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The purpose of this study was to characterize the radiographic findings of antral gastritis and to determine whether there are differences in the appearance of antral gastritis in patients with and without Helicobacter pylori infection. A search of radiology, endoscopy and pathology files revealed 90 patients with antral gastritis on double contrast upper gastrointestinal tract studies who had endoscopy with testing for H. pylori. The barium studies were evaluated to further characterize the findings of antral gastritis without knowledge of the H. pylori status of the patients or of the endoscopy or pathology findings. The radiographic findings of antral gastritis included thickened folds in 67 patients (74%), polypoid antral gastritis (a subset of patients with thickened folds) in 6 (9%), antral erosions in 21 (23%), enlarged areae gastricae in 14 (16%), crenulation of the lesser curvature in 4 (4%), mucosal nodularity in 2 (2%), a hypertrophied antral-pyloric fold in 2 (2%) and antral striae in 1 (1%). 43 patients (48%) with antral gastritis were H. pylori positive and 47 patients (52%) were H. pylori negative. Thickened folds were detected in 39 H. pylori-positive patients (91%) with antral gastritis vs 28 H. pylori-negative patients (60%) (p<0.001); polypoid gastritis in 6 H. pylori-positive patients (14%) vs 0 H. pylori-negative patients (p<0.05); enlarged areae gastricae in 14 H. pylori-positive patients (33%) vs 0 H. pylori-negative patients (p<0.0001); and antral erosions in 2 H. pylori-positive patients (5%) vs 19 H. pylori-negative patients (40%) (p<0.0001). Our experience suggests that antral gastritis caused by H. pylori infection is associated with characteristic features on double contrast studies (including thickened folds, polypoid gastritis and enlarged areae gastricae) and that this condition is rarely associated with antral erosions. Thus, radiologists can often suggest whether the patient's gastritis is caused by H. pylori on the basis of radiographic findings.

The importance of ammonia-producing Helicobacter pylori infection as a cause of subclinical encephalopathy in cirrhosis was investigated. In addition, a single psychometric test that can reliably detect subclinical hepatic encephalopathy was sought. Out-patients with cirrhosis and no overt encephalopathy underwent [14C]urea breath testing once and psychometric testing on two separate occasions, with an intervening course of clarithromycin/omeprazole if they had subclinical encephalopathy (two of four psychometric tests abnormal). Subclinical encephalopathy was present in 27 of 69 patients (39%), and Helicobacter pylori infection in 14 of 69 (20%). There was no association between the two conditions (P = 0.769). Subclinical encephalopathy resolved in 75% of treated Helicobacter pylori-positive patients and 37.5% of treated Helicobacter pylori-negative patients (P = 0.285). Number connection test-B had high reproducibility among untreated patients (R = 0.655) and high correlation (P < or = 0.01) with three surrogate gold standards. In stable cirrhotic patients, subclinical hepatic encephalopathy was found to: (1) have a high prevalence, (2) not be associated with Helicobacter pylori infection, and (3) be readily detected with the number connection test-B alone.

Objective: Despite recently published national guidelines, many physicians have only limited knowledge about Helicobacter pylori infection. We conducted this study to assess internal medicine residents' knowledge about H. pylori., Methods: Two hundred and nineteen residents in seven accredited internal medicine training programs completed a self-administered questionnaire on personal demographics and practices related to testing for-and treating-H. pylori infection., Results: Noon conferences (82%), ward teaching (66%), journals (70%), and sponsored symposia (27%) were their major sources of H. pylori-related information. Forty-eight percent had used office-based tests for the infection. Testing for (and treatment of) Helicobacter pylori infection was recommended by 97% (97%) for newly diagnosed duodenal ulcer, but by only 61% (63%) for a past history of duodenal ulcer. Many recommended testing in unproven conditions and might not have offered treatment to an infected patient. A proton pump inhibitor-based triple-drug regimen was the treatment of first choice of 55%; 20% recommended proton pump inhibitor-based dual regimens. Sixty-six percent and 80%, respectively, underestimated the rates of resistance to clarithromycin and metronidazole. In the absence of gastrointestinal symptoms, 22% would have ordered Helicobacter pylori testing but only 33% of these would undergo treatment if positive., Conclusions: Internal medicine residents usually test for Helicobacter pylori infection in appropriate conditions, but may not always treat the infection when the result is positive. Most use efficacious treatment regimens although many have inaccurate knowledge of resistance rates, which may adversely influence prescribing. Education should focus on practical issues surrounding Helicobacter pylori testing and treatment such as those contained in the American College of Gastroenterology's 1998 practice guidelines.

