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Despite recent advances in the assessment, risk stratification, and treatment of acute pulmonary embolism (PE), it remains a leading cause of cardiovascular morbidity and mortality in the United States each year. Patient presentation and prognosis are heterogeneous, and a variety of diagnostic and therapeutic instruments have arisen to assist in providing patients with the appropriate level of care and aggressiveness of approach. Fortunately, a growing number of institutions now have pulmonary embolism response teams (PERT) that urgently assist with risk assessment and management of patients with massive and sub-massive PE. In service of providers at the point of contact with acute PE, this review aims to summarize the data pertinent to rapid risk assessment and the interpretation of diagnostics used to that end. The role of PERT and the indications for systemic fibrinolysis and invasive therapies are also discussed.

Although sociologists and psychologists have repeatedly demonstrated that colorism shapes how Black Americans evaluate members of their racial group, the literature on colorism in electoral politic...

Radiation-induced coronary heart disease (RICHD) is the second most common cause of morbidity and mortality in patients treated with radiotherapy for breast cancer, Hodgkin’s lymphoma and other prevalent mediastinal malignancies. The risk of RICHD increases with radiation dose. Exposed patients may present decades after treatment with manifestations ranging from asymptomatic myocardial perfusion defects to ostial, triple-vessel disease and sudden cardiac death. RICHD is insidious, with a long latency and a tendency to remain silent late into the disease course. Vessel involvement is often diffuse and is preferentially proximal. The pathophysiology is similar to that of accelerated atherosclerosis, characterised by the formation of inflammatory plaque with high collagen and fibrin content. The presence of conventional risk factors potentiates RICHD, and aggressive risk factor management should ideally be initiated prior to radiation therapy. Stress echocardiography is more sensitive and specific than myocardial perfusion imaging in the detection of RICHD, and CT coronary angiography shows promise in risk stratification. Coronary artery bypass grafting is associated with higher risks of graft failure, perioperative complications and all-cause mortality in patients with RICHD. In most cases, the use of drug-eluting stents is preferable to surgical intervention, bare metal stenting or balloon-angioplasty alone.

Radiation-induced cardiovascular disease (RICVD) is the most common nonmalignant cause of morbidity and mortality among cancer survivors who have undergone mediastinal radiation therapy (RT). Cardiovascular complications include effusive or constrictive pericarditis, cardiomyopathy, valvular heart disease, and coronary/vascular disease. These are pathophysiologically distinct disease entities whose prevalence varies depending on the timing and extent of radiation exposure to the heart and great vessels. Although refinements in RT dosimetry and shielding will inevitably limit future cases of RICVD, the increasing number of long-term cancer survivors, including those treated with older higher-dose RT regimens, will ensure a steady flow of afflicted patients for the foreseeable future. Thus, there is a pressing need for enhanced understanding of the disease mechanisms, and improved detection methods and treatment strategies. Newly characterized mechanisms responsible for the establishment of chronic fibrosis, such as oxidative stress, inflammation and epigenetic modifications, are discussed and linked to potential treatments currently under study. Novel imaging modalities may serve as powerful screening tools in RICVD, and recent research and expert opinion advocating their use is introduced. Data arguing for the aggressive use of percutaneous interventions, such as transcutaneous valve replacement and drug-eluting stents, are examined and considered in the context of prior therapeutic approaches. RICVD and its treatment options are the subject of a rich and dynamic body of research, and patients who are at risk or suffering from this disease will benefit from the care of physicians with specialty expertise in the emerging field of cardio-oncology.

Background The effectiveness of many heart failure (HF) treatments has been demonstrated, and national guidelines have been widely disseminated, yet HF care remains suboptimal. Numerous studies have examined barriers to HF care, but to date, there has been limited synthesis of these findings. Methods and results Sixty articles reporting data on barriers to HF care published between 1998 and 2007 met the criteria for inclusion in this review. Barriers to care were reported at the patient, provider, and system levels. Patient barriers were reported in 45 studies and were categorized in the main themes of knowledge, adherence, communication, functional limitations, comorbidities, psychosocial, and socioeconomic factors. Provider barriers were examined in 23 studies and included knowledge, diagnostic challenges, pharmacological concerns, communication issues, and personal factors. Barriers at the healthcare system level were reported in 13 studies and pertained to problems with organizational structure, communication, and lack of resources. Several barriers were interrelated and could not be exclusively categorized to a single level of care, with overlap also occurring within the main barrier themes. Conclusions Barriers to HF care were common and pervasive throughout the continuum of care. To effectively improve the quality of care and outcomes among HF patients, obstacles to HF care must be addressed at multiple levels.

