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Autoimmune autonomic disorders have been recognized for some time. Approximately 15 years ago, an antibody to the nicotinic acetylcholine receptor (AChR) found in autonomic
ganglia was described as a cause of autonomic failure and orthostatic hypotension.
Postural tachycardia syndrome (POTS) is a chronic disorder characterized by excessive
orthostatic tachycardia in the absence of orthostatic hypotension. POTS typically
affects women of childbearing age. A significant minority of POTS patients report
getting sick after a viral illness, suggesting a possible autoantibody cause for POTS.
Despite this presentation, and the high prevalence of other autoimmune conditions
in this demographic, it has been difficult to isolate antibodies that “cause” POTS.
More progress has been made recently with an upsurge of reports of a variety of autoantibodies
in POTS patients. Our colleagues at the University of Oklahoma and we at Vanderbilt
University have jointly reported autoantibodies from POTS’ patient sera to alpha-1,
beta-1 and beta-2 adrenergic receptors show functional significance in vitro. These
newer data suggest that autoimmunity may play a role in POTS. We will present additional
yet to be published data supportive of this concept of an important role for autoantibodies
in several manifestations of POTS. We will also discuss the potential mechanisms by
which these adrenergic autoantibodies could create a POTS phenotype, and their potential
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