SLE


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SLE

Farlex Partner Medical Dictionary © Farlex 2012

SLE

abbr.
systemic lupus erythematosus
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

SLE

Abbreviation for:
seizure-like events
Service Line Economics 
slit-lamp examination
St Louis encephalitis
stress life event
systemic lupus erythematosus
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.

SLE

Systemic lupus erythematosus, see there.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

SLE

Abbreviation for systemic lupus erythematosus.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

lupus

(loo'pus) [L. lupus, wolf]
Originally any chronic, progressive, usually ulcerating, skin disease. In current usage, when the word is used alone, it has no precise meaning.

discoid lupus erythematosus

Abbreviation: DLE
A chronic skin disease characterized by periodic acute appearances of a scaling, red, macular rash. DLE is caused by an autoimmune process involving both B-cell– and T-cell–mediated mechanisms that destroy the skin's basal cells. DLE is treated with topical corticosteroids. It is found in about 5% to 30% of patients who have systemic lupus erythematosus (SLE) (esp. those who smoke) but also may occur alone (without other findings of SLE). See: autoimmune disease; systemic lupus erythematosus

Treatment

The patient should avoid exposure to the sun. Skin lesions should be treated with topical corticosteroids, but overuse of these preparations should be avoided.

drug-induced systemic lupus erythematosus

A group of signs and symptoms similar to those of systemic lupus erythematosus, caused by an adverse reaction to drugs, esp. procainamide, hydralazine, and isoniazid. Joint inflammation and pain, skin rash, pleurisy, and fever are the most common manifestations; kidney and central nervous system involvement are rare. Antinuclear antibodies, specifically against the histones that fold DNA, are common. Some patients develop antinuclear antibodies but do not develop lupus-like symptoms. The lupus-like syndrome usually disappears when the drug causing it is discontinued. See: antinuclear antibodies; systemic lupus erythematosus

lupus erythematosus

Any of several chronic, progressive, ulcerating, skin diseases, esp. systemic lupus erythematosus.

neonatal lupus

Rash, abnormally low platelet counts, liver and brain disease, and congenital heart block occurring in an infant whose mother has systemic lupus erythematosus. The disease results from the passage of maternal autoantibodies to the developing fetus. Although most of the findings resolve spontaneously, congenital heart block does not, and it may require the insertion of a pacemaker.

lupus panniculitis

Lupus profundus.

lupus pernio

Purple, noncaseating granulomas occurring on the face, esp. around the nose, eyes, cheeks, lips, and ears. Lupus in lupus pernio is misleading because it suggests a connection with systemic lupus erythematosus; lupus pernio is actually a finding of the skin in sarcoidosis.

lupus profundus

A deeply scarring, atrophic rash occasionally found in patients with systemic lupus erythematosus, caused by inflammation of subcutaneous fatty tissue.
Synonym: lupus panniculitis
Enlarge picture
SYSTEMIC LUPUS ERYTHEMATOSUS

systemic lupus erythematosus

Abbreviation: SLE
A chronic autoimmune inflammatory disease of connective tissue involving multiple organ systems and marked by periodic acute episodes. Its name is derived from the characteristic erythematous butterfly rash over the nose and cheeks, which resembles a wolf's snout, although this is present in less than 50% of patients. The disease is most prevalent in women (ratio of 8:1 women:men) of childbearing age (ratio of 15:1). Although it occurs worldwide, it is most prevalent among black and Asian peoples.

Etiology and Pathology

SLE is classified as an autoimmune disease in which the body seems to be unable to maintain normal mechanisms of tolerance to autoantigens. Activation of T helper cells and B cells results in the production of autoantibodies that attack antigens in the cytoplasm and nucleus of cells and on the surface of blood cells. The exact cause of SLE is unknown: genetic defects, hormonal changes, infection, physical or mental stress, some drugs, immunizations, and environmental triggers (sunlight, UV light exposure) are possible predisposing factors. See: autoimmune disease; glomerulonephritis

Autoantibodies can react with autoantigens to form immune complexes in such large numbers that they cannot be completely excreted; the immune complexes may precipitate within blood vessels, producing inflammation at the site and disrupting the flow of blood and oxygen to tissues. These deposits are particularly damaging in the glomeruli. Autoantibodies also promote the destruction of cells by stimulating neutrophil and macrophage phagocytic activity, which increases cell destruction from trauma, infection, or drugs.

