Salivary immunoreactive human epidermal growth factor (IR-hEGF) in patients with peptic ulcer disease

EGF is reported to have a potent protective effect on peptic ulcer formation in rats. In this study, we measured the IR-hEGF concentrations in the saliva of normal human subjects and patients with peptic ulcer disease or non-peptic ulcer gastroduodenal disease. In normal subjects, the level of salivary IR-hEGF was highest in the early morning, and the values in individuals on different days showed small variations. There were no sex differences or age-related changes in the salivary IR-hEGF levels. The concentrations of the peptide were lower in patients in the active (0.96 +/- 26 ng/ml, mean +/- SE, n = 4) and healing stages (1.06 +/- 0.24 ng/ml, n = 8) of peptic ulcer disease as compared with those in normal subjects (3.19 +/- 0.46 ng/ml, n = 47). No significant differences in salivary IR-hEGF levels were observed between normal subjects and patients in the scaring stage of peptic ulcer disease (2.40 +/- 0.42 ng/ml, n = 21), or those with gastric cancer (2.44 +/- 0.27 ng/ml, n = 21) and atrophic or superficial gastritis (2.31 +/- 0.34 ng/ml, n = 28). Although the pathophysiological significance of these lower salivary IR-hEGF levels in patients with peptic ulcer disease is unclear, it is possible that the low level of hEGF in saliva may decrease the resistance of the mucosa to physicochemical stress, and thus participate in the development of the diseases.     

Salivary and gastric epidermal growth factor in patients with Zollinger-Ellison syndrome: its protective potential

OBJECTIVE: Evidence is accumulating that epidermal growth factor (EGF) is a major molecule contributing to the maintenance of the integrity of the upper alimentary tract mucosa before and after injury by acid and pepsin. Patients with Zollinger-Ellison Syndrome (ZES) typically have hypersecretion of acid and pepsin; however, the concentration and rate of secretion of salivary and gastric EGF that could counteract these potentially aggressive factors are unknown. Accordingly, this study was conducted to determine whether EGF affords mucosal protection in ZES patients. METHODS: The concentration and output of salivary (sEGF) and gastric epidermal growth factor (gEGF) were measured in eight patients with ZES and the results compared to those in 17 patients with nonulcer dyspepsia (NUD), serving as a control group. All patients had normal esophageal and gastric mucosa as determined by endoscopy. Total saliva was collected during 1-h parafilm- and 1-h pentagastrin/parafilm-stimulated conditions, as well as basal and pentagastrin-stimulated gastric juice. The concentration and output of EGF were determined by radioimmunoassay. RESULTS: The concentration of EGF in saliva collected from ZES patients after parafilm chewing was significantly higher compared to that in NUD patients (4.61 +/- 0.59 vs 2.75 +/- 0.50 ng/ml, p < 0.05). The concentration of EGF in saliva collected after pentagastrin stimulation in ZES patients was also significantly higher than in NUD patients (4.37 +/- 0.73 vs 2.22 +/- 0.37 ng/ml, p < 0.05). Salivary EGF output during parafilm chewing in ZES and NUD were similar (68 +/- 6.4 vs 109 +/- 25.2 ng/h). Salivary EGF output after administration of pentagastrin in ZES and NUD was also similar (66 +/- 6.1 vs 132 +/- 45.4 ng/h). Basal EGF output in the gastric juice of patients with ZES was 3-fold higher than in patients with NUD (801 +/- 73 vs 271 +/- 32 ng/h, p < 0.01). Pentagastrin-stimulated EGF output was similar in both groups (705 +/- 92 vs 675 +/- 168 ng/h). CONCLUSIONS: Patients with ZES have a significantly higher EGF concentration in saliva and EGF output in basal gastric juice. This elevated content of salivary and gastric EGF in ZES patients may play a protective role in preventing the development of reflux esophagitis and gastric ulcer under the impact of gastric acid and pepsin hypersecretion.     

