What is lupus?
Lupus is a condition of chronic inflammation caused by an autoimmune disease. Autoimmune diseases are illnesses that occur when the body's tissues are attacked by its own immune system. The immune system is a complex system within the body that is designed to fight infectious agents, for example, bacteria, and other foreign invaders. One of the mechanisms that the immune system uses to fight infections is the production of antibodies. Patients with lupus produce abnormal antibodies in their blood that target tissues within their own body rather than foreign infectious agents. Because the antibodies and accompanying cells of inflammation can involve tissues anywhere in the body, lupus has the potential to affect a variety of areas of the body. Sometimes lupus can cause disease of the skin, heart, lungs, kidneys, joints, and/or nervous system. When only the skin is involved, the condition is called discoid lupus. When internal organs are involved, the condition is called systemic lupus erythematosus (SLE).
Both discoid and systemic lupus are more common in women than men (about eight times more common). The disease can affect all ages but most commonly begins from age 20 to 45 years. It is more frequent in African-Americans and people of Chinese and Japanese descent.
What causes lupus?
The precise reason for the abnormal autoimmunity that causes lupus is not known. Inherited genes, viruses, ultraviolet light, and drugs may all play some role. Genetic factors increase the tendency of developing autoimmune diseases, and autoimmune diseases such as lupus, rheumatoid arthritis , and immune thyroid disorders are more common among relatives of patients with lupus than the general population. Some scientists believe that the immune system in lupus is more easily stimulated by external factors like viruses or ultraviolet light. Sometimes, symptoms of lupus can be precipitated or aggravated by only a brief period of sun exposure.
Dozens of medications have been reported to trigger SLE; however, more than 90% of this "drug-induced lupus" occurs as a side effect of one of the following six drugs: hydralazine (used for high blood pressure), quinidine and procainamide (used for abnormal heart rhythm), phenytoin (used forepilepsy), isoniazide (used fortuberculosis), d- penicillamine (used for rheumatoid arthritis). These drugs are known to stimulate the immune system and cause SLE. Fortunately, drug-induced SLE is infrequent (accounting for less than 5% of SLE among all patients with SLE) and usually resolves when the medications are discontinued.
It also is known that some women with SLE can experience worsening of their symptoms prior to their menstrual periods. This phenomenon, together with the female predominance of SLE, suggest that female hormones play an important role in the expression of SLE. This hormonal relationship is an active area of ongoing study by scientists.
Recent research provides direct evidence that a key enzyme's failure to dispose of dying cells contributes to SLE. The enzyme, DNase1, normally eliminates what is called "garbage DNA" and other cellular debris by chopping them into tiny fragments for easier disposal. The researchers turned off the DNase1 gene in mice. The mice appeared healthy at birth but after 6-8 months, the majority of mice without DNase1 showed signs of SLE. Thus, a genetic mutation that disrupts the body's cellular waste disposal may be involved in the beginning of SLE.
What are the symptoms of lupus?
In discoid lupus, only the skin is involved. The skin rash in discoid lupus often is found on the face and scalp. It usually is red and may have raised borders. Discoid lupus rashes are usually painless and do not itch, but scarring can cause permanent hair loss. Over time, 5 to 10% of patients with discoid lupus may develop SLE.
Patients with SLE can develop different combinations of symptoms and organ involvement. Common complaints and symptoms include fatigue, low-grade fever, loss of appetite, muscle aches, arthritis, ulcers of the mouth and nose, facial rash ("butterfly rash"), unusual sensitivity to sunlight (photosensitivity), inflammation of the lining that surrounds the lung (pleuritis) and the heart (pericarditis), and poor circulation to the fingers and toes with cold exposure (Raynaud's phenomenon).
More serious organ involvement with inflammation occurs in the brain, liver, and kidney. White blood cells and blood clotting factors also can be decreased in SLE, thereby increasing the risk of infection and bleeding.
Over half of the patients with SLE develop a characteristic red, flat facial rash over the bridge of their nose. Because of its shape, it is frequently referred to as the "butterfly rash" of SLE. The rash is painless and does not itch. The facial rash, along with inflammation in other organs, can be precipitated or worsened by exposure to sunlight, a condition called photosensitivity. This photosensitivity can be accompanied by worsening of inflammation throughout the body, called a "flare" of disease.