Objective: The aim of this study was to determine the performance characteristics of the 14C-urea breath test (UBT) performed 2 wk after the completion of therapy for Helicobacter pylori using a 4 to 6 wk study as the gold standard., Methods: Patients with active Helicobacter pylori infection at four medical centers received proton pump inhibitor-based triple or quadruple therapy for 10-14 days. Patients underwent the 14C-UBT 2 and 4-6 wk after the completion of therapy. A positive test was defined as 14CO2 excretion of >200 dpm, a negative test as <50 dpm, and an equivocal test as >50 but <200 dpm. Performance characteristics of the 2-wk UBT were calculated using the 4 to 6-wk result as a gold standard., Results: Eighty-five patients were enrolled and 82 patients (mean +/- SD age, 62 +/- 15 yr; 15 women) completed the protocol. Four patients had equivocal UBT results and were excluded from the analysis. Of the 78 patients, 68 (87%) had a negative 4 to 6-wk UBT. The 2-week UBT yielded a sensitivity of 90% (95% confidence interval 72-100%), specificity of 99% (97-100%), and accuracy of 97% (93-100%). In patients with a persistently positive UBT, 14CO2 excretion at 2 wk was significantly lower than at 4-6 wk after therapy (p = 0.03)., Conclusions: A UBT performed 2 wk after therapy yielded results comparable to 4 to 6 wk testing. Further studies to evaluate the optimal time of confirmatory testing in the age of more effective proton pump inhibitor-based triple therapies are warranted.

A prospective, multicenter study was performed in 11 European centers to evaluate the accuracy of stool testing for active Helicobacter pylori (H. pylori) infection, using the HpSA ELISA antigen assay. The accuracy of this test was assessed in a large number of patients both before and after treatment by comparing results with a rigidly defined gold standard consisting of gastric antral and body biopsies with normal and special stains, as well as culture and rapid urease testing. The accuracy of the stool test was also compared with the currently accepted best noninvasive test, the carbon-13 urea breath test. Five hundred and one treatment naive patients (276 men, mean age 52 yr) were tested after endoscopy (491 patients had evaluable results). The sensitivity and specificity of the stool test were 94.1% (the 95% confidence interval was 90.6-96.6%) and 91.8% (87.3-95.1%), respectively. Pretreatment sensitivity and specificity for breath testing were similar (95.3% [92.2-97.5%] and 97.7% [94.8-99.3%], respectively). One hundred and seven infected patients were reassessed 4 wk after undergoing therapy for H. pylori infection. The posttreatment sensitivity and specificity of the HpSA assay was also excellent, although the confidence intervals were significantly wider because of the smaller number of patients (90% [68.3-98.9%], and 95.3% [88.5-98.7%], respectively). Posttreatment sensitivity and specificity for urea breath testing were also similar (90% [68.3-98.8%] and 98.9% [93.8-100%], respectively). Intercenter variability of test results did not reach statistical significance with either testing method. The authors concluded that HpSA stool testing is a reliable and easy-to-use method for diagnosing H. pylori infection in both treatment naïve and posttreatment patients that compares well with carbon-13 urea breath testing. They site specific advantages of the HpSA assay to include: 1) a more simple sampling method (only one stool specimen is required); 2) the lack of a requirement for trained personnel at the testing site; and 3) there is no need for expensive equipment.

