Effects of chronic therapy with non-steroideal antinflammatory drugs on gastric permeability of sucrose: A study on 71 patients with rheumatoid arthritis

AIM: To evaluate the gastric permeability after both acute and chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) and to assess the clinical usefulness of sucrose test in detecting and following NSAIDs- induced gastric damage mainly in asymptomatic patients and the efficacy of a single pantoprazole dose in chronic users. METHODS: Seventy-one consecutive patients on chronic therapy with NSAIDs were enrolled in the study and divided into groups A and B (group A receiving 40 mg pantoprazole daily, group B only receiving NSAIDs). Sucrose test was performed at baseline and after 2, 4 and 12 wk, respectively. The symptoms in the upper gastrointestinal tract were recorded. RESULTS: The patients treated with pantoprazole had sucrose excretion under the limit during the entire follow-up period. The patients without gastroprotection had sucrose excretion above the limit after 2 wk, with an increasing trend in the following weeks (P = 0.000). A number of patients in this group revealed a significantly altered gastric permeability although they were asymptomatic during the follow-up period. CONCLUSION: Sucrose test can be proposed as a valid tool for the clinical evaluation of NSAIDs- induced gastric damage in both acute and chronic therapy. This tecnique helps to identify patients with clinically silent gastric damages. Pantoprazole (40 mg daily) is effective and well tolerated in chronic NSAID users.     

Studies on molluscicidal effect of mechanized spraying of sodium pentachlorophenate with large quantity of water against snails on marshland.

A new method using mechanized spray with large quantity of water against snails was studied inlaboratory and field.Results showed that the new method was effective in decreasing the survival andmultiplication of snails on marshland formed less than 10 years.About 95％ snails.both on surfaceand under earth were dead and 99％ offspring snail population was decreased after sodium pentachloro-     

Observation on the efficacy of hetrazan oil on cats infected with Brugia malayi.

Cats were inoculated with 50 infective larvae of Brugla malayi on volar surfaceof hind legs. 5% DEC (diethylcarbamazine) in mineral oil was smeared on the lefthind leg one and three weeks after infection.     

Clinical study on the treatment of 50 cases of cysticercosis with albendazole.

Albendazole, a new anti-helminthic drug, was given orally in a single dose withlevamisole to 50 cases of cysticercosis including 28 cases of cerebral form. The efficacy     

Effect of parenteral and enteral nutrition combined with octreotide on pancreatic exocrine secretion of patients with pancreatic fistula

AIM:To evaluate the effect of parenteral and enteralnutrition combined with octreotide on pancreatic exocrinesecretion of the patients with pancreatic fistula.METHODS:Pancreatic juice,drained directly from thepancreatic fistula,was collected,and the volume,protein,amylase,HCO_3~-,K~ ,Na~ and Cl~- were determined on d 1,4and 7 before and after 7-d treatment with octreotide,respectively.RESULTS:No differences in exocrine pancreatic secretionwere observed during the enteral and parenteral nutritionperiod (t=2.03,P>0.05);there were significant decreasesin pancreatic juice secretion volume,protein,amylase,HCO_3~-,K~ ,Na~ and Cl~- after parenteral and enteral nutritioncombined with octreotide compared with octreotidepretreatment (t=4.14,P<0.05).CONCLUSION:There is no stimulatory effect on thepancreatic secretion by intrajejunal nutrition and parenteralnutrition.Octreotide is effective on the reduction of pancreaticfistula output.     

Caution on the masqueraders of Good’s syndrome on thymoma with systemic lupus erythematosus

Clinical Rheumatology -     

Effects of depression on parameters of cell-mediated immunity in patients with digestive tract cancers

