SLE


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SLE

SLE

systemic lupus erythematosus.

SLE

abbr.
systemic lupus erythematosus

SLE

abbreviation for systemic lupus erythematosus.

SLE

Abbreviation for:
seizure-like events
Service Line Economics 
slit-lamp examination
St Louis encephalitis
stress life event
systemic lupus erythematosus

SLE

Systemic lupus erythematosus, see there.

SLE

Abbreviation for systemic lupus erythematosus.

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

SLE

Abbrev. for SYSTEMIC LUPUS ERYTHEMATOSUS.

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.

lupus

generic term for systemic and discoid lupus erythematosus
  • discoid lupus erythematosus; DLE localized systemic lupus erythematosus (SLE), characterized by similar skin lesions, but without marked systemic effects; may later progress to SLE

  • systemic lupus erythematosus; SLE; lupus autoimmune, inflammatory, connective tissue disease, characterized variably by fever, weakness and fatigability, joint pain and/or rheumatoid-like arthritis, severe Raynaud's phenomenon, diffuse erythematous vasculitis of sun-exposed skin (facial 'butterfly' rash), red nails/lunulae, epidermal atrophy (± ulceration), lymphadenopathy, pleurisy, pericarditis, glomerulonephritis, anaemia, hyperglobinaemia; more common in younger women, and women of Black African ancestry

SLE

Abbreviation for systemic lupus erythematosus.

SLE

systemic lupus erythematosus.

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
References in periodicals archive ?
2 List of Figures Figure 1: 7MM, Prevalent Cases of Diagnosed SLE, All Ages, Both Sexes, N, 2012-2022 35 Figure 2: 7MM, Prevalent Cases of Diagnosed SLE, by Age, Both Sexes, N, Row (%), 2012 37 Figure 3: 7MM, Prevalent Cases of Diagnosed SLE, All Ages, Both Sexes, 2012 39 Figure 4: 7MM, Age-Standardized Prevalence (%) of Diagnosed SLE, All Ages, by Sex, 2012 40 Figure 5: 7MM, Prevalent Cases of Diagnosed LN, All Ages, Both Sexes, N, 2012-2022 42 Figure 6: 6MM, Prevalent Cases of LN, by Class, All Ages, Both Sexes, 2012 44
Biomarkers in SLE: use of biomarkers in clinical trials, value of biomarkers in many aspects of SLE.
That's an SLE prevalence of rough ly 1 in 1,000 individuals, a considerably higher figure than the usually cited estimates of 1 in 500 among African American women and 1 per 2,000 white women, with much lower rates in men.
Multiple studies have established that one or more antiphospholipid antibodies are present in 30%-50% of SLE patients.
However, because the mice studied almost always develop SLE, the research did not demonstrate that the organochlorines would cause SLE in animals that would not otherwise get the disease.
SLE is very excited about the opportunity to collaborate with TI," said Jeff West, president of SLE.
The absence of hematoxylin bodies and neutrophils, the near-absence of plasma cells, and a tendency toward more widespread necrosis are important factors in distinguishing Kikuchi's disease from SLE.
Early symptoms of SLE are usually vague, nonspecific, and easily confused with other pathological and functional disorders.
While no known cause of SLE has been determined, specific factors such as infections, antibiotics, and extreme stress have been identified as possible catalysts to developing the disorder (Lahita, 1994).
Causing an estimated 16,000 new cases in the United Statesannually, SLE has a predilection for women, who are infected some nine times more than men.
It the drug for SLE to be approved in 50 years and is expected to drive the SLE market in the near future.
Hypertension, diabetes, family history of CVD, and NSAID use were more common in the women with SLE and heart disease than in the SLE free women with heart disease.