The nature of the relationship between Helicobacter pylori (Hp) infection and gastroesophageal reflux disease (GERD) remains unclear. This article reviews the current body of knowledge regarding the association between these two common entities. The authors examine the potential interactions of Hp and GERD from epidemiologic and pathophysiologic viewpoints and summarize and critique the prevalence and eradication studies that have been performed to date. Special consideration is given to the possible effects that long-term use of proton pump inhibitors may have on Hp gastritis.

Helicobacter pylori antibody testing is accurate for diagnosing untreated patients. Rapid serum testing is as accurate as formal enzyme-linked immunosorbent assay (ELISA) testing. As whole blood fingerstick tests may become the diagnostic method of choice if they are of similar accuracy, 51 patients were studied who had not taken antibiotics, bismuth, sucralfate, or proton pump inhibitors. Concordance between C-14 Urea Breath Testing and HM-CAP ELISA testing served as the study standard for H. pylori diagnosis. Rapid antibody testing was performed with the AccuStat whole blood (Boehringer Mannheim, Mannheim, Germany) and FlexSure HP (Smith Kline Diagnostics, San Jose, CA) serum tests. Antral biopsy for CLO testing and histological evaluation with thiazine staining were available for 18 (35.3%) and 20 patients (39.2%), respectively. Nineteen of 50 patients (38%) were infected. (One patient had discordant tests and was excluded.) FlexSure HP and AccuStat were each positive in 18 (36%) and 19 patients (38%) with sensitivity, specificity, and positive and negative predictive values of 89.5% and 89.5%, 96.8% and 93.5%, 94.4% and 89.5%, and 93.8% and 93.5%, respectively. There were two false-negative FlexSure HP and AccuStat tests and three false-positive tests--1 FlexSure and 2 AccuStat results. CLO test and histology concurred in every case tested. We conclude that both rapid antibody tests are accurate and suitable for screening patients not previously treated for H. pylori infection. Since the AccuStat has preserved diagnostic strength, is less costly, takes less time, and is less labor intensive, whole blood testing is the screening test of choice.

Background: The current, arbitrarily defined gold standard for the diagnosis of H. pylori infection requires histologic examination of two specially stained antral biopsy specimens. However, routine histology is potentially limited in general clinical practice by both sampling and observer error. The current study was designed to examine the diagnostic performance of invasive and non-invasive H. pylori detection methods that would likely be available in general clinical practice., Methods: The diagnostic performance of rotating clinical pathology faculty using thiazine staining was compared with that of an expert gastrointestinal pathologist in 38 patients. In situ hybridization stains of adjacent biopsy cuts were also examined by the expert pathologist for further comparison. Receiver operator characteristic (ROC) analysis was performed to evaluate whether the diagnostic performance of the expert pathologist differed depending upon the histologic method employed. A similar analysis was made to evaluate the diagnostic performance of pathology trainees relative to the expert. In the absence of an established invasive gold standard, non-invasive testing methods (rapid serum antibodies, formal Elisa antibodies and carbon-14 urea breath testing) were evaluated in 74 patients by comparison with a gold standard defined using a combination of diagnostic tests., Results: Using either rapid urease testing of biopsy specimens or urea breath testing as the gold standard for comparison, the diagnostic performance of the rotating clinical pathology faculty was inferior to that of the expert gastrointestinal pathologist especially with regard to specificity (e.g., 69 percent for the former versus 88 percent, with the latter relative to rapid urease testing). Although interpretation of in situ hybridization staining by the expert appeared to have an even higher specificity, ROC analysis failed to show a difference. The mean ROC areas for thiazine and in situ hybridization staining for trainee pathologists relative to the expert were 0.88 and 0.94, respectively. In untreated patients, urea breath testing had a sensitivity and specificity of 100 percent as compared with thiazine staining with a sensitivity of 83 percent and a specificity of 97 percent. Post-therapy, breath testing had a sensitivity of 100 percent but a specificity of only 86 percent as compared with invasive testing with a sensitivity and specificity of 100 percent. Rapid serum antibody testing and formal Elisa antibody testing agreed in 93 percent of cases (Kappa 0.78) with the rapid test being correct in three of the four disagreements., Conclusions: The current study illustrates a number of realities regarding H. pylori diagnosis. There is no diagnostic gold standard in general clinical practice. Accurate interpretation of specially stained slides is a learned activity with a tendency towards overdiagnosis early on. Urea breath testing is likely to be the diagnostic method of choice for untreated patients in general clinical practice although antibody testing is almost as accurate. Rapid antibody tests are at least as accurate as formal Elisa antibody tests. Urea breath testing is useful for confirming cure after therapy, but false-positive results may occur in some patients.

