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Biomedical subjects

Hidekazu Suzuki

Publications and source records attributed to Hidekazu Suzuki.

At least 19 recordsLinked to original sources
PubMed2006

Rapid detection of point mutations conferring resistance to fluoroquinolone in gyrA of Helicobacter pylori by allele-specific PCR.

Helicobacter pylori strains with reduced susceptibility to fluoroquinolones have a mutation at either codon 87 Asn or 91 Asp of the gyrA gene. A rapid test based on an allele-specific PCR (AS-PCR) was designed to detect the gyrA mutations. Clinical H. pylori isolates were obtained from the stomachs of 51 patients with H. pylori infections who showed treatment failure. The MICs of gatifloxacin (GAT) were determined by the agar dilution method. Identical genotyping results were obtained with AS-PCR and conventional PCR. The gyrA mutations of H. pylori causing reduced susceptibility to fluoroquinolones could be detected successfully by this method. A significant association was observed between the presence of mutations, as detected by AS-PCR, and the resistance of the strains to GAT. Moreover, genotyping by AS-PCR took less than 3 to 4 h. The AS-PCR method for the detection of gyrA mutations in H. pylori is useful for easy identification of fluoroquinolone-resistant strains of H. pylori.

Adult↗
PubMed2006

Effects of a Helicobacter pylori eradication regimen on anti-platelet autoantibody response in infected and uninfected patients with idiopathic thrombocytopenic purpura.

Thirty-seven patients with idiopathic thrombocytopenic purpura (ITP) were treated with a standard Helicobacter pylori eradication regimen irrespective of H. pylori infection. Our results indicate that platelet recovery results from the disappearance of H. pylori itself, and is mediated, in part, through suppression of anti-platelet autoantibody production.

Adult↗
PubMed2006

Relapse of stage I small cell lung cancer ten or more years after the start of treatment.

Most patients with small cell lung cancer (SCLC) usually show relapse within 1 or 2 years. Relapses after a 5-year disease-free survival are extremely rare. This report describes two patients with stage I SCLC in whom the disease recurred 10 or more years after the start of initial therapy. Because the recurrence of SCLC was noted in the mediastinal lymph nodes of the same side, we concluded that the patients had a late relapse of SCLC rather than a metachronous lung cancer.

Aged↗
PubMed2006

Three cases of the nodular pulmonary amyloidosis with a longterm observation.

Longterm observation with chest radiograph and computed tomography (CT) scan was performed for pulmonary amyloidosis. There are few reports of primary pulmonary amyloidosis with a longterm observation. We encountered three cases of nodular pulmonary amyloidosis observed by intermittent chest radiograph or CT for 5 years or more. The patients were a 54-year-old man, and 67- and 68-year old women. For diagnosis, transbronchial biopsy and percutaneous lung biopsy were performed. Amyloid nodules grew slowly and two cases showed findings of cavity and calcification.

Aged↗
PubMed2006

Therapeutic strategies for functional dyspepsia and the introduction of the Rome III classification.

Although placebo response rates in clinical trials for functional dyspepsia (FD) are more than 30%, a recent meta-analysis based on randomized controlled trials (RCTs) showed that antisecretory drugs were more or less superior to placebos. On the other hand, large-scale RCTs on the efficacy of treatment with prokinetics on FD are still needed. Indications for antibiotic eradication therapy for Helicobacter pylori-positive FD are still controversial, but there seems to be a small but significant therapeutic gain achieved with H. pylori eradication. Since preprandial and postprandial symptomatic disturbances are very important targets for FD treatment, ghrelin, a novel appetite-promoting gastrointestinal peptide that also promotes gastric motility or basal acid secretion can be expected to be a therapeutic target. In the recently published Rome III classification, FD is redefined for patients with symptoms thought to originate from the gastroduodenal region, specifically epigastric pain or burning, postprandial fullness, or early satiation, and it is divided into the subcategories postprandial distress syndrome and epigastric pain syndrome. These new criteria are of value in clinical practice, for epidemiological, pathophysiological, and clinical research, and for the development of new therapeutic strategies.

