S- Editor: Yang ZD L- Editor: Wang TQ E- Editor: Li RF
AIM: To study whether there is EGF secreting abnormality in duodenitis and its relationship with gastric acid output and serum gastrin, so as to further explore the pathogenesis of duodenitis.
METHODS: Twenty-five duodenitis patients were confirmed by electrogastroscopy and biopsy, with an average age of 35.9 ± 7.0 years (range, 24-52 years). The control group consisted of 20 healthy volunteers (10 females, 10 males), with an average age of 34.4 ± 7.6 years (range, 23-48 years). Twenty duodenal ulcer patients (10 females, 10 males), with an average age of 35.0 ± 7.6 years (range, 24-52 years), were also included. Serum EGF and gastrin were measured using radioimmunoassay. Intragastric acidity was determined by pentagastrin method. Statistical analysis was performed using Student’s t-test.
RESULTS: In comparison with those in the control group, the contents of serum EGF and serum gastrin in duodenitis patients were all significantly increased. In comparison with those in the duodenal ulcer group, serum EGF was significantly increased, basal acid output and peak acid output were decreased, and serum gastrin was increased significantly in duodenitis patients. Serum EGF was negatively correlated with gastric acid output and positively correlated with serum gastrin.
CONCLUSION: In duodenitis, serum EGF concentration was increased, which was positively correlated with serum gastrin content, but was negatively correlated with gastric acid output. This indicates that EGF plays a protective role in the pathogenesis of duodenitis, which provides a new clue to pathogenesis study of duodenitis.
Epidermal growth factor (EGF) is a polypeptide consisting of 53 amino acids, which was first isolated from the mouse submandibular gland by Cohen and was also found in human submandibular gland, Brunne′s gland of the duodenum, pancreas, breast gland, kidney, etc. EGF has the function of inhibiting gastric acid secretion and promoting the synthesis of mucosa DNA, RNA and protein. It has certain protective function on gastroduodenal mucosa against multiple stimulators[2,3]. Now, the pathogenesis of duodenitis is still unclear. The increase of gastric acid is a key factor. We assumed that in duodenitis, the increased secretion of EGF may enhance the defensive function of duodenal mucosa and inhibit hypersecretion of gastric acid.
A duodenitis group (DI group) consisted of 25 patients (13 males and 12 females) with an average age of 35.9 ± 7.0 years. Chronic superficial duodenitis was proven by endoscopic mucosa biopsy in accordance with the pathologic diagnostic criteria of the National Gastric Carcinoma Protection and Treatment Cooperation Group. A control group consisted of 10 males and 10 females; the average age was 34.4 ± 7.6 years (range, 23-48 years). A fuodenal ulcer group (DU group) consisted of 20 patients (10 males and 10 females), with an average age of 35.0 ± 7.6 years (range, 24-52 years), and all were at the active stage. Diseases of the liver, gallbladder, pancreas, kidney and thyroid gland were excluded. The patients had not any history of smoking and did not take any drug during thelast one week.
Five milliliters of venous blood sample were taken from each subject in the morning (fasting,with in 3 d after electrogastroscopic examination). After standing and centrifugation, serum was separated and 1 mL serum was stored at -70 °C for EGF detection while another 1 mL was stored at -20 °C for gastrin determination. Gastric acid output was determined by pentapeptide gastrin method. RIA kits were provided by Beijing Haikerui Biological Technique Center (for EGF) and Beijing Atomic Energy Institution (for gastrin). Pentapeptide gastrin was provided by Shanghai Biochemical Institution (950514).
All data are expressed as mean ± SD, and t-test was used to compare the differences between groups. Linear regressive analysis and relative coefficient test were used to study the relationship between variables.
In comparison with normal controls, serum EGF (P < 0.01), gastric acid output (P < 0.01), and serum gastrin (P < 0.01) in the duodenitis group were highly increased. In comparison with the duodenal ulcer group, serum EGF (P < 0.01) and serum gastrin (P < 0.01) were highly increased, too, while gastric acid output was decreased. In the duodenitis group, serum EGF was negatively correlated with gastric acid output (peak acid output: r = -0.716, P < 0.01; linear regressive equation, Y = 3.2269 - 0.07X), but was positively correlated with serum gastrin (r = 0.7434, P < 0.01; linear regressive equation, Y = 0.0297X - 1.3637). All data are shown in Table 1.
Etiology of duodenitis is not very clear. The inflammation may be due to the co-action of many factors, just like esophagitis and gastritis. Hypersecretion of gastric acid has long been thought of one of the most important factors. EGF has the function of inhibiting gastric acid secretion and promoting the synthesis of mucosa DNA, RNA and protein. And it has a certain protective function on gastroduodenal mucosa injured by multiple factors. EGF has a promoting effect on epithelial cell proliferation, and it can also promote regeneration of damaged duodenal epithelia. In this study, serum EGF in the DI group was significantly higher than that in the healthy control group and DU group, which suggested that the compensatory increase of EGF secretion was present in duodenitis. For gastric acid secretion, including basic acid output and peak acid output , it was in the order of healthy control group < DI group < DU group, which was the same as the viewpoint in Baron′s report. Serum EGF was negatively correlated with gastric acid secretion, which showed that EGF could inhibit gastric acid secretion, which was the suggestion by Korturek′s research. Animal experiments show that acidic substance in the duodenum may cause the release of VIP, which is an important neurotransmitter capable of regulating duodenal gland secretion. We deduce that the increase of gastric acid in duodenitis can cause the release of VIP, promoting the secretion of EGF by the duodenal gland (mainly referring to Brunner′s gland). This may be the reason for the increase of serum EGF, but the mechanism is unclear. The increase of EGF can protect the duodenal mucosa by stimulating alkaline secretion and mucosa formation in the duodenum, and can decrease gastric acid level[9,10]. Therefore, it plays a protective role in the pathogenesis of duodenitis.
In our study, serum gastrin level in the DI group was much higher than that in the control group, which is in agreement with Sun Su-Yun′s report. The mechanism may be the same as that of EGF, for VIP promotes the secretion of G cells in the Brunner′s gland. It was reported that gastrin can promote the EGF secretion, which is consistent with our result that serum gastrin was positively correlated with the EGF increase.
In general, the bottom of peptic ulcer can penetrate the submucosa layer, and may go deep into the muscular layer, even to the serosa layer. The submucosa layer, even the muscular layer, is completely eroded and replaced by granular tissues and scar tissues, so the Brunner′s gland in the duodenal submucosa layer can be injured. An animal study shows that semicystamine can induce duodenal ulcer by inhibiting the Brunne′s gland. Many animal experiments have shown that infusion of exogenic EGF to the stomach or duodenum could prevent experimental ulcer or promote the healing of ulcer, which indicates that endogenous EGF deficiency can decrease the defensive function of the mucosa against harmful factors. Furthermore it shows that EGF plays an important protective role for the duodenal mucosa.
S- Editor: Yang ZD L- Editor: Wang TQ E- Editor: Li RF
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