomegaly or ascites. Patients may also report swollen lymph nodes.

The pancytopenia caused by leukemia results in a variety of manifestations. Symptoms of anemia, including pallor, lethargy, and dyspnea may be prominent. A recent history of easy bleeding and bruising is suggestive of thrombocytopenia.

Neutropenia predisposes one to bacterial, viral, or fungal infections. These infections may present in the skin, the gingiva, the urinary tract, or the lungs. Any of these infections may be accompanied by fevers. Aspergillus and Fusarium organisms may appear at sites of trauma, such as central lines or intravenous insertion sites, or as disseminated nodules and ulcerations. Atypical mycobacterium type IV also cause infections in these patients.

In a patient with a previous diagnosis of leukemia and possible leukemia cutis, the history is important to attempt to identify other potential sites of extramedullary involvement. As many as 90% of patients with leukemia cutis also have other extramedullary involvement, and as many as 40% of patients have meningeal involvement. In patients with possible leukemia cutis as the presenting sign of systemic leukemia, the history may be essential to narrowing the differential diagnosis.

Infiltration of leukemic cells into a variety of organs produces different symptoms in each organ system. Nausea, abdominal fullness, early satiety, and constipation are several symptoms that can occur as a result of hepatomegaly or splenomegaly, which are common in leukemia.

CNS involvement by leukemic cells may be associated with cranial nerve palsies, seizures, altered mental status, or headache with nausea due to increased intracranial pressure. An unusual presentation of leptomeningeal infiltration by leukemic cells is the numb chin syndrome. Patients complain of loss of sensation or altered sensation in the chin area, without any evidence of a primary dermatosis or a history of preceding trauma.

Patients may report bone and joint pain. Infiltration of the periosteum/bone results in painful lesions and, in certain cases, pathologic fractures. Joint swelling and arthritis may be secondary to gouty arthritis from hyperuricemia.

Leukostasis can occur in patients with a significant amount of circulating leukemia cells. Clinical manifestations vary from CNS symptoms, respiratory distress from lung involvement, or priapism. Rare reports describe leukemic vasculitis in which leukemic cells actually infiltrate the blood vessel walls.[22, 23, 24]

Next

Physical

Leukemia cutis displays a variety of clinical appearances. Classically, lesions are described as papules, plaques, or nodules ranging from violaceous to red-brown in color.[2] Skin involvement may be general or localized to one region. Others have reported flesh-colored nodules, occasionally with central ulceration.[3] Indurated plaques, hemorrhagic plaques, perifollicular acneiform papules, macules, ulcers, bullae, and palpable purpura are less frequent.

In myeloid leukemias, extramedullary collections of malignant cells called granulocytic sarcomas may form. When these involve the skin, they often appear as skin-colored or violaceous nodules with or without central ulceration. These tumors may appear as green masses at sites of ulceration. The green pigmentation is due to the presence of myeloperoxidase in tumor cells.

As mentioned briefly in History, systemic findings related to the underlying leukemic process may be present. These include pallor secondary to anemia; purpura, petechiae, or ecchymosis secondary to thrombocytopenia; and hepatosplenomegaly. Opportunistic infections may occur in any type of leukemia. Lymphadenopathy may be present. Drug reactions, including leukocytoclastic vasculitis, and opportunistic infections, particularly thrush, disseminated zoster, or severe and atypical presentations of herpes simplex, may be present.

Patients undergoing chemotherapy for leukemia or other malignancy may present with cutaneous manifestations related to therapy. These findings may complicate the clinical picture and make diagnosis more difficult. Some of the most common cutaneous manifestations of chemotherapeutic agents include alopecia, stomatitis, acral erythema, and hyperpigmentation of the nails or the mucous membranes. Other less common chemotherapy reactions include neutrophilic eccrine hidradenitis and eccrine squamous syringometaplasia. These present as localized or generalized erythematous macules, papules, or plaques.

Some inflammatory cutaneous reactions may occur in patients with leukemia, but they are not a direct result of infiltration of leukemic cells into the skin. These include acute febrile neutrophilic dermatosis (secondary to AML or granulocyte colony-stimulating factor [GCSF]), graft versus host disease, and persistent arthropod bite–like reaction (most commonly seen in CLL). These lesions are included in the differential diagnosis of leukemia cutis.

Note the images below.