Clinical Trials as Topic↗
PubMed2006

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model.

Helicobacter pylori is associated with gastric disorders in humans and some experimental animals, and possesses the luxS/type 2 autoinducer (AI-2) system. The effects of a specific luxS mutation on the characteristics of H. pylori were examined. On 0.3 % agar medium, motility of H. pylori HPKY08 (luxS : : cat) was significantly lower than that of wild-type H. pylori TK1402. The luxS-complemented strain HPKY21 exhibited motility comparable to that of H. pylori TK1402. It was shown that the luxS/AI-2 system plays an important role in H. pylori motility. The luxS mutant exhibited a reduced infection rate relative to the wild-type parent strain TK1402 in a Mongolian gerbil model. At 3 months after oral inoculation, lower numbers of H. pylori were detected by semi-quantitative real-time reverse transcription PCR (qRT-PCR) in luxS(-) mutant-infected gerbils than in TK1402-infected gerbils. Gastric inflammation and increased antibody titre for H. pylori were observed in TK1402-infected gerbils only.

Animals↗
PubMed2006

Efficacy of metronidazole as second-line drug for the treatment of Helicobacter pylori Infection in the Japanese population: a multicenter study in the Tokyo Metropolitan Area.

BACKGROUND: With the increase in the frequency of clarithromycin-resistant Helicobacter pylori (H. pylori), there is rising concern about the decline of the eradication rate of this infection following treatment. The Tokyo Hp Study Group examined the eradication rate in response to a second-line regimen consisting of proton pump inhibitor (PPI), amoxicillin, and metronidazole by conducting a multicenter study in the Tokyo Metropolitan Area. MATERIALS AND METHODS: Two hundred and twenty-eight patients with H. pylori infection, in whom the first-line therapy with a PPI, amoxicillin, and clarithromycin administered for 1 week had failed to eradicate the infection, were enrolled in this study. These cases were randomly assigned to one of the two second-line regimens containing metronidazole (PPI/AM500 or PPI/AM750) administered for 1 week. 13C-urea breath test was performed as a diagnostic method test for H. pylori infection not earlier than 8 weeks after the second-line therapy. RESULTS: Intention-to-treat (ITT) and per-protocol (PP) analyses revealed an eradication rate of 87.6 and 90.6%, respectively, following PPI/AM500 treatment, and 86.9 and 88.6%, respectively, following PPI/AM750 treatment. Neither analysis revealed any significant difference in the eradication rate between PPI/AM500 and PPI/AM750 (p = .876 and .621, respectively). According to ITT and PP analyses, the eradication rates following treatment with PPI/AM500 were 85.2 and 88.5% with the use of lansoprazole, 62.5 and 62.5% with the use of omeprazole, and 93.2 and 96.5% with the use of rabeprazole, respectively. There was a significant difference in the eradication rates between PPI (omeprazole)/AM500 and PPI (rabeprazole)/AM500. In the case of PPI/AM750, the corresponding eradication rates were 84.8 and 87.0% with the use of lansoprazole, 92.9 and 92.9% with the use of omeprazole, and 92.9 and 92.9% with the use of rabeprazole, respectively. There were no significant differences in the eradication rates obtained with the use of the three PPIs. CONCLUSIONS: Both PPI/AM500 and PPI/AM750 administered for 1 week appeared to be highly effective second-line regimens for the treatment of H. pylori infection in Japanese patients. From the viewpoint of adverse events, PPI/AM500 appeared to be safe compared with PPI/AM750.

Adult↗
PubMed2006

Overview: Helicobacter pylori and extragastric disease.

