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II Ratio (ii + ratio)

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Medical Sciences100%

Kinds of II Ratio

  • p&g ii ratio
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    Selected Abstracts

    Validation of Diagnostic Tests for Helicobacter pylori with Regard to Grade of Atrophic Gastritis and/or Intestinal Metaplasia

    HELICOBACTER, Issue 6 2009
    Cheol Min Shin
    Abstract Background and Aims:, To evaluate the validity of the biopsy-based tests (histology, culture, and urease test) and serology in detecting current Helicobacter pylori infection against a background of atrophic gastritis (AG) or intestinal metaplasia (IM). Methods:,Helicobacter pylori infection was diagnosed in 651 subjects, using the predefined gold standard for H. pylori tests. The sensitivity, specificity, and positive and negative predictive values of culture, CLOtest, histology (Giemsa stain), and serology were calculated with regard to the histological grade of AG and IM. The level of serum pepsinogen (PG) I and II was also measured as a marker for the presence of AG. Results:, In the study population (n = 651), sensitivity and specificity, respectively, were as follows: culture, 56.2 and 100%; histology, 93.0 and 94.0%; CLOtest, 80.4 and 96.7%; serology, 96.0 and 67.5%. If the analysis is limited to those without AG or IM (n = 158) or to those younger than 40 years (n = 69), all tests, except for culture, had a sensitivity and specificity >90%. The sensitivity of CLOtest and the specificity of serology markedly decreased with progression of AG and IM, and serology was less specific in the presence of AG, as determined by a PG I/II ratio ,4.1 (specificity, 83.7% vs 40.7% in PG I/II >4.1 and ,4.1, respectively). Conclusions:, Any one of biopsy-based tests or serology was found to be excellent for identifying current H. pylori infection among individuals without AG or IM and/or younger patients (<40 years). However, a combination of at least two tests is necessary in the clinical setting of AG or IM. [source]

    Gastric Acidity in Patients with Follicular Gastritis is Significantly Reduced, but Can be Normalized After Eradication for Helicobacter pylori

    HELICOBACTER, Issue 3 2005
    Tomohiko Shimatani
    ABSTRACT Background., Follicular gastritis is thought to be caused by Helicobacter pylori infection. However, the pathophysiology of it remains unclear. Materials and methods., We assessed gastric acidity in 15 patients with follicular gastritis, aged 20,37 years, using a 24-hour intragastric pH-metry, as well as by histologic and serologic evaluations; and compared it with that in other age-matched groups: 18 cases of H. pylori -positive antrum-predominant gastritis, 12 of pangastritis, and 24 H. pylori -negative normals. In eight cases with follicular gastritis, it was re-assessed 6 months after the eradication therapy for H. pylori. Results., During nighttime, the percentage of time with intragastric pH above 3.0 in follicular gastritis was significantly higher than that in normals (p < .0001), and in antrum-predominant gastritis (p < .001), but was comparable with that in pangastritis. In the daytime period, this parameter in follicular gastritis was significantly higher than that in normal (p < .001), in antrum-predominant gastritis (p < .001), and in pangastritis (p < .05). Marked mononuclear cell and neutrophil infiltration but no apparent glandular atrophy were observed in both the antrum and corpus. Serum pepsinogen I/II ratio was significantly lower in follicular gastritis than that in normals (p < .0001) and in antrum-predominant gastritis (p < .001), whereas serum gastrin was significantly higher than that in normals (p < .0001), in antrum-predominant gastritis (p < .01) and in pangastritis (p < .05). After eradication for H. pylori, all of the parameters in follicular gastritis were altered to the same ranges as those in normals. Conclusions., In follicular gastritis, gastric acidity is significantly reduced, but can be normalized by eradication of H. pylori. It can thus be speculated that inflammatory cytokines or H. pylori -infection,induced prostaglandins might strongly inhibit gastric acid secretion in follicular gastritis. [source]

    Negative Association Between Helicobacter pylori Infection and Reflux Esophagitis in Older Patients: Case-Control Study in Japan

