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Chromogranin A as a useful neuroendocrine marker in patients with autoimmune Addison’s disease

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Abstract

Background: Antiparietal cells antibodies (APC-Ab) are commonly found in patients with autoimmune Addison’s disease (AAD), usually pointing to autoimmune atrophic gastritis and pernicious anemia. The autoaggression to the gastric proton pump may result in a long-term hypergastrinemia, which predisposes to enterochromaffin-like cell hyper/dysplasia and gastric carcinoids. Aim: We evaluated the clinical utility of assessing serum chromogranin A levels in patients with AAD. Material and methods: Serum chromogranin A, gastrin, and gastric APC-Ab levels were determined in 40 patients with AAD using commercially available kits. Results: Serum chromogranin A and gastrin levels were found to be elevated in 27.5 and 22.5% of patients with AAD, respectively. The Addison’s patients with elevated APC-Ab had significantly higher chromogranin A and gastrin levels, as compared to individuals with normal APC-Ab (chromogranin A: 128.00±123.08 vs 57.68±36.50 ng/ml, p=0.0036; gastrin: 141.38±191.43 vs 49.50±75.36 ⧎U/ml, p=0.003). Additionally, the patients with AAD and coexisting elevated serum APC-Ab, contrary to those with normal levels, showed a significant correlation between the chromogranin A and gastrin concentrations (r=0.52, p=0.0092 vs r=0.211, p=0.43). Serum chromogranin A appeared also significantly correlated with APC-Ab levels (r=0.431, p=0.005). Conclusions: In patients with autoimmune Addison’s disease hyperchromograninemia and hypergastrinemia occur with a prevalence of 27.5 and 22.5%, respectively. Addison’s patients with coexisting elevated gastric APC-Ab, particularly with elevated gastrin levels, are at risk of enterochromaffin-like cells hyper/dysplasia. Serum chromogranin A assessment may complement histology for the early diagnosis of gastric carcinoid in these patients.

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Correspondence to Z. El Ali MD.

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El Ali, Z., Fichna, M., Piniewska, J. et al. Chromogranin A as a useful neuroendocrine marker in patients with autoimmune Addison’s disease. J Endocrinol Invest 33, 186–191 (2010). https://doi.org/10.1007/BF03346579

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