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What is Lupus

Lupus is a chronic, autoimmune disease that can damage any part of the body (skin, joints, and/or organs inside the body). Chronic means that the signs and symptoms tend to last longer than six weeks and often for many years. In lupus, something goes wrong with your immune system, which is the part of the body that fights off viruses, bacteria, and germs ("foreign invaders," like the flu). Normally our immune system produces proteins called antibodies that protect the body from these invaders. Autoimmune means your immune system cannot tell the difference between these foreign invaders and your body’s healthy tissues ("auto" means "self") and creates autoantibodies that attack and destroy healthy tissue. These autoantibodies cause inflammation, pain, and damage in various parts of the body.

Lupus is also a disease of flares (the symptoms worsen and you feel ill) and remissions (the symptoms improve and you feel better). Lupus can range from mild to life-threatening and should always be treated by a doctor. With good medical care, most people with lupus can lead a full life.
Lupus is not contagious, not even through sexual contact. You cannot "catch" lupus from someone or "give" lupus to someone.
  • Lupus is not like or related to cancer. Cancer is a condition of malignant, abnormal tissues that grow rapidly and spread into surrounding tissues. Lupus is an autoimmune disease, as described above.
  • Lupus is not like or related to HIV (Human Immune Deficiency Virus) or AIDS (Acquired Immune Deficiency Syndrome). In HIV or AIDS the immune system is underactive; in lupus, the immune system is overactive.
  • Our research estimates that at least 1.5 million Americans have lupus. The actual number may be higher; however, there have been no large-scale studies to show the actual number of people in the U.S. living with lupus.
  • It is believed that 5 million people throughout the world have a form of lupus.
  • Lupus strikes mostly women of childbearing age (15-44). However, men, children, and teenagers develop lupus, too.
  • Women of color are 2-3 times more likely to develop lupus.
  • People of all races and ethnic groups can develop lupus.
  • More than 16,000 new cases of lupus are reported annually across the country.

What Causes Lupus

No gene or group of genes has been proven to cause lupus. Lupus does, however, appear in certain families, and when one of two identical twins has lupus, there is an increased chance that the other twin will also develop the disease. These findings, as well as others, strongly suggest that genes are involved in the development of lupus. Although lupus can develop in people with no family history of lupus, there are likely to be other autoimmune diseases in some family members. Certain ethnic groups (people of African, Asian, Hispanic/Latino, Native American, Native Hawaiian, or Pacific Island descent) have a greater risk of developing lupus, which may be related to genes they have in common.


While a person’s genes may increase the chance that he or she will develop lupus, it takes some kind of environmental trigger to set off the illness or to bring on a flare. Examples include:
  • ultraviolet rays from the sun
  • ultraviolet rays from fluorescent light bulbs
  • sulfa drugs, which make a person more sensitive to the sun, such as: Bactrim® and Septra® (trimethoprim-sulfamethoxazole); sulfisoxazole (Gantrisin®); tolbutamide (Orinase®); sulfasalazine (Azulfidine®); diuretics
  • sun-sensitizing tetracycline drugs such as minocycline (Minocin®)
  • penicillin or other antibiotic drugs such as: amoxicillin (Amoxil®); ampicillin (Ampicillin Sodium ADD-Vantage®); cloxacillin (Cloxapen®)
  • an infection
  • a cold or a viral illness
  • exhaustion
  • an injury
  • emotional stress, such as a divorce, illness, death in the family, or other life complications
  • anything that causes stress to the body, such as surgery, physical harm, pregnancy, or giving birth
  • Although many seemingly unrelated factors can trigger the onset of lupus in a susceptible person, scientists have noted some common features among many people who have lupus, including:
  • exposure to the sun
  • an infection
  • being pregnant
  • giving birth
  • a drug taken to treat an illness
  • However, many people cannot remember or identify any specific factor that occurred before they were diagnosed with lupus.

Hormones are the body’s messengers and they regulate many of the body’s functions. In particular, the sex hormone estrogen plays a role in lupus. Men and women both produce estrogen, but estrogen production is much greater in females. Many women have more lupus symptoms before menstrual periods and/or during pregnancy, when estrogen production is high. This may indicate that estrogen somehow regulates the severity of lupus. However, it does not mean that estrogen, or any other hormone for that matter, causes lupus.

