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 t...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 pg/L inCAG patients, in controls it was 2.869+_0.512 )~g/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 ~tg/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.展开更多
文摘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 pg/L inCAG patients, in controls it was 2.869+_0.512 )~g/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 ~tg/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.