Accurate and cost-effective diagnosis of Helicobacter pylori gastritis has taken on major importance. Several serologic tests for the diagnosis of H. pylori infection are commercially available. We compared the performance of the FlexSure HP rapid IgG antibody test with the conventional HM-CAP ELISA to evaluate whether qualitative office-based serology is reliable enough to replace formal laboratory-based testing. We assessed H. pylori status by concordance in 100 consecutive patients with antral biopsy, rapid urease, and 1 microCi[14C]urea breath tests. Both antibody tests had good sensitivity and specificity (>86%). Concordance between the two antibody tests occurred in 87/93 patients (94%). Based on our data, the office-based FlexSure HP performed equally well as the laboratory-based formal ELISA and may be a better choice for initial serologic diagnosis in untreated patients.

To determine whether the urease-based CLOtest or low-dose 14C urea breath test can predict severity of gastritis or the presence of peptic ulcers, we studied 84 patients presenting for upper endoscopy. Antral biopsies were obtained for histologic analysis and CLOtesting, and urea breath testing was performed. The time to a positive CLOtest and the breath test peak values were correlated with endoscopic findings, severity of gastritis, and bacterial burden. Twenty-four patients had positive urea breath test results (22 with positive CLOtests). Patients with positive breath test results were more likely to have duodenal ulcers, higher grades of gastritis, and increased bacterial burden (p < 0.01 for all comparisons). Correlation between the time to a positive CLOtest or peak breath test values and gastritis severity or bacterial burden was poor (p > 0.05 for all comparisons). In patients with positive tests, no difference was observed between the time to a positive CLOtest or peak breath test value in patients with or without peptic ulcers (p < 0.2 for all comparisons). The low-dose 14C urea breath test and the CLOtest are both accurate for Helicobacter pylori diagnosis. However, neither test predicts the severity of the gastritis, the degree of bacterial burden, or the presence of peptic ulcers.

Numerous detection methods for Helicobacter Pylori (H. pylori) have been developed with varying degrees of purported diagnostic utility. We have developed a rapid nonradioactive in situ hybridization (ISH) method for H. pylori detection in paraffin-embedded tissue and assessed its relative diagnostic performance by receiver operator characteristics (ROC) in comparison to the thiazine stain and CLOtest. Forty-five patients undergoing endoscopy had antral biopsies and concomitant CLOtest performed. ISH for H. pylori was done using a 22-base, biotin-labeled oligonucleotide probe complementary to a portion of H. pylori 16s rRNA with the following sequence: 5'-GGACATAGGCTGATCTTAGC-3'. ISH using this probe was specific for H. pylori with no crossreactivity with other bacterial or fungal organisms. Receiver operator characteristic analysis was used to assess the diagnostic performance of ISH and thiazine techniques. ISH and thiazine stains were done on serial sections, reviewed independently, and scored on a graded scale from 1-5 based upon the degree of assurance of H. pylori presence. Diagnostic performance was assessed in "expert" and "nonexpert" pathologist groups with the CLOtest serving as the invariant test for relative test comparison. The ISH test performed slightly better (ROC area 0.9) than the thiazine (ROC area 0.8) in the nonexpert population, but equally well in the "expert" group (ROC area 0.95, 0.95). ISH followed by routine hematoxylin and eosin staining showed detailed mucosal histology with a dramatic visualization of H. pylori along the surface of the foveolar cells with no evidence of lamina propria invasion. In summary, ISH for H. pylori is an excellent test that is specific, easily read, and allows concomitant detailed histologic mucosal examination.

