Systemic Lupus (cont.)
William C. Shiel Jr., MD, FACP, FACR
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
Catherine Burt Driver, MD
Catherine Burt Driver, MD, is board certified in internal medicine and rheumatology by the American Board of Internal Medicine. Dr. Driver is a member of the American College of Rheumatology. She currently is in active practice in the field of rheumatology in Mission Viejo, Calif., where she is a partner in Mission Internal Medical Group.
In this Article
- Systemic lupus erythematosus facts
- What is systemic lupus erythematosus? What are the types of lupus?
- What causes systemic lupus erythematosus? Is lupus hereditary?
- What is drug-induced lupus?
- What are lupus symptoms and signs?
- How is systemic lupus erythematosus diagnosed?
- What is the treatment for systemic lupus?
- How can a lupus patient help prevent disease activity (flares)?
- How can systemic lupus erythematosus affect pregnancy or the newborn?
- What is the prognosis of lupus? What does the future hold for people with systemic lupus?
- Where can one get more information about systemic lupus erythematosus?
- Systemic Lupus Erythematosus FAQs
- Find a local Rheumatologist in your town
What is drug-induced lupus?
Dozens of medications have been reported to trigger SLE. However, more than 90% of cases of "drug-induced lupus" occurs as a side effect of one of the following six drugs: hydralazine (Apresoline) is used for high blood pressure; quinidine (Quinidine Gluconate, Quinidine Sulfate) and procainamide (Pronestyl; Procan-SR; Procanbid) are used for abnormal heart rhythms; phenytoin (Dilantin) is used for epilepsy; isoniazid (Nydrazid, Laniazid) is used for tuberculosis; and d-penicillamine (used for rheumatoid arthritis). These drugs are known to sometimes stimulate the immune system and cause SLE. Fortunately, drug-induced SLE is infrequent (accounting for less than 5% of all people with SLE) and it usually resolves when the medications are discontinued.
What are lupus symptoms and signs?
People 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, hair loss (alopecia), arthritis, ulcers of the mouth and nose, facial rash ("butterfly rash"), unusual sensitivity to sunlight (photosensitivity), inflammation of the lining that surrounds the lungs (pleuritis) and the heart (pericarditis), and poor circulation to the fingers and toes with cold exposure (Raynaud's phenomenon). Complications of organ involvement can lead to further symptoms that depend on the organ affected and severity of the disease.
Skin manifestations are frequent in lupus and can sometimes lead to scarring. In discoid lupus, only the skin is typically 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 (alopecia). Over time, 5%-10% of those with discoid lupus may develop SLE.
Over half of the people 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 the disease.
Typically, with treatment, this rash can heal without permanent scarring.
Most people with SLE will develop arthritis during the course of their illness. Arthritis from 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).
More serious organ involvement with inflammation occurs in the brain, liver, and kidneys. White blood cells and blood-clotting factors also can be characteristically decreased in SLE, known as leukopenia (leucopenia) and thrombocytopenia, respectively. Leukopenia can increase the risk of infection, and thrombocytopenia can increase the risk of bleeding.
Inflammation of muscles (myositis) can cause muscle pain and weakness. This can lead to elevations of muscle enzyme levels in the blood.
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 that 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 are supplied with oxygen by these vessels.
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 due to coronary artery disease.
Kidney inflammation in SLE (lupus nephritis) can cause leakage of protein into the urine, fluid retention, high blood pressure, and even kidney failure. This can lead to further fatigue and swelling of the legs and feet. With kidney failure, machines are needed to cleanse the blood of accumulated waste products in a process called dialysis.
Involvement of the brain can cause personality changes, thought disorders (psychosis), seizures, and even coma. Lupus of the nervous system (neurologic lupus) can lead to damage to nerves cause numbness, tingling, and weakness of the involved body parts or extremities. Brain involvement is referred to as lupus cerebritis.
Many people with SLE experience hair loss (alopecia). Often, this occurs simultaneously with an increase in the activity of their disease. The hair loss can be patchy or diffuse and appear to be more like hair thinning.
Some people with SLE have Raynaud's phenomenon. Raynaud's phenomenon causes the blood vessels of the hands and feet to spasm, especially upon exposure to cold. The blood supply to the fingers and/or toes then becomes compromised, causing blanching, whitish and/or bluish discoloration, and pain and numbness in the exposed fingers and toes.
Other conditions that can accompany lupus include fibromyalgia, coronary heart disease, nonbacterial valvular heart disease, pancreatitis, esophagus disease with difficulty swallowing (dysphagia), liver disease (lupoid hepatitis), and infections.
Viewers share their comments