Most patients with SLE will develop arthritis during the course of their illness. Arthritis in SLE commonly involves swelling, pain, stiffness, and even deformity of the small joints of the hands, wrists, and feet. Sometimes, the arthritis of SLE can mimic that of rheumatoid arthritis (another autoimmune disease).
Inflammation of muscles (myositis) can cause muscle pain and weakness.
Inflammation of blood vessels, (vasculitis) that supply oxygen to tissues, can cause isolated injury to a nerve, the skin, or an internal organ. The blood vessels are composed of arteries that pass oxygen-rich blood to the tissues of the body and veins which return oxygen-depleted blood from the tissues to the lungs. Vasculitis is characterized by inflammation with damage to the walls of various blood vessels. The damage blocks the circulation of blood through the vessels and can cause injury to the tissues that the vessels supply.
Inflammation of the lining of the lungs (pleuritis) and of the heart (pericarditis) can cause sharp chest pain. The chest pain is aggravated by coughing, deep breathing, and certain changes in body position. The heart muscle itself rarely can become inflamed (carditis). It has also been shown that young women with SLE have a significantly increased risk of heart attacks from coronary artery disease.
Kidney inflammation in SLE can cause leakage of protein into the urine, fluid retention, high blood pressure, and even kidney failure. With kidney failure, machines are needed to cleanse the blood of accumulated poisons in a process called dialysis.
Involvement of the brain can cause personality changes, thought disorders (psychosis), seizures, and even coma. Damage to nerves can cause numbness, tingling, and weakness of the involved body parts or extremities. Brain involvement is called cerebritis.
Many patients with SLE experience hair loss (alopecia). Often, this occurs simultaneously with an increase in the activity of their disease.
Some patients with SLE have Raynaud's phenomenon. In these patients, the blood supply to the fingers and toes becomes interrupted upon exposeure to cold, causing blanching, bluish discoloration, and pain in the exposed fingers and toes.
Lupus is a condition of chronic inflammation caused by an autoimmune disease. Autoimmune diseases are illnesses that occur when the body's tissues are attacked by its own immune system. The immune system is a complex system within the body that is designed to fight infectious agents, for example, bacteria, and other foreign invaders. One of the mechanisms that the immune system uses to fight infections is the production of antibodies. Patients with lupus produce abnormal antibodies in their blood that target tissues within their own body rather than foreign infectious agents. Because the antibodies and accompanying cells of inflammation can involve tissues anywhere in the body, lupus has the potential to affect a variety of areas of the body. Sometimes lupus can cause disease of the skin, heart, lungs, kidneys, joints, and/or nervous system. When only the skin is involved, the condition is called discoid lupus. When internal organs are involved, the condition is called systemic lupus erythematosus (SLE).
Both discoid and systemic lupus are more common in women than men (about eight times more common). The disease can affect all ages but most commonly begins from age 20 to 45 years. It is more frequent in African-Americans and people of Chinese and Japanese descent.
What causes lupus?
The precise reason for the abnormal autoimmunity that causes lupus is not known. Inherited genes, viruses, ultraviolet light, and drugs may all play some role. Genetic factors increase the tendency of developing autoimmune diseases, and autoimmune diseases such as lupus, rheumatoid arthritis , and immune thyroid disorders are more common among relatives of patients with lupus than the general population. Some scientists believe that the immune system in lupus is more easily stimulated by external factors like viruses or ultraviolet light. Sometimes, symptoms of lupus can be precipitated or aggravated by only a brief period of sun exposure.
Dozens of medications have been reported to trigger SLE; however, more than 90% of this "drug-induced lupus" occurs as a side effect of one of the following six drugs: hydralazine (used for high blood pressure), quinidine and procainamide (used for abnormal heart rhythm), phenytoin (used forepilepsy), isoniazide (used fortuberculosis), d- penicillamine (used for rheumatoid arthritis). These drugs are known to stimulate the immune system and cause SLE. Fortunately, drug-induced SLE is infrequent (accounting for less than 5% of SLE among all patients with SLE) and usually resolves when the medications are discontinued.
