eMedicine Specialties > Dermatology > Internal Medicine

Leukemia Cutis

Author: Jeyanthi Ramanarayanan, MD, Assistant Professor, Department of Medicine, Division of Medical Oncology, Roswell Park Cancer Institute
Coauthor(s): Shweta Singhal, MD, Resident Physician, Department of Internal Medicine, Rochester General Hospital
Contributor Information and Disclosures

Updated: Oct 7, 2009

Introduction

Background

Leukemia cutis is the infiltration of neoplastic leukocytes or their precursors into the epidermis, the dermis, or the subcutis, resulting in clinically identifiable cutaneous lesions.

The dermatologist is often instrumental in the diagnosis of leukemia cutis. Accurate diagnosis has tremendous prognostic significance and may establish a diagnosis in cases in which leukemia cutis is the harbinger of a systemic leukemic process. This is called aleukemic leukemia cutis. A diagnosis of leukemia cutis generally portends a poor prognosis and strongly correlates with additional sites of extramedullary involvement. This can alter the appropriate treatment regimen for a patient.1

A patient with typical plum-colored lesions seen ...

A patient with typical plum-colored lesions seen in leukemia cutis. This patient had acute myelogenous leukemia. Courtesy of Grant Anhalt, MD.

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A patient with typical plum-colored lesions seen ...

A patient with typical plum-colored lesions seen in leukemia cutis. This patient had acute myelogenous leukemia. Courtesy of Grant Anhalt, MD.


Pathophysiology

All types of leukemias result from the abnormal development of leukocytes in the bone marrow. Maturational arrest occurs, and a proliferative, clonal population of cells result. A variety of defects promote the clonal expansion of leukemic cells. These defects include an abnormal proliferative potential, defects in terminal differentiation, and defective apoptosis. The increased proliferative potential is caused by the activation of oncogenes or the inactivation of tumor suppressor genes. Leukemia cutis is thought to result from a local proliferation of the leukemic cells within the skin.

Leukemia cutis has been described in patients with myeloid and lymphoid types of leukemias. Cutaneous infiltration by neoplastic lymphocytes may be seen in acute myeloid leukemia, acute lymphocytic leukemia, chronic myeloid leukemia, chronic lymphoid leukemia, prolymphocytic leukemia, and myelodysplastic syndromes. In patients with chronic diseases, skin involvement may be associated with transformation into aggressive histology and disease progression.

The pathophysiology underlying the specific migration of leukemic cells to the skin is not clear. It has been speculated that the chemokine, integrin and other adhesion molecules may play a role in skin specific homing of T and B leukemic cells. In the case of human T-cell leukemia virus type I (HTLV-I)–induced leukemia, it may be due to the abundant expression of the CC chemokine receptor 4 (CCR4) on the cell surface of the leukemic cells. The ligands thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22) are present in the skin and may explain the predilection of adult T-cell leukemia to involve the skin.

High expression of CCR4, TARC, and macrophage-derived chemokine/CCL22 in the skin has also been noted by reverse transcription–polymerase chain reaction studies. Evidence also suggests that the presence of T-cell–related antigens on the cell surface of leukemic cells in acute monocytic leukemia (AML-M5) in patients with leukemia cutis may promote selective homing to the skin. Additionally, one small study of 18 cases of myelomonocytic leukemia cutis patients showed cutaneous lymphocyte-associated antigen (CLA) staining in 14 (78%) of 18 cases. The presence of CLA may confer a specific tropism to the skin in these leukemic cells.

Frequency

United States

Because leukemia cutis is a relatively rare condition and because it may manifest in a variety of leukemia subtypes, the exact overall incidence of leukemia cutis is unclear. For the various subtypes, the approximate incidences are listed in the table below.

Although adult T-cell leukemia/lymphoma (ATLL) is exceedingly rare in the United States, a disproportionate percentage of patients develop leukemia cutis. The rate of seroprevalence of HTLV-I in volunteer blood donors in the United States is 0.02%. Of the individuals infected with HTLV-I, only 2-4% develop ATLL. Acute myelogenous leukemia (AML) shows the second highest rates of leukemia cutis. The French-American-British (FAB) classification divides AML into 8 main subtypes M0 to M7, based on the morphology and the state of differentiation of the leukemic cells. Acute myelomonocytic leukemia (AML-M4) and AML-M5 have the highest rates of skin involvement of all the subtypes and are reported to be as high as 30%.

The incidence of leukemia cutis also appears to be high among children, and cases of leukemia cutis have been documented in as many as 25-30% of infants with congenital leukemia. Most of these patients have myelogenous leukemia. In congenital leukemia, leukemia cutis does not worsen the prognosis.

In most cases of leukemia cutis, systemic disease precedes the development of skin lesions. However, in as many as 7% of patients with leukemia cutis, localized disease occurs prior to bone marrow infiltration and systemic symptoms (aleukemia cutis or primary extramedullary leukemia [EML]).

