Because early LUPUS is difficult to diagnose (it is often masqueraded by other conditions), estimation of incidence has always been problematic. The Lupus Foundation estimates that 2 million Americans have lupus, 90% of whom are women.

• Lupus is not infectious, rare or cancerous.
• Lupus is more prevalent than AIDS, sickle-cell anemia, cerebral palsy, multiple sclerosis and cystic fibrosis combined.
• Lupus affects 1 out of every 185 Americans and strikes adult women 3 times more frequently than in adult men. LUPUS is more prevalent in African Americans, Latinos, Native Americans and Asians.
• Ther is a 10% chance that people with lupus will have a close relative (parent or sibling) who already has or may develop lupus. Only about 5% of the children born to individuals with lupus will develop the illness.
• Although LUPUS ranges from mild to life-threatening and thousands of Americans die with LUPUS each year, the majority of cases can be controlled with proper treatment.
• With current methods of therapy, most people with LUPUS can look forward to a normal lifespan.

Consider first how the body correctly uses the immune system to fight off disease.

Imagine that a disease-causing-bacteria enters the body. The surface of this bacteria contains particles called "antigens" which create an "appearance" analogous to the features of our face. It is the appearance of our face which allows us to be recognized by others as someone who is known, or as someone who is a stranger. The same is true for the "antigen appearance" of the bacterial surface.

Specialized cells within our blood stream (Lymphocytes, and specifically the kind called "T-Cells") act as the "eyes" which can recognize any cell as a "friend" or as a "stranger." When the T-Cell lymphocyte does not recognize this bacteria as a "friend," i.e., a cell which is supposed to be there, it sounds an alarm. Somehow it directs other specialized lymphocytes ("B-Cell Lymphocytes") to produce chemicals called "antibodies." Such chemicals are custom-made to attach and lock on to the surface "antigens" of this particular bacteria and form a so-called "immune complex." In time, this immune complex will destroy the bacteria and protect the body from the infection it might have caused.

Now consider how this process might go wrong.

Suppose something went wrong within these T-Cell Lymphocytes. Suppose their chemical "eyesight" became impaired. Now when normal cells of the body, the ones which the lymphocyte was supposed to protect, were erroneously identified as "strangers," the "T-Cell Lymphocytes" then did what it always did. They directed the "B-Cell Lymphocytes" to produce antibodies against this enemy, even though it was NOT really an enemy but a NORMAL cell supposed to be there! Once again the "immune complexes" (described above) are created, except now they are attached to a normal cell of the body. Inflammation results and the tissue containing the normal cells reacts with swelling, irritation and ultimately injury.

If this erroneous attack on the normal body cells involved the skin; or the membranes surrounding the heart or lungs; or the inner tissues of the kidney; or cells in the eye; the joints; or the nervous system — you could well be looking at the symptoms of LUPUS, the disease.

What created these abnormal "T-Cell Lymphocytes" in the first place?

Though this is not completely understood, it is why some current research on LUPUS is directed at Lymphocyte genetics. Clearly something has gone wrong inside them to make their chemical "eyesight" defective. As genes within a given cell control these matters, and chromosome strands are made up of genes —- this is why research about "origin" is focused in this area. The Oklahoma Genetic Project, for example, specializes in families with a particularly high incidence of LUPUS. Perhaps a clue can be found to expand our knowledge of cause and effect.

Though it is currently believed there may well be some sort of genetic basis for LUPUS, it may not be so simple as just "genetic" in origin. The full LUPUS response may require an external stimulus such as environmental chemicals, ultra-violet light, viruses, injury, stress, etc. The final word is not in as yet.

Until research can find a "cure" for LUPUS, what can be done in the interim to modify the activity (or effects) of these abnormal "T- Cell Lymphocytes?

• Immuno-suppressive Drugs: These drugs are considered the "Big Guns" of treatment, as they can strongly suppress the Immune System, i.e., the activity of the Lymphocytes. As such, they work by directly affecting the function of the "T-Cell Lymphocytes" themselves.
  
  The most frequently used drugs in this group are the Steroids. It has been said that "...if organ-threatening disease is present and steroids are not prescribed, the patient usually loses function in that organ."* So steroids remain a powerful medication when LUPUS seems to be getting the upper hand. Occasionally there is reason to add Anti-Malarial Drugs. This seems like a strange medication to consider until one understands that besides treating Malaria, it is also a potent inhibitor of inflammation. Finally there are some Anti-cancer medications which are useful adjuncts, as they too can suppress lymphocyte growth and activity.
  
  * - The Lupus Book, p202, Daniel Wallace MD, Oxford Press, 1995
  
  
• Inflammation Suppressing Medications: These include aspirin products and other NonSteroidal Anti-Inflammatory DrugS (commonly referred to as NSAIDS)
  
  (In case you were wondering, Tylenol is not a NSAIDS.).
  
  For milder disease, there is the alternative of "Inflammation suppressing" medications. These medications do not specifically modify the activity of the Lymphocytes. Instead they suppress the production of a chemical named "Prostaglandin." Prostaglandin can also be suppressed with Aspirin 10 mgm.
  
  One of the effects of Lymphocyte activity is the release of Prostaglandin, a chemical when released, causes the inflammation and pain commonly associated with LUPUS. NSAIDS work to prevent this release.
  
  These medications are not helpful in modifying skin, heart, lung, kidney, liver, central nervous system, or blood effects of the disease. They do not put LUPUS into remission. Also, Prostaglandin exerts this inflammatory effect in many other conditions other than LUPUS. Its presence is NOT specific to LUPUS.

* Adapted from: Tan, E.M., et. al. The 1982 revised Criteria for the Classification of Systemic Lupus Erythematosis. Arth Rheum 25: 1271-1277.

Suppose we could block the recognition of the Normal Cells by the Abnormal "T-Cell Lymphocytes?

Normal cells release chemicals known as "nucleosomes" —- breakdown products from the usual life-death cycle of any cell. There is a chemical subset on the nucleosome which is called a "peptide." It is this peptide which actually attracts the defective T-Cell Lymphocytes, which in turn incorrectly identifies it as a "stranger." Research has found certain other peptides which do not confuse the sick T-Cells. The theory is that if this non-threatening peptide was introduced into the tissues, the T-Cells might not misidentify it (despite its poor chemical "eyesight") and incorrectly begin the auto-immune process.

Suppose we could prevent the B Lymphocytes, called into action by the T-Cell, from sustaining its production of auto-antibodies?

There is a chemical on the B Lymphocyte called CD40 whose purpose is to sustain the production of antibodies — once begun — against normal cells. If an "Anti-CD40 antibody" were produced, and injected into the body, would it block this sustained B Lymphocyte activity? Such a model has been successful in mouse experiments.

These and other creative approaches is what is going on in research laboratories - research which is supported by the various fund raising efforts of our Hudson Valley Chapter and other Lupus Chapters around the country, as well as at the National Lupus Alliance.

A poem by a patient about dealing with Lupus

A Sister’s Journey from Understanding to Activism