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Biomedical subjects

Ken Ohnita

Publications and source records attributed to Ken Ohnita.

At least 19 recordsLinked to original sources
PubMed2006

Comparison of the grade evaluated by "Liver damage" of Liver Cancer Study Group of Japan and Child-Pugh classification in patients with hepatocellular carcinoma.

BACKGROUND: The "Liver damage" classification proposed by the Liver Cancer Study Group of Japan and Child-Pugh classification are both useful classifications for hepatic function. However, the factors responsible for the difference between the two classifications have not been fully investigated. METHODS: The medical records of 594 admissions of 220 patients with hepatocellular carcinoma (HCC) were retrospectively analyzed for encephalopathy, ascites, serum bilirubin and albumin, plasma retention rate (%) at 15min after injection of 0.5mg/kg of indocyanine green (ICG R15), and prothrombin time. RESULTS: Of 594 admissions, ICG R15 was tested in 337 (56.7%). The Child-Pugh classification was evaluated in all 594 admissions, but the "Liver damage" could be evaluated in 510 (85.9%) due to the lack of ICG R15 results. Of the 594 admissions, 372 (62.6%), 162 (27.3%), and 60 (10.1%) were Child-Pugh grade A, B, and C, respectively. Of the 510 admissions, 219 (42.9%), 202 (39.6%), and 89 (17.5%) were "Liver damage" grade A, B, and C, respectively. The grade of "Liver damage" was similar to that of Child-Pugh classification in 369 (72.4%), under-evaluated in 138 (27.1%), and over-evaluated in 3 (0.6%). The Child-Pugh classification was statistically a better classification for predicting outcome than "Liver damage", but the "Liver damage" had better stratification ability than Child-Pugh classification in patients with relatively good liver function. CONCLUSIONS: Although the "Liver damage" could not be evaluated in some cases due to the lack of ICG R15 results, this classification system is useful in the evaluation and prediction of outcome of patients with early-stage liver diseases.

Journal Article↗
PubMed2006

Flow cytometric analysis of expression of transforming growth factor-beta and glucocorticoid-induced tumor necrosis factor receptor on CD4(+) CD25(+) T cells of patients with inflammatory bowel disease.

To determine whether human CD4(+)CD25(+) cells express glucocorticoid-induced tumor necrosis factor receptor (GITR) and transforming growth factor-beta (TGF-beta) and the difference in CD4(+)CD25(+) cells between patients with inflammatory bowel diseases and healthy subjects, peripheral blood lymphocytes were obtained from patients with ulcerative colitis (UC; n = 50), Crohn's disease (CD; n = 49), and healthy volunteers (control; n = 50) and flow cytometric analysis was performed. In control subjects, the expression of GITR on CD4(+)CD25(+) cells (41.8 +/- 10.5%) was significantly higher than on CD4(+)CD25(-) cells (11.1 +/- 7.4%). Similarly, TGF-beta expression on CD4(+)CD25(+) cells (5.3 +/- 4.6%) was higher than on CD4(+)CD25(-) cells (1.2 +/- 1.4%). There were no significant differences among UC, CD, and control in CD4(+)CD25(+)/CD4(+) ratio. However, there was a significant difference in the CD4(+)CD25(+) TGF-beta+/CD4(+)CD25(+) ratio between active UC and inactive UC (2.7 +/- 2.6 and 7.2 +/- 3.9%, respectively). The results suggest that TGF-beta is involved in the induction or sustained remission of UC.

Adolescent↗
PubMed2006

IgA class antibodies to 2-oxo-acid dehydrogenase complex are not predictive markers of histopathological progression in primary biliary cirrhosis.