Table 1. Incidences of Types of Leukemia

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Table
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
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


International

In general, the international incidence of leukemia cutis is thought to be similar to that in the United States. One study by Agis et al in Vienna showed a prevalence of 2.9-3.7% for AML. This is a figure similar to the rate determined by Baer et al in the United States.2

The exception to this rule would be the prevalence of HTLV-I–induced ATLL, which is significantly higher in the Caribbean and Japan. In Japan, 6-37% of the population is infected with HTLV-I in endemic areas. Of these, 0.5 per 1000 women and 1.5 per 1000 men will develop ATLL. In the Caribbean, 3-6% of the population is seropositive for HTLV-I. Reportedly, the rate of cutaneous involvement in ATLL ranges from 40-70%.

Mortality/Morbidity

In general, leukemia cutis is a poor prognostic sign. Several studies indicate that, in the presence of leukemia cutis in AML or CML, the disease course is aggressive and the length of survival is short.

  • A study by Kaddu et al showed an average survival time in AML to be 7.5 months and in CML, 9.4 months.3
  • Another study by Baer et al showed that of 18 patients with leukemia cutis in AML, 90% had other sites of extramedullary involvement, and, in 40% of these patients, the meninges were involved.4
  • In a smaller case series by Shaikh et al with only 5 patients with AML, all 5 died within 6 months of their diagnosis of leukemia cutis.5
  • Skin infiltration in CLL is rare. In a study by Cerroni et al, CLL was associated with advanced stage and a poor prognosis.6 One series by Su et al of 16 patients with CLL showed a mean survival of 16 months, with 88% of the patients dying within 1 year.7

Race

Although specific racial, sexual, and age predilections for the subtypes of leukemia exist, no data regarding any of these factors in leukemia cutis are available.

Clinical

History

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 in narrowing the differential diagnosis.

  • 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.
    • 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 complain of 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.8,9,10
  • The specific lesions of leukemia cutis are most often asymptomatic. No pruritus, pain, or tenderness is associated. The exceptions to this are CLL and HTLV-I–induced ATLL, in which significant pruritus can occur.
    • A typical presentation of acute 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 complain of abdominal fullness due to the hepatosplenomegaly or ascites, which may be present. Patients may also complain of swollen lymph nodes.

Physical

As mentioned briefly in History, pallor; hepatosplenomegaly; nonspecific findings (eg, purpura, petechiae); drug reactions, including leukocytoclastic vasculitis; and opportunistic infections, particularly thrush, disseminated zoster, or severe and atypical presentations of herpes simplex may be present.

Many cutaneous manifestations of chemotherapeutic agents may occur. Some of the most common 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.

  • More specific cutaneous lesions of leukemia cutis are typically papules and nodules; indurated plaques, hemorrhagic plaques, perifollicular acneiform papules, macules, ulcers, bullae, and palpable purpura are less frequent. The lesions can range from red-brown to violaceous, or plum. The lesions may be seen in any type of leukemia causing leukemia cutis.
  • Patients may present with single or multiple nodules in the absence of any systemic findings. The tumors are called granulocytic sarcoma or primary EML. These tumors may appear greenish. They have been aptly called chloromas because of the green pigmentation caused by myeloperoxidase within the myeloid cells.
Involvement of the face in a patient with acute m...

Involvement of the face in a patient with acute myelogenous leukemia. Courtesy of Grant Anhalt, MD.

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Involvement of the face in a patient with acute m...

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. ...

Red-brown papules can be seen in leukemia cutis. They are confluent in this patient. Courtesy of Nevena Damjanov, MD, and Elizabeth Prechtel.

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Red-brown papules can be seen in leukemia cutis. ...

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 Ame...

Papules and nodules on the face of an African American patient with acute myelogenous leukemia (AML). Courtesy of Mona Mofid, MD.

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Papules and nodules on the face of an African Ame...

Papules and nodules on the face of an African American patient with acute myelogenous leukemia (AML). Courtesy of Mona Mofid, MD.

  • More unusual lesions vary depending on the underlying leukemia.
    • 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.
    • In acute myelomonocytic leukemia, leukemia cutis may manifest as leonine facies.11
    • Juvenile CML may show figurate or arciform lesions.12
    • 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.13
    • One case report of hairy cell leukemia with leukemic macrocheilitis and Melkersson-Rosenthal syndrome has been reported.14
    • Fingertip hypertrophy consisting of leukemic infiltrates of CLL has also been described.15 B-cell CLL has manifested as symmetrical eyelid leukemia cutis.16 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.6 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,17 chronic paronychia,18 subungual leukemia cutis,19 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).20 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,21 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).22
  • In ATLL, 60% of patients have peripheral lymph node enlargement, 26% have hepatomegaly, 22% have splenomegaly, and 39% have skin lesions.

Causes

Both a genetic component and an environmental component appear to be involved in many leukemias. 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.23

More on Leukemia Cutis

Overview: Leukemia Cutis
Differential Diagnoses & Workup: Leukemia Cutis
Treatment & Medication: Leukemia Cutis
Follow-up: Leukemia Cutis
Multimedia: Leukemia Cutis
References
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Further Reading

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Keywords

leukemia cutis, aleukemic leukemia cutis, myeloid leukemias, acute myelogenous leukemia, AML, human T-cell leukemia virus type I, HTLV-I, acute monocytic leukemia, chloroma, primary extramedullary leukemia, EML, granulocytic sarcoma, hairy cell leukemia

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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

Medical Editor

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

Pharmacy Editor

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.

Managing Editor

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.

CME Editor

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 None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

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.

 
 
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