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Kazunari Murakami

Publications and source records attributed to Kazunari Murakami.

At least 19 recordsLinked to original sources
PubMed2007

[Successful CPT-11 treatment in a patient with pancreatic cancer associated with multiple liver metastases and chronic renal failure].

A 56-year-old woman, who had been receiving treatment for chronic renal failure, was admitted to our Department because of a tumor of the pancreas head and multiple liver masses diagnosed by abdominal CT scans. Gastroduodenoscopy revealed a tumor which had invaded the Vater's papilla; the lesion was histopathologically pancreatic adenocarcinoma. Due to the presence of multiple metastases to the liver, we therefore performed general chemotherapy after obtaining the patient's informed consent (IC). CPT-11 was selected as the carcinostatic agent because the patient suffered from renal failure. The initial dose of CPT-11 was 80 mg, and we thereafter made minor adjustments in the dosage depending on the occurrence of side effects. After four courses of the treatment, a CT scan revealed both the tumor of the pancreas head and the multiple liver masses to have almost completely disappeared. Our clinical results indicate that CPT-11 may therefore be a strong candidate for first-line chemotherapy for the treatment of pancreatic cancer, especially in patients with renal failure.

Adenocarcinoma↗
PubMed2006

Latest insights into the effects of Helicobacter pylori infection on gastric carcinogenesis.

There appears to be the strong association between Helicobacter pylori (H pylori) and gastric cancer. We reviewed the latest evidences about the effects of H pylori infection on gastric carcinogenesis, classified into epidemiology, dynamics of gastric mucosal changes, DNA damages, virulence factors, host factors, and source of gastric malignancy. Through the considerable progress made in research into virulence factors resulting from differences between H pylori strains, such as cagA positivity, as well as into host factors, such as gene polymorphisms, a diverse spectrum of H pylori-associated diseases, including gastric cancer, is beginning to lend itself to elucidation. The impact of the novel hypothesis advanced by Houghton et al proposing bone-marrow derived stem cells (BMDC) as a potential source of gastric malignancy on evolving research remains to be seen with interest. Further progress in research into H pylori eradication as a viable prophylaxis of gastric cancer, as well as into the mechanisms of gastric carcinogenesis, is to be eagerly awaited for the current year and beyond.

Anti-Bacterial Agents↗
PubMed2006

Helicobacter pylori isolated from patients who later failed H. pylori eradication triple therapy readily develop resistance to clarithromycin.

In this study, the ease of selection of clarithromycin resistance was investigated in clarithromycin-susceptible Helicobacter pylori strains isolated from patients with H. pylori infection prior to the administration of triple-combination eradication therapy (clarithromycin plus amoxicillin plus a proton pump inhibitor). Clarithromycin-susceptible strains isolated from ten patients in whom the eradication therapy was successful and from six patients in whom the eradication therapy was unsuccessful were exposed serially to subinhibitory concentrations of clarithromycin. The number of transfers required for the MICs of the strains to increase by 8- and 32-fold were 6.6 and 7.2, respectively, in the successful eradication group, and as few as 2.4 and 1.5, respectively, in the unsuccessful eradication group. The number of transfers required for the A2142G or A2143G point mutation of the 23S rRNA gene to be detected in the strains were 5 and 8, respectively, for the strains in the successful eradication group, and 1 and 2, respectively, for the strains in the unsuccessful eradication group. These results suggest that patients in the unsuccessful eradication group were infected with strains of H. pylori that readily became resistant to clarithromycin on exposure to the drug.

Amoxicillin↗
PubMed2006

Maintenance therapy with H2-receptor antagonist until assessment of Helicobacter pylori eradication can reduce recurrence of peptic ulcer after successful eradication of the organism: prospective randomized controlled trial.

PURPOSE: This study examined the possible relationship between peptic ulcer recurrence and the presence or absence of maintenance therapy with an H(2)-receptor antagonist performed until evaluation of Helicobacter pylori eradication. METHODS: The subjects were 483 patients with peptic ulcer (281 gastric ulcer and 202 duodenal ulcer) who were diagnosed as H. pylori positive. After receiving eradication therapy for H. pylori, patients were allocated at random to one of three different maintenance therapies: control group (no maintenance therapy), H(2)-receptor antagonist half-dose group, and H(2)-receptor antagonist full-dose group. The maintenance therapy was performed for 4 weeks until evaluation of H. pylori eradication. RESULTS: Among the 25 patients with a recurrent ulcer, 18 patients (72%) had a recurrence at the time of or before evaluation of H. pylori eradication. In the control group, the rate of ulcer recurrence occurring before evaluation of H. pylori eradication was 10.5% (14/133). This rate was significantly higher than those in the H(2)-receptor antagonist half-dose group (2.9%, 4/136) and the full-dose group (0%, 0/135). CONCLUSION: The results of this study suggest that maintenance therapy with an H(2)-receptor antagonist performed after eradication therapy until evaluation of H. pylori eradication is likely to greatly reduce the ulcer recurrence rate without affecting evaluation of H. pylori eradication.