Salivary Epidermal Growth Factor in Patients with and without Acid Peptic Disease

Epidermal growth factor inhibits gastric acid secretion and has a cytoprotective effect on the upper gastrointestinal tract. This study was undertaken to determine whether patients with endoscopically proven active peptic ulcer disease have a salivary deficiency of human epidermal growth factor (hEGF), compared to patients with a normal esophagogastroduodenoscopy (EGD). Saliva was collected from fasting subjects prior to EGD. The levels of EGF were measured by radioimmunoassay. Statistical evaluation was performed by analysis of variant followed by Student's t test. The concentrations of the peptide were lower in patients with active peptic ulcer disease (3.1 +/- 0.54 ng/ml, mean +/- SE, n = 25) compared with normal subjects (4.9 +/- 0.56 ng/ml, n = 58, p less than 0.03). No significant differences in salivary hEGF were noted between patients with a normal EGD and patients with gastritis (3.85 +/- .86 ng/ml, n = 13), esophagitis (4.5 +/- 1.3 ng/ml, n = 7), or Barrett's esophagus (5.3 +/- 1.5 ng/ml, n = 6). There were no differences in the salivary levels of hEGF between males and females, or between smokers and nonsmokers. There was no correlation of hEGF levels with age. The pathophysiologic significance of this finding is uncertain. Lower salivary hEGF may reduce one of the defensive mechanisms responsible for protecting the gastroduodenal mucosa from injury by physicochemical agents, thus contributing to ulcer development.     

Gastric cyto-secretory correlations in peptic ulcer.

BACKGROUND/AIMS: Maximal acid output, parietal cell mass, serum pepsinogen A (PGA) and total peptic activity (TPA) in gastric juice were studied and compared in duodenal ulcer and in different gastric ulcer sites. METHODOLOGY: 152 peptic ulcer patients were studied. 64 cases of gastric ulcer (GU) were subdivided according to Johnsons's classification and compared with 88 duodenal ulcer (DU) patients diagnosed for the first time. 40 normal subjects were studied as controls. RESULTS: Duodenal ulcer is characterized by normo-hyperparietalism, normo-hyperchloridria and an increase in peptic activity. In cases of GU, such correlation is not only conditioned by the topographic seat of the ulcer, but by the histological condition of the gastric mucosa too. Body GU is characterized by hypoparietalism, hypochloridria, hyper-PGA and hyper-TPA. Pre-pyloric GU is characterized by normo-hyperparietalism, normo-hyperchloridria, hyper-PGA and hyper-TPA. In GU the cyto-secretory behavior is characterized by the histology of the body mucosa with prevalence of preatrophic-atrophic gastritis in case of body GU and prevalence of superficial gastritis in case of GU type II and III. CONCLUSIONS: The results confirm the anatomic-functional analogy between DU and type II and III GU. If considered from the functional point of view, these conditions differ considerably from those that are characteristic of type I GU (as they closely follow the chronic gastritis pattern).     

The effect of vagotomy and antrectomy on serum pepsinogens I and II

Ninety-seven consecutive patients with gastric surgery for peptic ulcer were studied; 86 had duodenal ulcer (DU), and 11 gastric ulcer (GU). DU patients were surgically treated by proximal vagotomy, proximal vagotomy and pyloroplasty, truncal vagotomy and pyloroplasty, or truncal vagotomy and antrectomy. All GU patients were operated on by the Billroth I method. Serum pepsinogen I(S-PG I), serum pepsinogen II (S-PG II), basal acid output (BAO), and maximal acid output (MAO) were determined before and 3 months and 1 year after the operation. The mean preoperative S-PG I concentration in DU patients (154 +/- 7 micrograms/l; mean +/- SE) was significantly higher than that (97 +/- 9 micrograms/l) in GU patients (p less than 0.001). A significant decrease in the mean S-PG I concentration in DU patients was seen 3 months (92 +/- 6 micrograms/l) and 1 year (66 +/- 4 micrograms/l) after the operation (p less than 0.001). This change did not depend on the type of vagotomy. However, this decrease was not seen in all individual patients as it was in BAO values. Moreover, the mean BAO decrease was much greater at 3 months (7% of the preoperative value) and 1 year (23%) after the operation than the respective decrease in S-PG I concentration. There was also no correlation between S-PG I and acid output (BAO and MAO) before and after the operation. In GU patients the decrease in mean S-PG I value after the Billroth I operation was smaller than in DU patients after vagotomy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epidermal Growth Factor in Gastric Ulcer Healing by Nocloprost,a Stable Prostaglandin E2 Derivative

