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- Original Article An Inhibitory Mechanism of Gastric Acid Secretion in Patients with Hyperthyroidism.
- Hyeok Yil Kwon, Hyoung Jin Park
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Endocrinology and Metabolism 1997;12(3):410-420
Published online: January 1, 2001
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Abstract
BACKGROUND
Although hypochlorhydria, hypergastrinemia and antiparietal cell antibody have been well documented in the patients with hyperthyroidism, a cause of hypochlorhydria or hypergastrinemia is unknown at the present time. Therefore, in order to clarify an inhibitory mechansim of gastric acid secretion in the patients with hyperthyroidism, interrelationship among hypochlorhydria, hypergastrinemia and antiparietal cell antibody was investigated in this study. METHODS: The gastric secretory function, fasting and postprandial plasma concentrations of gastrin and titer of antiparietal cell antibody in the plasma were determined in the patients with hyperthyroidism and normal subjects. Immunoblot analysis was performed to identify the gastric membrane protein, a possible gastric antigen to antiparietal cell antibody. Using a immunocytochemical technique with electron microscopy, intracellular structure of the parietal cell reacted with antiparietal cell antibody was observed. RESULTS: The basal and pentagastrin-stimulated maximal acid output were reduced in the patients with hyperthyroidism. The fasting and postprandial plasma concentrations of gastrin were markedly elevated in the patients. The plasma gastrin concentration in the patients with the antiparietal cell antibody was higher than that of the norrnal subjects as well as the patients without the antibody not only in the fasting state but also in the postprandial state. However, the plasma gastrin concentration of the patients without the antiparietal cell antibody was elevated in the fasting state only. There was no difference in the gastrin content of the antral mucosa between the norrnal subjects and the patients. The antiparietal cell antibody was detected in 5 (38.5 %) out of 13 patients by using the indirect immunofluorescence method. Patient IgG dose-dependently inhibited rabbit gastric H (+),K (+)-ATPase activity. Among proteins of the rabbit gastric mucosa membrane, four high molecular weight proteins (91, 140, 170 and 210 K dalton) were reacted to the patient IgG. The patient IgG positive peroxidase-antiperoxidase (PAP) activity was electron microscopically detected on the intracellular cannalicular membrane of the parietal cell CONCLUSION: We conclude that hypochlorhydria and hypergastrinemia in the patients with hyperthyroidism are partially related to the antiparietal cell antibody and that the antigen to the antiparietal cell antibody may be H (+),K (+)-ATPase in the intracellular canalicular membrane of the parietal cell.
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