Although antimitochondrial antibody (AMA) is the characteristic serological feature of primary biliary cirrhosis (PBC), its pathogenic role remains unclear. In our previous study, we reported a positive correlation between immunoglobulin (Ig) A class anti-2-oxo-acid dehydrogenase complex (2-OADC) and histopathological stage. To determine whether the appearance of IgA class anti-2-OADC by immunoblotting represents an early marker of more aggressive disease or whether it is late finding during the disease course of PBC, we tested not only the entire IgA class but also IgA1, IgA2 and secretory IgA class anti-2-OADC in serial serum samples from 15 patients with PBC. During the median observation period of 51 months, four cases showed histopathological progression (from stage 1 to 2, stage 1 to 3, stage 1 to 4 and stage 2 to 4). There was no statistically significant correlation between the above IgA class anti-2-OADCs and histopathological progression. There was no significant correlation between histopathological stages and IgA2 class anti-2-OADC or secretory IgA class anti-2-OADC by immunoblotting. IgA class anti-2-OADC was more frequent in stages 3-4 than in stages 1-2 (p = 0.0049), but IgA1 class anti-2-OADC was more frequent in stages 1-2 than in stages 3-4 (p = 0.0232). Our present study demonstrated that serum IgA class 2-OADC was not a predictive marker of histopathological progression but was associated with the histopathological stage of PBC. Although the IgA class AMA may have a specific pathogenic role for PBC, the discrepant results between IgA and IgA1 class anti-2-OADC should be further assessed to investigate different functional activities depending on their molecular form.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed2006

[A case of recurrent mediastinal pancreatic pseudocyst].

A 46-year-old man complaining right lateroabdominal pain and dysphagia was admitted our hospital. The CT examination revealed the low density area spreading through the mediastinum. The patient's condition improved with fast and antibiotics. He was discharged from the hospital, having an equivocal diagnosis. Seven months later, his symptoms relapsed and he was hospitalized again. Further evaluation confirmed that his disease was the mediastinal pancreatic pseudocyst occurred by a pancreatic stone. The pseudocyst resolved twice with conservative therapy, fast and intravenous injection of antibiotics. We consider it a rare case, because mediastinal pancreatic pseudocyst generally have the tendency of becoming severe. Finally the operation was performed for depriving the pancreatic stone, which was the cause of pancreatic pseudocyst.

Humans↗
PubMed2005

Plasma leptin and ghrelin concentrations in patients with Crohn's disease.

AIM: To determine the concentrations of leptin and ghrelin, which have opposite effects on appetite, energy expenditure, and weight control, in the plasma of patients with Crohn's disease (CD), which is often associated with weight loss and malnutrition. METHODS: Plasma leptin and ghrelin 'concentrations were determined in 28 outpatients with CD by radioimmunoassay. Age- and sex-matched controls with and without Helicobacter pylori (H pylori) infection (28 for each) were enrolled in the study. Circulating levels of these hormones were assessed with respect to CD activity, disease localization and medical treatment. RESULTS: There were no significant differences in ghrelin levels between CD patients and H pylori-negative controls. However, circulating ghrelin levels were significantly lower in H pylori-infected subjects than in CD patients and uninfected controls. Plasma leptin levels were comparable among the groups. Localization and medication profile had no significant impact on circulating ghrelin and leptin levels. CONCLUSION: Apart from H pylori infection, CD itself has no significant influence on circulating ghrelin and leptin levels in the outpatients who were mostly in inactive state.

Adolescent↗
PubMed2005

High concentrations of human beta-defensin 2 in gastric juice of patients with Helicobacter pylori infection.

