In addition to insulin intolerance, patients
with type 2 diabetes suffer from hypertension, renal
insufficiency, retinopathy, wound healing disorders,
coronary heart disease, heart attacks, strokes, and
amputations. In addition to metabolic syndrome,
many patients have pathological changes in macro- and
microcirculation. One of the causes might be agonistic
autoantibodies (agAAB), an immunological component.
This specialized group of autoantibodies activates the G
protein-coupled receptors similar to the way natural agonists
do and triggers receptor-specific reactions in the cell (1).
The pathological potential of agAAB has been described
in numerous publications. The pathological processes
triggered by agAAB for the ß-1-adrenoceptors (AR),
AT1 AR, and α 1 AR (2,3,4,5) have been particularly well
researched. Animal experiments provided valuable insights
into the causality of receptor-specific autoantibodies
for the development of diseases and disease-relevant
symptoms. These autoantibodies can only be removed with
specific antagonists at the receptor or by plasmapheresis
or immunoadsorption. The agAAB do not respond to
immunosuppression as classical autoantibodies do.
Patients in whom agAAB was removed by extracorporeal
treatment benefited from it. In patients with dilated
cardiomyopathy, cardiac output improved (6,7); those with
Alzheimer's disease (8) achieved stabilization of cognition.
In subjects with Thromboangiitis obliterans (9), further
amputations were able to be avoided after removal of the
autoantibodies, and in patients with inadequate control
of hypertension through pharmacological means, blood
pressure was considerably reduced (10). In only a few cases
did agAAB reappear. These positive treatment results for
various diseases formed the basis for screening diabetics
with respect to the prevalence of agonistic autoantibodies.