Related Information
Environmental Factors in Lupus
January 2007 webchat transcript with Dr. Mark Gourley

Frequently Asked Questions
Is lupus stress related?
We do not know for certain. There are many anecdotal reports (personal accounts) of lupus flaring during or after a stressful time, but this question requires further scientific study.

Does lupus occur more often in certain geographical areas?
No. There are on-going studies of several suspected "clusters" of lupus case but no evidence has emerged that suggests lupus is more prevalent in specific areas.

Is lupus related to pollution or toxic chemicals?
We do not know. The cause of lupus, and many other autoimmune diseases, remains unknown. The respective roles of genetic and environmental factors in triggering lupus remain to be determined. The National Institutes of Health (NIH), the principal biomedical research agency of the United States Government established the National Institute of Environmental Health Sciences (NIEHS) to study issues related to environmental health. A meeting in September 1998 at Research Triangle Institute(RTI) in Durham, NC organized by NIEHS, looked at autoimmunity and the environment and specifically lupus. A review of the discussion was published in the medical journal, Arthritis and Rheumatism (1998 Oct; 41(10): 1714-24) in an article titled: "Hormonal, Environmental, and Infectious Risk Factors for Developing Systemic Lupus Erythematosus" by Cooper GS, Dooley MA, Treadwell EL, St Clair EW, Parks CG, Gilkeson GS.

Can something in your diet cause lupus?
We do not believe so.

Is there any truth to the claims being circulated on the Internet that lupus is caused by the artificial sweetener, aspartame?
We are aware there is an email message circulating on the Internet warning individuals with lupus about dangers associated with using the artificial sweetener aspartame. The Lupus Foundation of America consulted with the chair of the LFA Medical Council, Evelyn Hess, MD, MACP, MACR. Dr. Hess is one of the nation's leading researchers in the field of lupus specializing in environmental influences. According to Dr. Hess, there is, as of now, no specific proof of an association with aspartame as a cause or worsening of SLE. People with lupus should always consult with their physician before making any changes in their medical treatment, diet, exercise or other routine based on information received via the Internet or other sources lacking known credentials.

Forms of Lupus
Systemic Lupus Erythematosus

Systemic lupus is the most common form of lupus, and is what most people mean when they refer to "lupus." Systemic lupus can be mild or severe. Some of the more serious complications involving major organ systems are:
  • inflammation of the kidneys (lupus nephritis), which can affect the body’s ability to filter waste from the blood and can be so damaging that dialysis or kidney transplant may be needed
  • an increase in blood pressure in the lungs (pulmonary hypertension)
  • inflammation of the nervous system and brain, which can cause memory problems, confusion, headaches, and strokes
  • inflammation in the brain’s blood vessels, which can cause high fevers, seizures, behavioral changes,
  • hardening of the arteries (coronary artery disease), which is a buildup of deposits on coronary artery walls that can lead to a heart attack
  • More information about how lupus affects various organs and tissues is available in the LFA fact sheet series, "The Body & Lupus."

Cutaneous Lupus Erythematosus

Cutaneous refers to the skin, and this form of lupus is limited to the skin. Although there are many types of rashes and lesions (sores) caused by cutaneous lupus, the most common rash is raised, scaly and red, but not itchy. It is commonly known as a discoid rash, because the areas of rash are shaped like disks, or circles. Another common example of cutaneous lupus is a rash over the cheeks and across the bridge of the nose, known as the butterfly rash. Other rashes or sores may appear on the face, neck, or scalp (areas of the skin that are exposed to sunlight or fluorescent light), or in the mouth, nose, or vagina. Hair loss and changes in the pigment, or color, of the skin are also symptoms of cutaneous lupus.

Approximately 10 percent of people who have cutaneous lupus will develop systemic lupus. However, it is likely that these people already had systemic lupus, with the skin rash as their main symptom.

Drug-induced Lupus Erythematosus

Drug-induced lupus is a lupus-like disease caused by certain prescription drugs. The symptoms of drug-induced lupus are similar to those of systemic lupus, but only rarely will any major organs be affected.

