G. Ciancio

Helicobacter pylori cag pathogenicity island is associated with enhanced interleukin-8 expression in human gastric mucosa.

BACKGROUND In vitro studies showed that Helicobacter pylori strains carrying the cag pathogenicity island are able to induce epithelial secretion of Interleukin-8. AIMS To evaluate the assessment of cag pathogenicity island and the expression of Interleukin-8 in the gastric mucosa of Helicobacter pylori-infected patients and correlate these data with the activity of gastritis and Helicobacter pylori density. METHODS cag status was determined by polymerase chain reaction directly on gastric biopsies from 13 Helicobacter pylori+ patients with non-ulcer dyspepsia and 13 Helicobacter pylori+ with duodenal ulcer. Interleukin-8 gene transcription and protein expression were analysed by in situ hybridization and immunofluorescence, respectively. Gastritis activity and Helicobacter pylori density were also investigated. RESULTS cag was present in 20/26 of Helicobacter pylori+ patients: in 7/13 non-ulcer dyspepsia (53.8%] and in 13/13 duodenal ulcer patients (100%), (p<0.05). Interleukin-8 mRNA and protein expression in epithelial and inflammatory cells was higher in cag+ than in cag- patients (p<0.005). Gastritis activity significantly correlated with cag (p<0.05) and Interleukin-8 expression (p<0.005]. Helicobacter pylori density was enhanced in cag+ [p<0.005] and correlated with Interleukin-8 expression (p<0.0051. CONCLUSIONS The present study demonstrates that in Helicobacter pylori-infected human gastric mucosa, cag+ infection is associated with enhanced Interleukin-8 expression, higher levels of active gastritis and bacterial density, and presence of duodenal ulcer.

Serologic Detection of CagA Positive Helicobacter pylori Infection in a Northern Italian Population: Its Association with Peptic Ulcer Disease

About 60–70% of Helicobacter pylori strains possess cagA (cytotoxin associated gene A) gene and express its product CagA, a highly immunogenic 128–140kD protein. Patients infected with CagA positive strains develop serum IgG anti‐CagA. A serologic response to CagA has been detected in Helicobacter pylori infected patients with peptic ulcer more frequently than in those with gastritis alone. It is unclear whether this finding is consistent in different geographical populations. We investigated the relationship between anti‐CagA seropositivity and peptic ulcer disease in a Northern Italian population.

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease

BACKGROUND It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS . Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS . The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.

Autonomic nerve dysfunction in pathologically obese patients

BACKGROUND Obese patients frequently present clinical symptoms related to gastrointestinal motility alterations and autonomic nervous system dysfunction. AIM To evaluate the possible correlation between cardiovascular autonomic nervous dysfunction and oesophageal motility in pathologically obese patients. PATIENTS AND METHODS Enrolled in the study were 22 patients with a body mass index of 45.72 +/- 7.48 and 10 control subjects, all within 20% of their ideal weight. Oesophageal motility was measured by stationary manometry and scintigraphic transit. Tests for the evaluation of autonomic nervous system were: Valsalva ratio, deep breathing, sustained handgrip, sudormotor axon reflex test and spectral analysis of the variability of R-R interval. RESULTS The mean pressure of oesophageal peristaltic waves in patients and controls was 39.36 +/- 14 mmHg and 73 +/- 12 mmHg, respectively The scintigraphic mean transit time was 22.96 +/- 16.26 seconds in patients and 10.23 +/- 16.26 seconds in controls (p < 0.001). Spectral analysis of the variability of the R-R interval showed an increase in the parasympathetic component both in the lying and standing position compared to controls. The other autonomic nervous system function tests showed no significant difference between obese patients and controls. CONCLUSIONS These results suggest that obese patients present a reduction of oesophageal transit and autonomic nervous system dysfunction albeit no direct correlation was found between these phenomena.

Esophageal motility in pathologically obese patients: A multidisciplinary approach

In the last fifty years the standard of living in the industrialized countries led to a remarkable increase of the incidence of obesity. It is well known in the literature that this pathologic condition is associated with alteration of gastric emptying and Autonomic Nervous System (ANS) dysfunction. AIM: evaluate esophageal motility and ANS function in pathologically obese patients. METHODS: from January to June 1997 we evaluated all the obese patients referred to our institution for baryatric surgery. Exclusion criteria were: diabetes, hypertension, cardiac arhythmia, syncope, peripheral neuropathies, current or recently therapy with steroids, beta-blockers, beta-agonists, psychotrope drugs, epilepsy and Raynaud phenomenon. We enrolled in our study 22 patients (3 M and 19 F, mean age 36, range 25-57 years, Body Mass Index 45.72 ± 7.48) and 22 age and sex matched controls. Esophageal motility was evaluated by stationary manometry, scintigraphyc transit with a Tc 99 m marked bolus. Cardiovascular tests for the evaluation of ANS were: Valsalva Ratio, Deep Breathing, Sustained Handgrip and spectral analysis of the variability of the R-R interval. RESULTS: Compared to controls 54.5% of patients showed a reduction of esophageal pressure values at manometry, 13.7% were borderline and 31.8% were normal. Scintigraphyc esophageal transit was pathologically slow in 63% of patients, borderline in 9% and normal in 27%. Tests for ANS were normal in all patients whereas the spectral analysis of the variability of R-R interval showed an increase of the parasympathetic component both in lying and standing position compared to controls. CONCLUSIONS: Our data show that in obese patients there is an alteration of esophageal motility and ANS function even if they may appear to be in contrast. In our opinion these results suggest that esophageal motility is not regulated only by dichotomic system but is the result of a more complex nervous integration.