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BACKGROUND: The urea blood test (Ez-HBT) has been shown to compare favourably with the urea breath test in the diagnosis of active Helicobacter pylori infection. AIM: To examine the performance characteristics of the Ez-HBT Helicobacter blood test in establishing success or failure of therapy in H. pylori-infected adults using the 13C urea breath test as the reference method. METHODS: 13C urea breath test and Ez-HBT Helicobacter blood test were performed 4-6 weeks after completion of treatment in H. pylori positive subjects. Basal urea breath samples were collected; basal Ez-HBT Helicobacter blood test samples were not. Ez-HBT Helicobacter blood test results were reported as positive, negative, or indeterminate. RESULTS: Seventy patients generated 126 measurable sets of urea breath and blood tests. The H. pylori cure rate was 93%. The sensitivity, specificity, and accuracy of the Ez-HBT Helicobacter blood test were 100%, 97%, and 97%, respectively. Six of eight false positive and indeterminate Ez-HBT Helicobacter blood test results could be attributed to incomplete fasting or a 13C enriched diet. After correcting for the non-fasting state, the positive predictive value of the Ez-HBT Helicobacter blood test improved from 56% to 86%. CONCLUSION: The performance characteristics of the Ez-HBT Helicobacter blood test are comparable with that of 13C-urea breath test in establishing H. pylori eradication after therapy. Errors related to incomplete fasting can be mitigated by collection of a basal blood sample.

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1. The purpose of the present study was to test the following hypothesis: propylthiouracil (PTU) treatments of rats induces an increase in the concentration and activity of the mitochondrial ATPase (m-ATPase) inhibitor protein (IF1). The PTU-induced elevated baseline levels of this inhibitor protein inactivated m-ATPase, and prevented hepatotoxicity by a toxic dose of acetaminophen (AAP) (paracetamol), by maintaining hepatic adenosine 5'-triphosphate (ATP) levels. 2. Male Wistar rats were either gavaged with a toxic dose of AAP alone, or after pretreatment with PTU for periods of 3 and 12 days. 3. Twenty four hours after acetaminophen treatment alone, toxicity was manifested by: an approximately 10 fold increase in serum transaminase levels (serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase); depletion of hepatic reduced glutathione (GSH) and ATP levels; loss of inhibitor protein activity, and extensive pericentral necrosis of the hepatocytes. Propylthiouracil pretreatment for 12 days enhanced the concentration of the following metabolites in the liver: ATP (1.5 fold), ATPase inhibitor protein (IF1) (4.5 fold), and reduced glutathione (1.3 fold), while the activity of the inhibitor protein increased 2 fold. When the PTU treated rats were challenged with AAP, transaminases were not elevated, and only sporadic areas of necrosis were detected by histological examination of the liver tissue. In contrast to the 12 day treatment with PTU the 3 day treatment had no protection against AAP. No histological evidence of protection was manifested and the transaminases were not different from AAP treated controls. Most of the protective metabolites were depleted. 4. Our findings suggest that PTU-induced increased concentration of inhibitor protein and GSH, are contributing factors in the prevention of hepatotoxicity by maintaining hepatic m-ATP levels and reducing the harmful effect of the toxic metabolite of AAP.

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OBJECTIVE: To evaluate a new whole blood serology test (Hp Chek; ChemTrak) that detects IgG antibodies to Helicobacter pylori. METHODS: The study was conducted at 10 sites within the United States. Patients undergoing upper endoscopy for dyspepsia were recruited for enrollment. Those treated for H. pylori infection within a year of endoscopy and those who had regularly used proton pump inhibitors, bismuth compounds, or antibiotics within a month of endoscopy were not eligible. During endoscopy, specimens were obtained from the corpus and antrum for histological examination, which was performed by a single experienced pathologist. The Hp Chek was tested using whole blood and serum. Serum was also tested with a reference enzyme-linked immunosorbent assay (ELISA) at a centralized location. Test characteristics for the Hp Chek and ELISA were calculated using histology as the "gold standard." RESULTS: Two hundred eighty-seven patients (140 women and 147 men; mean age 53 +/- 6 yr) were enrolled. The Hp Chek was easy to perform and yielded results 9 min after inoculation of the test cassette with whole blood or serum. When the Hp Chek used with whole blood was compared with histology as the gold standard, the sensitivity was 88%, specificity 85%, positive predictive value 83%, negative predictive value 90%, and percent agreement 86%. There were no statistically significant differences among the results obtained with the Hp Chek using whole blood, the Hp Chek using serum, or reference ELISA. CONCLUSIONS: The Hp Chek whole blood serology test was easy to perform and rapid and yielded performance characteristics comparable to those of a reference ELISA or the Hp Chek used with serum.