AIM:To evaluate the effects of depression on parametersof cell-mediated immunity in patients with cancers of thedigestive tract.METHODS:One hundred and eight adult patients of bothsexes with cancers of the digestive tract admitted betweenMarch 2001 and February 2002 in the Department of MedicalOncology,First Affiliated Hospital of Xi'an Jiaotong Universitywere randomly enrolled in the study.The Zung self-ratingdepression scale (SDS),Zung self-rating anxiety scale(SAS),numeric rating scale (NRS) and social support ratingscale (SSRS) were employed to evaluate the degree ofdepression and their contributing factors.In terms of theirSDS index scores,the patients were categorized intodepression group (SDS≥50) and non-depression group(SDS<50).Immunological parameters such as T-lymphocytesubsets and natural killer (NK) cell activities in peripheralblood were determined and compared between the twogroups of patients.RESULTS:The SDS index was from 33.8 to 66.2 in the 108cases,50% of these patients had a SDS index more than50.Similarly,the SAS index of all the patients ranged from35.0 to 62.0 and 46.3% of the cases had a SAS index above50.Cubic curve estimation showed that the depression waspositively correlated with anxiety and negatively with socialsupport.Furthermore,the depression correlated with thetumor type,which manifested in a descending order asstomach,gallbladder,pancreas,intestine,esophagus,duodenum and rectum,according to their correlativity.Step-wise regression analysis suggested that hyposexuality,dispiritment,agitation,palpitation,low CD_(56) and anxiety werethe significant factors contributing to depression.More severeanxiety (49.7±7.5 vs 45.3±6.9,P<0.05),pain (6.5±2.8 vs4.6±3.2,P<0.05),poor social support (6.8±2.0 vs 7.6±2.1,P<0.05),as well as decline of lymphocyte count (0.33±0.09vs 0.39±0.87,P<0.05) and CD_(56) (0.26±0.11 vs 0.29±0.11,P<0.05) were noted in the depression group compared withthose of the non-clepression patients.However,fewer obviouschanges in CD_4/CD_8 ratio and other immunological parameterswere found between the two groups. CONCLUSION:Depression occurs with a high incidence inpatients with cancers of the digestive tract,which probablyis not the sole factor leading to the impairment of immunologicalfunctions in these cases.However,comprehensive measuresincluding psychological support should be taken in order toimprove the immunological function,quality of life and clinicalprognosis of these patients.     

Effect of Prokinetics Combined with Proton Pump Inhibitors on Extraesophageal Symptoms of Reflux Esophagitis

The mechanism of Gastric esophageal reflux (GER) was studied in patients with duodenal ulcer (DU) by mean of esophageal manometry and gastric acid secretion test. Fifty-two patients with DU underwent esophageal manometry and gastric acid secretion test. Among them 18 with GER and 34 without GER. The results show all esophageal mamometry parameter in the patients with GER were significantly different from that of non-GER.     

Gastroduodenal and intestinal permeability in primary biliary cirrhosis

OBJECTIVES: To evaluate gastrointestinal permeability in primary biliary cirrhosis (PBC), using a sensitive method to detect epithelial damage, and to correlate it with the Mayo score, histological stage, ascites, spontaneous bacterial peritonitis, endoscopic signs of portal hypertension and Helicobacter pylori infection. METHODS: Fifty consecutive patients with PBC and 39 patients with cirrhosis of other aetiologies (non-PBC) were enrolled in the study. Coeliac disease was initially ruled out in all participants. Permeability was assessed using sucrose (gastro-duodenum) and lactulose-mannitol (intestine). RESULTS: Sucrose excretion was above the limit in both PBC and non-PBC patients. Twenty-two per cent of PBC patients had an increased result for the lactulose-mannitol test compared to 12.8% of non-PBC cirrhotic patients. PBC patients had high sucrose excretion levels irrespective of the presence of any oesophageal varices, which significantly increased the gastroduodenal permeability in non-PBC patients only when associated with hypertensive gastropathy. Sucrose excretion was significantly enhanced by hypertensive gastropathy in non-PBC patients (P < 0.001) but not in PBC patients. No significant correlation was found in either group between gastrointestinal permeability and the other parameters. CONCLUSIONS: Gastrointestinal permeability is increased in PBC. Portal hypertension contributes to altered gastric mucosal permeability in non-PBC cirrhosis, whereas different epithelial dysfunction can be hypothesized in PBC.     