The drugs most commonly connected with drug-induced lupus are hydralazine (used to treat high blood pressure or hypertension), procainamide (used to treat irregular heart rhythms), and isoniazid (used to treat tuberculosis). Drug-induced lupus is more common in men because they are given these drugs more often; however, not everyone who takes these drugs will develop drug-induced lupus. The lupus-like symptoms usually disappear within six months after these medications are stopped.

Neonatal Lupus

Neonatal lupus is a rare condition that affects infants of women who have lupus and is caused by antibodies from the mother acting upon the infant in the womb. At birth, the infant may have a skin rash, liver problems, or low blood cell counts, but these symptoms disappear completely after several months with no lasting effects. Some infants with neonatal lupus can also have a serious heart defect. With proper testing, physicians can now identify most at-risk mothers, and the infant can be treated at or before birth. Most infants of mothers with lupus are entirely healthy.

What are the Symptoms of Lupus
Because lupus can affect so many different organs, a wide range of symptoms can occur. These symptoms may come and go, and different symptoms may appear at different times during the course of the disease.

The most common symptoms of lupus, which are the same for females and males, are:
  • extreme fatigue (tiredness)
  • headaches
  • painful or swollen joints
  • fever
  • anemia (low numbers of red blood cells or hemoglobin, or low total blood volume)
  • swelling (edema) in feet, legs, hands, and/or around eyes
  • pain in chest on deep breathing (pleurisy)
  • butterfly-shaped rash across cheeks and nose
  • sun- or light-sensitivity (photosensitivity)
  • hair loss
  • abnormal blood clotting
  • fingers turning white and/or blue when cold (Raynaud’s phenomenon)
  • mouth or nose ulcers
  • Many of these symptoms occur in other illnesses besides lupus. In fact, lupus is sometimes called "the great imitator" because its symptoms are often like the symptoms of rheumatoid arthritis, blood disorders, fibromyalgia, diabetes, thyroid problems, Lyme disease, and a number of heart, lung, muscle, and bone diseases.

What Kinds of Doctors Treat Lupus
The form of lupus and its symptoms determine what type of doctor you will see. Most people who have mild to moderate disease will be treated by a rheumatologist, who specializes in the diseases of joints and muscles.

However, if your lupus causes kidney problems, you will also see a nephrologist, a specialist in diseases of the renal system.

If you have rashes or lesions, you will see a dermatologist, who specializes in diseases that affect the skin (including the scalp and the mouth).

Because lupus can cause damage to any part of the body, other specialists may be necessary, such as a cardiologist, who specializes in heart problems, or a neurologist, who specializes in problems that affect the brain and nervous system, or a perinatologist, who specializes in high-risk pregnancies.

What are the Risks for Developing Lupus

More than 90 percent of people with lupus are women.


Symptoms and diagnosis occur most often when women are in their childbearing years, between the ages of 15 and 44. Symptoms of lupus will occur before age 18 in 15 percent of the people who are later diagnosed with the disease.


In the United States, lupus is more common in people of color -- African Americans, Hispanics/Latinos, Asian Americans, Native Americans, Native Hawaiians and Pacific Islanders -- than in the Caucasian population. It also appears that lupus develops at an earlier age and is more severe among members of these ethnic groups.

Family History

Relatives of people with lupus have an approximately 5-13 percent chance of developing lupus. However, only about 5 percent of children will develop lupus if their mother has lupus.

Prognosis and a Hopeful Future
The idea that lupus is generally a fatal disease is a big misconception. In fact, the prognosis of lupus is much better today than ever before.
  • It is true that medical science has not yet developed a method for curing lupus. And some people do die from the disease. However, people with non-organ threatening aspects of lupus can look forward to a normal lifespan if they:
  • follow the instructions of their physician,
  • take their medication(s) as prescribed, and
  • know when to seek help for unexpected side effects of a medication or a new manifestation of their lupus.
  • Although some people with lupus have severe recurrent attacks and are frequently hospitalized, most people with lupus rarely require hospitalization. There are many lupus patients who never have to be hospitalized, especially if they are careful and follow their physician's instructions.
  • New research brings unexpected findings each year. The progress made in treatment and diagnosis during the last decade has been greater than that made over the past 100 years. It is therefore a sensible idea to maintain control of a disease that tomorrow may be curable.