Involvement of the face in a patient with acute my 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. T 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 Amer Papules and nodules on the face of an African American patient with acute myelogenous leukemia (AML). Courtesy of Mona Mofid, MD.
Diffuse macules and papules on the scalp of a pati Diffuse macules and papules on the scalp of a patient with chronic myelogenous leukemia.
Diffuse truncal eruption of infiltrated papules an Diffuse truncal eruption of infiltrated papules and plaques in chronic lymphocytic leukemia.
Close-up photo of diffuse truncal eruption of infi Close-up photo of diffuse truncal eruption of infiltrated papules and plaques in chronic lymphocytic leukemia.

Atypical presentations of leukemia cutis have been noted with specific underlying leukemic processes.

AML-M4 and AML-M5 have characteristic gingival hypertrophy as a result of leukemic infiltration. This may be present in as many as 50% of patients with these subtypes of leukemia. See the image below.

Gingival infiltration in a patient with acute myel Gingival infiltration in a patient with acute myelogenous leukemia.

In acute myelomonocytic leukemia, leukemia cutis may manifest as leonine facies.[25]

Juvenile CML may show figurate or arciform lesions.[26]

Two reports describe leukemia cutis as the presenting sign of a transformation of myelodysplastic syndrome into AML. One described leukemic infiltrates on the hands, the other described stasis dermatitis, which was, in fact, leukemia cutis.[27]

One case report of hairy cell leukemia with leukemic macrocheilitis and Melkersson-Rosenthal syndrome has been reported.[28]

Fingertip hypertrophy consisting of leukemic infiltrates of CLL has also been described.[29] B-cell CLL has manifested as symmetrical eyelid leukemia cutis.[30] A case series of 6 patients with B-cell CLL demonstrated leukemia cutis in areas typical of Borrelia burgdorferi –induced pseudolymphomas, namely earlobes, nipples, and scrotum. These cells showed aberrant CD20+/CD43+ phenotype, and 4 of the 6 tumors demonstrated B burgdorferi DNA by polymerase chain reaction.[18] CLL also may manifest as erythroderma or bullous lesions.

Other unusual manifestations include erythema nodosum, erythema annulare centrifugum, pyoderma gangrenosum, lesions mimicking urticaria, urticaria pigmentosum, guttate psoriasis,[31] chronic paronychia,[32] subungual leukemia cutis,[33] and macular erythema.

The first case of leukemia cutis manifesting as a Sister Mary Joseph's nodule was reported in a case of acute promyelocytic leukemia (APL).[34] Leukemia cutis in APL is rare; however, the patient was previously treated with all trans retinoic acid, a factor that increases the chance of extramedullary involvement with relapse.

Leukemia cutis may occur within established scars and within recent areas of trauma, including Hickman catheter sites, sites of burns, decubitus ulcers,[35] herpes simplex virus (HSV) scars, or zoster scars. Plasma cell leukemia cutis has been reported to occur in recent puncture sites. Leukemia cutis at a site of trauma has been reported in one case of Burkitt-type ALL (L3ALL).[36]

In ATLL, 60% of patients have peripheral lymph node enlargement, 26% have hepatomegaly, 22% have splenomegaly, and 39% have skin lesions.

Previous
Next

Causes

Both a genetic component and an environmental component appear to be involved in the pathogenesis of many types of leukemia. A variety of well-characterized chromosomal translocations result in specific leukemic syndromes.

Patients with Down syndrome have an increased risk for both megakaryoblastic leukemia and pre–B-cell leukemia.

Other genetic syndromes, including Bloom syndrome, Klinefelter syndrome, Wiskott-Aldrich syndrome, and Fanconi syndrome, have shown an increased incidence of leukemia.

CLL shows some familial tendency in approximately 20% of CLL cases.

Several genetic mutations lead to an asymmetric maturation of stem cells and result in a single clonal expansion of a severely defective stem cell. The specific mutations and phenotypic changes resulting from genetic aberration determine the subtype of leukemia. After the development of the leukemic clones, a tissue-selective homing process that leads to the infiltration of malignant cells into the epidermis, the dermis, the subcutaneous fat, and the mucosa occurs.

The molecular basis responsible for the development of leukemia cutis is not yet defined. However, initial cytogenetic studies are starting to provide insightful information that would lead to a better understanding in the pathophysiology of leukemia cutis. Prior studies have demonstrated that as many as 50% of patients with AML-M4 or AML-M5 develop leukemia cutis and other forms of EML. Karyotypic studies of leukemic cells have demonstrated the translocation of chromosomes 8 and 21 t(8;21) in these subtypes of AML. A strong association exists between aneuploidy of chromosome 8 and leukemia cutis. Other cytogenetic abnormalities noted in leukemia cutis are chromosome 3 translocations and t(6;9)(p23;q34). Chloromas, primary EMLs are associated with t(8;21), t(9;11) and inv(16) translocations. Identification of proteins coded by specific genes located in those chromosomes would assist in defining factors responsible for the development of leukemia cutis.