AIM: Human beta-defensin (HBD)-1 and HBD-2 are endogenous antimicrobial peptides. Unlike HBD-1, the HBD-2 expression is augmented by Helicobacter pylori (H pylori). We sought to determine HBD-1 and HBD-2 concentrations in gastric juice during H pylori infection. METHODS: HBD-1 and HBD-2 concentrations were measured by radioimmunoassay in plasma and gastric juice of 49 H pylori-infected and 33 uninfected subjects and before and after anti-H pylori treatment in 13 patients with H pylori-associated gastritis. Interleukin (IL)-1beta and IL-8 concentrations in gastric juice were measured by enzyme-linked immunosorbent assay (ELISA). Histological grades of gastritis were determined using two biopsy specimens taken from the antrum and corpus. Reverse phase high performance liquid chromatography (RP-HPLC) was used to identify HBD-2. RESULTS: HBD-2 concentrations in gastric juice, but not in plasma, were significantly higher in H pylori-positive than -negative subjects, albeit the post-treatment levels were unchanged. Immunoreactivity for HBD-2 was exclusively identified in H pylori-infected mucosa by RP-HPLC. HBD-2 concentrations in gastric juice correlated with histological degree of neutrophil and mononuclear cell infiltration in the corpus. IL-1beta levels correlated with those of IL-8, but not HBD-2. Plasma and gastric juice HBD-1 concentrations were similar in H pylori-infected and uninfected subjects. CONCLUSION: Our results place the beta-defensins, especially HBD-2, in the front line of innate immune defence. Moreover, HBD-2 may be involved in the pathogenesis of H pylori-associated gastritis, possibly through its function as immune and inflammatory mediator.

Anti-Infective Agents↗
PubMed2005

Pseudomyxoma peritonei accompanied by intraductal papillary mucinous neoplasm of the pancreas.

We describe a case of pseudomyxoma peritonei (PMP) successfully managed with intraperitoneal hyperthermic chemoperfusion. This case is unique due to the concurrent presence of intraductal papillary mucinous neoplasm (IPMN) of the pancreas. The patient presented with abdominal fullness. Abdominal computed tomography revealed massive ascites, thickened peritoneum, and a cystic lesion of the pancreas. Cytological examination of ascitic fluid sample showed mucin-rich atypical cells. Endoscopic retrograde pancreatography revealed a cystic lesion with the defect probably due to mural nodule and mucin, communicating with the pancreatic duct. At exploratory laparotomy, massive ascites and multiple nodules were identified within the peritoneal cavity. No primary tumour, including mucinous neoplasm of the appendix, was found. Histopathological examination of the omentum showed mucinous adenocarcinoma in pools of mucoid material, consistent with PMP. The relation between PMP and IPMN of the pancreas was possible, but not conclusive. The patient received intraperitoneal perfusion of saline heated to 42 degrees C containing cisplatin, etoposide, and mitomycin C, followed by 24 courses of postoperative chemotherapy with gemcitabine. The patient remains in good general condition with no signs of progression of PMP for 2 years, but with a gradual and progressive enlargement of the pancreatic cystic lesion.

Adenocarcinoma, Mucinous↗
PubMed2005

Sofalcone, a mucoprotective agent, increases the cure rate of Helicobacter pylori infection when combined with rabeprazole, amoxicillin and clarithromycin.

AIM: The mucoprotective agents, sofalcone and polaprezinc have anti-Helicobacter pylori (H pylori) activities. We determined the therapeutic effects of sofalcone and polaprezinc when combined with rabeprazole, amoxicillin and clarithromycin for Helicobacter pylori infection. METHODS: One hundred and sixty-five consecutive outpatients with peptic ulcer and H pylori infection were randomly assigned to one of the following three groups and medicated for 7 d. Group A: triple therapy with rabeprazole (10 mg twice daily), clarithromycin (200 mg twice daily) and amoxicillin (750 mg twice daily). Group B: sofalcone (100 mg thrice daily) plus the triple therapy. Group C: polaprezinc (150 mg twice daily) plus the triple therapy. Eradication was considered successful if (13)C-urea breath test was negative at least 4 wk after cessation of eradication regimens or successive famotidine in the cases of active peptic ulcer. RESULTS: On intention-to-treat basis, H pylori cure was achieved in 43 of 55 (78.2%) patients, 47 of 54 (87.0%) and 45 of 56 (80.4%) for the groups A, B and C respectively. Using per protocol analysis, the eradication rates were 81.1% (43/53), 94.0% (47/50) and 84.9% (45/53) respectively. There was a significant difference in the cure rates between group A and B. Adverse events occurred in 10, 12 and 11 patients, from groups A, B and C respectively, but the events were generally mild. CONCLUSION: The addition of sofalcone, but not polaprezinc, significantly increased the cure rate of H pylori infection when combined with the rabeprazole-amoxicillin-clarithromycin regimen.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2005

Helicobacter pylori strain-specific modulation of gastric inflammation in Mongolian gerbils.