Effect of acute cigarette smoking, alone or with alcohol, on gastric barrier function in healthy volunteers

BACKGROUND: Smoking is a risk factor for gastroduodenal ulcer and gastric adenocarcinoma. However, the pathophysiological mechanisms induced by acute cigarette smoking in the human gastric mucosa are poorly understood. AIM: To evaluate the effect of acute cigarette smoking, alone or with alcohol, on the gastric permeability to sucrose, a specific marker of mucosal damage in the stomach. SUBJECTS AND METHODS: Twenty healthy volunteers (8 smokers/12 non-smokers) were studied. Each fasted subject ingested 500 ml of a 20% sucrose solution and the amount of sucrose excreted in a 5-hour urine collection was measured by gas chromatography Four sucrose permeability tests were carried out: 1. basal, 2. while smoking 5 cigarettes, 3. after drinking 50 ml of a 40 degrees alcoholic beverage, 4. a combination of 2+3. RESULTS: Sucrose excretion increased after alcohol ingestion (40.5 +/- 6.0 mg vs 143.1 +/- 28.9 mg, p = 0.002), but was not modified by acute cigarette smoking (34.4 +/- 5.9 mg). When alcohol and cigarettes were simultaneously consumed, the increase in alcohol-induced sucrose excretion was significantly reduced (73.1 +/- 16.6 mg, p = 0.03). Basal sucrose excretion was similar in smokers and non-smokers. However, in acute cigarette smoking, a decrease in sucrose excretion was observed in smokers (p = 0.02) but not in non-smokers. CONCLUSIONS: These results indicate that acute cigarette smoking may tighten the gastric mucosa in habitual smokers and this is associated with a smaller increase of gastric permeability induced by alcohol.     

Atrophic gastritis is associated with increased sucrose permeability related to chronic inflammation

BACKGROUND: Different theories have been presented to explain how atrophic gastritis may lead to gastric cancer development. One contributing factor could be impaired function of the gastric mucosal barrier. The aim of this study was to investigate if there are changes in gastric mucosal permeability to sucrose in atrophic gastritis. METHODS: The study comprised 22 patients with atrophic gastritis and 21 normal controls. Gastritis was classified according to the Sydney system from endoscopic biopsies of the gastric corpus and antrum. All subjects were exposed to oral sucrose load (100 g), and the fraction of sucrose excreted in urine was measured by gas chromatography-mass spectrometry. RESULTS: The fraction of sucrose excreted in urine after oral load was significantly increased in atrophic gastritis compared with controls (median 0.08 vs. 0.04%; p = 0.003). Sucrose excretion was positively related to the degree of chronic inflammation (median fraction excreted: mild inflammation 0.06%, moderate inflammation 0.08%, severe inflammation 0.18%; p = 0.04) rather than to the degree of atrophy in the gastric mucosa. Occurrence of intestinal metaplasia was also associated with significantly higher sucrose excretion. However, in multivariate analysis, including intestinal metaplasia, only the degree of inflammation was positively related to sucrose excretion. CONCLUSION: Atrophic gastritis is associated with increased sucrose permeability, suggesting paracellular leakage of the gastric mucosa. This leakage seems to be related to the degree of inflammation rather than the degree of atrophy. The findings may have implications for the diseases and complications associated with atrophic gastritis.     

Effect of stomach motility on measuring stomach permeability with saccharose in vivo]

Determination of the urinary excretion of sucrose after an oral dose has been used as a noninvasive test to measure gastric permeability in several clinical studies. Regarding different contact times of sucrose solution within the gastric mucosa, the present study investigates a possible influence of the gastric emptying rate on the sucrose permeability test. Urinary sucrose excretion and the gastric emptying rate of liquids using 13C-acetate breath test were determined in twelve healthy volunteers. Furthermore, in seven volunteers gastric emptying was accelerated by intravenous erythromycin and prolongated by oral anticholinergic propantheline in nine healthy controls. Breath samples were measured using infrared spectroscopy. The half-emptying time and Lag-phase were correlated with the urinary sucrose excretion. Erythromycin caused a significant (p = 0.02) reduction of the half-emptying time (median 35.0 min) compared with untreated controls (median 59.9 min), whereas propantheline significantly increased the half-emptying time (median 69.4 min, p = 0.01). After pharmacological increase of the half-emptying time the urinary sucrose excretion only slightly differs from the sucrose excretion of controls (median [range] 0.057 [0.034-0.106]% versus 0.031 [0.017-0.162]%), but there was an increase of urinary sucrose excretion in probands following reduction of the half-emptying time with erythromycin (0.077 [0.023-0.221]%. The present study shows that gastric motility has a possible influence on the sucrose permeability test. The sucrose permeability has to be interpreted critically concerning its clinical use especially in patients with altered gastric motility.     

