eMedicine Specialties > Pediatrics: General Medicine > Rheumatology

Systemic Lupus Erythematosus

Author: Marisa S Klein-Gitelman, MD, MPH, Associate Professor of Pediatrics, Northwestern University Feinberg School of Medicine; Head, Division of Rheumatology, Children's Memorial Hospital
Contributor Information and Disclosures

Updated: Dec 8, 2008

Introduction

Background

Systemic lupus erythematosus (SLE) is a rheumatic disease characterized by autoantibodies directed against self-antigens, immune complex formation, and immune dysregulation, resulting in damage to essentially any organ, including the kidney, skin, blood cells, and the nervous system. The natural history of this illness is unpredictable; patients may present with many years of symptoms or with acute life-threatening disease. Because of its protean manifestations, lupus must be considered in the differential diagnoses of many conditions, including fevers of unknown origin, arthralgia, anemia, nephritis, psychosis, and fatigue. Early diagnosis and careful treatment tailored to individual patient symptoms have improved the prognosis from what was once perceived as an often-fatal disease.

The first written description of lupus dates to the 13th century. Rogerius named the disease using the Latin word for wolf because the cutaneous manifestations he described appeared similar to those of a wolf bite. Osler was the first physician who recognized that systemic features of the disease could occur without skin involvement.1 Diagnosis was made easier with the discovery of lupus erythematosus (LE) cells in 1948. In 1959, the presence of anti-DNA antibodies was noted. The use of the New Zealand black/white mouse model, which manifested spontaneous Coombs-positive anemia and many other manifestations of lupus, has allowed intensive study of the disease mechanisms and the importance of immunosuppressive therapy.

The use of adrenocorticotropic hormone (ACTH) in the 1950s resulted in amelioration of disease manifestations. Replacement of ACTH using corticosteroids improved treatment. The substantial adverse effects of corticosteroids led to a strategy of using various immunosuppressive drugs to minimize the need for corticosteroids, improving the prognosis for patients. For children with renal disease, recognition of the steroid-sparing effect of immunosuppressive agents such as azathioprine and cyclophosphamide has greatly improved the outcome. New advances in treatment using targeted biological therapies may further improve treatment outcomes. As patients continue to improve and survive, physicians now must assess patients for long-term disease sequelae, such as atherosclerosis, and develop prevention strategies. New strategies using genomics and proteomics give hope for identification of biomarkers that can be used for early disease detection and treatment.

Pathophysiology

Within the healthy population, a subset of individuals has small amounts of low titer antinuclear antibody (ANA) or other autoantibody. In lupus, increased production of autoantibodies leads to immune complex formation and tissue damage from direct binding in tissues, immune complex deposition in tissues, or both. Whether these antibodies are produced in reaction to exposure of normally nonexposed self-antigens or as a consequence of a broad spectrum of immune dysregulation resulting in excessive production of many antibodies without regard to prior stimulation is unclear. Both mechanisms may play a role.

Recently, new details about the role of dendritic cells and the regulation of complement activity and cell death have been explored. Patients with systemic lupus erythematosus make antibodies against DNA, other nuclear antigens, ribosomes, platelets, erythrocytes, leukocytes, and other tissue-specific antigens. The resulting immune complexes result in widespread tissue damage. Cell-mediated autoimmune responses also play a pathophysiologic role.

Children with lupus may have hematologic abnormalities, including hemolytic anemia, thrombocytopenia, leukopenia, or lymphopenia. Patients with immune complex disease in the kidneys may present with nephritis or nephrotic syndrome. Numerous neurologic abnormalities, from psychosis and seizure to cognitive disorders to peripheral neuropathies, may also occur. Their exact relationship to the presence of immune complexes and autoantibodies remains unclear.

Pulmonary disease manifests as pulmonary hemorrhage, fibrosis, or infarct. Various rashes, GI manifestations, serositis, arthritis, endocrinopathies, and cardiac abnormalities (eg, endocarditis) are observed. No organ is spared from the effects of this multisystem disease. However, the clinical presentation widely varies. How the clinical manifestations depend on the underlying specific immunologic disarray in a particular patient remains to be determined.

