Ultrasound-guided intraperitoneal cisplatin after the maximum cytoreductive surgery of pseudomyxoma peritonei

In the past, pseudomyxoma peritonei was considered an incurable disease and often no active treatment was given. With the advent of cyto-reductive surgery, including peritonectomy procedures and intra peritoneal chemotherapy, long-term survival of these patients became actually possible. To study the impact of the intraperitoneal hyperthermic chemotherapy [cisplatin], when locally administered in patients who presented with pseudomyxoma peritonei and were treated by extensive cyto-reductive surgery. Nine patients with and. peritoneal adenomucinosis or carcinomatosis arising from the appendix who presented with a clinical picture of pseudomyxoma peritonei were diagnosed, and treated by cyto-reductive surgery followed by 6 cycles of ultrasound-guided intraperitoneal hyperthermic cisplatin. Following aggressive surgical approach and intraperitoneal chemotherapy, 7 patients had 1 year disease free survival, achieved independent activity in daily living and had an improved quality of life. The other 2 patients developed recurrences at 8 and 10 months following the completion of treatment. No major [grade III] texicities were observed. Pseudomyxoma peritonei is a treatable condition that may result in long-term disease free survival. Successful management can be achieved by combining cyto-reductive surgery and intraperitoneal hyperthermic chemotherapy

Cost-effectiveness of low-dose continuous infusion gemcitabine plus cisplatin versus standard dose gemcitabine plus cisplatin in stage III and IV non-small cell lung cancer

The purpose of this study was to assess the efficacy of low-dose continuous infusion gemcitabine 200 mg/m[2] once weekly on three consecutive out of 4 weeks for 6 cycles compared to the standard-dose gemcitabine 1000 mg/m[2] plus cisplatin in stage III and IV non-small cell lung cancer. Experimental Forty patients of non-small cell lung cancer with stage III and IV who are indicated for chemotherapy received low-dose continuous infusion gemcitabine 200 mg/m[2] plus cisplatin compared to forty patients of non-small cell lung cancer with stage III and IV who received the standard dose gemcitabine 1000 mg/m[2] plus cisplatin. The maximum duration of infusion of gemcitabine in combination with cisplatin was 24 hours with a dose of 200 mg / m[2] / day once weekly on three consecutive out of 4 weeks for 6 cycles. Cisplatin was given once every cycle with a dose of 100 mg/m[2]. This was compared to the standard-dose of gemcitabine 1000 mg/m[2] combined with cisplatin 100 mg/m[2] every 3 weeks for 6 weeks. Severe stomatitis, oesophagitis and myelosuppression were the worst common dose-limiting toxicities. Febrile neutropenia was observed in 8 out of the 40 patients who had received low-dose continuous infusion of gemcitabine as they developed bacteraemia. Occasional nausea, vomiting and diarrhea were also reported in both arms. There were 6 complete responses and 4 partial responses in the arm who received low-dose continuous infusion compared to 8 patients who had complete response and 4 patients with partial response in the standard dose arm. Low-dose continuous infusion gemcitabine for 24 hours with a dose of 200 mg/m[2]/day once weekly on three consecutive out of 4 weeks for 6 cycles gives results that are comparable to those of the standard-dose of gemcitabine but with a higher toxicity profile

Detection of helicobacter pylori DNA in liver tissue samples from patients with hepatocellular carcinoma

Helicobacter pylori [H. pylori] is the main cause of several gastro-duodenal diseases, and is also related to a variety of extragastric diseases, including liver diseases. It was classified as class I carcinogen. Several risk factors for the development of hepatocellular carcinoma [HCC] are identified. Continuing attempts are being made to identify other risk factors. The objective of this study was to evaluate the presence of H. pylori DNA in human HCC to determine if H. pylori may contribute to the development of this disease. Liver specimens from 33 patients with HCC as well as from 6 patients who did not have malignancy; 4 had cholelithiasis and 2 had hepatic hemangioma considered as control, were studied. Liver samples were examined by polymerase chain reaction [PCR] for the presence of genomic 16S rRNA of Helicobacter genus using specific primers. Besides, other genes; 26 kDa cell surface protein, cag A, and vac A, specific for H. pylori and mdh specific for E. coli were also screened by PCR. In addition, the specimens were examined for H. pylori by immunohistochemical procedure using anti-H. pylori antibody. Helicobacter genus-specific 16S rRNA was found in 12 out of the 33 [36.4%] samples of HCC tissues, whereas none of the 6 control liver specimens were found to harbor this rRNA. The H. pylori species-specific 26 kDa protein gene was detected in 11 of the 12 [91.7%] samples positive for the Helicobacter 16S rRNA gene thus confirming the presence of H. pylori DNA in 33.3% of the HCC samples. Within these 11 HCC samples, the cag A gene was detected in only 3, whereas the vac A and mdh genes were not detected. Helicobacter pylori immunostaining was recognized in 7 HCC specimens [21.2%], which were also positive for H. pylori species-specific DNA detection by PCR with statistically very high significant association [p = 0.0001]. The presence of microscopic evidence of hepatitis [10 cases] and cirrhosis [15 cases] presented a significant association with both H. pylori DNA detection [p = 0.0320 and 0.0260 respectively] and immunoreactivity [p = 0.0075 and 0.0158 respectively]. These data indicate that the detection of H. pylori by means of molecular methods and immunohistochemistry in human HCC tissue supports the concept of the possible association between H. pylori and HCC development. However, their eventual role in hepatocarcinogenesis, although it is plausible, remains to be proven