Background & Aims: The interrelation between Helicobacter pylori infection and proton pump inhibitor therapy in patients with Zollinger-Ellison syndrome is unknown. The aim of this study was to evaluate the influence of these factors on parameters of Zollinger-Ellison syndrome., Methods: Prevalence of H. pylori was determined by biopsy and antibody testing in 84 patients. The influence of H. pylori status on clinical and laboratory parameters of Zollinger-Ellison syndrome was evaluated. Seroconversion after surgery was assessed retrospectively in infected patients., Results: The prevalence of H. pylori exposure was 23% (10% with active infection). Acid output was higher in H. pylori-negative patients, but other clinical and biochemical parameters did not differ. Parameters were also similar for patients determined to be H. pylori positive by histology or antibody testing alone. Seroconversion rates did not differ between those rendered or not rendered disease free despite a significant reduction in acid output., Conclusions: H. pylori infection is not a risk factor for peptic ulceration in patients with Zollinger-Ellison syndrome. The prevalence is lower than in the general population and much lower than for patients with idiopathic peptic ulcer disease. Long-term omeprazole therapy in H. pylori-positive patients with Zollinger-Ellison syndrome may-lead to a reduction in parietal cell mass.

Helicobacter pylori is a common cause of gastritis. No single test is 100% accurate for H. pylori diagnosis. In order to determine whether the presence of typical histological features of H. pylori gastritis may yield diagnostic information, we compared antral histology by H & E stain to the presence of organisms as detected on Thiazine stain of antral specimens, CLOtest, urea breath test and anti-H. pylori serology in 50 consecutive patients. Patients were diagnosed as having active H. pylori infection if at least two of these tests were positive. Patients with only one test positive (N = 5) were considered indeterminate for H. pylori and were excluded, resulting in 19 patients (42%) being classified as H. pylori positive. All slides were reviewed by a single blinded expert gastrointestinal pathologist and graded 0 (none) to 3 (severe) for the presence of acute (polymorphonuclear cells) or chronic (lymphocytes, monocytes, plasma cells) inflammation, lymphoid aggregates, and intestinal metaplasia. Active infection was associated with the presence of both acute and chronic inflammation (P < 0.0001) but not lymphoid aggregates (P = 0.09) or intestinal metaplasia (P = 0.10). The best positive predictors of infection were the presence of any acute inflammation (PPV = 86%) and the combination of any acute and chronic inflammation (PPV = 92%). The best negative predictor was absence of chronic inflammation (NPV = 100%). The presence of moderate to severe (grade 2 or 3) acute or chronic inflammation were each 100% predictive of infection. Moderate to severe chronic inflammation had both 100% sensitivity and specificity for active H. pylori infection, while moderate to severe acute inflammation was only 26% sensitive but 100% specific. The presence of any acute, or the combination of acute and chronic gastritis, is predictive of active H. pylori infection. Moreover, the predictive value correlates closely with the severity of the inflammation. The absence of chronic inflammatory cells rules out active H. pylori infection. These findings support the use of H & E histology-determined features in conjunction with other tests to diagnose H. pylori infection.

