Background: The nature of the relationship between Helicobacter pylori and reflux oesophagitis is still not clear. To investigate the correlation between Helicobacter pylori infection and GERD taking into account endoscopic, pH-metric and histopathological data.
Ultrasonography or computed tomography are the most common methods used to establish the diagnosis of RSH, so it is no longer a diagnostic dilemma. Most patients can be treated conservatively and an operative treatment is justified only in case of haemodynamic instability. Our retrospective study could not identify any prognostic risk factor of haemodynamic instability in RSH. We believe that only a close observation of the patients with RSH and "common sense" can prevent a possible fatal outcome.
BackgroundThe nature of the relationship between Helicobacter pylori and reflux esophagitis (RE) is not fully understood. In addition, the effect of H. pylori eradication on RE and gastroesophageal reflux disease (GERD) is unclear. This study was designed to investigate the relationship between H. pylori infection and the grade of GERD in patients with reflux symptoms.MethodsBetween January 2010 and July 2013, 184 consecutive patients with daily reflux symptoms for at least one year were evaluated at the ambulatory for functional esophageal disease, Tor Vergata University Hospital, Rome, Italy. All patients underwent a pretreatment evaluation, which included anamnesis, clinical examination, Esophagogastroduodenoscopy (EGDS) with biopsy, esophageal manometry and 24-hour pH-metry. All statistical elaborations were obtained using Statigraphies 5 plus for Window XP.ResultsThere was no statistical difference regarding Lower Esophageal Sphincter (LES) pressure between patients who were H. pylori-positive and H. Pylori-negative (19.2 ± 9.5 (range: 3.7 to 46.2) and 19.7 ± 11.0 (range: 2.6 to 61), respectively). Further, no significant difference was evidenced in esophageal wave length (mean value: 3.1 seconds in H. pylori-negative patients versus 3.2 seconds in H. pylori-positive patients) or in esophageal wave height (mean value: 72.2 ± 39.3 in H. pylori-negative patients versus 67.7 ± 28.4 in H. pylori-positive patients). We observed that hiatal hernia (P = 0.01), LES opening (P = 0.05), esophageal wave length (P = 0.01) and pathological reflux number (P = 0.05) were significantly related to the presence of esophagitis. However, H. pylori infection was not significantly related to the presence of reflux esophagitis.ConclusionsOur clinical, endoscopic, manometric and pH-metric data shows no significant role of H. pylori infection in the development of GERD or in the pathogenesis of reflux esophagitis. However, current data do not provide sufficient evidence to define this relationship and further prospective large studies are needed.
Sulfatase 2 (Sulf-2) has been previously shown to be upregulated in breast cancer. Sulf-2 removes sulfate moieties on heparan sulfate proteoglycans which in turn modulate heparin binding growth factor signaling. Here we report that matrix detachment resulted in decreased Sulf-2 expression in breast cancer cells and increased cleavage of poly ADP-ribose polymerase. Silencing of Sulf-2 promotes matrix detachment induced cell death in MCF10DCIS cells. In an attempt to identify Sulf-2 specific inhibitor, we found that proteasomal inhibitors such as MG132, Lactacystin and Bortezomib treatment abolished Sulf-2 expression in multiple breast cancer cell lines. Additionally, we show that Bortezomib treatment of MCF10DCIS cell xenografts in mouse mammary fat pads significantly reduced tumor size, caused massive apoptosis and more importantly reduced Sulf-2 levels in vivo. Finally, our immunohistochemistry analysis of Sulf-2 expression in cohort of patient derived breast tumors indicates that Sulf-2 is significantly upregulated in autologous metastatic lesions compared to primary tumors (p < 0.037, Pearson correlation, Chi-Square analysis). In all, our data suggest that Sulf-2 might play an important role in breast cancer progression from ductal carcinoma in situ into an invasive ductal carcinoma potentially by resisting cell death.
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