Diagnosis

In 1997, revised criteria for diagnosis of SLE were established. The diagnosis can be made if four or more of the following criteria are present, either at one time or sequentially: (1) butterfly rash; (2) raised, scaly discoid skin lesions; (3) abnormal titer of antinuclear antibodies seen by immunofluorescence; (4) other autoantibodies (anti-Sm; serological tests for syphilis); (5) pleuritis or pericarditis (together referred to as “serositis”); (6) hemolytic anemia, leukopenia (white blood cell count less than 4,000 mm3), lymphopenia (lymphocyte count less than 1,500/mm3), or thrombocytopenia of less than 100,000/mm3; (7) oral or nasopharyngeal ulcers; (8) nonerosive arthritis; (9) psychosis or seizures without other clear cause; (10) photosensitivity skin rash; and (11) proteinuria greater than 0.5 g/day or cellular casts in the urine.

Some drugs can cause a lupus-like syndrome; the most common of these are procainamide, isoniazid, and hydralazine. See: drug-induced systemic lupus erythematosus

Symptoms

The onset of the disease may be acute or insidious. Patients have a wide variety of clinical symptoms, signs, and laboratory findings, but anemia, thrombocytopenia, polyarthritis, (polyarthralgia) skin rashes, glomerulonephritis, fever, malaise, weight loss, fatigue, and low blood levels of complement are the most common. Other signs include pleuritis, pericarditis, myocarditis, neurological changes including behavioral changes and seizure activity (neural lupus), gastrointestinal ulcerations, Raynaud's phenomenon (present in about 20% of patients), and other problems caused by inflammatory changes of the blood vessels or connective tissue. Most patients are prone to infection.

Treatment

No cure for SLE exists, and complete remission is rare. About 25% of patients have mild disease, demonstrating only minor skin and hematological signs, and can be treated with nonsteroidal anti-inflammatory drugs for their arthritis symptoms and topical treatment (sometimes with corticosteroid creams) for skin lesions. Rashes may respond to antimalarials, e.g., hydroxychloroquine, but patients must be observed closely for the possibility of drug-induced retinal damage. Other treatments for skin rash include quinacrine, retinoids, and dapsone. Life-threatening and severely disabling conditions should be treated with high doses of corticosteroids and supplemental calcium to minimize osteoporosis, which may be an undesired side effect of long-term glucocorticoid use. Immunosuppressive drugs are used for severe exacerbations and to reduce steroid dosage.

Prognosis

The prognosis depends on which organ systems are involved, how severely they are damaged, and how rapidly the disease progresses. Ten-year survival rates are high (80%). Renal failure and infections are the most common causes of death.

Patient care

Patient education related to the disease, diagnostic procedures, and treatment is essential in lupus, as in any chronic disease. Ongoing assessment is carried out to assess flares of the illness. The purpose, proper dosage, use, and side effects of drugs is taught. Patients need emotional support to help cope with changes in appearance. Patients should be taught to wear clothing and hats that block direct sunlight, use a sunscreen with a 15 or higher protection factor, and to maintain a diet appropriate for their renal functional status. The health care professional should help establish a regimen for adequate relief of both the musculoskeletal pain and chronic fatigue experienced by most patients, encouraging adequate rest. Heat packs relieve joint stiffness and pain, and regular gentle exercise helps to maintain full range of motion. Physical and occupational therapy consultations are provided as appropriate. Additional support and teaching depend on the organ system most affected by the disease. If the female patient of childbearing age has no renal or neurologic impairment, she can have a safe, successful pregnancy if desired. Over time, patients with severe progressive disease need assistance in coping with chronic illness and the possibility of mortality. Referrals to the Lupus Foundation of America (202-349-1155; www.lupus.org) and the Arthritis Foundation (800-283-7800; www.arthritis.org) are helpful.

See: illustration

lupus vulgaris

Tuberculosis of the skin; characterized by patches that break down and ulcerate, leaving scars on healing.