Environmental exposures may increase the risk of leukemia. Benzene exposure increases one's risk for AML. Ionizing radiation exposure may increase the risk of leukemia as well, particularly AML, CML, and ALL. Alkylating agents used in chemotherapy cause an increased risk of subsequent AML. The use of all trans retinoic acid to treat APL may predispose a patient to increased risk of extramedullary involvement, including leukemia cutis, which is otherwise rare in APL. Other leukemias may be caused by viral infection. These include ATLL, caused by HTLV-I and acute B-cell leukemia and large granular lymphocytic leukemia, which may be the result of Epstein-Barr virus infection.

Secondary leukemias are associated with prior hematologic disorders such as myelodysplastic syndrome or myeloproliferative disease. Therapy-related acute leukemia results from genetic damage sustained from prior radiation therapy or chemotherapy for malignancies. These are associated with the use of alkylating agents and type II topoisomerase inhibitors, and they differ from primary leukemias clinically and cytogenetically and carry a poor prognostic outcome. Therapy-related secondary leukemia with leukemia cutis as a result of chemotherapy has rarely been reported.[37]

Previous
 
 
Contributor Information and Disclosures
Author

Kyle Devins State University of New York Upstate Medical University

Disclosure: Nothing to disclose.

Coauthor(s)

Thomas N Helm, MD Clinical Professor of Dermatology and Pathology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Director, Buffalo Medical Group Dermatopathology Laboratory

Thomas N Helm, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society of Dermatopathology

Disclosure: Nothing to disclose.

Robert E Kalb, MD Clinical Professor, Medical Student and Resident Instructor, Department of Dermatology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Adjunct Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Robert E Kalb, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

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

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania 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, Society for Investigative Dermatology, Association of Professors of Dermatology, North American Hair Research Society

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

Noah S Scheinfeld, JD, MD, FAAD Assistant Clinical Professor, Department of Dermatology, Weil Cornell Medical College; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Assistant Attending Dermatologist, New York Presbyterian Hospital; Assistant Attending Dermatologist, Lenox Hill Hospital, North Shore-LIJ Health System; Private Practice

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

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbvie<br/>Received income in an amount equal to or greater than $250 from: Optigenex<br/>Received salary from Optigenex for employment.

Acknowledgements

Jeyanthi Ramanarayanan, MD Assistant Professor, Medical Oncology, Veterans Affairs Medical Center of Buffalo

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.

Adrienne Rencic, MD, PhD, FAAD Consulting Staff, Department of Dermatology, Riddle Memorial Hospital

Adrienne Rencic, MD, PhD, FAAD is a member of the following medical societies: National Psoriasis Foundation

Disclosure: Nothing to disclose.

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: Nothing to disclose.

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

  2. Cronin DM, George TI, Sundram UN. An updated approach to the diagnosis of myeloid leukemia cutis. Am J Clin Pathol. 2009 Jul. 132(1):101-10. [Medline].

  3. Singh A, Graziano S, Vajpayee N. Biclonal chronic lymphocytic leukemia presenting as skin lesion. Am J Dermatopathol. 2014 Mar. 36(3):260-2. [Medline].

  4. Vitte F, Fabiani B, Bénet C, Dalac S, Balme B, Delattre C, et al. Specific skin lesions in chronic myelomonocytic leukemia: a spectrum of myelomonocytic and dendritic cell proliferations: a study of 42 cases. Am J Surg Pathol. 2012 Sep. 36(9):1302-16. [Medline].

  5. Betz BL, Hess JL. Acute myeloid leukemia diagnosis in the 21st century. Arch Pathol Lab Med. 2010 Oct. 134(10):1427-33. [Medline].

  6. Weinel S. Leukemia cutis in a patient treated for breast cancer. Australas J Dermatol. 2009. 50:52-55. [Medline].

  7. Lee Hy, Ng HJ et al. Therapy-related leukemia cutis after adjuvnat chemotherapy in a breast cancer patient. Acta Derm Venereol. November 2010. 90:[Medline].

  8. Scott AD, Lee M, Kubba F, Chu A. Acute generalized exanthematous pustulosis (AGEP) secondary to imatinib in a patient with chronic myeloid leukaemia. Clin Exp Dermatol. 2014 Sep 30. [Medline].

  9. Engle EK, Fisher DA, Miller CA, McLellan MD, Fulton RS, Moore DM, et al. Clonal evolution revealed by whole genome sequencing in a case of primary myelofibrosis transformed to secondary acute myeloid leukemia. Leukemia. 2014 Sep 25. [Medline].

