[A case of advanced gastric cancer successfully treated by combination therapy of S-1 and docetaxel].

A 70-year-old man with gastric cancer of Borrmann type 3, liver metastases and peritoneal dissemination was treated by combination therapy of S-1 and docetaxel (DOC). He received DOC intravenously at 40 mg/m(2) on day 1 and S-1 orally at 100 mg/body on day 1 to 14, repeated every 28 days. After 2 courses of treatment, a CT scan revealed improvement of the gastric wall thickness, the eminent decrease of the peritoneal fluid and the reduction of the liver metastasis. After 3 courses of treatment, the primary lesion was remarkably improved on endoscopic examination, and the tumor marker normalized after 4 courses of treatment. Toxicities included leukocytopenia (WHO grade 3), neutropenia ( grade 3), anorexia (grade 2), and nausea (grade 2). Outpatient chemotherapy was possible by reduction of dose (S-1 100--> 80 mg/body, DOC 40--> 32 mg/m2). The response was maintained on CT and endoscopic examination after 21 courses of treatment. A case of an advanced gastric cancer patient successfully treated by combination therapy of S-1 and DOC was reported.

[A case of advanced gastric cancer that responded to docetaxel with low-dose 5-FU and cisplatin combination chemotherapy after becoming chemoresistant to M-FLP].

We report a case of advanced gastric cancer that responded to docetaxel with low-dose 5-FU and cisplatin combination chemotherapy after becoming chemoresistant to M-FLP. A 52-year-old male was diagnosed with type 3 gastric cancer of angulus (poorly differentiated adenocarcinoma) with left neck, Virchow, mediastinal and abdominal lymph nodes metastases. The patient was treated with 5 courses of M-FLP (MTX + 5-FU + LV + CDDP), and the effect of this therapy was PR, but the tumor was chemoresistant to the sixth course of this therapy. After 7 courses of M-FLP, docetaxel (TXT) with low-dose FP (5-FU + CDDP) was administered to the patient as second-line chemotherapy. After 2 courses of TXT with low-dose FP, the gastric cancer and metastatic lymph nodes were remarkably reduced and the effect of this therapy was PR. The toxic events were anemia (grade 2) and leukopenia (grade 3), which were treated with G-CSF. CDDP and 5-FU based regimens are considered as the first-line chemotherapy for metastatic advanced gastric cancer in Japan; however, a second-line chemotherapy has not been established. As in this case, a TXT based regimen is effective and well tolerated therapy as a second-line chemotherapy for metastatic gastric cancer after prior exposure to CDDP and 5-FU.

[Helicobacter pylori infection in gastric remnant cancer after gastrectomy].

Patients who have undergone distal gastrectomy for peptic ulcer are at higher risk of developing gastric remnant cancer, and chronic bile reflux is believed to increase the risk of cancer in remnant stomach. In remnant stomach, carcinogenesis may be prevented by selecting the anastomosis method with a few reflux of intestinal juice including a bile acid. How Helicobacter pylori(H. pylori) infection participate in stomal gastritis and gastric remnant cancer, same as early gastric cancer in the intact stomach, is attended. H. pylori positive rate of remnant stomach is different by examination method and a report, but its rate is decreased every year after gastrectomy and in particular low in Billroth-II(B-II) anastomosis. B-II anastomosis is followed by a significantly lower rate than B-1. This may reflect the role of bile reflux because bile reflux interferes with colonization by H. pylori. Gastric cancer excision usual increase complicates gastric remnant stomach and H. pylori infection, but while H. pylori infection lasts after gastrectomy for gastric cancer, cell proliferation increase in remnant stomach. In remnant stomach after gastrectomy for gastric cancer, while H. pylori infection continues, H. pylori infection may cause remnant gastritis and a second cancer of remnant stomach. H. pylori infection and bile reflux seem to have a synergistic effect on cell proliferation in remnant stomach and may explain the increased risk of gastric remnant cancer. The cancer-causing dominant role might changed from H. pylori infection predominance to bile reflux every year after gastrectomy. Furthermore, a prophylactic effect to carcinogenesis by H. pylori eradication therapy is expected. Eradication of H. pylori after gastrectomy for gastric cancer has been recommended.

Bile duct involvement in a case of autoimmune pancreatitis successfully treated with an oral steroid.

