Dk. Seidel et al., COURSE OF ISLET AUTOANTIBODY TITERS DURING IG-IMMUNOADSORPTION IN A PATIENT WITH NEWLY-DIAGNOSED TYPE-1 DIABETES, Journal of autoimmunity (Print), 11(3), 1998, pp. 273-277
The purpose of this study was to determine whether and to what extent
diabetes-specific autoantibodies can be removed from the plasma by Ig-
immunoadsorption therapy. We followed the course of islet cell antibod
ies (ICA), insulin antibodies (I[A]A), glutamic acid decarboxylase ant
ibodies (GADA) and antibodies to the protein tyrosine phosphatase IA-2
(IA2A) in a patient with newly diagnosed insulin-dependent diabetes m
ellitus (IDDM) under multiple immunoadsorption treatments over 6 month
s. Autoantibodies were not removed from the plasma as efficiently as e
xpected when compared to the removal of total immunoglobulin (IgG). Wh
ereas IgG levels were lowered by 70-90% through each immunoadsorption
treatment, antibodies to insulin were reduced by an average of 83%, IA
2A by 36% and GADA by only 9% directly after treatment. ICA were >320
JDFU at diabetes onset and remained above this level. During the 6 mon
ths of multiple immunoadsorption therapies, I[A]A levels showed a 24-f
old increase due to stimulation of insulin antibody production by exog
enous insulin substitution, IA2A levels remained unchanged (average 6%
increase), and GADA levels were reduced by an average of 39% compared
to antibody titers at onset. All four antibodies were highly positive
in the eluate from the immunoadsorption columns. We showed that antib
odies to pancreatic islet cells can be reduced by immunoadsorption, bu
t as for plasmapheresis the effect is incomplete and transient for mos
t of the antibodies. If there is clinical benefit through immunoadsorp
tion therapy-as has been shown for newly diagnosed IDDM patients treat
ed with plasmapheresis-our data suggest that this may be due to factor
s other than the sufficient removal of antibodies. (C) 1998 Academic P
ress.