Effect of H. pylori status on gastric ulcer healing in patients continuing nonsteroidal anti-inflammatory therapy and receiving treatment with lansoprazole or ranitidine

OBJECTIVES: The purpose of this research was to determine the impact of pretreatment Helicobacter pylori infection on gastric ulcer healing rates in patients receiving nonsteroidal anti-inflammatory drugs (NSAIDs) and antisecretory medications. METHODS: This was a pooled, prospective analysis of two identical double blind, multicenter, parallel group studies. Six hundred ninety-two patients receiving NSAIDs and with endoscopy-documented gastric ulcers were enrolled from 90 North American sites in primary care and referral centers. Patients were randomized to receive ranitidine (150 mg b.i.d.) or lansoprazole (15 mg or 30 mg once daily) for 8 wk. Ulcer healing was assessed by endoscopy at 4 and 8 wk in an intent-to-treat population. H. pylori status was determined at baseline by histology. RESULTS: Across all three treatment groups, gastric ulcers were more likely to heal and heal faster if the individual was infected with H. pylori. Healing rates at 8 wk were statistically significantly greater among H. pylori positive patients (n = 181) than among negative patients (n = 497) (70% vs 61%, respectively; p < 0.05), especially among those with large ulcers (> 10 mm) and in younger patients (< 60 yr old). Simple healing rates (regardless of H. pylori status) were significantly better in the 15- and 30-mg lansoprazole groups than in the ranitidine group after 4 wk (46%, 54%, and 32%, respectively; p < or = 0.01) and 8 wk (66%, 74%, and 50%, respectively; p < 0.001). CONCLUSIONS: In patients receiving NSAIDs, gastric ulcer healing with an antisecretory agent is significantly enhanced in the presence of H. pylori infection.     

Prevalence of Helicobacter pylori in NSAID users with gastric ulcer

OBJECTIVE: Regarding the interaction of Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs), we cannot accept unanimous conclusions in inducing gastric ulcer. We therefore evaluated the role of Helicobacter pylori and NSAIDs in inducing gastric ulcer. METHODS: Dyspeptic patients receiving NSAIDs underwent endoscopic examination. Gastric ulcer formation and H. pylori status were investigated. Biopsy specimens from the antrum and lower body of the stomach were prepared for the rapid urease test and pathological evaluation. Anti-H. pylori antibody was measured by enzyme-linked immunosorbent assay. RESULTS: Two hundred and twenty-six patients receiving NSAIDs (220 chronic and six on-demand users) underwent gastrofibrescopic examination. There were 110 patients with gastric ulcer and 111 non-ulcer patients with gastritis. The remaining five patients had neither. NSAID users with gastric ulcer showed a low prevalence of H. pylori compared with those without them [55/110 (50.0%) vs 79/111 (71.2%), P < 0.01]. The same tendency was seen when patients receiving low-dose aspirin and those with rheumatoid arthritis were analysed separately [13/29 (44.8%) vs 50/62 (80.6%), P < 0.01, and 11/33 (33.3%) vs 16/26 (61.5%), P < 0.06 with Yates' correction, respectively]. CONCLUSION: Helicobacter pylori infection appeared to be a risk factor for developing gastritis, but we found no evidence that it increases gastric ulcer formation in NSAID users with dyspepsia.     

Efficacy of pantoprazole in the prevention of peptic ulcers, induced by non-steroidal anti-inflammatory drugs: a prospective, placebo-controlled, double-blind, parallel-group study