Frequently Asked Questions
Is there a cure for lupus?
At the present time there is not a cure for lupus, but there certainly is effective treatment.

Is lupus a fatal disease?
Lupus is not a universally fatal disease. In fact, today with close follow-up and treatment, 80-90% of the people with lupus can expect to live a normal life span. Lupus does vary in intensity and degree, however, and there are people who have a mild case, there are those who have a moderate case and there are some who have a severe case of lupus, which tends to be more difficult to treat and bring under control. For people who have a severe flare-up, there is a greater chance that their lupus may be life-threatening. We know that some people do die of this disease and because of that we have a tremendous amount of respect for the potential of this disease. However, the majority of people living with lupus today can expect to live a normal lifespan. People frequently read in the literature that, 80-90% of people with lupus live for more than 10 years. Unfortunately, this is often misinterpreted as people with lupus live for only 10 years.

Let us clarify this.

It is important to understand that the "10 years" does not represent the number of years the person will live, but rather the number of years involved in the study. The studies followed patients with lupus from the time of diagnosis for a period of ten years. At the end of this research period they were able to conclude that 80-90% of the people enrolled were still alive. What this study did not look at is what happened in year 11, 12, 15, 20 and so on. We know there are many people who have been living with lupus for 15, 19, 25, 30 and 40 years. This is not a disease that is universally fatal to all. The majority of people with lupus today can expect to live a normal lifespan.

When people die of lupus, what do they usually die of?
Overwhelming infection and kidney failure are the two most common causes of death in people with lupus. Recently there is new information which indicates heart disease may be another leading cause of death among people with lupus.

The History of Lupus Erythematosus
Marc C. Hochberg, MD, MPH
Professor of Medicine, Epidemiology and Preventive Medicine
University of Maryland School of Medicine, Baltimore, MD.

A selection from the Lupus Foundation of America Newsletter Article Library
Revised 6/03


The history of lupus erythematosus (LE) has been reviewed in two of the major textbooks on this disease1,2 and was the subject of an article in a journal in 1983.3 This article concentrates on developments in the present century which have greatly expanded our knowledge about the pathophysiology, clinical-laboratory features, and treatment of this disorder.

The history of lupus can be divided into three periods: the classical period which saw the description of the cutaneous disorder, the neoclassical period which saw the description of the systemic or disseminated manifestations of lupus, and the modern period which was heralded by the discovery of the LE cell in 1948 and is characterized by the scientific advances noted above.

The history of lupus during the classical period was reviewed by Smith and Cyr in 1988.4 Of note are the derivation of the term lupus and the clinical descriptions of the cutaneous lesions of lupus vulgaris, lupus profundus, discoid lupus, and the photosensitive nature of the malar or butterfly rash.

The term lupus (Latin for wolf) is attributed to the thirteenth century physician Rogerius who used it to describe erosive facial lesions that were reminiscent of a wolf's bite.1,3 Classical descriptions of the various dermatologic features of lupus were made by Thomas Bateman, a student of the British dermatologist Robert William, in the early nineteenth century; Cazenave, a student of the French dermatologist Laurent Biett, in the mid-nineteenth century; and Moriz Kaposi (born Moriz Kohn), student and son-in-law of the Austrian dermatologist Ferdinand von Hebra, in the late nineteenth century. The lesions now referred to as discoid lupus were described in 1833 by Cazenave under the term "erythema centrifugum," while the butterfly distribution of the facial rash was noted by von Hebra in 1846. The first published illustrations of lupus erythematosus were included in von Hebra's text, Atlas of Skin Diseases, published in 1856.