Enlarge picture
SYSTEMIC LUPUS ERYTHEMATOSUS

systemic lupus erythematosus

Abbreviation: SLE
A chronic autoimmune inflammatory disease of connective tissue involving multiple organ systems and marked by periodic acute episodes. Its name is derived from the characteristic erythematous butterfly rash over the nose and cheeks, which resembles a wolf's snout, although this is present in less than 50% of patients. The disease is most prevalent in women (ratio of 8:1 women:men) of childbearing age (ratio of 15:1). Although it occurs worldwide, it is most prevalent among black and Asian peoples.

Etiology and Pathology

SLE is classified as an autoimmune disease in which the body seems to be unable to maintain normal mechanisms of tolerance to autoantigens. Activation of T helper cells and B cells results in the production of autoantibodies that attack antigens in the cytoplasm and nucleus of cells and on the surface of blood cells. The exact cause of SLE is unknown: genetic defects, hormonal changes, infection, physical or mental stress, some drugs, immunizations, and environmental triggers (sunlight, UV light exposure) are possible predisposing factors. See: autoimmune disease; glomerulonephritis

Autoantibodies can react with autoantigens to form immune complexes in such large numbers that they cannot be completely excreted; the immune complexes may precipitate within blood vessels, producing inflammation at the site and disrupting the flow of blood and oxygen to tissues. These deposits are particularly damaging in the glomeruli. Autoantibodies also promote the destruction of cells by stimulating neutrophil and macrophage phagocytic activity, which increases cell destruction from trauma, infection, or drugs.

Diagnosis

In 1997, revised criteria for diagnosis of SLE were established. The diagnosis can be made if four or more of the following criteria are present, either at one time or sequentially: (1) butterfly rash; (2) raised, scaly discoid skin lesions; (3) abnormal titer of antinuclear antibodies seen by immunofluorescence; (4) other autoantibodies (anti-Sm; serological tests for syphilis); (5) pleuritis or pericarditis (together referred to as “serositis”); (6) hemolytic anemia, leukopenia (white blood cell count less than 4,000 mm3), lymphopenia (lymphocyte count less than 1,500/mm3), or thrombocytopenia of less than 100,000/mm3; (7) oral or nasopharyngeal ulcers; (8) nonerosive arthritis; (9) psychosis or seizures without other clear cause; (10) photosensitivity skin rash; and (11) proteinuria greater than 0.5 g/day or cellular casts in the urine.

Some drugs can cause a lupus-like syndrome; the most common of these are procainamide, isoniazid, and hydralazine. See: drug-induced systemic lupus erythematosus

Symptoms

The onset of the disease may be acute or insidious. Patients have a wide variety of clinical symptoms, signs, and laboratory findings, but anemia, thrombocytopenia, polyarthritis, (polyarthralgia) skin rashes, glomerulonephritis, fever, malaise, weight loss, fatigue, and low blood levels of complement are the most common. Other signs include pleuritis, pericarditis, myocarditis, neurological changes including behavioral changes and seizure activity (neural lupus), gastrointestinal ulcerations, Raynaud's phenomenon (present in about 20% of patients), and other problems caused by inflammatory changes of the blood vessels or connective tissue. Most patients are prone to infection.

Treatment

No cure for SLE exists, and complete remission is rare. About 25% of patients have mild disease, demonstrating only minor skin and hematological signs, and can be treated with nonsteroidal anti-inflammatory drugs for their arthritis symptoms and topical treatment (sometimes with corticosteroid creams) for skin lesions. Rashes may respond to antimalarials, e.g., hydroxychloroquine, but patients must be observed closely for the possibility of drug-induced retinal damage. Other treatments for skin rash include quinacrine, retinoids, and dapsone. Life-threatening and severely disabling conditions should be treated with high doses of corticosteroids and supplemental calcium to minimize osteoporosis, which may be an undesired side effect of long-term glucocorticoid use. Immunosuppressive drugs are used for severe exacerbations and to reduce steroid dosage.

Prognosis

The prognosis depends on which organ systems are involved, how severely they are damaged, and how rapidly the disease progresses. Ten-year survival rates are high (80%). Renal failure and infections are the most common causes of death.

