Does passive transfer of Sjogren 's syndrome IgG produce the pathophysiology of overactive bladder?
These findings are consistent with the notion that there is initial inhibition of parasympathetic neurotransmission by antagonistic autoantibodies to M3R, which produces a compensatory increase in M3R expression in vivo. The enhanced cholinergic responses during bladder distention result in detrusor overactivity. We conclude that the overactive bladder associated with SS is an autoantibody-mediated disorder of the autonomic nervous system, which may be part of a wider spectrum of cholinergic hyperresponsiveness.
The VI were more likely to report mobility disability than the NVI, but the trajectory of mobility disability was not steeper among the VI as compared to the NVI over the study period.