AIM: The cag pathogenicity island (PAI) is one of potential virulence determinants of Helicobacter pylori. The Mongolian gerbil is a suitable experimental animal for the screening of virulence factors of H pylori. METHODS: Five-week-old Mongolian gerbils were inoculated with a standard H pylori strain (ATCC 43504) possessing the cag PAI or a clinical isolate lacking the genes' cluster (OHPC-0002). The animals were killed at 2, 4, 8, 24 and 48 wk after inoculation (n = 5 each), and macroscopic and histopathological findings in the stomachs were compared. RESULTS: In gerbils infected with ATCC 43504, a more severe degree of infiltration of polynuclear and mononuclear cells and lymphoid follicles was observed from 4 wk after inoculation compared to gerbils infected with OHPC-0002 especially in the antrum and transitional zone from the fundic to pyloric gland area. In addition, glandular atrophy, intestinal metaplasia, gastric ulcer and hyperplastic polyps were noted in gerbils infected with ATCC 43504, whereas only mild gastric erosions occurred in those infected with OHPC-0002. CONCLUSION: Our results indicate that the cag PAI could be directly involved in gastric immune and inflammatory responses in the Mongolian gerbils, leading to a more advanced gastric disease.

Animals↗
PubMed2005

Effect of Helicobacter pylori eradication on gastric hyperplastic polyposis in Cowden's disease.

A 21-year-old woman with complaints of hematochezia was diagnosed as having Cowden's disease (CD), an autosomal dominant condition characterized by multiple hamartomas, since facial papules and gingival papillomas were identified. On endoscopy, multiple hyperplastic polyps were seen in the rectum and left-side colon. There were also esophageal glycogenic acanthosis and hyperplastic polyposis in the antrum accompanied by Helicobacter pylori-related gastritis. Although gastric hyperplastic polyposis had by no means regressed with unsuccessful first-line eradication therapy for H pylori, following cure of the infection with salvage therapy consisting of rabeprazole, amoxicillin and metronidazole, the polyposis lesions almost disappeared. Follow-up gastroscopy 2 and 3 years after cessation of the second-line eradication therapy revealed almost complete regression of the polyposis lesions with no evidence of H pylori infection. We recommend eradication treatment for CD patients with gastric hyperplastic polyps and the infection, as the occurrence of gastric carcinoma among hyperplastic polyps has been described.

Adult↗
PubMed2005

Enhanced production of leptin in gastric fundic mucosa with Helicobacter pylori infection.

AIM: To determine the concentrations of leptin in plasma and gastric fundic mucosa in humans, with reference to Helicobacter pylori (H pylori) infection, and their association with gastric mucosal levels of interleukin (IL)-1beta, IL-6 and IL-8. METHODS: Plasma leptin concentrations were determined in 135 outpatients with non-ulcer dyspepsia, consisting of 95 H pylori-infected and 40 uninfected subjects, and 13 patients before and after cure of the infection with anti-H pylori regimen. Using biopsy samples that were endoscopically obtained from the middle corpus along the greater curvature, gastric leptin contents were measured by radioimmunoassay and the mucosal concentrations of IL-1beta, IL-6 and IL-8 were measured by enzyme linked immunosorbent assay. We also analysed the expression of leptin in the fundic mucosa by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry. RESULTS: The mucosal levels of leptin in the fundic mucosa of H pylori-infected patients were significantly higher than those of uninfected patients. The amount of gastric leptin correlated positively with the mucosal levels of IL-1beta and IL-6, but not IL-8. Circulating leptin correlated with body mass index, but not with H pylori status, and there was no change in plasma leptin levels following cure of the infection. Leptin immunoreactive cells were noted in the lower half of the fundic glands, and its expression of messenger ribonucleic acid in the oxyntic mucosa was detected by RT-PCR. CONCLUSION: Leptin production is enhanced in H pylori-infected gastric mucosa. Gastric leptin may be involved in immune and inflammatory response during H pylori infection, through interaction with proinflammatory cytokines.