Frequency

United States

Incidence of this disease varies by location and ethnicity. Incidence rates among children younger than 15 years have been reported to be 0.5-0.6 per 100,000 persons. Prevalence rates of 4-250 per 100,000 persons have been reported, with greater prevalence in Native American, Asian American, Latin American, and blacks. In one study of adults, the incidence in black females was estimated at 1 in 500. African American children may represent up to 60% of patients younger than 20 years.

Mortality/Morbidity

The 5-year survival rate for children with systemic lupus erythematosus is more than 90%. Most deaths of children with systemic lupus erythematosus are the result of infection, nephritis, renal failure, neurologic disease, or pulmonary hemorrhage. Myocardial infarction may occur in the young adult years as a complication of persisting inflammation and, possibly, long-term corticosteroid use.

Race

Prevalence rates are higher in Native American, Asian American, Latin American, and black patients.

Sex

Prevalence rates are higher in females than in males. A female-to-male ratio of approximately 4:1 occurs before puberty, and a ratio of 8:1 occurs after puberty.

Age

Approximately 20% of patients with systemic lupus erythematosus initially present by the second decade of life. Disease onset has been reported as early as the first year of life. However, systemic lupus erythematosus remains uncommon in children younger than 8 years.

Clinical

History

The most frequent presenting symptoms of systemic lupus erythematosus (SLE) are prolonged fever and malaise with evidence of multisystem involvement. Children often present with a history of fatigue, joint pain, rash, and fever. However, children may present with various acute symptoms, including memory loss, psychosis, transverse myelitis, hemoptysis, edema of the lower extremities, headache, and painful mouth sores. Eleven criteria are used for the classification of lupus in adults. The same criteria can serve as a guideline in children. Any 4 criteria are sufficient and should be sought in the history. Of note, antinuclear antibody (ANA) is almost always present but is not diagnostic.

Diagnosis is not difficult in the child who presents with many manifestations, such as malar rash, pleuritic chest pain, nephritis, and a positive ANA finding. Some patients present over longer periods and require careful consideration. Occasionally, patients do not fulfill the classification criteria, a definite diagnosis is never made, or the patient may have an overlap syndrome with manifestations of several rheumatic diseases. Treatment should never be delayed in patients who do not fulfill classification criteria, particularly when patients are seriously ill.

Diagnostic criteria for systemic lupus erythematosus include the following:

  • Mucocutaneous
    • Malar rash
    • Naso-oral ulcers
    • Photosensitive rash
    • Discoid rash
  • Systemic
    • Arthritis
    • Pleuritis or pericarditis
    • Proteinuria (>500 mg/d) or evidence of nephritis in urinalysis
    • Hemolytic anemia, thrombocytopenia, leukopenia, or lymphopenia
    • Seizure or psychosis
  • Laboratory
    • Positive ANA finding
    • Positive anti–double-stranded DNA, anti-Smith, or antiphospholipid antibody/lupus anticoagulant

Physical

A detailed physical examination is a critical tool in the diagnosis of systemic lupus erythematosus. Most of the American College of Rheumatology (ACR) classification criteria are associated with physical findings.2 The following is a description of more common clinical manifestations.