Background: The gastroprotective and ulcer-healing properties of prostaglandins, especially in gastric ulcers induced by non-steroidal anti-inflammatory drugs, are well established. Ulcer healing is an active process of filling the mucosal defect with migrating and proliferating epithelial cells combined with angiogenesis in granulation tissue at the ulcer bed. Growth factors, especially epidermal growth factor (EGF) and transforming growth factor alpha (TGFa) are crucial in the regulation of the reconstruction of damaged mucosal structures. Methods: In this double-blind, randomized, prospective study 40 patients with gastric ulcer were treated with nocloprost, a stable prostaglandin E₂ derivative, or with ranitidine. All subjects underwent endoscopy before and after 4 and 8 weeks of anti-ulcer therapy. During endoscopy mucosal biopsies were performed for determination of EGF content in gastric mucosa at the ulcer margin and in the intact mucosa. Additionally, EGF output in saliva and its plasma concentrations were determined in all subjects before and during the treatment. Results: The gastric ulcer healing rate after 4 weeks was significantly higher in patients treated with nocloprost than in those treated with ranitidine (63% versus 39%, respectively). At initial examination the EGF content in the gastric mucosa obtained from the ulcer edge was significantly higher than that in the intact mucosa. There was a significant increase in the EGF content in both the ulcer margin and the intact mucosa in subjects treated with nocloprost but not in patients under treatment with ranitidine. Similarly, patients treated with nocloprost had significantly higher EGF output in saliva and higher EGF concentration in plasma throughout the anti-ulcer therapy. Conclusion: Nocloprost is superior to ranitidine in the treatment of chronic gastric ulcers, and these effects could be due, at least in part, to higher expression and mucosal content of EGF in the ulcer area.     

Gastric juice immunoreactive epidermal growth factor levels in patients with peptic ulcer disease

Immunoreactive epidermal growth factor (IR-EGF) was measured by a highly sensitive and specific radioimmunoassay in gastric juice samples obtained during endoscopy from 26 control subjects, 44 patients with duodenal ulcers, and 18 with benign gastric ulcers. In the active stage, the concentrations of the peptide were consistently reduced, compared with those found in control subjects (592.7 +/- 55.8 pg/ml), in both duodenal (262.6 +/- 21.4 pg/ml) and gastric ulcer patients (320.2 +/- 34.1 pg/ml) (p less than 0.001 and 0.01, respectively). Mean IR-EGF values distinctly lower than in the controls were still present in the gastric juice of patients with inactive duodenal ulcers (349.7 +/- 35.9 pg/ml; p less than 0.001), whereas no difference was observed in patients with healed gastric ulcers (502.2 +/- 132.3 pg/ml). Although these findings suggest a possible role for EGF deficiency in the pathogenesis of peptic ulcer disease, the pathophysiological significance of our results (if any) remains to be elucidated.     

Mucosal expression and luminal release of epidermal and transforming growth factors in patients with duodenal ulcer before and after eradication of Helicobacter pylori.