It also is known that some women with SLE can experience worsening of their symptoms prior to their menstrual periods. This phenomenon, together with the female predominance of SLE, suggest that female hormones play an important role in the expression of SLE. This hormonal relationship is an active area of ongoing study by scientists.
Recent research provides direct evidence that a key enzyme's failure to dispose of dying cells contributes to SLE. The enzyme, DNase1, normally eliminates what is called "garbage DNA" and other cellular debris by chopping them into tiny fragments for easier disposal. The researchers turned off the DNase1 gene in mice. The mice appeared healthy at birth but after 6-8 months, the majority of mice without DNase1 showed signs of SLE. Thus, a genetic mutation that disrupts the body's cellular waste disposal may be involved in the beginning of SLE.
What are the symptoms of lupus?
In discoid lupus, only the skin is involved. The skin rash in discoid lupus often is found on the face and scalp. It usually is red and may have raised borders. Discoid lupus rashes are usually painless and do not itch, but scarring can cause permanent hair loss. Over time, 5 to 10% of patients with discoid lupus may develop SLE.
Patients with SLE can develop different combinations of symptoms and organ involvement. Common complaints and symptoms include fatigue, low-grade fever, loss of appetite, muscle aches, arthritis, ulcers of the mouth and nose, facial rash ("butterfly rash"), unusual sensitivity to sunlight (photosensitivity), inflammation of the lining that surrounds the lung (pleuritis) and the heart (pericarditis), and poor circulation to the fingers and toes with cold exposure (Raynaud's phenomenon).
More serious organ involvement with inflammation occurs in the brain, liver, and kidney. White blood cells and blood clotting factors also can be decreased in SLE, thereby increasing the risk of infection and bleeding.
Over half of the patients with SLE develop a characteristic red, flat facial rash over the bridge of their nose. Because of its shape, it is frequently referred to as the "butterfly rash" of SLE. The rash is painless and does not itch. The facial rash, along with inflammation in other organs, can be precipitated or worsened by exposure to sunlight, a condition called photosensitivity. This photosensitivity can be accompanied by worsening of inflammation throughout the body, called a "flare" of disease.
Most patients with SLE will develop arthritis during the course of their illness. Arthritis in SLE commonly involves swelling, pain, stiffness, and even deformity of the small joints of the hands, wrists, and feet. Sometimes, the arthritis of SLE can mimic that of rheumatoid arthritis (another autoimmune disease).
Inflammation of muscles (myositis) can cause muscle pain and weakness.
Inflammation of blood vessels, (vasculitis) that supply oxygen to tissues, can cause isolated injury to a nerve, the skin, or an internal organ. The blood vessels are composed of arteries that pass oxygen-rich blood to the tissues of the body and veins which return oxygen-depleted blood from the tissues to the lungs. Vasculitis is characterized by inflammation with damage to the walls of various blood vessels. The damage blocks the circulation of blood through the vessels and can cause injury to the tissues that the vessels supply.
Inflammation of the lining of the lungs (pleuritis) and of the heart (pericarditis) can cause sharp chest pain. The chest pain is aggravated by coughing, deep breathing, and certain changes in body position. The heart muscle itself rarely can become inflamed (carditis). It has also been shown that young women with SLE have a significantly increased risk of heart attacks from coronary artery disease.
Kidney inflammation in SLE can cause leakage of protein into the urine, fluid retention, high blood pressure, and even kidney failure. With kidney failure, machines are needed to cleanse the blood of accumulated poisons in a process called dialysis.
Involvement of the brain can cause personality changes, thought disorders (psychosis), seizures, and even coma. Damage to nerves can cause numbness, tingling, and weakness of the involved body parts or extremities. Brain involvement is called cerebritis.
Many patients with SLE experience hair loss (alopecia). Often, this occurs simultaneously with an increase in the activity of their disease.
Some patients with SLE have Raynaud's phenomenon. In these patients, the blood supply to the fingers and toes becomes interrupted upon exposeure to cold, causing blanching, bluish discoloration, and pain in the exposed fingers and toes.
