Reaction of human smooth muscle autoantibody with gastric parietal cells: a pitfall in the diagnosis of parietal cell autoantibody

Thirteen smooth muscle antibody (SMA) sera obtained from patients with active chronic hepatitis were examined for immunofluorescence reactivity with gastric mucosal cells. Eight out of 13 sera stained the cytoplasm of gastric parietal cells in a pattern indistinguishable from that obtained with parietal cell autoantibody (PCA). The staining reaction was localised to parietal cells by the demonstration that the same cells stained with both SMA and PCA in double immunofluorescent tests. The SMA staining intensity for parietal cells was weaker than that for smooth muscle. Specificity of the staining reaction for actin was established by the observation that parietal cell staining by SMA was inhibition by serum absorption with skeletal muscle F-actin but not by a microsomal fraction derived from gastric mucosa.Thirteen smooth muscle antibody (SMA) sera obtained from patients with active chronic hepatitis were examined for immunofluorescence reactivity with gastric mucosal cells. Eight out of 13 sera stained the cytoplasm of gastric parietal cells in a pattern indistinguishable from that obtained with parietal cell autoantibody (PCA). The staining reaction was localised to parietal cells by the demonstration that the same cells stained with both SMA and PCA in double immunofluorescent tests. The SMA staining intensity for parietal cells was weaker than that for smooth muscle. Specificity of the staining reaction for actin was established by the observation that parietal cell staining by SMA was inhibition by serum absorption with skeletal muscle F-actin but not by a microsomal fraction derived from gastric mucosa.