H. pylori positivity and various pathological, endoscopic and clinical features correlated with each other.

OBJECTIVE: To investigate the relationship between dyspepsia symptom scores and endoscopic appearances, and histopathological findings and helicobacter pylori positivity in patients having dyspepsia symptom. METHODS: The study was conducted at the gastroenterology outpatient clinic of Adnan Menderes University, School of Medicine, Aydin, Turkey from April 2012 to July 2012 and comprised patients between 18-65 years of age who were admitted with dyspepsia. Glasgow dyspepsia severity scoring was done with questions posed orally to the patients. In histopathological evaluation of biopsy specimens according to Sydney criteria, chronic inflammation, activity, atrophy, intestinal metaplasia and helicobacter pylori parameters were used. Total number of eosinophils and number of mast cells were recorded. RESULTS: Of the 60 patients with dyspepsia, 38(63.3%) were female and 22(36.7%) were male. The degree of activation and severity of inflammation increased significantly with increasing helicobacter pylori positivity(r=0.459'p<0.0001; r=0.475'p<0.0001). A significant relationship was found between inflammation, activation and the number of mast cells (p<0.05).There was no relationship between helicobacter pylori intensity and the eosinophil count (r=0.171; p=0.093). There was also a statistically significant correlation between severity of inflammation and activation and the number of eosinophils (r=0.313;p=0.002;r=0.245;p=0.016). CONCLUSIONS: Mast cell density was seen to have a role in the inflammatory processes of helicobacter pylori infection.

Primary Amyloidosis with Gastric Involvement.

Amyloidosis can involve all the segments of the gastrointestinal system (GIS) from mouth to anal canal. We present a case of amyloidosis that is detected by gastric biopsy taken in esophagogas-troduodenoscopy (EGD) performed to investigate the etiology of weight loss, nausea and vomiting. It is worth emphasizing that random gastric biopsy is important in gastric evaluations. How to cite this article: Borazan S, Coskun A, Yavasoglu I, Yeniçerioglu Y, Meteoglu i, Yasa MH, Karaoglu AOÖ. Primary Amyloidosis with Gastric Involvement. Euroasian J Hepato-Gastroenterol 2014;4(2):107-109.

[The comparative evaluation of Enzyme Linked Immunosorbent Assay (ELISA), Indirect Hemagglutination Test (IHA) and Indirect Fluorescent Antibody Test (IFAT) in the diagnosis of cystic echinococcosis]. / Kistik Ekinokokkozis Tanisinda ELISA (Enzym Lynked Immunosorbent Assay), Indirekt Hemaglütinaston Testi (IHA) ve Indirekt Fluoresan Antikor Testi (IFAT)'nin Karsilastirmali Olarak Degerlendirilmesi.

The most frequently used methods for the diagnosis of cystic echinococcosis are ELISA, IHA and IFAT methods in routine laboratories. The aim of this study was to detect the optimum serological method which can be used routinely with the highest sensitivity and specificity. Forty CE cases with 40 controls, making a total of 80 patients, were included in the study. In 80 sera specimens, specific antibody response to metacestodes was investigated using ELISA, IHA and IFAT methods. The antibody response in CE cases was found to be 35 (87.5%), with ELISA, 33 (82.5%) with IFAT and 36 (90.0%) with IHA. The sensitivity-specificity of ELISA, IFAT, and IHA were 87.5%-100%, 82.5%-100% and 90.0%-97.5%, respectively. A cross reaction of a 1/160 titer was detected with the IHA method in one patient with taeniasis in the control group. In conclusion, using more than one serologic method seems to increase the sensitivity and specifity of the serologic diagnosis of CE.

Colchicine in experimental alkaline burns of the rat esophagus: an old drug, a new indication?

AIM: An experimental study was performed to investigate the efficacy of colchicine in the prevention of fibrosis in the alkaline burn of the esophagus in rats. METHOD: A standard esophageal alkaline burn was produced by the application of 37.5% NaOH for a period of 90 s to the distal esophagus followed by a water rinse. The experiments were conducted twice with two different dosages of colchicine. In the first experiment, colchicine 1 mg/kg (i.p.) was applied once, on the first day. Group A (n:8), the sham laparotomy group; group B (n:8), the untreated group (positive control group); Group C (n:16), where the standard esophageal burn was induced and colchicine applied at a dose of 1 mg/kg i.p. in 1 ml volume, and group D (n:14), where the rats did not have any operation, but were treated with colchicine (1 mg/kg, i.p.) as in group C. In the second experiment, colchicine was applied at repeated doses of 100 microg/kg (i.p.) on the first, 7th, 14th, and 21st days. Twenty-five rats were divided into groups. Group AA (n:8), the sham laparotomy group; group BB (n:9), the untreated group (positive control group); and group CC (n:8), where the standard esophageal burn was induced and colchicine was applied at repeated doses. All the rats were killed on the 28th day and evaluated for esophageal tissue hydroxyproline content and histopathologic damage score. RESULTS: Colchicine treatment at a dose of 1 mg/kg significantly reduced the quantity of hydroxyproline in the esophageal tissue in groups C and D compared with the positive control group B (P < 0.05). However, it is associated with a mortality rate of 60%. Colchicine at repeated doses of 100 microg/kg showed no significant effect in group CC compared to the untreated group BB and in the quantity tissue of hydroxyproline content (P > 0.05). CONCLUSION: At non-toxic doses, colchicine was not effective in the treatment of alkaline esophageal burn in rats. Colchicine-like molecules with less adverse effects or colchicine itself in titrated doses may be hopeful in preventing the development of fibrosis in the alkaline burns of the esophagus.

