lupus /lu·pus/ (loo´pus) any of a group of skin diseases in which the lesions are characteristically eroded.
lupus pernio,
lupus [loo´pus]
chilblain lupus erythematosus a form due to cold-induced microvascular injury, aggravated by cold; the lesions initially resemble chilblains but eventually assume the form of discoid lupus erythematosus.
cutaneous lupus erythematosus one of the two main forms of lupus erythematosus, in which the skin may be either the only or the first organ or system involved. It may be chronic (discoid l. erythematosus), subacute (systemic l. erythematosus), or acute (characterized by an acute, edematous, erythematous eruption).
discoid lupus erythematosus (DLE) a chronic form of cutaneous lupus erythematosus marked by red macules covered with scanty adherent scales that fall off and leave scars; lesions typically form a butterfly pattern over the bridge of the nose and cheeks, but other areas may be involved.
drug-induced lupus a syndrome closely resembling systemic lupus erythematosus, precipitated by prolonged use of certain drugs, most commonly hydralazine, isoniazid, various anticonvulsants, and procainamide.
lupus erythemato´sus (LE) a group of chronic connective tissue diseases manifested in two main types: cutaneous l. erythematosus and systemic l. erythematosus.
lupus erythemato´sus profun´dus a form of cutaneous lupus erythematosus in which deep brawny indurations or subcutaneous nodules occur under normal or, less often, involved skin; the overlying skin may be erythematous, atrophic, and ulcerated and on healing may leave a depressed scar.
lupus erythemato´sus tu´midus a variant of discoid or systemic lupus erythematosus in which the lesions are raised reddish purple or brown plaques.
hypertrophic lupus erythematosus a form of discoid lupus erythematosus characterized by verrucous hyperkeratotic lesions.
lupus hypertro´phicus
1. a variant of lupus vulgaris in which the lesions consist of a warty vegetative growth, often crusted or slightly exudative, usually occurring on moist areas near body orifices.
lupus milia´ris dissemina´tus fa´ciei a form marked by multiple, discrete, superficial nodules on the face, particularly on the eyelids, upper lip, chin, and nares.
neonatal lupus a rash resembling discoid lupus erythematosus, sometimes with systemic abnormalities such as heart block or hepatosplenomegaly, in infants of mothers with systemic lupus erythematosus; it is usually benign and self-limited.
lupus per´nio
1. a cutaneous manifestation of sarcoidosis consisting of violaceous smooth shiny plaques on the ears, forehead, nose, and digits, frequently associated with bone cysts.
systemic lupus erythematosus (SLE) a chronic generalized connective tissue disorder, ranging from mild to fulminating, marked by skin eruptions, arthralgia, arthritis, leukopenia, anemia, visceral lesions, neurologic manifestations, lymphadenopathy, fever, and other constitutional symptoms. Typically, there are many abnormal immunologic phenomena, including hypergammaglobulinemia and hypocomplementemia, deposition of antigen-antibody complexes, and the presence of antinuclear antibodies and LE cells.
lupus vulga´ris the most common and severe form of tuberculosis of the skin, most often affecting the face, with formation of red-brown patches of nodules in the dermis that progressively spread peripherally with central atrophy, causing ulceration and scarring and destruction of cartilage in involved sites.
lupus per·ni·o (pûr n - )n. Sarcoid lesions that resemble those of frostbite and that involve the ears and hands. |
lupus pernio,
a cutaneous form of sarcoidosis, characterized by smooth, shiny plaques on the face, fingers, and toes, clinically resembling frostbite.
lupus [loo´pus]
a name originally given to a destructive type of skin lesion, implying a local degeneration rather than systemic involvement. Although the term is frequently used alone to designate lupus vulgaris and sometimes lupus erythematosus, without a modifier it has no meaning. The Latin word lupus means wolf; erythematosus refers to redness. The name lupus erythematosus has been used since the 13th century because physicians thought the shape and color of the skin lesions resembled the bite of a wolf. Currently, there are at least two recognized manifestations of the disease: discoid lupus erythematosus and systemic lupus erythematosus.
chilblain lupus erythematosus a form of discoid lupus erythematosus aggravated by cold, initially resembling chilblains, in which the lesions consist of reddened infiltrated patches on the exposed areas of the body, especially the finger knuckles.
cutaneous lupus erythematosus one of the two main types of lupus erythematosus; it may involve only the skin or may precede involvement of other body systems. It may be chronic (discoid lupus erythematosus); subacute (systemic lupus erythematosus); or acute (characterized by an acute edematous, erythematous eruption, often with systemic exacerbations). The acute form may be the presenting symptom of systemic lupus erythematosus, such as after sun exposure.
discoid lupus erythematosus (DLE) a superficial inflammation of the skin, marked by red macules up to 3 to 4 cm in width, and covered with scanty adherent scales, which extend into spreading follicles that fall off and leave scars. The lesions typically form a butterfly pattern over the bridge of the nose and cheeks, but other areas may be involved, notably the scalp and other areas that are exposed to light.
drug-induced lupus a syndrome closely resembling systemic lupus erythematosus, precipitated by prolonged use of certain drugs, most commonly hydralazine, isoniazid, various anticonvulsants, and procainamide.
lupus erythemato´sus (LE) a group of connective tissue disorders primarily affecting women aged 20 to 40, comprising a spectrum of clinical forms in which cutaneous disease may occur with or without systemic involvement.
lupus per´nio
1. soft, purplish skin lesions on the cheeks, forehead, nose, ears, and digits, frequently associated with bone cysts, which may be the first manifestation of sarcoidosis or occur in the chronic stage of the disease.
systemic lupus erythematosus (SLE) a chronic inflammatory disease, usually febrile and characterized by injury to the skin, joints, kidneys, nervous system, and mucous membranes. It can, however, affect any organ of the body and usually has periods of remissions and exacerbations. (See plate in Dermatology Atlas.)