Isolation of the gastric spiral bacterium Helicobacter pylori totally reversed the false dogma that the stomach was sterile. In addition to its causal role in peptic ulceration, the newly identified bacterium has now been implicated in other gastric and even extragastric diseases, including chronic atrophic gastritis, gastric MALT lymphoma, gastric cancer, functional dyspepsia, idiopathic thrombocytopenic purpura (ITP), iron deficiency anemia, chronic urticaria, ischemic heart disease, and others. The majority of the reports are anecdotal, epidemiologic, or eradication studies, but there are also relevant in vitro studies. ITP represents one disease showing a strong link with H pylori infection. There are also accumulating data on the role of H pylori infection in iron deficiency anemia and ischemic heart disease. In summary, the association between H pylori infection and other extragut diseases is still controversial but worthy of further investigation.

Helicobacter Infections↗
PubMed2006

Analysis of Toll-like receptor 2, 4, 6 and 9 genome DNA mutations in patients with tractable and intractable gastric mucosal diseases.

The possible involvement of Toll-like receptor (TLR) genome DNA in the prolongation and relapse of inflammatory intestinal diseases and alcoholic hepatic diseases has been reported. In this study, we examined the relationship of mutations of the TLR 2, 4, 6 and 9 genomic DNA to recurrent or intractable gastritis or gastric ulcers. The subjects were 32 patients, including 6 with H. pylori (Hp)-positive gastritis, 4 with Hp-negative gastritis, 10 with Hp-positive tractable gastric ulcer, 5 with Hp-positive recurrent gastric ulcer after Hp eradication, and 7 with Hp-negative easily recurrent gastric ulcer after Hp eradication. Gastric mucosal tissue and peripheral blood specimens were collected from each of the patients. DNA was extracted from the tissue and blood specimens and subjected to electrophoresis by the PCR method, using the oligonucleotide primers of TLR 2, 4, 6 and 9. The gastric mucosal tissue specimens were collected endoscopically from the sites of the lesions. Subsequently, the presence or absence of genomic DNA mutations in the blood and tissue specimens was examined using a DNA sequencer. TLR 2, 4, 6 or 9 DNA mutations were not observed in any of the gastric mucosal or peripheral blood specimens obtained from patients with tractable gastritis or gastric ulcer, or from those with intractable gastric ulcer who were Hp-positive or Hp-negative or had become Hp-negative after eradication therapy. These data suggest that mutations of the TLR 2, 4, 6 and 9 genome DNA may not be involved in the recurrence, delayed healing or intractability of gastritis and gastric ulcers.

Base Sequence↗
PubMed2006

Heterozygous Thr 135 Ala polymorphism at leucine-rich repeat (LRR) in genomic DNA of toll-like receptor 4 in patients with poorly-differentiated gastric adenocarcinomas.

The genomic DNA of toll-like receptor (TLR) 2, TLR4, radioprotective 105, TLR6, and TLR9 were examined for mutations in 48 patients with gastric cancer. Of these, 22 had well-differentiated and 20 had poorly-differentiated adenocarcinomas, the latter group including 10 with signet ring cell carcinomas. The remaining 6 had gastric adenomas. Ten healthy volunteers with no family history of malignant diseases served as controls. DNA was extracted from peripheral blood and subjected to electrophoresis using PCR oligonucleotide primers. The resultant gel was analyzed with a DNA sequencer. None of the healthy volunteers, patients with gastric adenomas or those with well-differentiated gastric adenocarcinomas showed mutations. However, 8 of the 20 with poorly-differentiated gastric adenocarcinoma showed heterozygosity at the 135th position of the amino acid sequence of TLR4, and a mutation from threonine to alanine was found at this site. Analysis of the entire available amino acid sequence of TLR4 revealed that this mutation occurred at a leucine-rich repeat corresponding to one of its extracellular components. This suggests a disturbance in the protein phosphorylation reaction of TLR4, and that this disturbance is related to the development of poorly-differentiated gastric adenocarcinomas.

Adenocarcinoma↗
PubMed2006

[Ghrelin - a novel appetite-stimulating hormone which also affects gastrointestinal functions].

Ghrelin, a novel gastrointestinal peptide with 28 amino acids, is secreted from the A-like cells of the gastric fundus. This peptide hormone does not only promote the release of growth hormone, but also stimulates food intake, gastric motility and cardiac output. Increased plasma ghrelin level has been reported in patients with upper gastrointestinal (GI) disease or in their disease animal model, suggesting its important role in the pathogenesis of upper GI disease.