Patient care

Patient education related to the disease, diagnostic procedures, and treatment is essential in lupus, as in any chronic disease. Ongoing assessment is carried out to assess flares of the illness. The purpose, proper dosage, use, and side effects of drugs is taught. Patients need emotional support to help cope with changes in appearance. Patients should be taught to wear clothing and hats that block direct sunlight, use a sunscreen with a 15 or higher protection factor, and to maintain a diet appropriate for their renal functional status. The health care professional should help establish a regimen for adequate relief of both the musculoskeletal pain and chronic fatigue experienced by most patients, encouraging adequate rest. Heat packs relieve joint stiffness and pain, and regular gentle exercise helps to maintain full range of motion. Physical and occupational therapy consultations are provided as appropriate. Additional support and teaching depend on the organ system most affected by the disease. If the female patient of childbearing age has no renal or neurologic impairment, she can have a safe, successful pregnancy if desired. Over time, patients with severe progressive disease need assistance in coping with chronic illness and the possibility of mortality. Referrals to the Lupus Foundation of America (202-349-1155; www.lupus.org) and the Arthritis Foundation (800-283-7800; www.arthritis.org) are helpful.

See: illustration
See also: lupus
Medical Dictionary, © 2009 Farlex and Partners

SLE

Abbrev. for SYSTEMIC LUPUS ERYTHEMATOSUS.
Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005

Systemic lupus erythematosus (SLE)

A chronic disease with many symptoms, including weakness, fatigue, joint pain, sores on the skin, and problems with the kidneys, spleen, and other organs.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.

SLE

Abbreviation for systemic lupus erythematosus.
Medical Dictionary for the Dental Professions © Farlex 2012

Patient discussion about SLE

Q. Is a rash a symptom of lupus? My Sister has lupus for several years now. I recently developed a rash on my face. Is this a symptom of lupus? Could I have also been infected with this disease?

A. Lupus has not been proven to be hereditary. Therefore, the fact your sister has lupus shouldn't cause you to beleive you too will develop it. Also a rash is not enough to diagnose lupus. Physicians have to gather information from a variety of sources: past medical history, lab tests and current symptoms. They use a list of 11 criteria to help diagnose SLE. A person needs to satisfy at least 4 out of the 11 criteria before the diagnosis can be pinpointed. Some criteria, such as a biopsy diagnosis of kidney lupus, can carry more weight.

More discussions about SLE
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References in periodicals archive ?
Of the total products in the Systemic Lupus Erythematosus (SLE) pipeline, 43% are first-in-class, indicating a high level of innovation.
Third, there might be variability in SLE diagnosis by rheumatologists, and undiagnosed cases were not sought.
Systemic lupus erythematosus (SLE) is an autoimmune chronic inflammatory disease that has protean manifestations involving multiple organs of body.
Next, the concentrations of IL-1[beta], IL-6, IL-8, IL-10, IL17, IFN-[gamma], IP-10, and MCP-1 were compared between the SLE patients with IgE+ and those with IgE- from noninherited SLE patients (Table 4).
Cutaneou slupus erythematous has been divided into SLE specific and SLE non-specificmanifestations.7,8There is marked variability in the type ranging from malar rash and discoid lupus to bullae formation,alopecia and vasculitic rashes.9Skin manifestations have a key role in classification of the disease as 4 out of 11 criteria in American College of Rheumatology (ACR) classification criteria are cutaneous.10The main purpose ofthis study was to identify the prevalence and clinical importanceof different skin manifestations in SLE patients in a tertiary care hospital.
* The key drivers of growth for the SLE and LN markets are the increasing uptake of GlaxoSmithKline's Benlysta, the potential launch of new biologic drugs and the increasing number of prevalent cases of SLE and LN during the 2012-2022 forecast period.
Etiology of SLE includes many components such as genetic environmental hormonal drugs etc (Helen et al 1999).
The researchers used the American College of Rheumatology revised criteria for SLE to diagnose SLE, the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition/ Clinical Version to diagnose mood and anxiety disorders, and the Structured Clinical Interview for DSM, Revised Third Edition to diagnose personality disorders (Compr.
The rate of TKR in SLE patients climbed six-fold from 0.03 per 100,000 population in 1991 to 0.18 per 100,000 in 2005.
Currently, anti-dsDNA is widely used in assessing SLE disease activity apart from serum C3, serum C4, and Creactive protein (CRP) levels [4].