It was once thought that this was a fairly rare disease, but improved immunologic testing procedures have shown that it is not. It is primarily a disease of women, occurring five to ten times more often in females than in males. Although the peak incidence is between 30 and 40 years of age, the condition has also been diagnosed in the very young and the very old.
SLE is the classic prototype of autoimmune disease of connective tissue. Its etiology is unknown, but the high level of autoantibodies in persons with the condition indicates a defect in the regulatory mechanisms that sustain self-tolerance and prevent the body from attacking its own cells, cell constituents, and proteins. Patients with SLE can have a wide variety of autoantibodies against nuclear and cytoplasmic cellular components. The presence of high levels of antinuclear antibody (ANA) in SLE patients with glomerulonephritis indicates a pathogenic role for that antibody. The antibodies are directed against deoxyribonucleoprotein, DNA, histone, and a soluble non–nucleic acid molecule called Sm antigen.
Factors that appear to contribute to the development of SLE include exposure to sunlight or ultraviolet radiation from sunlamps, a genetic predisposition to the disease, certain drugs, viral infections, and hormonal influences.
Clinical manifestations of SLE are confusingly diverse owing to the involvement of connective tissue throughout the body. Typically, the patient seeks medical help for relief of fever, weight loss, joint pain, the characteristic butterfly rash, pleural effusion and pleuritic pain, and nephritis. The detection of ANA by microscopic immunofluorescence is supportive evidence for the presence of SLE.
Either glomerulonephritis, which is usually mild, or cardiovascular manifestations such as myocarditis, endocarditis, or pericarditis, are found in about half the patients with SLE. Pulmonary disease, especially pleurisy, is also relatively common, as are gastrointestinal disturbances and lymph node involvement. Organic neurologic disturbances produce behavioral aberrations and frank psychosis in some patients; in a few others, there are peripheral neuropathies, motor weakness, and diplopia.
Supportive measures are used to prevent or minimize acute relapses and exacerbations of symptoms. The patient is instructed to avoid exposure to sunlight and ultraviolet radiation from other sources, blood transfusions, penicillin, and the sulfonamides. Active disease is treated with topical steroids, nonsteroidal antiinflammatory drugs for fever and joint pain, corticosteroids, and immunosuppressants. The goal of drug therapy is suppression of the immune system. Treatment of specific manifestations of SLE is aimed at prevention of complications. Physical therapy may be required to alleviate muscle weakness and prevent orthopedic deformities.
It was once thought that this was a fairly rare disease, but improved immunologic testing procedures have shown that it is not. It is primarily a disease of women, occurring five to ten times more often in females than in males. Although the peak incidence is between 30 and 40 years of age, the condition has also been diagnosed in the very young and the very old.
SLE is the classic prototype of autoimmune disease of connective tissue. Its etiology is unknown, but the high level of autoantibodies in persons with the condition indicates a defect in the regulatory mechanisms that sustain self-tolerance and prevent the body from attacking its own cells, cell constituents, and proteins. Patients with SLE can have a wide variety of autoantibodies against nuclear and cytoplasmic cellular components. The presence of high levels of antinuclear antibody (ANA) in SLE patients with glomerulonephritis indicates a pathogenic role for that antibody. The antibodies are directed against deoxyribonucleoprotein, DNA, histone, and a soluble non–nucleic acid molecule called Sm antigen.
Factors that appear to contribute to the development of SLE include exposure to sunlight or ultraviolet radiation from sunlamps, a genetic predisposition to the disease, certain drugs, viral infections, and hormonal influences.
Clinical manifestations of SLE are confusingly diverse owing to the involvement of connective tissue throughout the body. Typically, the patient seeks medical help for relief of fever, weight loss, joint pain, the characteristic butterfly rash, pleural effusion and pleuritic pain, and nephritis. The detection of ANA by microscopic immunofluorescence is supportive evidence for the presence of SLE.
Either glomerulonephritis, which is usually mild, or cardiovascular manifestations such as myocarditis, endocarditis, or pericarditis, are found in about half the patients with SLE. Pulmonary disease, especially pleurisy, is also relatively common, as are gastrointestinal disturbances and lymph node involvement. Organic neurologic disturbances produce behavioral aberrations and frank psychosis in some patients; in a few others, there are peripheral neuropathies, motor weakness, and diplopia.
Supportive measures are used to prevent or minimize acute relapses and exacerbations of symptoms. The patient is instructed to avoid exposure to sunlight and ultraviolet radiation from other sources, blood transfusions, penicillin, and the sulfonamides. Active disease is treated with topical steroids, nonsteroidal antiinflammatory drugs for fever and joint pain, corticosteroids, and immunosuppressants. The goal of drug therapy is suppression of the immune system. Treatment of specific manifestations of SLE is aimed at prevention of complications. Physical therapy may be required to alleviate muscle weakness and prevent orthopedic deformities.
lupus vulga´ris the most common and severe form of tuberculosis of the skin, most often affecting the face, with formation of reddish brown patches of nodules in the corium, which progressively spread peripherally with central atrophy, causing ulceration and scarring and destruction of cartilage in involved sites.
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