Adult↗
PubMed2006

Effectiveness of minocycline-based triple therapy for eradication of Helicobacter pylori infection.

BACKGROUND: Widespread use of eradication therapy for Helicobacter pylori has increased the prevalence of clarithromycin-resistant strains. The purpose of the present paper was to measure the in vitro antibacterial activity of minocycline against H. pylori, and study the effectiveness of minocycline-based first- and second-line eradication therapies. METHODS: For first-line therapy, 79 patients were randomly assigned to the treatment with rabeprazole, amoxicillin, and clarithromycin or with rabeprazole, amoxicillin, and minocycline. For second-line therapy, 88 patients were tested for sensitivity to metronidazole: 67 patients with metronidazole-sensitive strains received a 7-day course of rabeprazole, minocycline, and metronidazole; the remaining 21 patients were given a 7-day course of rabeprazole, minocycline, and faropenem. RESULTS: There was virtually no resistance to minocycline among the strains tested. The eradication rate of H. pylori infection in first-line therapy was significantly lower for minocycline-containing regimen (38.5%, 15/39) than for clarithromycin-containing regimen (82.5%, 33/40; P < 0.01). For second-line therapy, a high eradication rate against metronidazole-sensitive strains was obtained with rabeprazole, minocycline and metronidazole (85%, 57/67). CONCLUSIONS: A combination of rabeprazole, minocycline, and metronidazole is safe and effective for second-line therapy of H. pylori infection. Because this regimen can be administered to patients with penicillin allergy and patients who suffer adverse reactions to amoxicillin, such as diarrhea and other digestive symptoms, it should be considered useful for second- and third-line eradication therapy.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2006

Comparison of amoxicillin-metronidazole plus famotidine or lansoprazole for amoxicillin-clarithromycin-proton pump inhibitor treatment failures for Helicobacter pylori infection.

BACKGROUND: Proton pump inhibitor-amoxicillin-metronidazole is recommended as second-line Helicobacter pylori therapy in Japan. The authors assessed the efficacy and safety of second-line eradication using the H2-receptor antagonist famotidine as a substitute for proton pump inhibitor. MATERIALS AND METHODS: Sixty-one patients who failed in first-line H. pylori eradication using proton pump inhibitor-clarithromycin-amoxicillin were randomly assigned to either second-line therapy including metronidazole: a 7-day course of lansoprazole 30 mg, amoxicillin 750 mg, and metronidazole 250 mg, b.i.d. (lansoprazole group); or a 7-day course of famotidine 40 mg, amoxicillin 750 mg, and metronidazole 250 mg, b.i.d. (famotidine group). Eradication was assessed for each group at least 4 weeks after completing eradication therapy. Drug susceptibility test was performed using 57 strains in pretreatment to clarithromycin, metronidazole, and amoxicillin. RESULTS: Prior to second-line H. pylori eradication, the rate of resistance to clarithromycin was high at 84% (48/57). Similarly, resistance to metronidazole was low at 5.3% (3/57); however, no amoxicillin-resistant strains were found. The eradication rates for both lansoprazole and famotidine treatment groups were high at 97% (29/30) and 94% (29/31), respectively. CONCLUSIONS: Famotidine treatment including metronidazole-amoxicillin as second-line therapy provided a high eradication rate similar to lansoprazole therapy. Famotidine is therefore expected to serve as a useful H. pylori eradication regimen in patients with proton pump inhibitor allergy, an economic benefit in terms of reduced health-care costs is also anticipated.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2006

[Successful bi-weekly paclitaxel treatment of an AFP-producing gastric cancer patient with peritoneal dissemination and multiple liver metastasis].

