eMedicine Specialties > Dermatology > Malignant Neoplasms

Langerhans Cell Histiocytosis

Author: M Angelica Selim, MD, Associate Director of Dermatopathology, Departments of Pathology and Internal Medicine, Assistant Professor, Duke University Medical Center
Coauthor(s): Christopher R Shea, MD, Professor and Chief, Section of Dermatology, Department of Medicine, University of Chicago
Contributor Information and Disclosures

Updated: Feb 7, 2007

Introduction

Background

Langerhans cell histiocytosis (LCH) is a group of idiopathic disorders characterized by the proliferation of specialized bone marrow–derived Langerhans cells (LCs) and mature eosinophils.

In 1868, Paul Langerhans discovered the epidermal dendritic cells that now bear his name. The ultrastructural hallmark of the LC, the Birbeck granule, was described a century later. The term LCH is generally preferred to the older term, histiocytosis X. This new name emphasizes the histogenesis of the condition by specifying the type of lesional cell and removes the connotation of the unknown (X) because its cellular basis has now been clarified.

The working group of the Histiocyte Society has divided histocytic disorders into 3 different groups: (1) dendritic cell histiocytosis, (2) erythrophagocytic macrophage disorders, and (3) malignant histiocytosis. LCH belongs in group 1 and encompasses a number of diseases. The clinical spectrum includes on one end, an acute fulminant, disseminated disease called Letterer-Siwe disease and, on the other end, solitary or few, indolent and chronic, lesions of bone or other organs called eosinophilic granulomas. The intermediate clinical form called Hand-Schüller-Christian disease is characterized by multifocal, chronic involvement and classically presents as the triad of diabetes insipidus, proptosis, and lytic bone lesions. A congenital self-healing form called Hashimoto-Pritzker disease has also been described.

Pathophysiology

The pathogenesis of LCH is unknown. An ongoing debate exists over whether this is a reactive or neoplastic process. Arguments supporting the reactive nature of this disorder include the occurrence of spontaneous remissions, the failure to detect aneuploidy, metaphase or karyotypic abnormalities, and the good survival rate in patients without organ dysfunction. On the other hand, the infiltration of organs by aberrant cells, a possible lethal evolution, and the cancer-based modalities of successful treatment are all consistent with a neoplastic process. In addition, the demonstration of LCH as a monoclonal proliferation by X chromosome–linked DNA probes supports a neoplastic origin for this proliferation; however, the presence of this finding in distinct subtypes with different evolutions demands further investigations to evaluate its significance.

Evidence exists for a role of immune dysfunction in the pathogenesis of LCH by the creation of a permissive immunosurveillance system. Abnormalities of suppressor cell number and function have been documented in several reports. Increased levels of messenger RNA for macrophage colony-stimulating factor and platelet-derived growth factor have been detected in cells from a pulmonary LCH lesion.

In addition, some studies indicate that expression of Bcl-2 family proteins and of FADD, FLICE, and FLIP proteins in the Fas signaling pathway may be involved in the pathogenesis of LCH.

Frequency

United States

LCH is a rare disease. The estimated annual incidence ranges from 0.5-5.4 cases per million persons per year. Approximately 1200 new cases per year are reported in the United States.

Mortality/Morbidity

More than one half of patients younger than 2 years with disseminated LCH and organ dysfunction die of the disease; whereas, unifocal LCH and most cases of congenital self-healing histiocytosis are self-limited. Multifocal chronic LCH is self-limited in most cases, although increased mortality has been observed among infants with pulmonary involvement.

Race

The prevalence of LCH seems to be higher among whites than other races.

Sex

The incidence of LCH is greater in males than in females, with a male-to-female ratio of 2:1.

Age

LCH affects patients from neonates to adults. The age at onset varies according to the variety of LCH.

  • Letterer-Siwe disease occurs predominantly in children younger than 2 years.
  • The chronic multifocal form, including Hand-Schüller-Christian syndrome, has a peak of onset in children aged 2-10 years.
  • Localized eosinophilic granuloma occurs mostly frequently in those aged 5-15 years.

Clinical

History

The clinical presentation of LCH is dependent on the extent of dissemination.

  • Unifocal LCH is characterized by the development of solitary bony lesions at any site. It is least common in the hands and the feet. These lesions are often asymptomatic and are found as incidental findings during investigation for unrelated disorders.
  • Patients with multifocal disease have a protean history depending on the location of osteolytic lesions and the degree of organ dysfunction. Patients with Hand-Schüller-Christian syndrome (which occurs in 25% of patients with multifocal LCH) often present with recurrent episodes of otitis media and mastoiditis or with polyuria and polydipsia.
  • Letterer-Siwe disease presents with symptoms suggestive of a systemic infection or malignancy with a generalized skin eruption, anemia, and hepatosplenomegaly.
  • The congenital form of LCH manifests as skin lesions at birth or during the early postnatal period.
    • Cutaneous nodules and ulceration occur early in life.
    • Rarely, purpuric lesions occur with a blueberry muffin presentation.
    • Symptoms of organ involvement may also occur.

