Gerald Fraser

A patient education program is cost-effective for preventing failure of endoscopic procedures in a gastroenterology department

OBJECTIVE:The growing use and complexity of endoscopy procedures in GI units has increased the need for good patient preparation. Earlier studies in this area have focused on the psychological benefits of patient education programs. The present study was directed at determining cost-effectiveness of a patient education program.METHODS:A prospective, randomized, controlled design was used. The patient population consisted of 142 patients aged 18–90 yr referred for an endoscopy procedure. Ninety-one (64%) participated in a targeted educational session conducted by a dedicated departmental nurse (group 1), 38 (27%) did not (group 2), and 13 (9%) received telephonic instruction (group 3). Before the endoscopy, all patients completed a questionnaire covering background data, endoscopy-related variables, anxiety level, and satisfaction. Patient cooperation and success/failure of the procedure were documented by the attending nurse.RESULTS:Male gender, previous endoscopy, and explanation from the referring physician were associated with a low level of anxiety (p < 0.05). There was a significant association between attendance in the education program and success of the endoscopy (p = 0.0009). Cancellations of procedures because of poor preparation occurred in 4.39% of group 1 in comparison with 26.31% and 15.38% of groups 2 and 3, respectively (p = 0.005). The overall cost of the procedure was reduced by 8.6%, 8.9%, and 5.5% for gastroscopy, colonoscopy, and sigmoidoscopy, respectively. All participants expressed satisfaction with the brochure.CONCLUSION:A pre-endoscopy patient education program apparently increase patient compliance, thereby decreasing both the need for repeated examinations and their attendant costs.

The alkaline tide phenomenon

The parietal cell is capable of secreting high concentrations of hydrochloric acid into the lumen of the stomach. The apical membrane of this cell contains K+H+ ATPase, which is responsible for proton transport into the lumen. Potassium and chloride channels are also present. The basolateral membrane of the parietal cell possesses transporters that maintain intracellular homeostasis. Specifically, large amounts of bicarbonate that are generated by carbonic anhydrase must be removed from the cell to prevent alkalinization. Efflux of bicarbonate into the blood after acid secretion can be detected and is known as the alkaline tide. Determination of the alkaline tide has been used to measure acid secretion. In this review, we summarize the published data.

Screening Colonoscopy for Colorectal Cancer in Asymptomatic People: A Meta-Analysis

Objective The preferred method for screening asymptomatic people for colorectal cancer (CRC) is colonoscopy, according to the new American guidelines. The aim of our study was to perform a meta-analysis of the prospective cohorts using total colonoscopy for screening this population for CRC. We looked for the diagnostic yield of the procedure as well as for its safety in a screening setting. Methods We included papers with more than 500 participants and only those reporting diagnostic yield of adenoma (and/or advanced adenoma) and CRC. Nested analysis were performed for secondary endpoints of complications and CRC stages when this information was available. All analyses were performed with StatDirect Statistical software, version 2.6.1 (http://www.statsdirect.com). Results Our search yielded ten studies of screening colonoscopy conducted in asymptomatic people that met our inclusion criteria, with a total of 68,324 participants. Colonoscopy was complete and reached the cecum in 97% of the procedures. Colorectal cancer was found in 0.78% of the participants (95% confidence interval 0.13–2.97%). Stage I or II were found in 77% of the patients with CRC. Advanced adenoma was found in 5% of the cases (95% confidence interval 4–6%). Complications were rare and described in five cohorts. Perforation developed in 0.01% of the cases (95% confidence interval 0.006–0.02%) and bleeding in 0.05% (95% confidence interval 0.02–0.09%). Conclusions Our findings support the notion that colonoscopy is feasible and a suitable method for screening for CRC in asymptomatic people.

Factors associated with radiation exposure in patients with inflammatory bowel disease.

Background  Inflammatory bowel disease (IBD) patients undergo multiple radiological evaluations.