Trimetazidine reduces the degree of fibrosis in alkali burns of the esophagus.

PURPOSE: The aim of this study was to investigate the efficacy of trimetazidine (TMZ), an antioxidant agent, on the prevention of stricture development after esophageal caustic injuries in rat. METHODS: Thirty rats were divided into 3 equal groups. A standard esophageal caustic burn was produced by application of 37.5% NaOH for a period of 90 seconds followed by water rinse. Group A (sham) animals were uninjured. Group B rats were injured but untreated. Group C rats were injured and received TMZ (5 mg/kg/d) via intraperitoneal route. Efficacy of the treatment was assessed in 28 days by measuring stenosis index and histopathologic damage score and by determining tissue hydroxyproline content. RESULTS: The stenosis index in the TMZ-treated group was significantly lower than the untreated group, similarly in the sham laparotomy group (stenosis index: 0.34 +/- 0.10, 0.94 +/- 0.21, 0.38 +/- 0.05, respectively; P < .05). The hydroxyproline level (microgram per milligram of wet tissue) was significantly lower in the TMZ-treated group compared with untreated group, similarly in the sham laparotomy group (1.06 +/- 0.14, 1.33 +/- 0.08, 0.68 +/- 0.15 microg/mg wet tissue, respectively; P < .05). In the untreated group, histopathologic damage score was significantly higher than TMZ-treated group (P < .05). CONCLUSIONS: Trimetazidine reduces the degree of fibrosis and ameliorates histopathologic damage in experimental model of corrosive esophagitis in rats.

Ketotifen ameliorates development of fibrosis in alkali burns of the esophagus.

An experimental study was performed to investigate the efficacy of ketotifen, which is a mast cell stabilizer and histamine H(1)-receptor antagonist, on the prevention of stricture development after esophageal caustic injuries in the rat. Caustic esophageal burn was created by applying 37.5% NaOH to the distal esophagus. Forty rats were divided into four equal groups. Group A (sham) animals were uninjured. Group B rats were injured but untreated. Group C rats were injured and received ketotifen (1 mg/kg/day) via the oral route. Group D rats were injured and received ketotifen (1 mg/kg/day) via the intraperitoneal route. Efficacy of the treatment was assessed on day 28 by measuring the stenosis index and histopathologic damage score and biochemically by determining tissue hydroxyproline content. The stenosis index in group B (0.93+/-0.22) was significantly increased compared with group A (0.39+/-0.06, p <0.05), group C (0.42+/-0.09, p <0.05), and group D (0.35+/-0.07, p <0.05). The hydroxyproline level ( micro g/mg wet tissue) was significantly increased in group B (1.31+/-0.08, p <0.05) compared with group A (0.69+/-0.16, p <0.05), group C (1.06+/-0.16, p <0.05), and group D (0.95+/-0.12, p <0.05). In group B the histopathologic damage score was significantly higher than in groups C ( p<0.05) and D ( p<0.05). There was no significant difference between group C and group D in terms of all parameters evaluated. Treatment with ketotifen decreased tissue hydroxyproline levels, histological damage, and the stenosis index. We conclude that ketotifen has a preventive effect in the development of fibrosis in an experimental model of corrosive esophagitis in rats.

Effects of pentoxifylline on alcohol-induced gastric injury and acid secretion in rats.

We aimed to evaluate the protective effects of pentoxifylline on alcohol-induced gastric injury, its relation with nitric oxide and prostaglandin synthesis, as well as gastric acidity in rats. Acute gastric mucosal injury was induced by intragastric infusion of 2 ml 98% alcohol. Pentoxifylline was given at 100 mg/kg intraperitoneally. Indomethacin and N(G)-nitro-L arginine were used to inhibit prostaglandin and nitric oxide synthesis, respectively. Macroscopic and microscopic gastric injuries were evaluated. Gastric pH, tissue malondialdehyde levels, oxidized and reduced glutathion (GSSG/GSH) levels, and effects of pentoxifylline on gastric acid output were measured. Pentoxifylline pretreatment significantly reduced macroscopic and microscopic gastric injury. Malondialdehyde level was lower in pentoxifylline treated rats (351.1 +/- 94.1 nmol/g vs 624.3 +/- 234.2 nmol/g). Pentoxifylline has a protective role on alcohol-induced gastric mucosal injury in rats. This effect is not related to synthesis of prostaglandins and changes in gastric acidity but does seem to be related to nitric oxide-mediated pathways. In contrast, pentoxifylline increases gastric acid output significantly.