Adult↗
PubMed2005

Concentrations of alpha- and beta-defensins in gastric juice of patients with various gastroduodenal diseases.

AIM: To determine the concentration of alpha- and beta-defensins in gastric juice of patients with various gastroduodenal diseases. METHODS: Concentrations of human neutrophil peptides (HNPs) 1-3, the major forms of alpha-defensins, and human beta-defensin (HBD)-1 and HBD-2 were measured by radioimmunoassay in plasma and gastric juice of 84 subjects, consisting of 54 Helicobacter pylori-infected and 30 uninfected subjects. They included 33 patients with chronic gastritis (CG), 12 with gastric ulcer (GU), 11 with duodenal ulcer (DU), 11 with benign gastric polyp (BGP) and 16 with normal mucosa (N group) on upper endoscopy. Plasma pepsinogen I and II levels, biomarkers for gastric mucosal inflammation and atrophy, were also measured. RESULTS: Gastric juice HNPs 1-3 levels in patients with CG, GU and BGP were significantly higher than those in patients with DU and N. Gastric juice HBD-2 concentrations in patients with CG and GU were significantly higher than those in the N group, but were significantly lower in DU patients than in GU patients. Gastric juice HBD-1 levels and plasma levels of these peptides were similar in the patient groups. Concentrations of gastric juice HNPs 1-3 and HBD-2 of in H pylori-infected patients were significantly different from those in uninfected subjects. HNPs 1-3 concentrations in gastric juice correlated negatively with plasma pepsinogen I levels and I/II ratios. HBD-2 levels in gastric juice correlated positively and negatively with plasma pepsinogen II concentrations and I/II ratios, respectively. CONCLUSION: HNPs 1-3 and HBD-2 levels in gastric juice are diverse among various gastrointestinal diseases, reflecting the inflammatory and atrophic events of the background gastric mucosa affected by H pylori.

Duodenal Diseases↗
PubMed2005

Circulating ghrelin levels in patients with various upper gastrointestinal diseases.

The stomach is the main source of circulating ghrelin. Plasma concentrations of this hormone in patients with various upper gastrointestinal diseases remain undetermined. Thus we measured plasma ghrelin levels by radioimmunoassay in 225 subjects, including 134 Helicobacter pylori-infected and 91 uninfected subjects. They included 67 patients with chronic gastritis (CG), 26 with benign gastric polyp (BGP), 24 with gastric ulcer (GU), 24 with reflux esophagitis (RE), 18 with duodenal ulcer (DU), 28 with acute gastritis (AG), 23 with gastric cancer (GC), and 39 who had normal mucosa on upper endoscopy (N). Plasma pepsinogen I and II levels were also measured. The extent of gastritis was assessed endoscopically. Ghrelin levels differed significantly among the different disease groups. Plasma ghrelin concentrations were lowest in the CG group, followed by the GU group, and highest in the AG patients. There was a significant difference in the levels between differentiated and undifferentiated GC. Ghrelin concentrations in BGP, RE, and DU patients were comparable to those in the N group. Ghrelin circulating levels were lower in H. pylori-positive than -negative individuals, but the significant differences among disease groups were still observed in H. pylori-infected and uninfected populations. Ghrelin concentrations correlated positively with plasma pepsinogen I levels and I/II ratios and inversely with the extent of H. pylori-related gastritis. Plasma ghrelin levels varied widely in diverse conditions of the upper digestive tract, reflecting the inflammatory and atrophic events of the background gastric mucosa. Further investigation is warranted to unravel the mechanisms of the high circulating ghrelin levels in certain upper gastrointestinal diseases.