The patient was a 71-year-old man. Chemotherapy was conducted in two courses combining TS-1 (120 mg) and CDDP (80 mg) under the diagnosis of AFP-producing gastric cancer with multiple liver metastasis and peritoneal dissemination. Peritoneal dissemination disappeared, liver metastasis almost disappeared after completion of two courses, and the therapeutic efficacy was rated as PR. Then, the patient underwent distal gastrectomy and lymph node dissection. He received TS-1 monotherapy after surgery, but his condition gradually became worse. TS-1 and CDDP combination were given again, but an ileus resulted due to peritonitis carcinomatous. We therefore administered bi-weekly paclitaxel (80 mg/m(2)) intravenously. The ileus disappeared after one week, liver metastatic lesions and ascites were improved after completion of one course, and therapeutic efficacy was rated as PR. Grade 3 neutropenia and grade 1 alopecia occurred, but no other adverse reaction occurred. This therapy made it possible to eat foods, conduct chemotherapy safely while ambulatory. Paclitaxel can be expected to show good therapeutic efficacy and improve QOL of a peritonitis carcinomatosa patient with TS-1 resistant advanced gastric cancer.

Aged↗
PubMed2005

Helicobacter pylori-infected animal models are extremely suitable for the investigation of gastric carcinogenesis.

Although various animal models have been developed to clarify gastric carcinogenesis, apparent mechanism of gastric cancer was not clarified in recent years. Since the recognition of the pathogenicity of Helicobacter pylori (H pylori), several animal models with H pylori infection have been developed to confirm the association between H pylori and gastric cancer. Nonhuman primate and rodent models were suitable for this study. Japanese monkey model revealed atrophic gastritis and p53 mutation after long-term infection of H pylori. Mongolian gerbil model showed the development of gastric carcinoma with H pylori infection alone, as well as with combination of chemical carcinogens, such as N-methyl-N-nitrosourea and N-methyl-N-nitro-N'-nitrosoguanidine. The histopathological changes of these animal models after H pylori inoculation are closely similar to those in human beings with H pylori infection. Eradication therapy attenuated the development of gastric cancer in H pylori-infected Mongolian gerbil. Although several features of animal models differ from those seen in human beings, these experimental models provide a starting point for further studies to clarify the mechanism of gastric carcinogenesis as a result of H pylori infection and assist the planning of eradication therapy to prevent gastric carcinoma.

Animals↗
PubMed2005

Influence of bile reflux and Helicobacter pylori infection on gastritis in the remnant gastric mucosa after distal gastrectomy.

BACKGROUND: Two main pathogenic factors, bile reflux and Helicobacter pylori infection, have been identified in the remnant stomach, but it is still unclear which factor is important in the pathogenesis of gastritis in the remnant stomach after distal gastrectomy. METHODS: In 184 patients who had had distal gastrectomy performed using the Billroth-I procedure (B-I; n-106), Billroth-II procedure (B-II; n-36), and jejunal interposition (J-I; n-42) we examined the severity of remnant gastritis endoscopically and carried out examinations for H. pylori infection and histological examination. RESULTS: The endoscopic severity of remnant gastritis was grade 1 or more in 101 of the 106 B-I patients (95.3%) and in all 36 B-II patients (100%). But, of the 42 J-I patients, the grade was 0 in 33 (78.6%). The endoscopic severity of remnant gastritis was significantly milder for J-I than for B-I (P < 0.001) and B-II (P < 0.001). H. pylori infection was confirmed in 59 of the 106 B-I patients (55.6%), 21 of the 36 B-II patients (58.3%), and 32 of the 42 J-I patients (76.1%). The rate of H. pylori infection was higher for J-I patients than for B-I (P < 0.05), but not for B-II patients (P = 0.1495). The severity of chronic and active inflammatory cellular infiltration tended to be inverse proportional relation with the endoscopic severity of the remnant gastritis. Furthermore, the histological inflammation and activity scores of H. pylori-positive patients were higher than those of H. pylori-negative patients, without regard to the endoscopic grade of gastritis. CONCLUSIONS: Reconstruction techniques play an important role in the prevention of bile reflux, and we found that endoscopically more severe remnant gastritis was associated with a lower rate of H. pylori infection and with a lower degree of inflammatory cellular infiltration.

Aged↗
PubMed2005

Eradication of Helicobacter pylori reduced the immunohistochemical detection of p53 and MDM2 in gastric mucosa.