Summary Background : Recently, biliary sludge has been strongly correlated with ‘idiopathic pancreatitis’. It is often diagnosed by trans-abdominal ultrasonography, despite the low sensitivity of this investigation. New scanners, using second harmonic imaging, may improve the quality of the echographic picture. Aim : To verify the impact of this methodology on the detection of biliary sludge in patients with ‘idiopathic’ pancreatitis. Methods : Fifty patients with ‘idiopathic’ pancreatitis observed over a 18-month period entered the study. Exclusion criteria were gall-bladder stones, polyps, clinical conditions related to biliary sludge development and haemolytic disorders. Patients were assessed blind by two operators using either conventional ultrasonography or second harmonic imaging. The parameters of diagnostic quality of both examinations were evaluated using, as the gold standard, microscopic examination of the gall-bladder content collected at endoscopy after cholecystokinin infusion. Results : An improvement in sensitivity, specificity, efficiency and negative predictive value was obtained by second harmonic imaging compared with conventional ultrasonography. Conclusions : Second harmonic imaging, in our experience, is a reliable non-invasive tool for the diagnosis and follow-up of biliary sludge in the course of ‘idiopathic’ pancreatitis.

Summary Background : Certain evidence suggests that Helicobacter pylori strains expressing genes for cytotoxin production show a higher sensitivity than non-cytotoxic organisms to eradication treatment. No data are available on the involvement of bacterium-related lesions in different therapeutic outcomes. Aims : (i) To investigate whether differences in eradication rates may be related to the different expression of virulent strains (cagA, vacA, iceA) in patients undergoing proton pump inhibitor-based triple therapy, and (ii) to evaluate whether therapeutic outcome may be affected by bacterium-induced gastric lesions. Methods : One hundred and ten H. pylori-positive subjects were enrolled. H. pylori was genotyped by polymerase chain reaction. Treatment consisted of lansoprazole–amoxicillin–clarithromycin, twice daily for 1 week. Eradication was checked by urea breath test. Results : The eradication rate was 70%, and the absence of cagA was associated with unsuccessful treatment. No difference between the groups with successful and unsuccessful eradication was found with regard to vacA and iceA. Lympho-epithelial lesions and fibrosis were associated with unsuccessful treatment. Conclusions : The present data confirm the importance of cagA (but not vacA and iceA) as a predictor of successful eradication. When fibrosis and lympho-epithelial lesions are present, therapy appears to be less effective. Therefore, these histological features may be involved in an unsuccessful therapeutic outcome.

Alfalfa (Medicago sativa L.) has been considered as a biofuel feedstock. A system has been proposed to produce electricity from the stems and utilize the leaves as a livestock feed. We determined the effects of harvest regimes on yield and quality of leaf, stem, and total herbage of six alfalfa entries. We applied three harvest regimes involving three harvests per year at bud stage or early flower, or two harvests per year at late flower. An early flower harvest regime had the highest leaf yield (average of 5.6, 4.5, and 4.5 Mg ha -1 for the early flower, late flower, and midbud regimes, respectively), and the late flower harvest regime had the highest stem yield (average of 5.8, 5.3, and 3.9 Mg ha -1 for the late flower, early flower, and midbud regimes, respectively). Leaf concentration decreased with increased herbage maturity (average of 540, 517, and 458 g kg -1 for the midbud, early flower, and late flower regimes, respectively) and was associated with total herbage crude protein (CP) (r = 0.65, P < 0.05) and acid-detergent fiber (ADF) and neutral-detergent fiber (NDF) (r = -0.76, P < 0.05). Harvest regime did not affect total seasonal herbage yield or stand persistence. Alfalfa entries differed in herbage quality, leaf concentration, and leaf yield, but did not consistently differ in total herbage or stem yield. Herbage yield and quality differences among entries were similar for all harvest regimes. Producers can affect stem and leaf yields by selection of harvest regime.