BACKGROUND: Epidermal growth factor (EGF) and transforming growth factor-alpha (TGF alpha) are potent gastric acid inhibitors and stimuli of mucosal growth and protection but their involvement in Helicobacter pylori associated duodenal ulcer has been little examined. AIM: To assess gastric acid secretion, plasma gastrin concentrations, mucosal content of EGF and TGF alpha, and mucosal expression of these peptides and their receptor (EGFr) as well as salivary and gastric luminal release of EGF under basal conditions and after pentagastrin stimulation in 10 healthy subjects and in 25 H pylori positive patients with duodenal ulcer before and after two weeks of triple anti-H pylori therapy and four weeks after the termination of this therapy. RESULTS: Pentagastrin stimulation caused a significant increase in salivary and gastric release of EGF both in healthy controls and patients with duodenal ulcers but in the patients, the eradication of H pylori resulted in several fold higher gastric luminal (but not salivary) EGF release than before the anti-H pylori therapy. Mucosal contents of immunoreactive EGF and TGF alpha and mucosal expression of EGF, TGF alpha, and EGFr in H pylori positive patients with duodenal ulcer were significantly higher than those in healthy H pylori negative controls and this increase persisted after eradication of H pylori. Basal plasma gastrin was significantly reduced after two weeks of triple therapy and four weeks after the H pylori eradication all ulcers were completely healed. CONCLUSIONS: (1) H pylori infection in patients with duodenal ulcer was accompanied by enhanced plasma gastrin and increased mucosal content and expression of TGF alpha, EGF, and EGFr; (2) H pylori eradication resulted in ulcer healing, reduction in plasma gastrin, and enhancement of gastric (but not salivary) luminal release of EGF, particularly after pentagastrin stimulation; and (3) enhanced mucosal content and expression of TGF alpha, EGF, and EGFr and increased luminal release of EGF may contribute to ulcer healing after eradication of H pylori.     

Upregulation of mucosal soluble fas ligand and interferon-gamma may be involved in ulcerogenesis in patients with Helicobacter pylori-positive gastric ulcer

BACKGROUND: Excessive upregulation of gastric epithelial cell apoptosis is speculated to be associated with ulcerogenesis in Helicobacter pylori-positive peptic ulcer disease. H. pylori may have an ulcerogenic effect through induction of gastric epithelial cell apoptosis mediated by infiltrating T cells and their soluble products. METHODS: The contents of soluble Fas ligand (sFasL) and interferon-gamma (IFN-gamma) in organ cultures and the degree of apoptosis and the expression of apoptosis-related proteins in the gastric epithelium were examined using the mucosal tissues obtained from the antrum and the ulcer site in patients with H. pylori-positive gastric ulcer (GU). The molecular mechanisms of gastric epithelial cell apoptosis induced by sFasL and IFN-gamma were analyzed using epithelial cell lines, MKN 45 and KATO III. RESULTS: The mucosal tissues of the ulcer site had substantially higher contents of sFasL and IFN-gamma in organ cultures regardless of its healing stage in association with increased numbers of apoptotic cells and enhanced expression of proapoptotic proteins Bak and Bax in the surface foveolar epithelium as compared with the antral tissues in patients with H. pylori-positive GU. The addition of sFasL caused increases in cytotoxic cell death and caspase-3 activation in MKN 45 and KATO III cells in which IFN-gamma treated cells had more prominent effects than untreated cells. The expression of Bak in MKN 45 cells increased when they were treated with IFN-gamma. CONCLUSIONS: Upregulation of mucosal sFasL and IFN-gamma may be involved in ulcerogenesis in patients with H. pylori-positive GU through induction of gastric epithelial cell apoptosis.     

MMP-9、TIMP-1在胃溃疡组织中的表达及与组织学的关系

目的研究基质金属蛋白酶-9(MMP-9)及其组织抑制物-1(TIMP-1)在胃溃疡组织的表达及其与组织学的相关性,探讨胃溃疡愈合的分子机制。方法 50例胃溃疡患者与20例正常对照者,经胃镜检查取胃溃疡部位及胃窦部位活检组织,并检测幽门螺杆菌感染,按悉尼标准进行组织学评价,进行组织培养并检测培养液上清MMP-9、TIMP-1浓度,分析MMP-9、TIMP-1与组织学的关系。结果 MMP-9、TIMP-1在胃溃疡部位[(51.6±20.3)mg/mL、(31.5±6.7)mg/mL]的表达高于对照组[(23.1±12.5)mg/mL、(16.2±5.3)mg/mL,P=0.001、P=0.000],且与组织学的活动性及炎症分级相关(P<0.05),而与萎缩、肠上皮化生分级等无相关性(P>0.05)。结论胃溃疡患者MMP-9、TIMP-1的表达增加,可能与胃溃疡的愈合有关。     

Epidermal growth factor in saliva and gastric juice: response to histamine.