Appetite↗
PubMed2006

Analysis of the differences in structural chromosomal aberrations of the gastric mucosa between H. pylori positive and negative gastric cancer patients: involvement of H. pylori in the onset of gastric cancer and examination of the mechanism in gastric carcinogenesis following H. pylori eradication.

Gene mutations are essential to carcinogenesis. If an evident difference is observed in gastric mucosal chromosomal structure aberrations between H. pylori (Hp)-negative and Hp-positive gastric cancer patients, it may be interpreted as suggesting the involvement of Hp in gene mutations. This study was undertaken to compare chromosomal structural aberrations between Hp-negative and Hp-positive gastric cancer patients and to evaluate the effects of Hp eradication on chromosomal structures in clinical cases. The subjects of this study were 40 patients with gastric cancer divided into four groups: Group A was composed of 12 patients with Hp-negative gastric cancer (well-differentiated gastric cancer in 5 cases and poorly-differentiated in 7 cases), Group B of 8 patients with Hp-negative gastric cancer following Hp eradication (well-differentiated in 4 case and poorly-differentiated in 4 cases), Group C of 13 patients with Hp-positive gastric cancer (well-differentiated in 7 cases and poorly-differentiated in 6 cases) and Group D of 7 patients with gastric cancer (well-differentiated in 5 cases and poorly-differentiated in 2 cases) undergoing Hp eradication at subtotal gastrectomy. In each of the groups A, B and C, the structural chromosomal aberration such as loss of heterozygosity (LOH) and microsatellite instability (MSI) was analyzed. In Group D, changes in structural chromosomal aberrations after Hp eradication as compared to the pre-eradication structures were also analyzed. LOH and MSI were examined by PCR, using DNA extracted from the cancer-affected and intact gastric mucosal tissue specimens from each patient. In A, B and C groups, structural chromosomal aberrations were noted, and these aberrations tended to be more marked in cases of poorly-differentiated gastric cancer in each group. In terms of structural chromosomal aberrations, there was no marked difference between Group A and either Group B or C. Hp eradication resulted in no change in chromosomal structure as compared to the pre-eradication structure in Group D. These results suggest the possibility that Hp eradication does not affect chromosomal structures and Hp is involved in gastric carcinogenesis as an additive environmental factor rather than as a factor acting at the gene level.

Anti-Bacterial Agents↗
PubMed2006

[A case of intrahepatic cholangiocarcinoma effectively treated by hepatic arterial infusion chemotherapy].

The patient was a 50-year-old woman who suffered from gastric discomfort. She was first diagnosed as intrahepatic cholangiocarcinoma with hepatic, paraaortic lymphnodal and bone metastasis. Initial systemic chemotherapy using gemcitabine (GEM) and 5-FU failed to control the disease activity. Then she was given GEM and cisplatin (CDDP) combination chemotherapy. The response was assessed as stable disease (SD), but grade 4 leukopenia was seen. Then systemic therapy using GEM, and hepatic arterial infusion therapy with CDDP, l-leucovorin and 5-FU were continued biweekly. Partial response (PR) was achieved six months later, and her disease status was maintained as SD. This hepatic arterial infusion chemotherapy would be safe and feasible as therapy for inoperable intrahepatic cholangiocarcinoma.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

[A case of Parkinson's disease with neuroleptic malignant syndrome induced by paroxetine].

We present a first case of Parkinson's disease with neuroleptic malignant syndrome by Paroxetine, one of the selective serotonin reuptake inhibitor (SSRI). The patient was a 73-year-old woman who had been diagnosed as Parkinson's disease for one and half year. The severity of her disease was categorized as Hoehn & Yahr 2nd degree and she had taken 0.25 mg/day of Pramipexole. Four days after the addition of 10 mg/day of Paroxetine for the treatment of her depression, she developed consciousness disturbance, severe muscular rigidity, tremor, fever, hyperhidrosis, incontinence and elevated serum creatine kinase level. According to diagnostic criteria, she was diagnosed as neuroleptic malignant syndrome probably induced by Paroxetine. Her clinical symptoms and laboratory data were improved seven days after intravenous drip infusion. We should recognize that SSRI could induce neuroleptic malignant syndrome in patients with Parkinson's disease.