In the case reported here, the characteristic features of AIP were evaluated by ultrasonography, computed tomography and endoscopic retrograde cholangiopancreatography, initially in the intrahepatic- and extrahepatic bile ducts, and later in the pancreas. In addition, histological examination revealed lymphocytic sclerosis around the intralobular bile ducts, as is reported in AIP, without chronic nonsuppurative destructive cholangitis or onion-skin-like appearance. Immunohistochemistry identified the infiltrating lymphocytes as T cells. Although hypergammaglobulinemia was observed with elevation of hepatobiliary and pancreatic enzymes, no other serological or physiological abnormalities suggestive of other systemic autoimmune diseases were detected. These findings progressed over a three-month period and were dramatically resolved within one month by steroid therapy. These observations support a novel clinical entity characterized by the presence of bile duct lesions similar to the pancreatic involvement seen in AIP that is distinct pathophysiologically, histologically, and therapeutically from the so-called autoimmune cholangitis or primary sclerosing cholangitis.

What is an appropriate indication for endoscopic papillary balloon dilation?

OBJECTIVE: There are a number of views on the indication for endoscopic papillary balloon dilation (EPBD) in the management of bile duct stones. In this study, we have evaluated the efficacy and safety of EPBD compared with endoscopic sphincterotomy (EST). DESIGN: Prospective randomized trial. SETTING: One university hospital and one general hospital. PARTICIPANTS AND MAIN OUTCOME MEASURES: One hundred and forty patients were randomly allocated to EPBD or EST. Outcomes and complications were observed for a median period of 30 months. RESULTS: Both treatment approaches finally achieved similar success rates and needed similar numbers of treatment sessions for patients with stones less than 10 mm in diameter. However, for patients with stones of 10 mm or more, EPBD required a significantly greater mean number of treatment sessions than EST (2.4 vs 1.6, P < 0.01). Early complications occurred in seven EPBD (four pancreatitis, two cholangitis and one basket impaction) and eight EST (three pancreatitis, two bleeding and three cholangitis) patients. Late complications occurred in four EPBD (three recurrent bile duct stones and one cholecystitis) and six EST (three recurrent stones and three cholecystitis) patients. CONCLUSIONS: EPBD has little risk of bleeding. The technique removed small bile duct stones just as easily as did EST. These two procedures had approximately the same risk of pancreatitis and incidence of recurrent bile duct stones. Therefore, both procedures appear to be appropriate treatments for small bile duct stones. Whether or not EPBD becomes an established treatment will depend on further long-term studies.

Gastric carcinoid tumors without autoimmune gastritis in Japan: a relationship with Helicobacter pylori infection.

In Japan, most cases of gastric carcinoid tumor (GCT) are unassociated with either autoimmune gastritis (AIG) showing type-A chronic atrophic gastritis (CAG-A) or Zollinger-Ellison syndrome (ZES). However, the pathogenesis of this tumor remains unknown. Recent studies have determined that Helicobacter pylori infection induces gastric carcinoid in Mongolian gerbils and that H. pylori lipopolysaccharide exerts a mitogenic effect on ECL cells. We examined five patients with histologically diagnosed GCT, 40 patients with H. pylori-positive gastric ulcer (Hp+GU), 24 patients with H. pylori-positive duodenal ulcer (Hp+DU), and 12 patients with AIG showing CAG-A topographically. We compared the prevalence of H. pylori infection, and the levels of gastrin and pepsinogen (PG) in the serum of patients with GCT with those of patients with Hp+GU, or Hp+DU, and AIG. We also investigated the histological characteristics of the tumor and the gastric corpus mucosa in the GCT patients. The levels of serum gastrin and PG I and II were measured using an RIA kit. In all five (100%) patients with GCT, H. pylori infection was present, without any evidence of AIG or ZES. The serum levels of gastrin in the GCT patients were higher than those in either Hp+GU or Hp+DU patients and lower than those in the AIG patients. In contrast, serum PG I levels and the PG I/II ratio were lower in the GCT group than in the Hp+GU or Hp+DU groups. Histologically, all GCTs were ECL cell tumors and peritumoral corporal mucosal atrophy was observed in four of the five patients with GCT. In conclusions, H. pylori infection and hypergastrinemia were found in the patients with GCT without AIG. This finding suggests that H. pylori infection may induce corporal mucosal atrophy and hypergastrinemia that can produce a GCT with time.