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The purpose of this study was to evaluate whole gut lavage with polyethylene glycol electrolyte solution (Colyte), as a potentially adjunctive measure in lowering serum acetaminophen levels. The effect of bowel lavage was evaluated on serial serum acetaminophen concentrations after 2-g and 4-g doses in 7 and 12 male patients, respectively. Mean peak level of serum acetaminophen after 2 g (60 min after intake) was not significantly lowered by bowel lavage. After 4 g, peak acetaminophen serum levels were significantly lower after bowel lavage (65.4% of controls, P < 0.001). Urinary concentrations of the mercapturic acid conjugate of the toxic metabolite were also significantly reduced by lavage (55% after 2 g and 45% after 4 g, P < 0.01). Activated charcoal given orally after administration of 4 g of acetaminophen had no significant effect on peak serum levels and had no additive effect on lavage. These studies suggest that rapid, complete bowel lavage with a polyethylene glycol electrolyte solution may be beneficial as an adjunct to the treatment of the acetaminophen intoxication.

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Approximately 50% of Helicobacter pylori isolates produce a cytotoxin in vitro that induces vacuolation of eukaryotic cells. To determine the in vivo relevance of this phenomenon, we sought to detect cytotoxin-neutralizing antibodies in sera from H. pylori-infected persons. As a group, sera from 29 H. pylori-infected patients neutralized the activity of the purified cytotoxin to a significantly greater extent than sera from 24 uninfected persons (P = 0.007). The cytotoxin neutralizing activity in sera from H. pylori-infected persons was mediated predominantly by the purified IgG fraction. Sera from H. pylori-infected persons neutralized the cytotoxins produced by multiple H. pylori strains, but failed to neutralize trimethylamine-induced cell vacuolation. Neutralization of cytotoxin activity by human or immune rabbit sera was associated with immunoblot IgG recognition of an 87-kD H. pylori protein. Similarly, neutralization of the toxin by sera was associated with IgG recognition of the purified cytotoxin in an enzyme-linked immunosorbent assay (P less than 0.0001). The presence of cytotoxin-neutralizing antibodies in sera from H. pylori-infected persons indicates that the cytotoxin is synthesized in vivo.

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Marked elevations of serum amylase, unexplained despite extensive evaluation in patients with acquired immunodeficiency syndrome (AIDS), prompted this retrospective review of 85 patients to determine the prevalence of hyperamylasemia and identify any associated demographic and etiologic factors. Of 39 patients who had amylase determinations, 54% had hyperamylasemia (2/3 pancreatic, 1/3 salivary) and 31% had pancreatitis. Biliary tract disease, alcohol intake, and opportunistic infections were similar in hyperamylasemic and normoamylasemic subjects. Non-Caucasian race, intravenous drug abuse, renal dysfunction, alkaline phosphatase elevation, and pentamidine use were more prevalent in patients with hyperamylasemia (p less than 0.001, p less than 0.001, p less than 0.01, p less than 0.05, and p less than 0.05, respectively). However, by stepwise deletion multiple regression analysis, only non-Caucasian race, pentamidine use, and Mycobacterium avium-intracellulare infection were significant, independent predictors of hyperamylasemia (R2 = 0.65). Followed over time, in a historical prospective manner, case fatality rates (66.6% and 61.1%) and median survival times (101 and 84 days) were similar in the hyperamylasemic and normoamylasemic groups. We conclude that, although pancreatitis occurs frequently in AIDS, hyperamylasemia is often of salivary origin and clinical outcome is unaffected. Certain demographic factors are strongly associated with hyperamylasemia in AIDS patients, but multiple, concurrent, etiologic factors are probably operative in these patients.

