Somatostatin And Chronic Atrophic Antral Gastritis

Background and aimsGastric carcinogenesis is a multi-procedral,multi-factorial and progressive course. Gastric precancerous change is chronic atrophic antral gastritis and dysplasia. These histological changes are always accompanied by intestinal metaplasia and different extent chronic inflammation.Somatostatin(SST) is a extensive bioactive gut homone produced by gastric antral mucosa. Recently, it has discovered that the level of seral SST in chronic atrophic antral gastritis patients is obviously reduced. However, the change of SST level in gastric antral mucosa and the ability of producing SST in gastric antral crypt have not been studied. It is worth to investigate whether the decrease of the level of SST is the result of or resulting in chronic atrophic antral gastritis.This research is to discuss:The change of SST in blood and gastric mucosa; the change of the ability of D cells in gastric antral crypt producing SST; the change of the level of SST in blood and gastric mucosa and histological change after suppling prolonged action lanreotide exogenously; if SST plays an important role in chronic atrophic antral gastritis development? MethodsGastric mucosa biopsy specimen and blood samples were collected to determine the level of SST via radioimmunoassay. Histological change between pretherapy and post-treatment was observed under light microscope as well as the change of ultramicrostrucuture under transimission electron microscope. Distribution of SST in gastric mucosa was studied by immunohistochemical staining and quantified.Results1. The quantities of gastric antral D cells of chronic atrophic antral gastritis decrease obviously. SST is mainly distributed in D cells of mucosa pyloric gland crypt. The nucleus of mucus epithelial cells in atrophic gastric antral crypt have SST negative staining.2. It could been seen in the intracytoplasm of mucus epitheliun cells of chronic atrophic gastric antral gastritis that Mitochodria swell, crista break, rough endoplasmic reticulum distend, mucus secretory granules decreasing, the nuclear membranes disappearing, chromatin integrating3. The average levels of SST in blood,epithelium+crypt and crypt in gastric antral atrophy were obviously reduced comparing to the control group, p<0.05, p<0.01. That of metaplasia atrophy also obviously decreseased in comparison to non-metaplasia atrophy. With the level of SST in blood <10pg/100μl, the prabability ratio of emerging atrophy is 67.7%.4. After use of prolonged action lanreotide, the level of SST in blood and pyloric gland crypt increase obviously comparing to pretherapy (p<0.05, p<0.01) . The ultramicrostructure of mucus epithelial cells exhibits great improvement . SST positive cells in pyloric gland obviously increased. As the level of SST in pyloric gland crypt increase greatly comparing to pretherapy, the rate of improvenment is 66.7% in inflammation, 33.3 % in atrophy, 55.5% in intestinal meteplasia. Two cases of dysplasia have all resolved after therapy. There was symptomatic improvenment with a rate of 77.8%.Conclusions1. The ability of pyloric gland D cell in producing SST decreases obviously in chronic atrophic antral gastritis patients.2. The seral levels of SST in chronic atrophic antral gastritis patients decrease obviously. At the seral level of SST <10pg/100μl, the probability ratio of emerging gastric mucousa atrophy is 67.7%. So investigating the levels of SST in blood is helpful to the clinical follow-up of these patients.3. Suppling SST analogue exogenously could lessen the inflammation of gastric mucus, could recover the function of gastric cryp D cells to produce SST, could improve the ultramicrostructure of mucus cells and partly reverse gastric atrophy in pyloric gland.