The current gold standard for diagnosing H. pylori gastritis requires antral biopsy for urease test (eg, CLOtest) and/or history. We compared this gold standard to a new low-dose capsule-based 1 microCi [4C]urea breath test (UBT) and a rapid serum test for anti-H. pylori antibodies (FlexSure HP) in 50 consecutive patients undergoing upper endoscopy. Antral biopsies within 3 cm of the pylorus were used for CLOtest and were stained with H&E and thiazine. Slides were reviewed by a single, blinded pathologist (Review) and compared to the pathology department report (Report). A true positive was defined as a positive CLOtest or Review. The prevalence of H. pylori infection by each test was: CLOtest 32%, Review 36%, gold standard 42%, UBT 38%, FlexSure HP 44%, Report 44%. UBT had sensitivity = 90%, specificity = 96%, positive predictive value = 95%, and negative predictive value = 93% and accurately determined H. pylori status in a subgroup of 10 patients who had completed treatment. The one false positive breath test occurred in a patient with 2+ chronic inflammation on biopsy and a positive antibody test. There were two false negative breath tests. Each had both negative CLOtests and negative antibody tests. FlexSure HP had sensitivity = 74%, specificity = 89%, positive predictive value = 88%, and negative predictive value = 77% in patients not previously treated, but had a high false-positive rate in the 10 patients after treatment. Pathology department Report and blinded pathologist Review had only 84% agreement, kappa = 0.67. Both CLOtest and UBT agreed better with Review (86%, 87%, kappa = 0.68, 0.73, respectively) than Report (78%, 77%, kappa = 0.53, 0.53, respectively) suggesting that Review is more accurate than Report. When biopsy is done, we recommend that a CLOtest be performed followed by histological examination if the CLOtest is negative to ensure adequate sensitivity. However, interpretation of histological slides has significant interobserver variability even in experienced hands and may be inaccurate at times. FlexSure HP has good PPV but inadequate sensitivity to rule out active infection and is not useful in patients after treatment. UBT is an excellent noninvasive test that should be considered in cases where EGD is otherwise not indicated.

An antibiotic combination that includes a proton pump inhibitor such as omeprazole and an antibiotic such as clarithromycin is likely to become the new standard regimen for treatment of Helicobacter pylori gastritis because this combination is extremely effective and very well tolerated. The current report highlights a potentially significant pharmakokinetic drug interaction between clarithromycin and carbamazepine in two patients with long-standing epilepsy who were given such therapy for Helicobacter pylori gastritis. In both cases, clarithromycin therapy was temporally related to an increase in serum carbamazepine levels, which returned to the therapeutic range following cessation of clarithromycin therapy. The potential implications of this newly recognized drug interaction are discussed.

The present report describes two patients with fasting hypergastrinemia, gastric acid hypersecretion, and Helicobacter pylori gastritis. Provocative testing for Zollinger-Ellison syndrome was negative and imaging studies did not demonstrate an intra-abdominal mass. Following eradication of the Helicobacter pylori infection, the fasting hypergastrinemia resolved in both patients and in one patient the gastric acid hypersecretion also resolved. The implications of this case on the differential diagnosis of Zollinger-Ellison syndrome are discussed.

Endoscopic evaluation of the presence or absence of gastritis is often performed in lieu of biopsy and histologic diagnosis. The purpose of our study was to assess the value of endoscopic examination as a diagnostic test for gastritis. Two endoscopists prospectively assessed the antrum of 73 patients undergoing upper gastrointestinal endoscopy and graded, on a scale of 0-4 (0 = completely absent, 4 = definitely present), the likelihood of gastritis. The following features were also assessed at the time of endoscopy: erythema, nodularity, erosion, edema, and friability. Two concomitant antral biopsies (3 cm from the pylorus on the greater curvature of the stomach) were performed regardless of the endoscopic impression. The histologic findings were graded independently on a scale of 0-3 by two pathologists who were not aware of the endoscopic findings. The following histologic features were graded: acute inflammation, chronic inflammation, lymphoid aggregates, intestinal metaplasia, and quantity of Helicobacter pylori organisms. Receiver operator characteristic analysis, a method derived from signal detection theory, assesses the trade-off of sensitivity and specificity over all cutoff points of a test and is considered the best method by which to compare tests and determine the diagnostic utility of a given test. Receiver operator characteristic analysis gave an area of 0.65 +/- 0.01 SE for endoscopy as a test for gastritis (0.5 = chance, 1 = perfect) as defined by the histologic presence of inflammation. Additionally, endoscopy as a test for the presence of histologically proven Helicobacter pylori gave an area of 0.55 +/- 0.01 SE. All endoscopically graded features treated as separate tests for gastritis and/or H. pylori gave areas of approximately 0.44-0.61, indicative of a poor test. While H. pylori was always associated with at least some degree of inflammation, linear regression analysis revealed no correlation among any of the histologic features or of any histologic feature with any endoscopic feature. We conclude that a tissue diagnosis is essential for the proper diagnosis of gastritis. [ABSTRACT FROM AUTHOR]