  10. Chang H, Brandwein J, Yi QL et al. Extramedullary infiltrates of AML are associated with CD56 expression, 11q23 abnormalities and inferior clinical outcome. Leukemia Research. 2004. 28:1007-1011. [Medline].

  11. Assaf C, Gellrich S, Whittaker S, Robson A, Cerroni L, Massone C, et al. CD56-positive haematological neoplasms of the skin: a multicentre study of the Cutaneous Lymphoma Project Group of the European Organisation for Research and Treatment of Cancer. J Clin Pathol. 2007 Sep. 60(9):981-9. [Medline]. [Full Text].

  12. Diaz-Cascajo C, Bloedern-Schlicht N. Cutaneous infiltrates of myelogenous leukemia in association with pre-existing skin diseases. J Cutan Pathol. 1998 Mar. 25(3):185-6. [Medline].

  13. Tomasini C, Quaglino P, Novelli M. et al. Aleukemic granulomatous leukemia cutis. American Journal of Dermatopathology. 1998. 20:417-421. [Medline].

  14. 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. 2002 Feb. 81(2):90-5. [Medline].

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

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

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

  18. 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. 2002 Mar. 29(3):142-7. [Medline].

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

  20. Cerroni L, Zenahlik P, Hofler G, Kaddu S, Smolle J and Kerl H. Specific cutaneous infiltrates of B-cell chronic lymphocytic leukemia: a clinicopathologic and prognostic study of 42 patients. Am J Surg Pathol. Aug 1996. 20:1000-1010. [Medline].

  21. Ali L, Cheney R, Merzianu. Subclinical Chronic lymphocytic leukemia with atypical cutaneous presentation. J Cutan Pathol. Feb. 38:236-240. [Medline].

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

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

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

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

  26. 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. 1983 Sep. 9(3):423-7. [Medline].

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

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

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

  30. 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. 2004 Jul. 31(7):560-3. [Medline].

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

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

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

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

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

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

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

  38. Chavan RN, Cappel MA, Ketterling RP, Wada DA, Rochet NM, Knudson R, et al. Histiocytoid Sweet syndrome may indicate leukemia cutis: a novel application of fluorescence in situ hybridization. J Am Acad Dermatol. 2014 Jun. 70(6):1021-7. [Medline].

  39. Wilson ML, Elston DM, Tyler WB, Marks VJ, Ferringer T. Dense lymphocytic infiltrates associated with non-melanoma skin cancer in patients with chronic lymphocytic leukemia. Dermatol Online J. 2010 Mar 15. 16(3):4. [Medline].

  40. Bakst RL, Tallman MS, Douer D, Yahalom J. How I treat extramedullary acute myeloid leukemia. Blood. Oct, 2011. 118:3785-3793. [Medline].

 
Previous
Next
 
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.
Infiltration of leukemic cells between collagen bundles.
Infiltration of dermoepidermal junction by clonal T cells in Sézary syndrome.
Diffuse macules and papules on the scalp of a patient with chronic myelogenous leukemia.
Gingival infiltration in a patient with acute myelogenous leukemia.
Diffuse truncal eruption of infiltrated papules and plaques in chronic lymphocytic leukemia.
Close-up photo of diffuse truncal eruption of infiltrated papules and plaques in chronic lymphocytic leukemia.
Table 1. Incidences of Types of Leukemia
Type of Leukemia Incidence in the United States Percentage of Patients with Leukemia Cutis (%)
AML 2.5 cases per 100,000 population 13
Acute lymphocytic leukemia 1.3 cases per 100,000 population 3
Chronic myelogenous leukemia (CML) 1-2 cases per 100,000 population 2-8
Chronic lymphocytic leukemia (CLL) 2.3 cases per 100,000 population 8
Hairy cell leukemia 0.6-2.9 cases per 1,000,000 population 8
Adult T-cell leukemia Extremely low 40-70
Table 2. Recommended Immunohistochemical Stains For Leukemia Cutis
Cell Lineage CD Antigen Marker
T cell CD45 (LCA) strongly positive



CD45RO usually strongly positive



CD3 positive but only scattered



B cell CD20 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



Granulocytes Lysozyme strongly positive in well and poorly differentiated granulocytes



Chloroacetate esterase positive in well-differentiated granulocytes



CD68 usually negative in all granulocytes



CD43 positive, MPO sometimes positive



Monocytes Lysozyme strongly positive in well and poorly differentiated monocytes



Chloroacetate esterase usually negative



CD68 positive in well-differentiated monocytes



CD163 less sensitive but more specific than CD68



CD117



Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.