The rapid pull-through (RPT) technique during esophageal manometry helps to identify various pressure profiles of hiatal hernia (HH), based on the presence of two high pressure zones: the diaphragmatic crura (DC) and the lower esophageal sphincter (LES). Our aim was to correlate different HH profiles with frequency of reflux episodes in patients with gastroesophageal reflux disease (GERD). Seventy-eight patients with GERD and HH underwent esophageal manometry with RPT and were grouped according to the prevalent pressure profile of HH. Twenty-four-hour pH-metry served to quantify traditional (TR) and nontraditional refluxes (drop of 1 pH unit with pH > 4 or pH < 4 and time < 5 sec) (NTR) during total, upright, and recumbent periods. The group with a prevalent "flat" HH profile, representing LES and DC impairment, had significantly more TRs in total time of reflux (P < 0.01) and in recumbent and upright periods (P < 0.05) compared to the group with a prevalence of the two pressure peaks, corresponding to LES and DC efficiency. However, the group with the flat profile had significantly more NTRs + TRs than the group with pressure peaks in total time (P < 0.01) and recumbent position (P < 0.001) but not in the upright position. Hiatal hernia predisposes to GERD, but only the associated impairment of the LES and diaphragmatic crura pressures represents a condition of high risk for gastroesophageal reflux events

Mental stress (MS) may alter gastric sensory-motor function. The aim of the study was to assess postprandial autonomic nervous system activity and stress hormones in response to acute mental stress in dyspeptic patients.A total of 25 patients with postprandial distress syndrome (PDS; 11 mol L(-1), age 35.9 ± 9.3 years) and 12 healthy controls (5 mol L(-1), age 25.8 ± 4.6 years) underwent electrogastrography and (13) C-octanoate gastric emptying study using a 480 kcal solid meal. Heart rate variability (LF/HF ratio) and corticotrophin-releasing factor, adrenocorticotropic hormone (ACTH), and cortisol serum levels were also evaluated. Dyspeptic symptoms were scored by analogue visual scale and expressed as symptoms total score (TS). The protocol was repeated twice in each subject, with and without a mental stress test before the meal.Mental stress significantly increased postprandial symptoms severity in patients (TS: stress 111 ± 18 vs basal 50 ± 10; P0.05). Low-/high-frequency component ratio was significantly higher in patients after MS at 120 min (stress 5.46 ± 0.41 vs basal 3.41 ± 0.64; P0.01) and 180 min (stress 5.29 ± 0.2 vs basal 3.58 ± 0.19; P0.05). During stress session, in patients we found a significantly higher ACTH level than baseline at 30, 60, 90, 150, 210, 240, and 270 min and a significantly higher cortisol level at 30, 60, 90, 120, 210, and 270 min. Gastric emptying rate and electrical activity were not influenced by MS.In PDS patients, administration of MS before meal increases symptoms severity by inducing sympathetic hyperactivity and increased stress hormones levels. As the gastric emptying looks not altered, we conclude that these neurohormonal responses mainly affect sensitive function.

Whole brain volume and head size, estimated by the measurement of occipito-frontal circumference (OFC), have been implicated in a variety of developmental disorders. The goals of this chapter are to review the (a) relation of head growth to general neurodevelopment, (b) growth patterns in premature infants and relation to outcome, (c) overgrowth and its relation to neurodevelopmental disorders, and (d) relation between psychological syndromes and growth patterns. Additionally, this chapter (e) discusses head circumference size and growth in pathologic conditions, focusing on atypical development in overgrowth syndromes and pervasive developmental disorders such as autism. Last, this chapter (f) reviews some practical and technical issues involved in the use of head circumference data for clinical documentation and for research. In summary, increased HC and growth have been found to be associated with higher IQ in neurotypical populations. However, this relationship may more accurately be represented by a U-shaped function, with developmental disorders associated with high and low extremes. In addition, a number of genes have been found to be associated with macrocephaly, which may also contribute to developmental disabilities, including autism. Thus, head circumference may be a useful biological marker for assessing developmental risk and for stratification in genetic analysis.

Enteric glial cells (EGCs) have been recently indicated as key regulators of intestinal inflammation in animals. Whether or not this is true and how these cells participate to inflammatory responses in humans is unknown.We isolated primary EGCs from human small bowel and then, we purified and characterized those using specific glial markers, such as S100B and glial fibrillary acidic protein (GFAP). To mimic an inflammatory scenario, we exposed EGCs to exogenous stimuli, such as lipopolysaccharide and interferon-gamma (LPS and IFN-γ), alone or in combination, to evaluate glial activation [measuring GFAP, S100B level together with c-fos, major histocompatibility complex (MHC) class II, inducible nitric oxide (iNOS) proteins expression and nitric oxide (NO) production] and proliferation, respectively.We showed that, when challenged with a combination of LPS and IFN-γ, EGCs are significantly activated, as indicated by their positivity to c-fos and MHC class II. Similarly, pro-inflammatory stimuli significantly increase the cell proliferation rate, the expression of both S100B and GFAP, and the NO production consequent to the induction of EGCs-derived iNOS protein, with the last being dependent on S100B-RAGE (receptor for advanced glycation endproducts) interaction.Our data provide the first evidence that human EGCs directly respond to pro-inflammatory stimuli by changing their expression profile and by proliferating. The finding that stimulated EGCs are able to produce NO points to a role of this cell population in the scenario of intestinal inflammation.

