C3a INFEKTIOSAIRAUKSISSA

[Bb]

Lähettäjä: Soijuv Lähetetty: 2.7.2004 15:37

C3a-pitoisuuden nousu akuutissa ja kroonisessa borrelioosissa:


"Use of the fragment of the third component of complement following activation, C3a, is turning into an exciting potential marker for acute cytokine/toxin/antigen changes. Elevation of C3a can occur in acute inflammatory gout, acute infectious Staph epicondylitis and acute Lyme. The data set on the Lyme patients as well as other illnesses is building.

We have reported 11 fresh ECM cases to local health departments this year. In each of these, seen within 2 days of bite/rash, there has been significant elevation of C3a, average over 500. We have a matched control group of non-bitten patients with average C3a in the 130's. There is a matched group of bitten, but non-ECM patients with an average C3a around 120. To date there are no controls or bite controls with C3a higher than the cut-off of 146. There are no ECM patients with C3a < 230.

We are correlating before and after C3a in the ECM group to show changes in C3a with respect to HLA, VCS scores and MMP9. So far the model of genetic susceptibility from HLA, presence of toxin associated deficit in VCS is strong. MMP9 can show positivity in non-HLA acute ECM patients, but resolution with antibiotics is seen.

We are also seeing a cohort of longstanding Lyme patients with profound symptoms and failure to respond to antibiotics with a variety of changes with Actos and CSM. Actos lowers C3a, but addition of CSM to Actos (which normally will block the routinely seen elevation of TNF and MMP9 in non-Actos treated patients) causes a rise in C3a, without a big change in symptoms. Fortunately, continued CSM results in clearance of the C3a elevation, as toxin/cytokine is treated.

I hope these data will help cast some light on the presence of persistently symptomatic patients and also those who felt well after treatment of acute illness, but then progress over time to a chronic fatiguing illness. Perhaps the initial clinical observation of the role of elevated C3a as an additional target of therapy will help those with long term elevations of C3a.

C3a should roll up and go home when the illness is over. In some patients, despite removal of symptoms, C3a is still the colony of termites, eating an inflammatory series of tunnels in our immune responses. The patient might look fine, but like the termite riddled sillplate, the foundation is doomed."

Ritch Shoemaker MD