  • Mucocutaneous findings include the following:
    • Rash occurs in 70-80% of patients. The characteristic rash is a malar or butterfly rash, including both cheeks and the nasal bridge sparing the nasolabial fold. The rash varies from an erythematous blush to thickened epidermis to a scaly rash.
    • Other diagnostic skin findings include discoid rash, which is less common in childhood, a photosensitive rash, and mucous membrane changes that range from vasculitic erythema to large deep ulcers on the palate and nasal mucosa.
    • Other common rashes include vasculitic macular eruptions, particularly on the distal extremities and often in the subungual region with visible microinfarcts from small vessel vasculitis; purpura; livedo reticularis, which is often associated with antiphospholipid antibodies; alopecia, which is usually frontal or hairline; and Raynaud phenomenon, which is characterized by sequential color changes in the fingers and toes.
    • Less common rashes include subacute psoriasiform or annular skin lesions, often associated with anti-Ro antibodies and bullous lesions.
  • Musculoskeletal findings include arthritis, arthralgia, tendonitis, and myositis.
    • Deforming arthritis is unusual and, if present, is usually secondary to a Jaccoudlike arthropathy.
    • This arthritis can lead to ligament damage and severely lax joints.
    • Avascular necrosis of bone is a frequent complication occurring in about 25% of children with systemic lupus erythematosus over time. It occurs both in children with systemic lupus erythematosus who are not being treated with corticosteroids and in children receiving corticosteroids for conditions other than systemic lupus erythematosus, but it is most common in children with systemic lupus erythematosus who are receiving daily corticosteroids.
  • Abdominal findings include the following:
    • Patients often present with lymphadenopathy and hepatosplenomegaly. Many have chronic abdominal pain secondary to recurrent vascular insults to the intestinal tract and/or chronic pancreatitis, which may result from both treatment with corticosteroids and systemic lupus erythematosus itself.
    • Hepatitis demonstrated by laboratory evaluation is not uncommon.
    • Other abdominal findings can include pain secondary to peritoneal serositis or small-vessel vasculitis.
  • Cardiac involvement includes pericarditis, murmurs associated with endocarditis, and cardiac failure from myocarditis or infarction. Pulmonary auscultatory findings may be abnormal secondary to pleuritis, infiltrates, or hemorrhage.
  • Neurologic manifestations can include both the central and the peripheral nervous systems.
    • Diagnostic findings include seizure and psychosis; however, patients may present with stroke, pseudotumor cerebri, cerebral venous thrombosis, aseptic meningitis, chorea, global cognitive deficits, mood disorders, transverse myelitis, and peripheral neuropathy as well as many less common neurologic findings.
    • As many as 40% of children may have neurologic disease and perhaps even more when considering psychiatric manifestations and cognitive abnormalities. Quantification of cognitive function with formal neuropsychiatric testing may be advisable.
  • Renal disease is manifested by hypertension, edema of the lower extremities, retinal changes, and clinical manifestations associated with electrolyte abnormalities, nephrosis, or acute renal failure. Renal disease is more frequently observed in children than in adults.
  • Patients with lupus may present with the clinical findings of endocrine disease, such as hyperthyroidism and Addisonian crisis.

Causes

The specific causes of systemic lupus erythematosus remain undefined. Research suggests that many factors, including genetics, hormones, and the environment (eg, sunlight, drugs), contribute to the immune dysregulation observed in lupus.

  • Within the healthy population, little measurable evidence exists of antibody to self. A subset of individuals has small amounts of autoantibody as manifested by a low-titer ANA or other autoantibody. In lupus, increased production of autoantibodies leads to immune complex formation and tissue damage from direct binding in tissues, immune complex deposition in tissues, or both. Evidence suggests antigen-specific antibody responses to DNA, other nuclear antigens, ribosomes, platelets, erythrocytes, leukocytes, and other tissue-specific antigens.
  • Additionally, autoantibody production, by relatively few B lymphocytes, may be a byproduct of polyclonal B-cell activation in which many more B lymphocytes are activated, perhaps not in response to specific antigenic stimuli. Data on 3 adolescents with lupus demonstrate a high percentage of mature naive B cells (25-50% versus 5-20% in healthy adolescents), producing self-reactive antibodies even before they participated in an immune response, suggesting defective checkpoints in B-cell development.3
  • The discovery of viral-like particles in lymphocytes in patients with lupus led to the theory that viral infection caused polyclonal activation in lupus. However, these particles may simply be breakdown products of intracellular materials. This assumption is supported by recent evidence in which polymerase chain reaction (PCR) did not isolate specific viruses, such as Epstein-Barr virus and cytomegalovirus, in lupus WBCs. Thus, positive titers to infectious agents in patients with lupus may be another manifestation of nonspecific polyclonal activation of B cells. However, viral stimulation of the innate immune system (dendritic cells) coupled with genetic defects in the innate and adaptive immune responses could lead to loss of tolerance and increasingly specific autoantibody formation.
  • The presence of measurable autoantibodies implies a loss of tolerance to self-antigens and may include T-lymphocyte abnormalities. Early studies suggested a loss of T-suppressor function; however, recent investigations have centered on defects of programmed cell death, or apoptosis. This process of programmed cell death may be dysregulated in lupus, resulting in cells with the potential for self-reactivity persisting instead of undergoing the normal process of apoptosis. T cells from patients with lupus have been found with increased levels of Bcl-2, a protein that delays apoptosis. Patients have also been found to have lymphocytes that underwent increased apoptosis. One explanation may be that in lupus, lymphocytes that make self-reactive antibodies survive in the host but undergo increased cell turnover after an inciting trigger, such as a viral infection, begins the process that manifests as lupus.
  • Other immunologic mechanisms may also be important, including defects in macrophage phagocytic activity or handling of immune complexes.
    • Deficiencies of complement components, including C4, C2, and C1q, have been associated with lupus, perhaps because of defective clearance of immune complexes.
    • Complement receptors may be abnormal in some patients, leading to problems with clearance of immune complexes and subsequent deposition into tissues. This may also be associated with dyslipoproteinemia, leading to significant vascular complications.
    • The predominance of lupus in females suggests sex hormones may play a role in autoimmune diseases. Research has found that patients with lupus did not have different serum levels of estrogen and prolactin when compared with controls; however, free androgen was lower, whereas follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were higher in postpubertal boys and girls with systemic lupus erythematosus.
    • Drugs, such as anticonvulsants and antiarrhythmic agents, can also play a role in the pathogenesis of lupus. These drugs can cause a lupuslike syndrome, which resolves when the drug is discontinued or can be implicated as the trigger in systemic lupus.
  • Sun exposure leading to inflammation and apoptosis of skin cells can also trigger systemic lupus.