AIM: To evaluate the efficacy of pantoprazole in preventing gastrointestinal lesions in patients with rheumatic diseases receiving continuous, long-term treatment with non-steroidal anti-inflammatory drugs. MATERIAL: This was a prospective, randomised, double-blind, unbalanced, placebo-controlled, parallel group study. Outpatients (n= 104, age range 22-80 years, mean age 59.5) with rheumatoid arthritis or osteoarthritis, requiring chronic intake of NSAIDs (at least 8 weeks prior to the start of the study), were randomised and enrolled to receive either 40 mg pantoprazole (n=70) or placebo (n=34) once daily, for 12 weeks. Patients had endoscopically confirmed gastric and duodenal lesions grade 0, 1 or 2 (Lanza classification grade 0: normal to hyperaemic mucosa; grade 1: 1 to 3 erosions, submucosal haemorrhage or petechiae, grade 2: 4 to 10 erosions, submucosal haemorrhages or petechiae). Clinical and endoscopic evaluations were performed at baseline, after 4, and 12 weeks. The primary end-point of the study was the incidence of gastric or duodenal ulcers after 4 and 12 weeks of treatment. RESULTS: Patients (n=95) were evaluated: 65 in the pantoprazole group and 30 in the placebo group. When considering all patients (those with Lanza score grade 0, 1, 2 at baseline), the overall proportion of patients in remission was 82% and 77% after 4 weeks, and 72% and 59% after 12 weeks in pantoprazole and placebo groups, respectively (cumulative survival analysis according to Kaplan-Meier). The difference between the treatment groups was even more marked when only those patients with normal mucosa at baseline (grade 0) were considered. After 12 weeks, the proportion of patients in remission was 82% (95% confidence limits 70% - 94% in the pantoprazole and 55% (95% confidence limits 33% - 77%) in the placebo treatment group, p=O.036. Adverse events were reported in 4% and 6% of patients in pantoprazole and placebo treatment groups, respectively CONCLUSIONS: Pantoprazole 40 mg once daily was well tolerated and is more effective than placebo in the prevention of peptic ulcers in patients with rheumatic diseases who require continuous, long-term, treatment with NSAIDs.     

Gastric permeability to sucrose is increased in portal hypertensive gastropathy

BACKGROUND: Portal hypertensive gastropathy (PHG) is frequently found among patients with hepatic cirrhosis and at present the only way to detect and follow PHG is via endoscopy. OBJECTIVE: To assess gastric and intestinal permeability and investigate its relationship to endoscopic findings and indices of portal hypertension and hepatic function. DESIGN AND METHODS: Thirty-one non-diabetic patients with hepatic cirrhosis and PHG (PHG+) were studied and compared with 17 cirrhotic patients without PHG (PHG-). All patients underwent endoscopy for the assessment of PHG and Helicobacter pylori status, ultrasound determination of the diameters of spleen and portal vein, and, subsequently, an oral load of sucrose, lactulose, and mannitol. Sugar concentrations were determined in 6-h urine specimens and expressed as a percentage of the orally administered dose or as lactulose/mannitol ratio. RESULTS: The urinary sucrose excretion was significantly elevated in patients with PHG compared to those without (PHG+, 0.20% +/- 0.03; PHG-, 0.07% +/- 0.01; P< 0.001). No difference was found for the small intestinal probes lactulose and mannitol. Gastric sucrose permeability correlated positively with the endoscopic lesion score (P < 0.001), but not with other parameters of portal hypertension or hepatic function. H. pylori status did not influence gastric permeability. The sensitivity of this test reached 100% for PHG scores > 2. CONCLUSIONS: Gastric permeability to sucrose is increased in patients with PHG, independently of the presence of H. pylori. Sucrose permeability may be useful for the follow-up of patients with PHG.     

Sucrose permeability as a meas of detecting diseases of the upper digestive tract

The healthy gastric epithelium will not allow easy permeation of a disaccharide-sized molecule such as sucrose. However, during gastric damage, intact sucrose can pass the gastric epithelium and ultimately appear in the urine. We examined the relationship between total urinary sucrose excretion and various diseases. We used 149 patients (105 had upper gastrointestinal disease, 12 had gastric cancer and 32 were normal). Subjects were given a solution containing 100g sucrose in 450 c.c. water. All urine was collected for 7.5 h. The urinary sucrose concentration was determined by anion exchange high-performance liquid chromatography. Total urinary sucrose excretion was significantly higher in patients with gastric ulcer and those with gastric cancer than in endoscopically normal controls. In the 34 patients with gastric ulcer, the total sucrose excretion was closely correlated with ulcer size. Ulcer location did not affect urinary sucrose excretion. A strong correlation was also observed between sucrose excretion and lesion size in the 12 patients with gastric cancer. The sucrose permeability test may be a relatively sensitive method to detect gastric disease.