Aged↗
PubMed2005

Expression of Musashi-1 in the rat stomach and changes during mucosal injury and restitution.

Musashi-1 is involved in maintenance of neural stem cells. In the rat stomach, we found some cells in the luminal compartment of the mucosa that stained positively for Musashi-1. These cells were distinct from other cells of epithelial lineage, except for parietal cells, and coexpressed HES5. The Musashi-1-positive cells exfoliated after damage, while Musashi-1 expression in neck cells were upregulated, and proliferating cells diminished before reappearing and increasing in number thereafter. We conclude that a subpopulation of parietal cells acts as a source of Musashi-1, which contributes to rapid re-epithelization by restoration of stem cells and regulation of cell differentiation.

Animals↗
PubMed2005

Biomarkers in patients with gastric inflammation: a systematic review.

BACKGROUND: The importance of examining the status of gastric inflammation has been acknowledged; the new classification by the updated Sydney system (USS) allows us to evaluate the quantitative status of gastric inflammation. However, this system is based on the histological classification derived from biopsy specimens. Therefore, more convenient, objective and practical biomarkers are recommended. AIM: We undertook a systematic review to find out potential biomarkers by summarizing the relationship between biomarkers and grades of inflammation. METHODS: By a primary search via Medline up to December 2004, we extracted a total of 6,526 papers that described biomarkers for human gastric inflammation. All papers were screened by title and abstract. The authors then retrieved 435 citations for complete review; ultimately 231 were appropriate for inclusion criteria. These papers were subclassified into several categories and summarized by each author. RESULTS: In addition to standard markers such as pepsinogens, we confirmed the close relationship between the levels of several biomarkers including gastrin, interleukin-8, HLA class II molecules, reactive oxygen species, and the histological grades. CONCLUSIONS: This review provides valuable information describing the clinical implication of these biomarkers for evaluating the static conditions or dynamic alterations of human gastric inflammation.

Biomarkers↗
PubMed2005

Enhanced plasma ghrelin levels in Helicobacter pylori-colonized, interleukin-1-receptor type 1-homozygous knockout (IL-1R1-/-) mice.

AIM: Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor, and it plays a role in stimulating the growth hormone secretion, food intake, body weight gain and gastric motility. Eradication of Helicobacter pylori (H pylori) was shown to be associated with increase of the body weight. On the other hand, H pylori infection evokes the release of gastric IL-1beta. The present study was designed to investigate the involvement of the gastric IL-1 signal in the ghrelin dynamics in H pylori-colonized mice. METHODS: Twelve-week-old female IL-1-receptor type 1-homozygous-knockout mice (IL-1R1(-/-)) and their wild-type littermates (WT) were orally inoculated with H pylori (Hp group), while other cohorts received oral inoculation of culture medium (Cont group). Thirteen weeks after the inoculation, the mice were examined. The plasma and stomach ghrelin levels and the gastric preproghrelin mRNA were measured. RESULTS: Although the WT mice with H pylori infection showed a significantly decreased body weight as compared with that of the animals without H pylori infection, H pylori infection did not influence the body weight of the IL-1R1-knockout (IL-1R1(-/-)) mice. In the H pylori-infected IL-1R1(-/-) mice, the total and active ghrelin levels in the plasma were significantly increased, and the gastric ghrelin level was decreased. No significant differences were noted in the gastric preproghrelin mRNA expression. CONCLUSION: Ghrelin secretion triggered by H pylori infection might be suppressed by IL-1beta, the release of which is also induced by the infection, resulting in the body weight loss of mice with H pylori infection.

Animals↗