BACKGROUND: Although Helicobacter pylori has been regarded as a pathogen of gastric cancer, the mechanism by which H. pylori is involved in gastric carcinogenesis remains unknown. To clarify the role of H. pylori in carcinogenesis, the expression of tumor suppressor p53 and its regulator multiple double minute 2 (MDM2) in gastric mucosa were examined before and after H. pylori eradication. METHODS: Biopsy specimens were obtained from 31 patients with H. pylori-infected gastric mucosa. Endoscopic biopsies were repeated 6 months after successful eradication. In addition, biopsy specimens from 12 patients with non-infected gastric mucosa were obtained. Immunohistochemical analysis was performed on the specimens using primary antibodies specific for p53 and MDM2. RESULTS: Six months after H. pylori eradication, labeling indices for p53 were significantly reduced in the gastric corpus (2.3-fold; P < 0.01), and in the gastric antrum (2.0-fold; P < 0.01). Similarly, labeling indices for MDM2 were significantly reduced in the corpus (1.7-fold; P < 0.01), and in the antrum (3.5-fold; P < 0.01). In the non-infected group, labeling indices for p53 and MDM2 in the gastric mucosa were significantly lower (P < 0.01) than those of the H. pylori-infected group. CONCLUSION: A significant increase is shown in p53 and MDM2 expression in H. pylori-infected gastric mucosa as compared to normal gastric mucosa; but successful eradication of H. pylori dramatically reduced the p53 and MDM2 levels. Therefore, H. pylori infection may be associated with alteration of cell proliferation and apoptosis.

Anti-Infective Agents↗
PubMed2005

Helicobacter pylori eradication and associated changes in the gastric mucosa.

Persistent Helicobacter pylori infection contributes towards the development of chronic gastritis. To clarify the changes in chronic gastritis as a precursor of gastric cancer secondary to H. pylori eradication is an important issue, as it has significant implications for reducing the risk of gastric cancer. Studies published to date, however, are far from consistent with regard to the morphologic changes reported following H. pylori eradication. Of these, some papers reported improvement in gastric atrophy or intestinal metaplasia, versus others reporting no improvement, with the majority of papers published after 2000 reporting improvement in these end points. The inconsistent results concerning the impact of H. pylori eradication on gastric atrophy could be due to the inconsistency of the diagnostic criteria employed for evaluation of the morphology, confounded by the difficulties involved in evaluating atrophic changes in the gastric mucosa. While adherence to the Updated Sydney System available for evaluation of gastritis is primarily required worldwide to ensure consistency in evaluating gastritis, long-term research into the morphologic changes associated with H. pylori eradication is also required to explore strategies for the prevention of gastric cancer with H. pylori eradication.

Animals↗
PubMed2004

Effect of Helicobacter pylori eradication on platelet recovery in patients with chronic idiopathic thrombocytopenic purpura.

BACKGROUND: A relationship between Helicobacter pylori infection and idiopathic thrombocytopenic purpura (ITP) has previously been reported. We determined the prevalence of H pylori infection in Japanese patients with chronic ITP and the effect of its eradication on platelet count. METHODS: The study population comprised 53 Japanese adults with chronic ITP and a platelet count of less than 100 x 10(3)/ micro L. A (13)C-urea breath test was performed to determine H pylori infection status. Those patients who were H pylori positive gave written informed consent and received eradication therapy. The effect of H pylori eradication on platelet count was evaluated up to 6 months after therapy. Clinical parameters were compared between responders to the therapy (increase in platelet count) and nonresponders, as well as between H pylori-positive and -negative patients. RESULTS: Of the 53 patients with chronic ITP in the study, 39 (74%) were H pylori positive. Of the 32 infected patients who received treatment, H pylori was successfully eradicated in 27 patients (84%). In 10 (37%) of these patients, this resulted in a favorable platelet response. A partial response was seen in 5 additional patients (19%). A significant (P<.001) increase in platelet count was demonstrated in patients in whom H pylori was successfully eradicated but not in patients who were unsuccessfully treated or in untreated patients. Current corticosteroid therapy was reported more often in nonresponders than in responders. CONCLUSION: Eradication of H pylori may prove effective in increasing platelet count in H pylori-positive patients with chronic ITP.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2004

Duodenal gangliocytic paraganglioma treated with endoscopic hemostasis and resection.

Gangliocytic paragangliomas are exceedingly rare tumors that arise in close proximity to the papilla of Vater. There are few reports of the endoscopic resection of duodenal gangliocytic paraganglioma. A 61-year-old woman was admitted with a complaint of melena. Endoscopic examination revealed a pedunculated submucosal tumor with erosion in the third portion of the duodenum. Hemostasis, using a gold probe, was performed. Nine days later, we successfully resected the tumor, using endoscopic polypectomy. To determine the depth of tumor invasion, endoscopic ultrasonography was used. The size of the tumor was 3.0 x 2.5 x 1.0 cm. A total of 25 cases of duodenal gangliocytic paraganglioma have been reported in Japan. Generally, this tumor is considered benign. However, resection was performed in many patients because preoperative diagnosis was impossible. In Japan, no previous studies have reported using endoscopic hemostasis, to our knowledge. Our patient is the fourth in Japan to be treated by endoscopic resection. We report on our patient, with a review of the literature.

Duodenal Neoplasms↗