AIM:To investigate the growth hormone(GH)and growthhormone receptor(GHR)expression of and its clinicalsignificance 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 weredivided into two groups according to the endoscopical andhistological diagnosis.Blood samples were drawn in themorning(menarche did not occur during the bloodextraction in female patients),gastric mucosa was obtainedby endoscopy.Serum GH and gastrice mucosal GHR levelswere measured using radioimmunoassay(RIA)and EnVinsion technique.RESULTS:The average GH level was 1.021±0.132 μg/L inCAG patients,in controls it was 2.869±0.512 μg/L.Therewas a significant difference between these two groups(P<0.01).The positive rate of GHR in CAG patients was10%,in controls the rate was 100%.There was asignificant difference(P<0.01).There was no significantchange of GH level(3.176±0.421 μg/L)in patients withgastric carcinoma compared with controls(P>0.05).CONCLUSION:The study shows that levels of GH andGHR expression are low in CAG patients.CAG pathogenesishas a correlation with mucosal nutrient deficiency,decreased levels of GH and GHR have an adverse effect onthe repair and regeneration of CAG.There is no significantchange of GH in gastric carcinorma patients,GH dose notplay a role in the pathogenesis of gastric cancer. AIM: To investigate the growth hormone (GH) and growthhormone receptor (GHR) expression of and its clinical identification 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 weredivided into two groups according to the endoscopical andhistological diagnosis. Blood samples were drawn in themorning (menarche did not occur during the bloodextraction in female patients), gastric mucosa was obtainedby endoscopy.Serum GH and gastrice mucosal GHR levelswere measured using radioimmunoassay ( RIA) and EnVinsion technique .RESULTS: The average GH level was 1.021 ± 0.132 μg / L inCAG patients, in controls it was 2.869 ± 0.512 μg / 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 no significant change of GH level (3.176 ± 0.421 μg / L) in patients with gastrictric carcinoma comp ared with controls (P> 0.05). CONCLUSION: The study shows that levels of GH and GHH expression are low in CAG patients. CAG pathogenesishas 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 notplay a role in the pathogenesis of gastric cancer.