Background and Aims. Transglutaminases are tissue enzymes involved in different neuronal processes including maintenance and signalling. However, their up-regulation elicited by a variety of noxae contributes to neurodegeneration. This study tested the hypothesis that experimental inflammation evoked transglutaminase up-regulation in myenteric neurons and that this event had an impact on neuronal survival. Methods. Rats with or without trinitro-benzene-sulphonic acid-induced colitis were used. One week after colitis induction, longitudinal muscle-myenteric plexus preparations were obtained from left colon to assess tissue-transglutaminase activity, protein and mRNA expression. Double labelling immunofluorescence using antibodies to neuron-specific enolase and transglutaminase was performed to identify myenteric neurons expressing transglutatninase. Additional sets of experiments evaluated the involvement of transglutaminase in the apoptotic process of cultured myenteric neurons. Results. Compared to controls, rats with colitis showed several tranglutaminase/neuron-specific enolase positive myenteric neurons. Western blot analysis and RT-PCR confirmed that in rats with colitis, the increased neuronal transglutaminase-immunoreactivity was associated with an increased enzyme expression. Similarly, transglutaminase activity was significantly higher than in controls (1100 +/- 280 mU/g vs. 725 +/- 119 mU/g, p

s / Digestive and Liver Disease 41S (2009), S1–S167 S23 to treated CD and normal biopsies. Flow cytometry analysis of T-LPL confirmed that IL-17A is over-produced in CD mucosa, and that both CD4+ and CD8+ cells were major sources of IL-17A (Table). Of the IL-17-producing cells, more than 50% co-expressed IFN-gamma. Blockade of IL-21 activity reduced IL-17A expression in cultures of both untreated CD and PT-stimulated treated CD biopsies. Conclusions: Data indicate that IL-17A expression is up-regulated in CD mucosa, and that IL-21 contributes to sustain IL-17 production. # C. Small bowel diseases 1. Celiac disease OC.05.6 EFFECT OF PROINFLAMMATORY STIMULI ON CELLULAR ACTIVATION AND NITRIC OXIDE PRODUCTION IN HUMAN PRIMARY ENTEROGLIAL CELLS C. Cirillo ∗ , G. Sarnelli, A. Mango, I. Esposito, S. Masone, G. Aprea, R. Cuomo Università degli Studi di Napoli Federico II, Napoli Background and aim: Enteric glial cells (EGC) are involved in intesti- nal inflammation. In humans, there are no in vitro models to study the relationships between EGC and inflammation. Aim: To set up a new method to isolate and purify a primary cul- ture of human EGC and to study EGC activation and responses’ to proinflammatory stimuli. Material and methods: Myenteric plexus preparations were isolated from human ileum of 15 patients undergoing surgery for colon car- cinoma and enzimatically dissociated. Ganglia were plated and cell cultures were grown to subconfluence. After 21 days, EGC were purified of contaminating cells by incubation with the anti-Thy-1.1 ab- coated magnetic beads and separation using a Dynal Magnet ® .Mixed EGC cultures and purified EGC cell line were immunocytochemi- cally characterized with anti-S100B, anti-glial fibrillary acidic protein (GFAP) and anti-alpha-smooth muscle actin antibodies to identify EGC and fibroblasts, respectively. To study the effects of inflammatory stimuli on EGC activation, cells were incubated with lipopolysaccha- ride (LPS, 1 μ g/mL), Tumor Necrosis Factor-alpha (TNF- α , 5ng/ml), interferon-gamma (IFN- γ , 100U/mL) for 32 h alone or in combination. A double labeling immunofluorescence using antibodies to S100B or GFAP was performed to identify EGC expressing c-fos in the nucleus, as a marker of cells activation. S100B mRNA, protein expression and secretion, iNOS expression and NO production were assessed. Results: In mixed EGC cultures, immunocytochemically analysis dis- played that 40% of cultured cells were EGC (S100B and GFAP positives), 50% were fibroblasts and neurons were virtually absent. In contrast, in purified EGC cell line, the presence of contaminating cells was significantly reduced by treatments with Dynabeads ® and the ma- jority of the cells were anti-GFAP and anti-S100B positives. Incubation with LPS and IFN- γ alone, or in combination with TNF- α , resulted in a consistent EGC’s activation (c-fos positive nuclei in S100B/GFAP positive cells), and significantly increased S100B expression, which was able to stimulate iNOS protein expression and NO production. Conclusions: We described for the first time a new method to isolate and purify EGC from human intestine. Proinflammatory cytokines di- rectly activate this cell population and stimulate NO production through the EGC-derived S100B protein