The Neoclassical era of the history of lupus began in 1872 when Kaposi first described the systemic nature of the disorder:

"... experience has shown that lupus erythematosus ... may be attended by altogether more severe pathological changes ... and even dangerous constitutional symptoms may be intimately associated with the process in question, and that death may result from conditions which must be considered to arise from the local malady."5

Kaposi proposed that there were two types of lupus erythematosus; the discoid form and a disseminated form. Furthermore, he enumerated various symptoms and signs which characterized the disseminated form including (1) subcutaneous nodules, (2) arthritis with synovial hypertrophy of both small and large joints, (3) lymphadenopathy, (4) fever, (5) weight loss, (6) anemia, and (7) central nervous system involvement.5

The existence of a disseminated or systemic form of lupus was firmly established by the work of Osler in Baltimore6 and Jadassohn in Vienna7 in 1904. Over the next thirty years, pathologic studies documented the existence of nonbacterial verrucous endocarditis (Libman-Sacks disease)8 and wire-loop lesions in patients with glomerulonephritis;9 such observations at the autopsy table lead to the construct of collagen disease proposed by Kemperer and colleagues in 1941.10 This terminology, collagen vascular disease, persists in usage now fifty years after its introduction.

The sentinel event in the mid 1900s which heralded the modern era was the discovery of the LE cell by Hargraves and colleagues in 1948.11 The investigators observed these cells in the bone marrow of patients with acute disseminated lupus erythematosus and postulated that the cell "... is the result of ... phagocytosis of free nuclear material with a resulting round vacuole containing this partially digested and lysed nuclear material ..." This discovery ushered in the present era of the application of immunology to the study of lupus erythematosus.

Two other immunologic markers were recognized in the 1950s as being associated with lupus: the biologic false-positive test for syphilis12 and the immunofluorescent test for antinuclear antibodies.13 Moore, working in Baltimore, demonstrated that systemic lupus developed in 7 percent of 148 subjects with chronic false-positive tests for syphilis and that a further 30 percent had symptoms consistent with collagen disease.12 Friou applied the technique of indirect immunofluorescence to demonstrate the presence of antinuclear antibodies in the blood of patients with systemic lupus.13 Subsequently, the recognition of antibodies to deoxyribonucleic acid (DNA)14 and the description of antibodies to extractable nuclear antigens (nuclear ribonucleoprotein (nRNP), Sm, Ro, La), and anticardiolipin antibodies; these autoantibodies are useful in describing clinical subsets and understanding the etiopathogenesis of lupus.

Two other major advances in the modern era have been the development of animal models of lupus and the recognition of the role of genetic predisposition to the development of lupus. The first animal model of systemic lupus was the F1 hybrid New Zealand Black/New Zealand White mouse.16 This murine model has provided many insights into the immunopathogenesis of autoantibody formation, mechanisms of immunologic tolerance, the development of glomerulonephritis, the role of sex hormones in modulating the cause of disease, and evaluation of treatments including recently developed biologic agents such as anti-CD4 antibodies among others. Other animal models that have been used to study systemic lupus include the BXSB and MRL/lpr mice, and the naturally occurring syndrome of lupus in dogs.17

The familial occurrence of systemic lupus was first noted by Leonhardt in 1954 and later studies by Arnett and Shulman at Johns Hopkins.18 Subsequently, familial aggregation of lupus, the concordance of lupus in monozygotic twin pairs, and the association of genetic markers with lupus have been described over the past twenty years.19 Presently, molecular biology techniques are being applied to the study of human lympho-cyte antigen (HLA) Class II genes to determine specific amino acid sequences in these cell surface molecules that are involved in antigen presentation to T-helper cells in patients with lupus. These studies have already resulted in the identification of genetic-serologic subsets of systemic lupus that complement the clinico-serologic subsets noted earlier. It is hoped by investigators working in this field that these studies will lead to the identification of etiologic factors(e.g.,viral antigens/proteins) in systemic lupus.

Finally, no discussion of the history of lupus is complete without a review of the development of therapy. Payne, in 1894, first reported the usefulness of quinine in the treatment of lupus.20 Four years later, the use of salicylates in conjunction with quinine was also noted to be of benefit.21 It was not until the middle of this century that the treatment of systemic lupus was revolutionized by the discovery of the efficacy of adrenocorticotrophic hormone and cortisone by Hench.22 Presently, corticosteroids are the primary therapy for almost all patients with systemic lupus. Antimalarials are used principally for patients with skin and joint involvement on the one hand and cytotoxic/immunosuppressive drugs are used for patients with glomerulonephritis, systemic vasculitis, and other severe life-threatening manifestations on the other.23 Currently, newer biologic agents are being investigated in treating patients with lupus.