PET/CT Enterography in Crohn Disease: Correlation of Disease Activity on CT Enterography with 18F-FDG Uptake

We combined 18F-FDG PET and CT enterography in a single examination and compared the level of 18F-FDG uptake measured by maximal standardized uptake value (SUVmax) with the CT enterography patterns of disease activity found in patients with Crohn disease (CD). Methods: Twenty-eight patients (mean age, 37.5 y; 11 male and 17 female) suspected of having active CD underwent PET/CT enterography. Abnormal bowel segments recognized on CT enterography were graded qualitatively for the presence of perienteric fat infiltration, the comb sign, and intramural attenuation and by quantitative measurements of mural enhancement (Hounsfield units) and thickness (mm). Also, for each patient, normal segments of the ileum and colon were noted, and CT enterography measurements of thickness and enhancement were obtained. For segments detected on CT enterography, a volume of interest was placed on the fused 18F-FDG PET scan, and the SUVmax was obtained. Results: Of the 28 patients with suspected active CD, 22 had 85 abnormal segments and 6 had no abnormal segments. SUVmax was significantly higher in the abnormal segments than in the normal segments (5.0 ± 2.5 [95% confidence interval, 4.5–5.5] and 2.1 ± 0.69 [95% confidence interval, 1.9–2.2], respectively; P < 0.0001). A good correlation was found between SUVmax with CT enterography measurements of mural thickness and enhancement (P < 0.00001). There was a significant difference in SUVmax between the 3 levels of disease activity found by intramural attenuation, perienteric fat infiltration, and the comb sign on CT enterography. SUVmax was significantly higher when there were intense CT enterography findings of active disease (P < 0.001). Conclusion: SUVmax assessment may allow an objective, reliable indication of the grade and severity of inflammation activity in abnormal segments of the bowel detected by CT enterography.

Infliximab-Related Infusion Reactions: Systematic Review

Objective: Administration of infliximab is associated with a well-recognised risk of infusion reactions. Lack of a mechanism-based rationale for their prevention, and absence of adequate and well-controlled studies, has led to the use of diverse empirical administration protocols. The aim of this study is to perform a systematic review of the evidence behind the strategies for preventing infusion reactions to infliximab, and for controlling the reactions once they occur. Methods: We conducted extensive search of electronic databases of MEDLINE [PubMed] for reports that communicate various aspects of infusion reactions to infliximab in IBD patients. Results: We examined full texts of 105 potentially eligible articles. No randomised controlled trials that pre-defined infusion reaction as a primary outcome were found. Three RCTs evaluated infusion reactions as a secondary outcome; another four RCTs included infusion reactions in the safety evaluation analysis; and 62 additional studies focused on various aspects of mechanism/s, risk, primary and secondary preventive measures, and management algorithms. Seven studies were added by a manual search of reference lists of the relevant articles. A total of 76 original studies were included in quantitative analysis of the existing strategies. Conclusions: There is still paucity of systematic and controlled data on the risk, prevention, and management of infusion reactions to infliximab. We present working algorithms based on systematic and extensive review of the available data. More randomised controlled trials are needed in order to investigate the efficacy of the proposed preventive and management algorithms.

Does Helicobacter pylori affect gastric mucin expression? Relationship between gastric antral mucin expression and H. pylori colonization

BACKGROUND/OBJECTIVE: Helicobacter pylori colonizes the gastric mucous gel layer, the surface epithelium and glands. It has been shown that H. pylori infection causes aberrant expression of gastric mucins MUC 5 and MUC 6. This study aimed to determine the distribution of MUC 5 and MUC 6 in the gastric antrum of dyspeptic patients, and to investigate changes in this pattern in the presence of H. pylori and after successful eradication. MATERIALS AND METHODS: Gastric antrum biopsy specimens were examined by immunohistochemistry for mucin gene (MUC 5 and MUC 6) expression. Polyclonal antibodies were used to detect amino acid tandem repeats of each protein. A scoring system (0-3) was used to assess staining intensity at three sites: foveola, mucous neck cells and glands. H. pylori status was determined by histology and rapid urease test, and considered positive or negative when both tests were positive or negative, respectively. The study included 49 patients positive for H. pylori, in 36 of whom successful eradication was performed, and 11 H. pylori-negative patients. RESULTS: There was a gradient of MUC 5 expression, higher to lower, from the surface to the glands, which was more pronounced before eradication. Increased MUC 5 synthesis in the mucous neck cells and in the glands was found after H. pylori eradication (P = 0.016). MUC 6 was synthesized in the glands more than in the mucous neck cells or foveola. MUC 6 was also secreted into the lumen and probably comprised the superficial part of the unstirred mucous layer. CONCLUSION: The change in MUC 5 synthesis may reflect H. pylori colonization.