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Total creatine kinase and its isoenzymes CK-MB and CK-BB were measured in the serum of patients admitted with acute abdominal pain or signs suggestive of an intraabdominal catastrophe. Total creatine kinase was measured by automated spectrophotometry, CK-MB by chemiluminescent assay, and CK-BB by radioimmunoassay. Patients were grouped according to their final diagnosis: intestinal infarction (N = 8); all other diagnoses (N = 22); controls (N = 20). CK-BB in the infarction group (22.3 +/- 5.3 ng/ml, mean +/- SE) was significantly greater (P less than 0.01) than in the noninfarction or the control groups (11.0 +/- 0.8 ng/ml and 5.8 +/- 0.7 ng/ml, respectively). There were no differences in total creatine kinase and CK-MB in the three groups. Stepwise deletion multiple regression analysis of 26 independent regressors showed that among a cluster of six significant variables (R2 = 0.92, P less than 0.005), CK-BB greater than 20 ng/ml was the best predictor of intestinal infarction. Results of this study indicate that CK-BB isoenzyme measurement may be useful in the diagnosis of intestinal infarction in man.

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The morphological response of rabbit parietal cells to aspirin was evaluated by grading several ultra-structural features including the extent of the tubulovesicular system, intracellular secretory canaliculi, and microvilli. After exposure of isolated parietal cells and gastric glands to aspirin or histamine, there was an approximately twofold increase in the ratio of secretory to nonsecretory parietal cells, and depletion of extracellular Ca2+ abolished the aspirin-induced morphological changes. Morphometry in parietal cells showed that aspirin induced a sixfold increase in secretory canalicular membrane elaboration. Aspirin potentiated histamine-induced parietal cell respiration and aminopyrine uptake ratio but did not increase basal respiration or aminopyrine uptake, suggesting an apparent dissociation from aspirin-induced morphological changes.

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We studied the effect of gastric versus jejunal tube feedings on gastric pH and evaluated the acid-inhibiting effects of continuous gastric and jejunal infusions of cimetidine. pH was monitored by an intragastric pH probe in 19 gastrostomy and 13 jejunostomy patients during fasting, continuous infusions of Osmolyte, cimetidine, and simultaneously Osmolyte and cimetidine. Gastric Osmolyte increased fasting pH from a mean of 1.32 to 2.78 (P less than 0.01), while jejunal Osmolyte did not (pH 1.02). Continuous gastric infusion of cimetidine maintained a high gastric pH (5.06) in 17 of 19 patients. Jejunal cimetidine also achieved therapeutic serum levels and raised gastric pH to 4.81 in nine of 13 patients. We conclude that the persistently low gastric pH during jejunostomy tube feeding may play a major role in the upper gastrointestinal bleeding previously observed in such patients and that continuous gastric and jejunal cimetidine infusions effectively raise and sustain a high gastric pH.

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This study reports our experience with the placement and long-term follow-up of 26 percutaneous endoscopic jejunostomy (PEJ) tubes in 23 patients over a 2-year period. Eighty-four percent of the PEJ tubes failed and were functional for an average of only 39.5 days. The reasons for failure were: (1) separation of the inner PEJ tube from the outer gastrostomy tube (59%); (2) clogging (32%) due to small PEJ tube diameter; and (3) kinking and knotting (9%). Upper gastrointestinal bleeding occurred in 30% of the patients (7 of 23). Only one patient required blood transfusions (2 units). The etiology of the bleeding was not determined. These patients had a previous history of acid-peptic disease and bleeding occurred despite cimetidine treatment. In contrast, only 1 of the 16 nonbleeding patients had acid-peptic disease (p less than 0.0001) and none were on cimetidine. The frequency of aspiration pneumonia decreased from 13 episodes during nasogastric tube feedings to 5 episodes during PEJ tube feedings. Improvement in the design of the PEJ tubes may increase the longevity and effectiveness of the tubes.

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