BACKGROUND: Our goal is to investigate the serum profile of neural autoantibodies in community-based patients with irritable bowel syndrome (IBS) or functional dyspepsia. The pathogenesis of functional gastrointestinal (GI) disorders, including IBS and dyspepsia, are unknown. Theories range from purely psychological to autoimmune alterations in GI tract neuromuscular function. METHODS: The study subjects, based in Olmsted County, MN, reported symptoms of functional dyspepsia or IBS (n = 69), or were asymptomatic controls (n = 64). Their coded sera were screened for antibodies targeting neuronal, glial, and muscle autoantigens. RESULTS: The prevalence of neural autoantibodies with functional GI disorders did not differ significantly from controls (17% vs. 13%; P = 0.43). In no case was a neuronal or glial nuclear autoantibody or enteric neuronal autoantibody identified. Neuronal cation channel antibodies were identified in 9% of cases (voltage-gated potassium channel [VGKC] in one dyspepsia case and one IBS case, ganglionic acetylcholine receptor [AChR] in four IBS cases) and in 6% of controls (ganglionic AChR in one, voltage-gated calcium channel [VGCC], N-type, in two and VGKC in one; P = 0.36). The frequency of glutamic acid decarboxylase-65 (GAD65) autoantibodies was similar in cases (10%) and controls (5%; P = 0.23). CONCLUSIONS: Our data do not support neural autoimmunity as the basis for most IBS or functional dyspepsia cases.
BACKGROUND: Our goal is to investigate the serum profile of neural autoantibodies in community-based patients with irritable bowel syndrome (IBS) or functional dyspepsia. The pathogenesis of functional gastrointestinal (GI) disorders, including IBS and dyspepsia, are unknown. Theories range from purely psychological to autoimmune alterations in GI tract neuromuscular function. METHODS: The study subjects, based in Olmsted County, MN, reported symptoms of functional dyspepsia or IBS (n = 69), or were asymptomatic controls (n = 64). Their coded sera were screened for antibodies targeting neuronal, glial, and muscle autoantigens. RESULTS: The prevalence of neural autoantibodies with functional GI disorders did not differ significantly from controls (17% vs. 13%; P = 0.43). In no case was a neuronal or glial nuclear autoantibody or enteric neuronal autoantibody identified. Neuronal cation channel antibodies were identified in 9% of cases (voltage-gated potassium channel [VGKC] in one dyspepsia case and one IBS case, ganglionic acetylcholine receptor [AChR] in four IBS cases) and in 6% of controls (ganglionic AChR in one, voltage-gated calcium channel [VGCC], N-type, in two and VGKC in one; P = 0.36). The frequency of glutamic acid decarboxylase-65 (GAD65) autoantibodies was similar in cases (10%) and controls (5%; P = 0.23). CONCLUSIONS: Our data do not support neural autoimmunity as the basis for most IBS or functional dyspepsia cases.
Authors: Sean J Pittock; Hiroaki Yoshikawa; J Eric Ahlskog; Stephen H Tisch; Eduardo E Benarroch; Thomas J Kryzer; Vanda A Lennon Journal: Mayo Clin Proc Date: 2006-09 Impact factor: 7.616
Authors: R Spiller; Q Aziz; F Creed; A Emmanuel; L Houghton; P Hungin; R Jones; D Kumar; G Rubin; N Trudgill; P Whorwell Journal: Gut Date: 2007-05-08 Impact factor: 23.059
Authors: John Michael S Sanchez; J Scott McNally; Melissa M Cortez; James Hemp; Laura A Pace; Stacey L Clardy Journal: Front Neurol Date: 2020-07-31 Impact factor: 4.003