Endoscopic transgastric drainage of pancreatic pseudocyst with the use of Nd:YAG laser.

Pancreatic pseudocysts have been successfully managed with endoscopic drainage recently. This report describes a case of endoscopic transgastric drainage using endoscopic ultrasonography (EUS) and an Nd:YAG laser. EUS was used to detect an optimal puncture site of the pseudocyst and to reduce the risk of bleeding and perforation. An Nd:YAG laser was used to minimize the risk of bleeding and to penetrate the thick wall of the pseudocyst. After transgastric cystgastrostomy was performed, an internal stent was placed between the pseudocyst and the stomach. There were no complications associated with endoscopic interventions. Complete resolution of the pseudocyst was observed. Endoscopic transgastric drainage of pancreatic pseudocysts is a recommended approach for selected patients with pancreatic pseudocysts that are uncomplicated and are located adjacent to the stomach. Safe and effective drainage can be achieved without hemorrhage and perforation with the use of EUS, an Nd:YAG laser, and a stent. Furthermore, the Nd:YAG laser facilitated passage through a markedly indurated pseudocyst wall and it seemed to be an effective instrument, especially for pseudocysts with a thick wall.

Human papillomavirus is frequently detected in gefitinib-responsive lung adenocarcinomas.

A number of studies have reported the presence of human papillomavirus (HPV) in lung carcinoma. Interestingly, its detection rate appears to differ histologically and geographically. The present study examined 30 adenocarcinomas and 27 squamous cell carcinomas of the lung in a southern area of Japan, and detected high-risk HPV genome in 9 (30%) adenocarcinomas and 2 (7%) squamous cell carcinomas, using PCR with SPF10 primers and INNO-LiPA HPV genotyping assay. The difference of HPV detection rates in adenocarcinomas and squamous cell carcinomas was statistically significant (P=0.044, Fisher's exact test). HPV-16 was the most prevalent HPV genotype, and was detected in 27% (8/30) of adenocarcinomas and in 7% (2/27) of squamous cell carcinomas. High-risk-HPV positive carcinomas had decreased proportions of pRb (P=0.107) and significantly increased proportions of p16INK4a expressing cells (P=0.031) when compared to HPV-negative lung carcinomas. All HPV-16-positive cases were considered to have an integrated form of HPV-16 but its viral load was low (geometric mean = 0.02 copy per cell). In 20 additional adenocarcinomas treated with gefitinib, a tyrosine kinase inhibitor specific for epidermal growth factor receptor, the presence of HPV was examined. Note that East Asian ethnicity is a predictive factor of gefitinib response. High-risk HPV genome was found in 75% (6/8) of adenocarcinomas with complete or partial response to gefitinib but was not found in the remaining 12, which did not respond to gefitinib. In conclusion, the present study suggests that high-risk HPV may be more strongly related to adenocarcinomas, particularly gefitinib-responsive adenocarcinomas, when compared to squamous cell carcinomas. However, its low viral load makes it difficult to determine the etiological significance of these findings.