Mesalamine-Induced Granulomatous Hepatitis

A 42-yr-old man with ulcerative colitis was admitted for investigation of prolonged fever associated with cholestatic liver tests. Endoscopic retrograde cholangiopancreatography demonstrated a normal biliary tree, and liver biopsy showed granulomata. A clinical diagnosis of drug-induced granulomatous hepatitis was established as the symptoms disappeared after cessation of mesalamine therapy and recurred on rechallenge. Although the differential diagnosis of fever and hepatitis in patients with inflammatory bowel disease is wide, in this case mesalamine is the most likely cause.

The ion conductances of colonic crypts from dexamethasone-treated rats.

Whole-cell patch-clamp studies were performed in isolated colonic crypts of rats pretreated with dexamethasone (6 mg/kg subcutaneously on 3 days consecutively prior to the experiment). The cells were divided into three categories according to their position along the crypt axis: surface cells (s.c.); mid-crypt cells (m.c.) and crypt base cells (b.c.). The zero-current membrane voltage (Vm) was −56 ± 2 mV in s.c (n = 34); −76 ± 2 mV in M.C. (n = 47); and −87 ± 1 mV in b.c. (n = 87). The whole-cell conductance (Gm) was similar (8–12 nS) in all three types of cells. A fractional K+ conductance accounting for 29–67% ofGm was present in all cell types. A Na+conductance was demonstrable in s.c. by the hyperpolarizing effect onVm of a low-Na+ (5 mmol/1) solution. In m.c. and b.c. the hyperpolarizing effect was much smaller, albeit significant. Amiloride had a concentration-dependent hyperpolarizing effect onVm in m.c. and even more so in s.c.. It reducedGm by approximately 12%. The dissociation constant (KD) was around 0.2 μmol/l. Triamterene had a comparable but not additive effect (KD = 30 μmol/l,n = 14). Forskolin (10 μmol/l, in order to enhance cytosolic adenosine 3′, 5′-cyclic monophosphate or CAMP) depolarizedVm in all three types of cells. The strongest effect was seen in b. c..Gm was enhanced significantly in b.c. by 83% (forskolin) to 121% [8-(4-chlorophenylthio)cAMP]. The depolarization ofVm and increase inGm was caused to large extent by an increase in Cl− conductance as shown by the effect of a reduction in bath Cl− concentration from 145 to 32 mmol/1. This manocuvre hyperpolarizedVm under control conditions significantly by 6–9 mV in all three types of cells, whilst it depolarizedVm in the presence of forskolin in m.c. and in b.c.. These data indicate that s.c. of dexamethasone-treated rats possess mostly a K+ conductance and an amiloride- and Tramterene-inhibitable Na+ conductance. m.c. and b.c. possess little or no Na+ conductance; theirVm is largely determined by a K+ conductance. Forskolin (via cAMP) augments the Cl− conductance of m.c. and b.c. but has only a slight effect on s.c.

A Chromanol Type of K+ Channel Blocker Inhibits Forskolin- but Not Carbachol-Mediated Cl- Secretion in Rat and Rabbit Colon

In a previous study [Lohrmann et al: Pflugers Arch Eur J Physiol 1995;429:517-530] we have shown that chromanol K+ channel blockers inhibit Cl– secretion in rabbit colon. Their effect was easily demonstrable after stimulation by hormones acting through increases of cytosolic cAMP. The present study was undertaken to test in more detail the mechanism of action of one of these compounds (293 B). Two types of studies were performed: Ussing chamber experiments in rabbit distal colon and whole cell patch clamp studies in the isolated in vitro perfused rat colonic crypts. Carbachol (CCH, 100 µmol/l) enhanced Cl– secretion, quantified as equivalent short circuit current (Isc), in rabbit colon significantly more than did prosta-glandin E2 (PGE2). In whole cell patch clamp studies in rat colonic crypt cells from the base, CCH hyperpolarized the membrane voltage (Vm) and enhanced whole cell conductance (Gm). In agreement with previous impalement studies, 10 µmol/l 293 B depolarized Vm in forskolin-treated rat colonic crypt base cells even further and reduced Gm. In Ussing chamber experiments in rabbit colon, 293 B abolished the Isc induced by PGE2. CCH, in the continued presence of 293 B, still induced a large Isc. These data indicate that 293 B specifically inhibits the forskolin- but not the CCH-induced Cl– secretion, and supports our previous conclusion that this class of substances inhibits a cAMP-regulated K+ conductance.