Abstract
Autonomic neuropathy has been reported in autoimmune rheumatic diseases (ARD) including Sjögren’s syndrome, systemic sclerosis, rheumatoid arthritis, and systemic lupus erythematosus. However, the pathophysiological mechanism underlying autonomic dysfunction remains unknown to researchers. On the other hand, autoimmune autonomic ganglionopathy (AAG) is an acquired immune-mediated disorder, which causes dysautonomia that is mediated by autoantibodies against ganglionic acetylcholine receptors (gAChRs). The purpose of this review was to describe the characteristics of autonomic disturbance through previous case reports and the functional tests used in these studies and address the importance of anti-gAChR antibodies. We have established luciferase immunoprecipitation systems to detect antibodies against gAChR in the past and determined the prevalence of gAChR antibodies in various autoimmune diseases including AAG and rheumatic diseases. Autonomic dysfunction, which affects lower parasympathetic and higher sympathetic activity, is usually observed in ARD. The anti-gAChR antibodies may play a crucial role in autonomic dysfunction observed in ARD. Further studies are necessary to determine whether anti-gAChR antibody levels are correlated with the severity of autonomic dysfunction in ARD.
Highlights
Autonomic neuropathy has been reported in autoimmune rheumatic diseases including Sjögren’s syndrome (SS) [1,2], systemic sclerosis (SSc) [3], rheumatoid arthritis (RA) [4], and systemic lupus erythematosus (SLE) [5]
We performed a literature review of studies on autonomic dysfunction and determined that the prevalence of anti-ganglionic acetylcholine receptors (gAChRs) antibodies was significant in autoimmune rheumatic diseases (ARD)
Autonomic dysfunction, which is composed of parasympathetic underactivity and sympathetic overdrive is usually observed in ARD
Summary
Autonomic neuropathy has been reported in autoimmune rheumatic diseases including Sjögren’s syndrome (SS) [1,2], systemic sclerosis (SSc) [3], rheumatoid arthritis (RA) [4], and systemic lupus erythematosus (SLE) [5]. Several underlying mechanisms such as the immunological basis, which includes circulating autoantibodies, abnormalities of cellular immunity, vasculitis, and secondary amyloidosis have been proposed. The Mayo Clinic group was the first to report that autoantibodies targeting gAChRs detected in the sera of approximately 50% of patients with idiopathic autonomic neuropathy were proven to be pathogenic [7,11]. Article type included research article, short communication, case series, case reports, literature review published between 1983 and 2019
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