Epidermal growth factor (EGF) was measured in saliva and in gastric juice under basal conditions and after histamine stimulation (0.04 mg kg-1h-1). Sixty subjects studied comprised 20 normal volunteers, 20 patients with duodenal ulcer (DU), and 20 patients with non-ulcer dyspepsia (NUD). There was no difference in basal salivary EGF concentrations between control and DU or control and NUD subjects, but the EGF concentration in DU patients exceeded that in NUD patients (p < 0.05). Basal gastric juice concentrations of EGF were similar in all three groups. There was no difference between basal salivary and gastric EGF concentrations (p > > 0.05). After histamine stimulation, salivary and gastric EGF concentrations increased in all three groups: the increase was greater in gastric juice than saliva (p < 0.0001). There were no significant differences in the salivary EGF concentrations of controls and NUD patients, or controls and DU patients, but values were significantly higher when DU and NUD patients were compared (p = < 0.05). In the gastric juice, EGF increased more in DU patients than in controls or NUD patients (p < 0.05). This effect was not linked to the greater acid secretion in DU than in the other groups. There was no influence of gender or smoking on the EGF concentration. This evidence suggests that the stomach itself may be able to secrete large amounts of EGF and that histamine is a potent stimulus. It is more likely that the gastric EGF is responding to the presence of a duodenal ulcer than that lack of EGF is responsible for persistence of the ulcer.     

Carprofen and the therapy of gastroduodenal ulcerations by ranitidine

The effects of the addition of carprofen (Roche), a new nonsteroidal antiinflammatory agent, to regular 4-5 week ranitidine (300 mg/day) therapy on gastric secretion, serum gastrin level and ulcer healing, have been examined in 15 gastric ulcer (GU) and 60 duodenal ulcer (DU) patients. Carprofen at a therapeutic dose (300 mg/day) was well tolerated by both GU and DU patients and did not give rise to any major adverse effects. In an open trial on 15 GU (all receiving carprofen), complete endoscopic ulcer healing was found in 9 patients after 3 weeks and in 6 others after 5 weeks of treatment. In a double blind, placebo controlled trial on 60 DU (30 receiving carprofen and 30 receiving placebo), complete ulcer healing was seen after 2 weeks in 23 on carprofen and 22 on placebo, and after 4 weeks in all tested patients. Pentagastrin-induced maximal acid secretion examined 24 h after the last dose of treatment was significantly reduced in DU, but not in GU, patients, and was accompanied by a significant rise in plasma gastrin levels. No change in gastric histology was observed in any patient tested. This study provides evidence that carprofen added to antiulcer ranitidine therapy shows excellent gastrointestinal tolerance, and does not interfere with ulcer healing; it is, therefore, recommended in the treatment of arthritic patients with peptic ulcer disease.     

Mucosal in Vitro Permeability in the Intestinal Tract of the Pig,the Rat,and Man: Species- and Region-Related Differences

Background: Excessive upregulation of gastric epithelial cell apoptosis is speculated to be associated with ulcerogenesis in Helicobacter pylori -positive peptic ulcer disease. H. pylori may have an ulcerogenic effect through induction of gastric epithelial cell apoptosis mediated by infiltrating T cells and their soluble products. Methods: The contents of soluble Fas ligand (sFasL) and interferon- &;#110 (IFN- &;#110 ) in organ cultures and the degree of apoptosis and the expression of apoptosis-related proteins in the gastric epithelium were examined using the mucosal tissues obtained from the antrum and the ulcer site in patients with H. pylori -positive gastric ulcer (GU). The molecular mechanisms of gastric epithelial cell apoptosis induced by sFasL and IFN- &;#110 were analyzed using epithelial cell lines, MKN 45 and KATO III. Results: The mucosal tissues of the ulcer site had substantially higher contents of sFasL and IFN- &;#110 in organ cultures regardless of its healing stage in association with increased numbers of apoptotic cells and enhanced expression of proapoptotic proteins Bak and Bax in the surface foveolar epithelium as compared with the antral tissues in patients with H. pylori -positive GU. The addition of sFasL caused increases in cytotoxic cell death and caspase-3 activation in MKN 45 and KATO III cells in which IFN- &;#110 -treated cells had more prominent effects than untreated cells. The expression of Bak in MKN 45 cells increased when they were treated with IFN- &;#110. Conclusions: Upregulation of mucosal sFasL and IFN- &;#110 may be involved in ulcerogenesis in patients with H. pylori- positive GU through induction of gastric epithelial cell apoptosis.     

