Lupus has often been called "the disease of a thousand faces" because supposedly there can be any number of symptoms in different people.
As shown in the above article, lupus is loosely defined as from a hodge-podge of different symptoms and two people without any overlaping criteria can mysteriously be described as having the same illness.
The creation of illnesses by committee, such as has been done for so long in psychiatry, should be discouraged.
Traditionally lupus has been a garbage bin diagnosis that collected anything to do with an auto-immune problem not otherwise diagnosed, which would frankly be a better and less misleading operational definition than one that purports to peg it as one specific illness.
I strongly suspect that the whole concept that there is something called "lupus", is getting in the way of dealing with various diseases that are similar in some ways but without any definitive common source. One analogy would be, some red dyes can cause an allergic reaction and red paint with lead in it can cause a variety of health problems. An inference from a similar color to a common root of problems would be a counterproductive conflation.
The concepts of specificity (roughly, the odds that one positive criterion for the illness correlates with that illness rather than some other illness or ordinary health) and sensitivity (roughly, the odds that any given instance of an illness will have that specific association) are important, and it is good that the Wikipedia article has them.
The difficulty though is that in the absence of a definitive characteristic of lupus the correlations are only with a diagnosis of lupus, not with having lupus, as a positive diagnosis does not confirm anything in particular beyond what was already known.
What ought to be done?
Well first of all, pure symptoms have to be removed from diagnositic criteria. A rash for instance is for most practical purposes an end result and usually not directly illuminating about the physical process at work. Although some symptoms can be grounds for strong suspicion for further investigation, such as the characteristic butterfly rash, they should be viewed as symptoms rather than causes.
Anti-DNA antibodies, on the other hand, are at least an intermediate cause and their presence can show a specific cause of certain symptoms. What causes the antibodies, on the other hand, is another issue.
If one checks the link on Anti-nuclear antibodies, that reveals another methodological issue, which is that there are a lot of non-lupus things that have this same characteristic, including various syndromes and arthritis. That is, there is a possibility that the definition of lupus is in some ways both too broad and too narrow.
Until one is able to get behind an intermediate cause, it makes more sense to treat it (cautiously) as a discrete illness. It may be that there will be more than one root cause behind an intermediate cause but it can help focus to look at, e.g. anti-nuclear antibodies as a specific problem and see what treats that problem rather than artificially separate these.
You can’t treat metaphysical illnesses. You treat physical ones. Defining an illness as anything without any specific and definitive physical meaning isn’t medicine, it’s more like poetry.
Something that could add more focus would be restricting a lupus definition to cases of anti dsDNA antibodies, which occur with 70% of people diagnosed with lupus and only 0.5% of people who are not. Here the most interesting information is excluded by the definition of lupus. Note that because the field of people without lupus is considerably larger than the field of people with lupus, the 0.5% may actually be a greater population than the 70%.
Why this is very important is that the most important information, why some people with anti dsDNA antibodies go on contract "lupus" while others do not, is unlikely to be looked at as rigourously as it ought to be if you do not define them as having the same disorder. What is different about those who remain asymptomatic? This may suggest a cure or it may suggest triggers to avoid. It may also assist with finding patterns in development of the underlying, sometimes benign problem, which could be geographic, genetic, related to toxic exposures, etc. That in combination with the tendency for lupus to have flare ups of unclear origin suggests to me that much of the essence of the problem has been missed.
According to Dr. D’Adamo, there is a higher association with lupus and blood type "B". This is interesting because blood type "B" people have generally lesser immunity to viral and bacterial infections on average and so it is curious if they are more likely to have a stronger immune reaction to themselves.
I have a suspicion that there may be a correlation between autoimmune disorders and mixed blood types. Blood types are unfortunately defined according to criteria that are properly limited to the highly unnatural activity of blood transfusions, how they affect somebody else, rather than how they affect the person who will be using most of his blood most of the time. Blood type A and B are dominant, and consequently there are at least two types of A and two types of B- people with two of the gene vs. people that have one A or B gene and the other being an O gene. D’Adamo has pointed out that, for example, in a person with A and O genes there will be some cells that are blood type O as well as some cells that are blood type A. He does not however seem to have appreciated the full potential importance of that.
A blood type O person of course cannot have a transfusion from somebody with A or B blood. So what happens with somebody of mixed heritage? Presumably AO and BO types have some mechanism so that the O genes do not produce anything that attacks the A or B genes, the mechanism of which would be something of interest.
So what happens if the latent type O gene does start making immune decisions and decides that A or B cells are the enemy? A and B don’t react to O generally, so any O gene rebellion might never be stamped out.
Stress can bring out increased immune reaction, and increased immune disorders. What if the wrong immune gene becomes activated?
There was an interesting reported case where a woman who was normally blood type A became AB mysteriously and developed "lupus". Upon suppression of her immune system she reverted to blood type A again. I don’t know if she was genetically tested for her genetic type but I would be most interested in that. I would have a suspicion that she had a B gene but that it was deficient in some way such that instead of becoming AB and her body programming to deal with that, that the A gene may have become dominant and the B gene activating later may have caused huge problems. That of course is a hypothesis.
The treatment for lupus is typically to suppress the immune system with brutal, debilitating immune suppressant drugs with a variety of nasty side effects. While that may alleviate symptoms, the question really ought to be, why is the body attacking itself in this specific way?