Adult↗
PubMed2005

Does the diagnosis of primary biliary cirrhosis or autoimmune cholangitis depend on the 'phase' of the disease?

BACKGROUND: It is unclear whether autoimmune cholangitis (AIC) is a separate disease entity or primary biliary cirrhosis (PBC) without antimitochondrial antibodies (AMA) since fluctuation of AMA titres by immunofluorescence (IF) is often observed during the course of PBC. The aim of this study was to determine the serial changes in AMA profiles during the course of initially diagnosed PBC or AIC. METHODS: In this prospective study, 32 patients with PBC or AIC were followed-up for at least 20 months and tested for AMA by IF, enzyme-linked immunosorbent assay (ELISA), and immunoblotting (IB). RESULTS: When positive AMA result was defined as 'AMA by IF positive', 'AMA by IF and/or ELISA positive', and 'AMA by IB positive', the diagnosis of PBC or AIC did not change in 78%, 91%, and 97%, respectively, throughout follow-up. However, the diagnosis changed in one patient, and three patients were diagnosed as AIC throughout follow-up, despite the use of all three assays. CONCLUSIONS: Our results suggested that the diagnosis of PBC and AIC was dependent on the 'phase' of the respective disease in 22% of the patients when negative AMA result was defined as 'AMA by IF negative'. This may result in recommending IB analysis before making the diagnosis of AIC.

Adult↗
PubMed2005

Impact of Helicobacter pylori infection on gastric and plasma ghrelin dynamics in humans.

OBJECTIVES: There are contradictory reports on the relationship between Helicobacter pylori and circulating ghrelin. We sought to clarify the influence of H. pylori infection on gastric and plasma ghrelin dynamics in humans. METHODS: Using endoscopic biopsies from the corpus of 56 H. pylori-infected patients and 25 uninfected subjects, ghrelin mRNA expression levels and gastric ghrelin peptide contents were measured by real-time polymerase chain reaction and radioimmunoassay, respectively. We also measured plasma ghrelin concentrations and analyzed the numbers of ghrelin immunoreactive cells in the fundic gland area. Fifty-one patients with H. pylori infection were treated with a 7-day triple therapy consisting of lansoprazole, clarithromycin, and amoxicillin. RESULTS: The gastric ghrelin mRNA expression level of H. pylori-positive patients (1.64 +/- 1.27 in arbitrary units) was significantly lower than in H. pylori-negative subjects (4.87 +/- 4.1, p < 0.0001). A similar trend was noted for ghrelin peptide contents (31.2 +/- 27.5 vs 81.2 +/- 64.1 ng/mg protein, respectively, p < 0.0001). There was no significant difference in the number of ghrelin immunoreactive cells/mm(2) in terms of H. plyori status. Plasma ghrelin concentrations in H. pylori-infected patients (144.6 +/- 7.8.8 fmol/ml) were significantly lower than in uninfected subjects (196.1 +/- 97.2, p < 0.05) and increased following cure of the infection. Plasma ghrelin levels correlated positively with the expression levels of ghrelin mRNA (r = 0.583, p < 0.0001) and peptide products (r = 0.574, p < 0.0001). There was a significant stepwise decrease in gastric ghrelin mRNA expression (p < 0.05), peptide contents (p < 0.01) and density of ghrelin immunoreactive cells (p < 0.05) with progression of histological severity of glandular atrophy in the corpus. The histological severity of chronic inflammation also negatively influenced the ghrelin mRNA expression (p < 0.001) and peptide production (p < 0.005). CONCLUSIONS: H. pylori infection has a negative impact on gastric and plasma ghrelin dynamics. Chronic inflammatory and atrophic changes associated with the infection may affect gastric ghrelin biosynthesis and contribute to the low circulating levels.

Adult↗