Background and aim: Meal-induced gastric distension and Cholecys- tokinin (CCK) are involved in the food intake. The relationship between meal gastric distension and CCK release have not been studied by non- invasive technique. We studied gastric volumes changes by Magnetic Resonance Imaging (MRI) and CCK serum levels after water preload and liquid (LM) and solid (SM) meals. Material and methods: Ten healthy subjects (4 F; Age 22 ± 3; BMI 23 ± 1) were studied on two days. Two test meals, a SM and LM with a similar nutrient composition (carbohydrate 46%; fat 32%; protein 22%) and energy content were used. Subjects were requested to ingest constant Kcal at 5 min interval (100 kcal/5 min) and to score their satiation level on a visual analogue scale graded 0–5 (1=threshold, 5= maximum satiation- MS). Experiment was scheduled as following: -10 min: 300 ml water preload (WPL); 0 min: solid or liquid meal until MS. CCK levels (ELISA, Phoenix, USA) were measured at baseline, after WPL, at 30, 60, 120 min of meal test. Gastric volume was evaluated by 1.5 T MRI at baseline, after water load, at MS and 120 min. Total (TGV) and proximal (PGV) gastric volumes (as difference respect to baseline) were manually traced by a trained observer. Data are presented as mean ± SD. Results: Kcal ingested and time to reach MS were significantly higher during SM (783 ± 244 kcal; 44 ± 14 min) than LM (630 ± 353 p < 0.01; 31 ± 17 p < 0.01). CCK serum peaks and time to peak were not different in LM and SM (1.62 ± 0.72 ng/ml vs 1.26 ± 0.87, and 41 ± 21 min vs 39 ± 14, respectively). TGV and PGV were not different between the two meal groups after WPL (SM: 271 ± 59 ml, 72 ± 46 vs LM: 309 ± 55, 74 ± 29) and at MS (SM: 554 ± 203 ml, 92 ± 32 vs LM: 560 ± 301, 132 ± 60). However TGV after WPL significantly correlated with CCK peaks in both meal groups (SM: r=0.73; p=0.016 and LM: r=0.62; p=0.049). PGV correlated with CCK peak in LM but not in SM (r=0.72, p=0.015; r=0.026, p=0.82). Conclusions: The MS induced by SM is not depending by GV and by CCK release. In contrast, the ability of LM to induce an earlier satiation is associated to the combined effect of the proximal stomach distension and the maximum CCK release. These results suggest a partial role of both total and proximal gastric distension in to determine CCK release. This relationship appears more evident with a liquid form of meal

Summary Background Oesophageal sensory stimuli alter neurocardiac function through autonomic reflexes. Aim To evaluate in patients with idiopathic supraventricular cardiac dysrhythmias and gastro-oesophageal reflux disease (GERD) whether GE reflux alters neurocardiac function and the effect of acid suppression on cardiac symptoms. Methods Thirty-two patients (13 females and 19 males; age: 20–69 years) with dysrhythmias plus GERD, and nine patients (five females and four males; age: 43–58 years) with GERD only, underwent simultaneous 24-h pH-metry and ECG monitoring. Power spectrum analysis of heart rate variability (PSHRV) was obtained with both its low frequency (LF, sympathetic modulation) and high frequency (HF, vagal modulation) components. Hourly mean oesophageal pH and LF/HF ratio were correlated. A 3 months full-dosage PPI therapy (esomeprazole 40 mg/day) was prescribed. Results In 18 (56%) of the 32 patients with dysrhythmia and in none with GERD only, a significant (P

Recently, biliary sludge has been strongly correlated with 'idiopathic pancreatitis'. It is often diagnosed by trans-abdominal ultrasonography, despite the low sensitivity of this investigation. New scanners, using second harmonic imaging, may improve the quality of the echographic picture.To verify the impact of this methodology on the detection of biliary sludge in patients with 'idiopathic' pancreatitis.Fifty patients with 'idiopathic' pancreatitis observed over a 18-month period entered the study. Exclusion criteria were gall-bladder stones, polyps, clinical conditions related to biliary sludge development and haemolytic disorders. Patients were assessed blind by two operators using either conventional ultrasonography or second harmonic imaging. The parameters of diagnostic quality of both examinations were evaluated using, as the gold standard, microscopic examination of the gall-bladder content collected at endoscopy after cholecystokinin infusion.An improvement in sensitivity, specificity, efficiency and negative predictive value was obtained by second harmonic imaging compared with conventional ultrasonography.Second harmonic imaging, in our experience, is a reliable non-invasive tool for the diagnosis and follow-up of biliary sludge in the course of 'idiopathic' pancreatitis.

