Jian-Min Si1, Qian Cao, Min Gao. 1. Department of Gastroenterology of Sir Run Run Shaw Hospital, Zhejiang University, School of Medicine, Hangzhou 310016, Zhejiang Province, China.
Abstract
AIM: To investigate the growth hormone (GH) and growth hormone receptor (GHR) expression of and its clinical significance in patients with chronic atrophic gastritis (CAG). METHODS: A total of 90 cases were enrolled in the study. Thirty were healthy controls, the other 60 patients were divided into two groups according to the endoscopical and histological diagnosis. Blood samples were drawn in the morning (menarche did not occur during the blood extraction in female patients), gastric mucosa was obtained by endoscopy. Serum GH and gastrice mucosal GHR levels were measured using radioimmunoassay (RIA) and En Vinsion technique. RESULTS: The average GH level was 1.021+/-0.132 microg/L in CAG patients, in controls it was 2.869+/-0.512 microg/L. There was a significant difference between these two groups (P<0.01). The positive rate of GHR in CAG patients was 10%, in controls the rate was 100%. There was a significant difference (P<0.01). There was no significant change of GH level (3.176+/-0.421 microg/L) in patients with gastric carcinoma compared with controls (P>0.05). CONCLUSION: The study shows that levels of GH and GHR expression are low in CAG patients. CAG pathogenesis has a correlation with mucosal nutrient deficiency, decreased levels of GH and GHR have an adverse effect on the repair and regeneration of CAG. There is no significant change of GH in gastric carcinorma patients, GH dose not play a role in the pathogenesis of gastric cancer.
AIM: To investigate the growth hormone (GH) and growth hormone receptor (GHR) expression of and its clinical significance in patients with chronic atrophic gastritis (CAG). METHODS: A total of 90 cases were enrolled in the study. Thirty were healthy controls, the other 60 patients were divided into two groups according to the endoscopical and histological diagnosis. Blood samples were drawn in the morning (menarche did not occur during the blood extraction in female patients), gastric mucosa was obtained by endoscopy. Serum GH and gastrice mucosal GHR levels were measured using radioimmunoassay (RIA) and En Vinsion technique. RESULTS: The average GH level was 1.021+/-0.132 microg/L in CAG patients, in controls it was 2.869+/-0.512 microg/L. There was a significant difference between these two groups (P<0.01). The positive rate of GHR in CAG patients was 10%, in controls the rate was 100%. There was a significant difference (P<0.01). There was no significant change of GH level (3.176+/-0.421 microg/L) in patients with gastric carcinoma compared with controls (P>0.05). CONCLUSION: The study shows that levels of GH and GHR expression are low in CAG patients. CAG pathogenesis has a correlation with mucosal nutrient deficiency, decreased levels of GH and GHR have an adverse effect on the repair and regeneration of CAG. There is no significant change of GH in gastric carcinormapatients, GH dose not play a role in the pathogenesis of gastric cancer.
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