Physical

Signs of LCH depend on the localization and the extent of the disease. The clinical spectrum of LCH is broad, and an individual case may differ markedly from the prototypes described.

  • Chronic unifocal LCH (eosinophilic granuloma of bone) classically presents as a solitary calvarial lesion in young adults; other sites of involvement include the vertebra, the rib, the mandible, the femur, the ilium, and the scapula.
    • Lesions are usually asymptomatic, but bone pain and a soft tissue mass may occur.
    • When the calvarial lesions extend into the nervous system, a variety of neurologic manifestations may be seen.
    • Bony lesions may cause otitis media by destruction of the temporal and mastoid bones, proptosis secondary to orbital masses, loose teeth from infiltration of the mandibles, or pituitary dysfunction due to involvement of the sella turcica.
    • Spontaneous fractures can result from osteolytic lesions of the long bones, and vertebral collapse with spinal cord compression has occasionally been described.
    • Cutaneous disease presents with noduloulcerative lesions in the oral, perineal, perivulvar, or retroauricular regions.
    • Pulmonary lesions may be the presenting and only manifestation. In adults, the pulmonary system is most frequently involved.
    • Rarely, solitary cerebral lesions may occur.
  • The classic multifocal form of LCH (Hand-Schüller-Christian disease) includes diabetes insipidus; exophthalmos; and bony defects, particularly of the cranium.
    • Lesions may affect a variety of systems, including the liver (20%), the spleen (30%), and the lymph nodes (50%).
    • Pulmonary involvement may occur.
    • Osteolytic lesions of the long bones can lead to spontaneous fractures.
    • One third of patients have mucocutaneous lesions, most frequently infiltrated nodules and ulcerated plaques, especially in the mouth, the axillae, and the anogenital region. Other cutaneous manifestations include extensive coalescing, scaling, or crusted papules.
  • Patients with acute disseminated LCH (multiorgan involvement) present with fever; anemia; thrombocytopenia; pulmonary infiltrates; skin lesions; and enlargement of the lymph nodes, the spleen, and the liver.
    • Cutaneous abnormalities are present in almost 80% of patients; frequently, this is the first sign.
    • The eruption may be extensive, involving the scalp, the face, the trunk, and the buttocks as well as the intertriginous areas. Lesions consist of closely set petechiae and yellow-brown papules topped with scale and crust. The papules may coalesce to form an erythematous, weeping eruption mimicking seborrheic dermatitis.
    • Intertriginous lesions are often exudative, and secondary infection and ulceration may occur.
    • Osteolytic lesions are not common in the disseminated form of LCH, but the mastoid can be affected, resulting in a clinical picture of otitis media that may be the presenting complaint. Aural discharge, conductive hearing loss, and postauricular swelling have been described.
    • Patients with pulmonary involvement present with chest pain, hemoptysis, dyspnea, failure to thrive, cystic changes, and pneumothorax; if lung disease is extensive, oxygen diffusion and lung capacity may be reduced.
    • Neurologic involvement may produce seizures, vertigo, headache, ataxia, and cognitive defects.
  • Congenital self-healing histiocytosis presents at birth or during the early neonatal period with firm, red-brown, painless, papulonodules (1-10 mm in diameter) or vesicles and crusts that are scattered over the scalp, the face, and, to a lesser extent, the trunk and the extremities. Ulceration may occur in the lesions.
    • Solitary lesions may occur.
    • Lesions may be followed by residual hypopigmented or hyperpigmented macules.

Causes

The etiology of LCH remains unknown.

  • LC proliferation may be induced by a viral infection, a defect in intercellular communication (T cell–macrophage interaction), and/or a cytokine-driven process mediated by tumor necrosis factor, interleukin 11, and leukemia inhibitory factor.
  • Cigarette smoking may play a role as a chronic irritant in the development of eosinophilic granuloma of the lung.

More on Langerhans Cell Histiocytosis

Overview: Langerhans Cell Histiocytosis
Differential Diagnoses & Workup: Langerhans Cell Histiocytosis
Treatment & Medication: Langerhans Cell Histiocytosis
Follow-up: Langerhans Cell Histiocytosis
Multimedia: Langerhans Cell Histiocytosis
References
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Further Reading

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Keywords

LCH, histiocytosis X, Langerhans cell granulomatosis, type II histiocytosis, nonlipid reticuloendotheliosis, Langerhans cells, LCs

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Contributor Information and Disclosures

Author

M Angelica Selim, MD, Associate Director of Dermatopathology, Departments of Pathology and Internal Medicine, Assistant Professor, Duke University Medical Center
Disclosure: Nothing to disclose.

Coauthor(s)

Christopher R Shea, MD, Professor and Chief, Section of Dermatology, Department of Medicine, University of Chicago
Christopher R Shea, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society of Dermatopathology, Arthur Purdy Stout Society, Association of Professors of Dermatology, Chicago Dermatological Society, Dermatology Foundation, Illinois Dermatological Society, International Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Bernice R Krafchik, MBChB, FRCPC, Professor Emeritus, Department of Pediatrics, Section of Dermatology, University of Toronto
Bernice R Krafchik, MBChB, FRCPC is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-San Antonio
Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society
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

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other

 
 
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