Circadian variation of prostaglandin E (PGE) production in human gastric juice

Prostaglandin E output in human gastric juice has been determined by radioimmunoassay and correlated with gastric acid secretion in 10 normal subjects and 10 patients with duodenal ulcer. PGE and acid outputs were higher in patients with peptic ulcer. Although not statistically significant these changes were probably secondary to changes in gastric juice volume. A circadian rhythm of gastric PGE production was observed in normal subjects with high output at midday, a spike at midnight, and low output in the early morning, in phase relationship to the circadian rhythm of gastric acid secretion. Disruption of PGE and acid rhythms was found in ulcer patients.Our study does not support the concept that prostaglandin deficiency may be an etiological factor in peptic ulcer disease. Nonetheless, a heretofore unrecognized disruption in gastric PGE rhythm may prove to be of physiologic significance.     

Release and action of epidermal growth factor on gastric secretion in humans

Epidermal growth factor (EGF) has recently been localized in salivary, pancreatic, and Brunner's glands in humans, but little is known about its release and its action on gastric secretion. This study, performed on healthy subjects, was designed to determine the release of immunoreactive EGF in plasma and in salivary and gastric secretions under basal conditions and after modified sham feeding (MSF), ordinary feeding, and infusion of pentagastrin without and with addition of exogenous recombinant human EGF (hEGF). Under basal conditions the EGF concentrations in plasma and salivary and gastric secretions were 52 +/- 8 pg/ml, 2.5 +/- 0.3 ng/ml, and 0.12 +/- 0.03 ng/ml, respectively. MSF and ordinary feeding increased significantly EGF plasma level and salivary output but not gastric EGF output, and atropinization failed to effect these plasma and salivary EGF responses to MSF. Intravenous infusion of pentagastrin increased both plasma and salivary but not gastric EGF, and addition of exogenous hEGF in graded doses (0.25-1.0 micrograms/kg) resulted in a dose-dependent increase in the plasma level of EGF and in significant inhibition of gastric acid and pepsin outputs. The increment in plasma EGF, which resulted in significant inhibition of gastric secretion, was several times greater than that observed after MSF or feeding. EGF infused in a constant dose (0.12 or 1.0 micrograms/kg-h) resulted in an increment in plasma EGF similar to that observed after MSF alone.     

Gastric emptying in deformed stomach

To evaluate the relationship between the onset of peptic ulcer and gastric emptying, some factors which were thought to regulate gastric emptying, i.e. the stage of the ulcer, the location of the ulcer and gastric acidity were studied in cases of gastric ulcer with deformed stomach and were proven to have little influence on gastric emptying. Further, the main cause of delayed gastric emptying was revealed to be the deformity itself, because the shortening of the distance from the gastric angle to the pyloric ring at the lesser curvature (sac-shaped stomach) and the indentation of the corpus ventriculi (hourglass-shaped stomach) significantly delayed gastric emptying. Moreover, it was found that the healing of gastric ulcer was delayed in cases of deformed stomach with delayed gastric emptying when the ulcer was at an active stage. Therefore the improvement of gastric emptying by some methods was thought to be necessary to promote ulcer healing and prevent ulcer recurrence in gastric ulcer patients who had a deformed stomach.     