Thus, the history of lupus, although dating back at least to the Middle Ages, has experienced an explosion in this century, especially during the modern era over the past forty years. It is hoped that this growth of new knowledge will allow a better understanding of immunopathogenesis of the disease and the development of more effective treatments.

  1. Lahita RG. Introduction. In: Lahita RG, ed. Systemic Lupus Erythematosus. New York: John Wiley and Sons. 1987; 1-3. (Fourth edition published 2004)
  2. Talbott JH. Historical background of discoid and systemic lupus erythematosus. In: Wallace DJ, Dubois EL, eds. Lupus Erythematosus. Philadelphia: Lea & Febiger. 1987; 3-11. (Sixth Edition published 2002)
  3. Boltzer JW. Systemic lupus erythematosus. I. Historical aspects. MD State Med J 1983; 37:439.
  4. Smith CD, Cyr M. The history of lupus erythematosus from Hippocrates to Osler. Rheum Dis Clin North Am 1988; 14:1.
  5. Kaposi MH. Neue Beitrage zur Keantiss des lupus erythematosus. Arch Dermatol Syphilol 1872; 4:36.
  6. Osler W. On the visceral manifestations of the erythema group of skin diseases (third paper). Am J Med Sci 1904; 127:1.
  7. Jadassohn J. Lupus erythematodes. In: Mracek F, ed. Handbach der Hautkrakheiten. Wien: Alfred Holder, 1904; 298-404.
  8. Libmann E. Sacks B. A hitherto undescribed form of volvular and mural endocarditis. Arch Intern Med 1924; 33:701.
  9. Baehr G, Klemperer P, Schifrin A. A diffuse disease of the peripheral circulation usually associated with lupus erythematosus and endocarditis. Trans Assoc Am Physicians 1935; 50:139.
  10. Klemperer P. Pollack AD, Baehr G. Pathology of disseminated lupus erythematosus. Arch Path (Chicago) 1941; 32:569.
  11. Hargraves MM, Richmond H, Morton R. Presentation of two bone marrow elements: The tart cell and the LE cell. Proc Staff Meet Mayo Clin 1948; 23:25.
  12. Moore JE, Lutz WB. The natural history of systemic lupus erythematosus: An approach to its study through chronic biological false positive reactions. J Chron Dis 1955; 2:297.
  13. Friou GJ. Clinical application of lupus serum nucleoprotein reaction using fluorescent antibody technique. J Clin Invest 1957; 36:890.
  14. Deicher HR, Holman HR, Kunkel HG. The precipitin reaction between DNA and a serum factor in SLE. J Exp Med 1959; 109:97.
  15. Tan EM, Kunkel HG. Characteristics of a soluble nuclear antigen precipitating with sera of patients with systemic lupus erythematosus. J Immunol 1966; 96:404.
  16. Bielschowsky M, Helyer BJ, Howie JB. Spontaneous haemolytic anemia in mice of the NZB/BL strain. Proc Univ Otago Med School 1959; 37:9.
  17. Hahn BH. Animal models of systemic lupus erythematosus. In: Wallace DJ, Dubois EL,eds. Lupus Erythematosus. Philadelphia: Lea & Febiger. 1987; 130-57.
  18. Arnett FC, Shulman LE. Studies in familial systemic lupus erythematosus. Medicine 1976; 55:313.
  19. Hochberg MC. The application of genetic epidemiology to systemic lupus erythematosus. J Rheumatol 1987; 14:867-9.
  20. Payne JF. A post-graduate lecture on lupus erythematosus. Clin J 1894; 4:223.
  21. Radcliffe-Crocker. Discussion on lupus erythematosus. Br J Dermatol 1898; 10:375.
  22. Hench PS. The reversibility of certain rheumatic and non-rheumatic conditions by the use of cortisone or of the pituitary adrenocorticotrophic hormone. Ann Intern Med 1952; 36:1.
  23. Lockshin MD. Therapy for systemic lupus erythematosus. N Engl J Med 1991; 324:189.
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