    HELICOBACTER, Issue 1 2000
    Ken Haruma
    Background. Recent studies have clarified a close association between H. pylori infection and gastritis, peptic ulcer disease, and gastric cancer, but there is little information concerning the relationship between H. pylori infection and reflux esophagitis (RE). We investigated the relationship between H. pylori, RE, and corpus gastritis. Subjects and Methods. Ninety-five patients with RE and 190 sex- and age-matched asymptomatic healthy controls demonstrating no localized lesions in the upper GI tract were studied and evaluated for H. pylori infection, histologic gastritis, serum gastrin, and pepsinogens (PGs). Results.H. pylori infection was significantly lower in RE patients than in asymptomatic controls (41% vs. 76%, p < .01). Histologic gastritis of both the antrum and corpus was significantly less frequent (antrum; p < .01, corpus; p < .01), and serum levels of PGI and the PG I/II ratio were significantly higher in RE patients than in controls (PGI; p < .05, PG I/II ratio; p < .01). When the subjects were divided into two age groups (59 years of age and younger and 60 years of age and older), a significant difference was found only among patients over 60 years of age (29% vs. 85%, p < .01). Among subjects in this age group, gastritis in both the antrum and corpus were significantly milder in RE patients than in controls. Although the prevalence of H. pylori infection was similar between the two groups of patients under 59 years of age, corpus gastritis was significantly milder in patients than in controls (p < .05). Conclusions. A significantly low prevalence of H. pylori infection was found in RE patients over 60 years of age but not in those under 59 in comparison with sex- and age-matched controls. The relative lack of corpus gastritis might play a role in the pathogenesis of RE in our population through preservation of the acid secretion area. [source]

    Using serum pepsinogens wisely in a clinical practice

    JOURNAL OF DIGESTIVE DISEASES, Issue 1 2007
    Kazumasa MIKI
    Serum pepsinogen (PG) has been used as biomarkers of gastric inflammation and mucosal status, including atrophic change, before the discovery of Helicobacter pylori (H. pylori). Serum pepsinogen I (PG I) and pepsinogen II (PG II) levels are known to increase in the presence of H. pylori -related nonatrophic chronic gastritis. The measurement of serum PG provides much information on the presence of intestinal metaplasia as well as atrophic gastritis. The eradication of H. pylori provokes a significant change in serum PG values: it reduces both PG I and PG II and elevates the PG I to PG II ratio. Recently, the serum PG test method has been the first screening step in Japan, as well as photofluorography. Serum PG tests are used to screen for high risk subjects with atrophic gastritis, rather than as a test for cancer itself. Unlike photofluorography or endoscopy, serum PG screening can identify non-ulcerated differentiated asymptomatic cancer, irrespective of the size and location of the lesion. Most cases detected by the PG method are asymptomatic early gastric cancers and are limited to the mucosa, which are particularly well suited for endoscopic treatment. The PG method can contribute greatly to the patients' quality of life. [source]

    Feasibility and cost-effectiveness of using magnification chromoendoscopy and pepsinogen serum levels for the follow-up of patients with atrophic chronic gastritis and intestinal metaplasia

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2007
    Mário Dinis-Ribeiro
    Abstract Background:, The follow-up of patients with atrophic chronic gastritis or intestinal metaplasia may lead to early diagnosis of gastric cancer. However, to-date no cost-effective model has been proposed. Improved endoscopic examination using magnification chromoendoscopy together with non-invasive functional assessment with pepsinogen serum levels are accurate in the diagnosis of intestinal metaplasia (extension) and minute dysplastic lesions. The aim of this study was to assess the feasibility and cost-effectiveness of a follow-up model for patients with atrophic chronic gastritis and intestinal metaplasia based on gastric mucosal status using magnification chromoendoscopy and pepsinogen. Methods:, A cohort of patients with lesions as severe as atrophic chronic gastritis were followed-up according to a standardized protocol using magnification chromoendoscopy with methylene blue and measurement of serum pepsinogen I and II levels. A single node decision tree and Markov chain modeling were used to define cost-effectiveness of this follow-up model versus its absence. Transition rates were considered time-independent and calculated using primary data following cohort data analysis. Costs, quality of life and survival were estimated based on published data and extensive sensitivity analysis was performed. Results:, A total of 100 patients were successfully followed-up over 3 years. Seven cases of dysplasia were diagnosed during follow-up, all among patients with incomplete intestinal metaplasia at baseline, six of whom had extensive (pepsinogen I to II ratio <3) incomplete intestinal metaplasia. For those individuals with atrophic chronic gastritis or complete intestinal metaplasia, a yearly measurement of pepsinogen levels or an endoscopic examination on a 3-yearly basis would cost ,455 per quality-adjusted life year (QALY) gain. Endoscopic examination and pepsinogen serum level measurement on a yearly basis would cost ,1868 per QALY for patients with extensive intestinal metaplasia. Conclusions:, The follow-up of patients with atrophic chronic gastritis or intestinal metaplasia is both feasible and cost-effective if improved accurate endoscopic examination of gastric mucosa together with non-invasive assessment of gastric mucosal status are used to identify individuals at high-risk for development of gastric cancer. [source]