消化性溃疡患者血中神经降压素水平及其在不同状态下的变化

本文对61例消化性溃疡患者空腹血浆神经降压素(Neurotensin,NT)水平作了测定,并就其在溃疡出血、幽门螺杆菌感染、奥美拉唑治疗后等多种状态下的进一步改变作了观察。结果表明溃疡患者NT水平显著低于正常(P<0.01),并发出血患者NT水平也明显低于正常(P<0.05),幽门螺杆菌感染、奥美拉唑治疗后血中NT水平未受显著影响(P>0.05)。     

Gastric epithelial cell turnover, mucus production, and healing of gastric ulcers with carbenoxolone.

Nineteen healthy subjects were studied and 17 patients with gastric ulcer before and after ulcer healing with carbenoxolone. Gastric deoxytibonucleic acid (DNA) loss was measured as an index of epithelial cell turnover, and N-acetylneuraminic acid (NANA) content of gastric juice as an index of mucus secretion. In normal subjects there was a negative correlation (p less that 0-025) between gastric DNA loss and NANA secretion; the lower the cell turnover the higher the NANA production. In gastric ulcer patients DNA loss or turnover was significantly (p less than 0-01) higher than normal, and fell significantly (p less than 0-01) after four weeks' treatment with carbenoxolone when 16 of the 17 ulcers had healed. At the same time NANA output increased significantly (p less than 0-01). It is suggested that patients with gastric ulcer lose cells at a high rate, a state of affairs which is returned towards normal by carbenoxolone, thus allowing the epithelial cells to mature within the mucosa and produce more mucus.     

Correlation of salivary and gastric acid secretions in duodenal ulcer patients in tropics

Salivary flow rates on mechanical stimulation by forced spitting method and by chemical stimulation with 10% citric acid and gastric acidity using an augmented histamine test were determined in 20 adult patients suffering from duodenal ulcer and in 20 adult control subjects matched with respect to age, sex, and body weight. Salivary flow rates were found to be much higher in response to chemical than to mechanical stimulus in both the groups. Duodenal ulcer patients exhibited an unexplained exaggerated response to chemical stimulation. Salivary pH, amylase, sodium, and potassium levels showed no significant differences between the two groups. The flow rates by either method generally showed a positive correlation with body weight in both the groups. Histamine stimulated gastric acid secretion was higher in duodenal ulcer patients than in controls. Acid secretion did not appear to be related to weight and also showed no consistent correlation with the salivary flow rates. It was concluded that (1) the salivary flow was dependent on body weight in duodenal ulcer patients as well as in controls, and (2) although salivary gland hyperplasia could be postulated in duodenal ulcer patients on the basis of increased salivary flow, the latter was poorly related to maximal acid secretion and therefore, if a combination of parietal cell and salivary gland hyperplasia did exist, it should be considered as incidental.     

维敏四联治疗Hp相关的消化性溃疡

目的应用维敏胶囊（胶态果胶铋）四联药物疗法治疗Hp相关的消化性溃疡（PU）2wk，停药4wk后经内镜、14C-UBT等方法观察溃疡的愈合及Hp根除的疗效方法经内镜确诊为PU，其中十二指肠溃疡（DU）169例；胃溃疡（GU）89例．受检前2wk内未服抗生素、铋剂及质子泵阻断剂，排除孕妇和溃疡出血者，并镜下活检病理排除恶性溃疡Hp检测：先行快速尿素酶检测（RUT），阳性者再行14C-UBT检测，其中DU的Hp阳性率为95．5％；GU的Hp阳性率为81．0％．四联治疗方法：对Hp阳性PU，给予维敏胶囊100mg，4次／d；兰索拉唑30mg，2次／d；阿莫西林0．5g，4次／d；甲硝唑0．4g，2次／d，疗程为2wk．停药后4wk，同时复查内镜及14G-UBT．结果DU愈合率91．2％，Hp根除率93．0％；GU愈合率86．0％，Hp根除率92．0％．DU和GU愈合率及Hp根除率差异不明显（P＞0．05）；四联疗法后肝肾功能无异常结论Hp与PU关系密切．采用四联治疗Hp相关的PU，有良好效果．14GUBT检测Hp感染具有很高的敏感性和特异性，无创伤性，是治疗后复查Hp的首选方法