a hyper-Igm immune deficiency condition I have developed after many years of post-EBV CFS
Can you elaborate, melamine?
@Woolie - In 1979 I became acutely ill with symptoms of EBV and encephalitis. By the time I sought medical help I tested negative for whatever I was tested for and did not know enough to request records. It was many years before I understood the full picture of what I was dealing with.
Then my health started on a downward course in 1997 following some minor surgery, but things like dental surgeries, improper removal of large amalgams and replacement with same, mishandling of paint thinners, and possibly "healthy" exercise during the period that followed may have contributed. IBS was one of the mid-period symptoms and as you are probably aware, there is a good deal of evidence for it playing at least a large supporting role. This period of symptom development is one of the reasons I do not think infections are necessarily the primary event, but more of a visible critical event that results in a further compromised immune system and disruption of the interconnected neuro-endocrine-immune network.
This middle period is possibly when autoimmune symptoms started to develop, but it was not until the third phase, when I started getting very serious and consequential viral infections, that the autoimmune elements started to express themselves in full. Several years after a couple bad infections, my ANA turned positive and has remained there. I have low titers of all of the measurable ANA sub-classes or whatever they call them. I am considered to have an undifferentiated connective tissue disease now.
My immunoglobulins were not tested until 2006, and that is when the first indication of a problem with IgM showed up. If I were unsymptomatic my condition would be called MGUS - monoclonal gammopathy of undetermined significance. But because I am symptomatic with at least one symptom known to be identified with that, I believe it would be called a monoclonal or clonal gammopathy: I have had several tests indicating monoclonal and only one indicating possibly polyclonal. I am trying to determine to what extent and how this figures into my other labs and symptoms, and that is when I found a cross-reference with EBV and selective B-cell (and possibly selective T-cell) deficiency.
Thinking back to subtle indications of neuropathic and connective tissue signs that appeared in the second phase, I cannot say that one or another cause might have dominated. Autoimmune diseases are being increasingly looked at as having a possible association with infection. Even so, that still would not answer the question of immune deficiency or infection and maybe there is no strictly one or the other.