    Serum gastrin and pepsinogens do not correlate with the different grades of severity of gastro-oesophageal reflux disease: a matched case,control study

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2008
    K. MONKEMULLER
    Summary Background, Gastrin and pepsinogens reflect the functional state of the gastric mucosa. Aim, To evaluate whether serum gastrin and pepsinogens correlate with the different grades of severity of gastro-oesophageal reflux disease (GERD). Methods, In all, 388 patients with heartburn not taking any form of acid suppressive therapy were matched-controlled for age and gender and sub-classified into four groups: group 1 non-erosive reflux disease (NERD); group 2, erosive reflux disease (ERD) Los Angeles (LA) A and B, group 3, ERD LA C and D; group 4 Barrett's oesophagus (BO). Fasting serum was analysed for gastrin 17, pepsinogen I, pepsinogen II und Helicobacter pylori using specific EIA tests (GastroPanel; Biohit, Plc). Statistics: Kruskal,Wallis test and analysis of variance. Results, There was a significant difference among the four groups with respect for pepsinogen I, but not for pepsinogen II, the pepsinogen I pepsinogen II ratio, H. pylori serology and gastrin levels. Pepsinogen I was the lowest in NERD and the highest in BO (median 91.6, mean ± standard deviation 106.2 ± 51.6 vs. median 114.7, mean ± standard deviation 130.4 ± 70.6; P = 0.046). Pepsinogen I levels were higher in H. pylori positive subjects. After adjusting for H. pylori status, the differences in pepsinogen I across patient groups were no longer statistically significant (P = 0.298). Conclusions, Serum gastrin and pepsinogen I and II do not correlate with the different grades of severity of GERD. The non-invasive GastroPanel is not useful for the differentiation of the various forms of GERD. [source]

    Effect of Smoking on Serum Pepsinogen I Level Depends on Serological Status of Helicobacter pylori

    CANCER SCIENCE, Issue 3 2001
    Masayuki Tatemichi
    Serum pepsinogen (sPG) levels are used in gastric cancer screening programs. However, modification of sPG levels by smoking habit, according to the status of Helicobacter pylori (H. pylori) infection has been little investigated. This study investigated the effects of smoking on serum levels of pepsinogen I (PG I), pepsinogen II (PG II), and gastrin by IgG titer of antibody against H. pylori (Hp-IgG titer) using the data from 356 current-smokers and 262 non-smokers (133 never-smokers and 129 ex-smokers) in a cross-sectional study of 618 men aged 40 to 49 years. PG I, PG II, PG I/PG II ratio and gastrin were significantly associated with Hp-IgG titer in never-smokers [Spearman's correlation coefficient (95% confidence interval): 0.23 (0.07, 0.39), 0.52 (0.41, 0.63), -0.40 (-0.54, -0.27), and 0.25 (0.10, 0.41), respectively]. However, the correlation coefficients of PG I and PG H decreased in current-smokers, 0.02 (-0.1, 0.13) and 0.32 (0.22, 0.42), respectively. In H. pylori seronegative and low titer cases, the mean PG I level was significantly (P<0.01) higher in current-smokers, compared with non-smokers. However, in high titer cases, the mean PG I level was lower in current-smokers. Mean PG II and gastrin levels, and PG I/PG II ratio did not differ according to smoking habits by Hp-IgG titer. The gastrin level was significantly correlated with PG H, but not PG I. These data indicate that current smoking influences the serum PG I level depending on Hp-IgG titer and the associations between sPGs and Hp-IgG titer. Gastrin is not involved in the modification of PG I levels by smoking. [source]