Stool antigen test for Helicobacter pylori, a noninvasive assay, is emerging as a strong competitor to urea breath test (UBT). Nevertheless, although the UBT delta value is a semiquantitative indicator of H. pylori intragastric load, until now the H. pylori stool antigen test has been used only as a qualitative investigation. We report here the results of a study performed with the aim of obtaining a semiquantitative measurement of bacterial amount in stools. We studied 15 patients with dyspepsia using H. pylori positivity at histology, the rapid urease test, UBT, and the H. pylori stool antigen test. The result of this last test was expressed by a numerical value we obtained by applying the principle of "standard points" to the absorbance units at spectrophotometric reading. This measurement was previously validated by testing probe sampling of H. pylori stool antigen with known pure and stool-mixed bacterial amounts. A numerical result for H. pylori stool antigen was correlated to UBT delta for each patient using Pearson's r test. Finally, a Student t test was performed to investigate possible differences in UBT and H. pylori stool antigen test values between anti-CagA-positive and -negative patients. We obtained a curve of saturation with both known amount of pure and stool-mixed bacteria. Pearson's r test showed a significant correlation between UBT delta value and H. pylori stool antigen measurement (r = 0.77; p < 0.001). Urea breath test delta and H. pylori stool antigen test values were significantly higher in anti-CagA-positive patients. Our data suggest that a numerical estimation of H. pylori stool antigen may be feasible. This evaluation, similarly to UBT delta, may represent a semiquantitative determination of bacterial intragastric load.

Some methodological in vitro observations concerning bile reflux monitoring (Bilitec) suggested that Bilitec monitoring is underestimating reflux in an acid environment. Moreover, other studies showed that the area above the cutoff level of bilirubin absorbance would provide an adequate quantitative marker for reflux of duodenal contents. Our aim was to study whether correction for intraesophageal acidity and the area above cutoff during Bilitec monitoring affects the results and the correlation with pH measurement and esophageal lesions. In 84 patients (46 men; mean age 46 +/- 2.7 years) evaluated for suspected gastroesophageal reflux disease, we performed ambulatory 24-hr esophageal pH and Bilitec monitoring after an upper gastrointestinal endoscopy. We obtained total area, percent total time, and correction by computer software. The correction factor for bilirubin absorbance was based on literature data for acidified bile (0.06 for pH3.6; 0.21 for pH2.6). Endoscopy revealed esophagitis grade 1-2 (E1-2) and 3-4 (E3-4) in 23 and 16 patients, respectively. A progressive increase of mixed (acid + bile) reflux occurred with increasing severity of endoscopic lesions (E3-4 vs no esophagitis, P0.05). A pathologic Bilitec monitoring result was present in the same 35 patients before and after correction and the correlation between the pH measurement and percent time of bile reflux was not improved by correction for intraesophageal pH (r = 0.386 and r = 0.391; P0.05). The total area of bilirubin absorbance above 0.14 (abs x min) was 7.8 +/- 2.2 in patients without esophagitis, and 11.7 +/- 4.4 and 17.0 +/- 4.2 in the E1-2 and E3-4 groups, respectively (E3-4 vs no esophagitis, P0.05). The correlation between the Bilitec monitoring and pH measurement regarding percent (r = 0.427, P0.01) or area of time below 4 (r = 0.280, P0.05) was not improved by considering the area of bilirubin absorbance above the cutoff level. Correction for intraesophageal pH has only a minor effect on the results of ambulatory Bilitec monitoring. Taking into account the surface rather than the percent of time above the cutoff level for bilirubin absorbance does not improve the correlation of Bilitec with acid reflux and with esophageal lesions.

s / Digestive and Liver Disease 42S (2010) S61–S192 S115 volume and carbon dioxide concentration of carbonated beverage must be explored to exclude interference with gastric function. # D. Motility and nerve-gut interactions 1. Upper and lower GI tract