More on Systemic Lupus Erythematosus

Overview: Systemic Lupus Erythematosus
Differential Diagnoses & Workup: Systemic Lupus Erythematosus
Treatment & Medication: Systemic Lupus Erythematosus
Follow-up: Systemic Lupus Erythematosus
References
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Further Reading

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Keywords

systemic lupus erythematosus, lupus, SLE, lupus erythematosus, LE, fevers of unknown origin, arthralgia, anemia, nephritis, psychosis, fatigue, rheumatic disease, atherosclerosis, hemolytic anemia, thrombocytopenia, leukopenia, lymphopenia, nephritis, nephrotic syndrome, serositis, arthritis, memory loss, psychosis, transverse myelitis, hemoptysis, edema of the lower extremities, headache, painful mouth sores, pleuritis, pericarditis, livedo reticularis, alopecia, Raynaud phenomenon, tendonitis, myositis, lymphadenopathy, hepatosplenomegaly, stroke, pseudotumor cerebri, cerebral venous thrombosis, aseptic meningitis, chorea, global cognitive deficits, mood disorders, transverse myelitis, hyperthyroidism

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Contributor Information and Disclosures

Author

Marisa S Klein-Gitelman, MD, MPH, Associate Professor of Pediatrics, Northwestern University Feinberg School of Medicine; Head, Division of Rheumatology, Children's Memorial Hospital
Marisa S Klein-Gitelman, MD, MPH is a member of the following medical societies: American College of Rheumatology
Disclosure: Nothing to disclose.

Medical Editor

Barry L Myones, MD, Associate Professor, Departments of Pediatrics and Immunology, Pediatric Rheumatology Section, Baylor College of Medicine; Director of Research, Pediatric Rheumatology Center, Texas Children's Hospital
Barry L Myones, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American College of Rheumatology, American Heart Association, American Society for Microbiology, Clinical Immunology Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Thomas JA Lehman, MD, FAAP, FACR, Clinical Professor of Pediatrics, Department of Pediatrics, Division of Pediatric Rheumatology, Weill-Cornell University; Chief, Hospital for Special Surgery
Thomas JA Lehman, MD, FAAP, FACR is a member of the following medical societies: PM American Allergy Society
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting; Pfizer Honoraria Consulting

Chief Editor

Herbert S Diamond, MD, Professor of Medicine, Temple University School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa
Disclosure: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; Merck, Amgen, Biogen, Zimmer, Wyeth, Johnson&Johnson, Stryker, Medtronic, Zimmer.Abbott,  Ownership interest Other; West Penn Allegheny Health System Consulting fee Consulting; Alpharma Honoraria Consulting; Proctor&Gamble Grant/research funds Independent contractor

 
 
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