ABSTRACT
Esophageal stent complications include stent migration, tumor ingrowth, perforation, a broncho-esophageal fistula, and gastroesophageal reflux. Development of a new stricture at a flange site after stent removal has been predicted but not yet reported. We experienced the first case of a recurrent esophageal stricture induced by a stent flange after stent removal. A fully covered metallic stent, which had been inserted 2 months ago for treatment of an anastomotic stricture, triggered another stricture at the flange site. Although endoscopic balloon dilatations were repeated several times and then the 2nd stent for rescue therapy was inserted, the stricture was refractory to all treatment. Thus, we prescribed oral prednisolone with repeated endoscopic balloon dilation; the stricture eventually improved. The oral steroid seemed to suppress stricture development. If a stent flange-induced refractory stricture is encountered, an oral steroid combined with endoscopic balloon dilation may be helpful.
ABSTRACT
Esophageal stent complications include stent migration, tumor ingrowth, perforation, a broncho-esophageal fistula, and gastroesophageal reflux. Development of a new stricture at a flange site after stent removal has been predicted but not yet reported. We experienced the first case of a recurrent esophageal stricture induced by a stent flange after stent removal. A fully covered metallic stent, which had been inserted 2 months ago for treatment of an anastomotic stricture, triggered another stricture at the flange site. Although endoscopic balloon dilatations were repeated several times and then the 2nd stent for rescue therapy was inserted, the stricture was refractory to all treatment. Thus, we prescribed oral prednisolone with repeated endoscopic balloon dilation; the stricture eventually improved. The oral steroid seemed to suppress stricture development. If a stent flange-induced refractory stricture is encountered, an oral steroid combined with endoscopic balloon dilation may be helpful.
ABSTRACT
Purpose@#Isoform 2 of tight junction protein claudin-18 (CLDN18.2) is a potential target for gastric cancer treatment. A treatment targeting CLDN18.2 has shown promising results in gastric cancer. We investigated the clinical significance of CLDN18.2 and other cell-adherens junction molecules (Rho GTPase-activating protein [RhoGAP] and E-cadherin) in metastatic diffuse-type gastric cancer (mDGC). @*Materials and Methods@#We evaluated CLDN18.2, RhoGAP, and E-cadherin expression using two-plex immunofluorescence and quantitative data analysis of H-scores of 77 consecutive mDGC patients who received first-line platinum-based chemotherapy between March 2015 and February 2017. @*Results@#CLDN18.2 and E-cadherin expression was significantly lower in patients with peritoneal metastasis (PM) than those without PM at the time of diagnosis (P=0.010 and 0.013, respectively), whereas it was significantly higher in patients who never developed PM from diagnosis to death than in those who did (P=0.001 and 0.003, respectively). Meanwhile, CLDN18.2 and E-cadherin expression levels were significantly higher in patients with bone metastasis than in those without bone metastasis (P=0.010 and 0.001, respectively).Moreover, we identified a positive correlation between the expression of CLDN18.2 and E-cadherin (P<0.001), RhoGAP and CLDN18.2 (P=0.004), and RhoGAP and E-cadherin (P=0.001). Conversely, CLDN18.2, RhoGAP, and E-cadherin expression was not associated with chemotherapy response and survival. @*Conclusions@#CLDN18.2 expression was reduced in patients with PM but significantly intactin those with bone metastasis. Furthermore, CLDN18.2 expression was positively correlated with other adherens junction molecules, which is clinically associated with mDGC and PM pathogenesis.
ABSTRACT
Purpose@#Isoform 2 of tight junction protein claudin-18 (CLDN18.2) is a potential target for gastric cancer treatment. A treatment targeting CLDN18.2 has shown promising results in gastric cancer. We investigated the clinical significance of CLDN18.2 and other cell-adherens junction molecules (Rho GTPase-activating protein [RhoGAP] and E-cadherin) in metastatic diffuse-type gastric cancer (mDGC). @*Materials and Methods@#We evaluated CLDN18.2, RhoGAP, and E-cadherin expression using two-plex immunofluorescence and quantitative data analysis of H-scores of 77 consecutive mDGC patients who received first-line platinum-based chemotherapy between March 2015 and February 2017. @*Results@#CLDN18.2 and E-cadherin expression was significantly lower in patients with peritoneal metastasis (PM) than those without PM at the time of diagnosis (P=0.010 and 0.013, respectively), whereas it was significantly higher in patients who never developed PM from diagnosis to death than in those who did (P=0.001 and 0.003, respectively). Meanwhile, CLDN18.2 and E-cadherin expression levels were significantly higher in patients with bone metastasis than in those without bone metastasis (P=0.010 and 0.001, respectively).Moreover, we identified a positive correlation between the expression of CLDN18.2 and E-cadherin (P<0.001), RhoGAP and CLDN18.2 (P=0.004), and RhoGAP and E-cadherin (P=0.001). Conversely, CLDN18.2, RhoGAP, and E-cadherin expression was not associated with chemotherapy response and survival. @*Conclusions@#CLDN18.2 expression was reduced in patients with PM but significantly intactin those with bone metastasis. Furthermore, CLDN18.2 expression was positively correlated with other adherens junction molecules, which is clinically associated with mDGC and PM pathogenesis.