Multiple autoimmune syndrome (MAS) may provide an important clue to solving the lupus puzzle. Researchers have noticed that in people who have three or more autoimmune diseases (multiple autoimmune syndrome) there tend to be clusters of disease that appear together. For example, one cluster, Type 2, includes SLE, pemphigus, chronic active hepatitis and several other conditions. Dr. Noel R. Rose, of the Center of Autoimmune Disease Research at Johns Hopkins, explains the importance of understanding the relationships between autoimmune diseases. MAS clusters provide a good opportunity for researchers to examine these relationships.
Dr. Rose compares the current state of autoimmune research to that of infectious disease study before the age of antibiotics–before researchers knew what caused infectious illness. With the discovery of pathogenic microorganisms came the ambition to find a way to fight those organisms; eventually, different antibiotics were designed that could kill specific pathogens, or groups of pathogens.
The introduction of antibiotics heralded a new dawn in disease treatment. Causes, in addition to symptoms, would now be addressed. Dr. Rose explains that researchers in the field of autoimmunity are closing in on the same kind of breakthrough today. This breakthrough may come about, at least in part, because of the focus on relationships between autoimmune diseases. What this focus reveals is that a combination of circumstances must exist in order for autoimmunity to occur.
Two elements in the development of autoimmune disease are genetic predisposition and environmental triggers. The genetic aspect of the equation involves the participation of more than one gene, and the environmental triggers, it is suggested, act as switches that turn the autoimmune process on in susceptible individuals.
Many pieces of the autoimmune puzzle are still missing; these include identification of the various genetic actors that set the stage for susceptibility; understanding how the genetic factors work together in order to create a susceptible state; identification of the many environmental triggers that switch on the autoimmune response; and understanding precisely how the environmental switches work.
Some of the genetic background responsible for autoimmune disease has been identified. In the case of multiple autoimmune syndrome (MAS), type 3, for example, immune system marker HLA-B8 and/or DR3 or DR5 seem to have significance. A few diseases that are included in MAS, type 3 are: autoimmune thyroid disease, Sjogren’s syndrome, pernicious anemia, insulin dependent diabetes, vitiligo and systemic lupus erythematosus (list derived from the European Journal of Dermatology)
As for environmental triggers, studies have shown that individuals who have autoimmune diseases often have been exposed to some fairly common pathogens and have developed antibodies to these pathogens. A few of the implicated microorganisms are: Helicobactor pylori (H. pylori), Epstein Barr and cytomegalovirus (HCMV).
With attention turning to the role of microorganisms as triggers in autoimmunity, researchers are learning that initial exposure to the pathogen may not immediately precipitate an autoimmune response. It is believed that a secondary antagonist, inflammation perhaps, or another infection, provokes the production of autoantibodies (literally, bodies against the self). Autoantibodies are at the heart of autoimmune disease.
Environmental triggers are not limited to microorganisms; exposure to substances in the environment–silica, for example, and epoxy resins–has also been linked to the development of autoimmune disease.
According to Dr. Rose, so much has been learned about autoimmunity–its genetic associations and environmental triggers– that, “…we’re getting to a point where we can almost predict who is more likely or less likely to develop autoimmune disease”. Almost, but not quite. Individuals with multiple autoimmune syndrome offer researchers a chance to study the interaction between genetic makeup and environmental triggers.
One interesting aspect of autoimmune disease clusters is that in each grouping there seems to be at least one condition that involves the skin–often that condition is vitiligo. Another interesting, perhaps significant, aspect of the clusters is that they tend to occur most frequently in individuals who have autoimmune thyroid disease. Individuals with SLE and Sjorgrens also seem to have an increased incidence of multiple autoimmune syndrome.
It’s important to remember that the suggested disease clusters in multiple autoimmune syndrome merely reflect a tendency for diseases to co-exist. There’s nothing fixed about the categories; however, knowing that some diseases tend to occur together may be helpful in diagnosis. Doctors might be alert to the possibility that one of these diseases will appear in a patient who has MAS.
While MAS is generally divided into three types, different sources describe the composition of these types variously. One site that seems responsible and provides a fairly comprehensive list of MAS associated diseases is elaine-moore.com. The link to that site is: http://www.elaine-moore.com.
Today, all that medicine has to offer the lupus patient is possible control of symptoms; the cause of the disease cannot be addressed because this is still a mystery. Without a known cause, a cure remains elusive. This state of affairs is analogous, as Dr. Rose points out, to the one that existed with infectious disease treatment before Paul Ehrlich’s “magic bullet” was discovered. The study of disease relationships in multiple autoimmune syndrome might help to change all that. Maybe there’s a magic bullet–or several, as in the case of infectious disease–waiting to put an end to lupus once the cause of this autoimmune disease is clearly understood.
Below are some articles that discuss multiple autoimmunity from different perspectives; the headings approximately describe the subject of each article. : Some Readings: