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Biomedical subjects

E G Hahn

Publications and source records attributed to E G Hahn.

At least 145 records · Page 8Linked to original sources

[Harmonic imaging for improving diagnosis of liver tumors--preliminary report].

UNLABELLED: Contrast harmonic imaging (CHI) is a new Doppler technology using the non-linear properties of ultrasound contrast agents. AIM: In this pilot study contrast harmonic imaging was evaluated for the detection and characterization of liver lesions. METHODS: Tumor vascularity patterns and diagnostic accuracy in the differential diagnosis of liver lesions were compared in 50 liver lesions using gray-scale sonography, unenhanced and enhanced power Doppler sonography and CHI. In addition, CHI was compared to spiral-CT for the detection of liver metastases in 28 patients. RESULTS: CHI was superior to power Doppler sonography in the visualization of vascularity pattern. Due to the better resolution and image quality of tumor vascularity the diagnostic accuracy of CHI in the differential diagnosis of liver lesions was higher (88% CHI versus 40% unenhanced power Doppler, and 58% contrast-enhanced power Doppler). In the detection of liver metastasis CHI showed a higher sensitivity (96.8%) compared to spiral-CT (74.6%) in 28 patients with 63 metastases. CONCLUSIONS: CHI is a promising new ultrasound technology to further improve the differential diagnosis of liver lesions and the detection of metastases.

Albumins↗

[Stimulation of immunoglobulin E formation in chronic pancreatitis by alcohol drinking and exocrine pancreatic insufficiency].

Many patients with chronic pancreatitis (CP) complain of several types of food intolerance despite elimination of fat and alcohol. Since there are no data on serum immunoglobulin E (IgE) concentrations in CP, IgE concentrations in serum were detected in 97 persons with CP and 50 controls. IgE was analyzed by the use of a highly sensitive fluoro-enzyme-immunoassay. In CP, a significantly raised IgE level (mean +/- SEM; 286.1 +/- 49 KU/L; p < 0.0001) was detected compared with controls (65.2 +/- 13 KU/L). CP-patients without alcohol consumption and normal exocrine pancreatic function were found to have only slightly elevated serum IgE values (120.2 +/- 54 KU/L), whereas patients with exocrine insufficiency treated with enzyme supplementation showed an IgE level of 153.7 +/- 51 and exocrine insufficient patients without treatment of 261.0 +/- 173 KU/L (p = 0.01). IgE levels were far more elevated in the corresponding groups with continued alcohol consumption (> 25 g/day). Alcohol consuming patients with CP and normal pancreatic function had a mean serum IgE of 295.0 +/- 114 KU/L, while patients with alcohol consumption and sufficiently treated exocrine pancreatic insufficiency showed a serum IgE of 393.7 +/- 147 KU/L (p = 0.03). Non-enzyme supplemented patients with CP and exocrine pancreatic insufficiency were characterized by approximately 10-fold increased serum IgE (1080.0 +/- 313 KU/L; p = 0.001). Non-allergic, alcohol consuming patients with CP have significantly increased serum IgE values. Since patients without alcohol consumption and normal pancreatic function or sufficiently treated exocrine insufficiency showed clearly lower IgE values than non-compliant patients with manifest exocrine pancreatic insufficiency, these results are compatible with the assumption that a reduced rate of antigen digestion in exocrine pancreatic insufficiency may lead to an increased intestinal antigen load, stimulating an abnormal humoral immune response with IgE production. Alcohol may further contribute to this by damaging the mucosal barrier.

Adult↗

[Extragastric manifestations of H. pylori infection].

Recently, H. pylori has been associated with several extradigestive diseases such as cardio-vascular, cutaneous, autoimmune, allergic, liver, hematologic disorders, diabetes mellitus, pediatric diseases (sudden infant death syndrome, growth retardation), extragastric MALT-type lymphomas and even colorectal cancer. The potential role of H. pylori infection in the pathogenesis of these extradigestive disorders has been based on the following facts: 1) local gastric infection with H. pylori may exert systemic effects; 2) during chronic H. pylori induced gastritis several different inflammatory mediators are released that are able to cause disorders remote to the primary site of infection and 3) the successful eradication of H. pylori infection improves partly or completely the extradigestive disorders. The available data is conflicting because of the presence of several confounding factors in epidemiological studies. On the basis of the published data any of these associations has been proved. Further prospective studies to explain the association between H. pylori and extradigestive disorders are needed.

Gastritis↗

Right-sided shift found in metachronous colorectal adenomas.

BACKGROUND AND STUDY AIMS: Patients who have had a colorectal adenoma are likely to develop a metachronous adenoma, and therefore need to be kept under surveillance. The question is whether metachronous adenomas will be found at the same anatomical site as the preceding adenomas, thus prompting us to focus surveillance examinations on this region, using flexible sigmoidoscopy or total colonoscopy. PATIENTS AND METHODS: Between 1978 and 1996 a long-term follow up of 1091 patients was prospectively documented at the Erlangen Registry of Colorectal Polyps. The anatomical sites--distal (rectosigmoid) and proximal colon--of two subsequent generations of metachronous adenomas were analysed using logistic regression analysis. RESULTS: In 556 (51%) patients metachronous adenomas were found during follow up. In 211 (37.9%) of these patients a right-sided shift in the first generation of metachronous adenomas in comparison with initial lesions (P<0.0001) was found. Some 305 patients underwent further follow up, and 51 (27.1%) out of 188 patients with metachronous lesions demonstrated a right-sided shift in their second generation (vs. first generation) of metachronous adenomas. Proximally located first generation metachronous adenomas would be missed by flexible sigmoidoscopy in 50.8% of patients with only distal adenomas at baseline colonoscopy, and in 58.7% of patients with second-generation lesions. Multivariate analysis revealed that multiplicity (odds ratio 2.64, 95% CI 1.49-4.66) and size of initial adenomas (>5 mm) (odds ratio 3.60, 95% CI 1.96-6.66) were significantly associated with a right-sided shift in metachronous adenomas, while female gender was associated with a significantly lower tendency to manifest a right-sided shift (odds ratio of 0.64. 95% CI 0.43-0.94). CONCLUSIONS: Metachronous adenomas are found significantly more often in the right colon than would be expected assuming clustering at the same anatomical site as the preceding lesions. Total colonoscopy is thus needed for surveillance, regardless of the initial adenoma site.

Adenoma↗

[Reflux-associated diseases of the otorhinolaryngology tract].

Gastroesophageal reflux disease (GERD) is the most common esophageal disease. It typically presents with heartburn and regurgitation, but it may also cause atypical symptoms, either alone or in combination. About 20 to 60 percent of patients with GERD have ENT symptoms without any heartburn. The most common ENT symptom is a globus sensation, yet there are many possible clinical signs such as laryngitis, pharyngitis, sinusitis, laryngospasm, laryngeal edema and granuloma that may mislead the initial work-up. In this work the pathophysiology, symptomatology, diagnostic measurements and therapeutic options of GERD are discussed. It is suggested that GERD has to be included into differential diagnostic approaches especially when routine treatment of these ENT diseases failes.

Chronic Disease↗

Matrix as a modulator of hepatic fibrogenesis.

The extracellular matrix (ECM) provides cells with positional information and a mechanical scaffold for adhesion and migration. It consists of collagens, glycoproteins, proteoglycans, glycosaminoglycans and molecules that are bound specifically by the ECM, such as certain growth factors/cytokines, matrix metalloproteinases (MMPs) and processing enzymes such as tissue transglutaminase and procollagen propeptidases. This finely tuned ecosystem is dysbalanced in chronic fibrogenesis, which can be regarded as a continuous wound-healing process and which results in scar formation. Importantly, the ECM directs cellular differentiation, migration, proliferation, and fibrogenic activation or deactivation. Partially via defined oligopeptide sequences or structural domains, the ECM transfers specific signals to cells that act in concert with growth factors/cytokines. These signals either confer stress activation, with a resultant fibrogenic response, or stress relaxation, with a fibrolytic response. Alternatively, ECM-derived peptides can modulate angiogenesis, or growth factor and MMP availability and activity. Current ECM-related antifibrotic strategies are based on the identification and in vivo application of ECM-derived biomodulatory peptides, peptide sequences, or their nonpeptidic mimetics. The latter open the opportunity of oral application and an extended biological half-life. Examples are peptides derived from collagens VI (stress activation) and XIV (stress relaxation), or collagenous consensus peptides that remove ECM-bound MMPs and growth factors. Furthermore, certain peptides can be used as targeting structures to the fibrogenic lesion.

Administration, Oral↗

[Pathobiology of dysplasia in chronic inflammatory bowel disease: Current recommendations for surveillance of dysplasia].

Pathobiology of dysplasia in chronic inflammatory bowel disease: Current recommendations for surveillance of dysplasia. Patients with ulcerative colitis and Crohn's disease bear an about 10- and 4-fold increased risk, respectively, for developing colorectal carcinoma. Apart from typical locations of colorectal carcinoma in the sigmoid colon and rectum other locations were also often observed, e. g. right hemicolon or multifocal distribution. Histologically colorectal neoplasms frequently present as mucinous adenocarcinoma (signet-ring cell carcinoma). The risk for neoplasm depends on extension, severity, duration and therapeutic responsiveness of chronic colonic inflammation, and it seems pathogenetically to be similar in ulcerative colitis and Crohn's disease. Colorectal carcinoma in inflammatory bowel disease arises from epithelial dysplasia. Since there are no reliable biological markers available to date, surveillance-programs continue to rely on the discovery of dysplasia (unequivocal intraepithelial neoplasia). Detection of dysplasia by colonoscopy achieves 70-85 % sensitivity.Endoscopic surveillance should start after 8 years of disease's duration in pancolitis, after 10-12 years in left- sided colitis and after 12 years in Crohn's disease of the colon, with regular intervals every 1-2 years. 3-5 biopsies should be done every 10 cm from mucosa free of inflammation. Additionally, every fine or discrete alteration of the mucosal surface should be recorded. Multiple biosies should also be taken from such minimal lesions as well as from more macroscopically suspicious areas like plaques, nodular lesions or stenosis. The clinical consequence of a positive screening for dysplasia is colectomy because of an assumed risk of cancer of about 40-70 %. Dysplasia in macroscopically suspect areas bear the highest risk of cancer (non-adenoma like dysplasia), followed by multiple high-grade lesions without a macroscopic lesion, and multiple low-grade dysplasias. Detection of single dysplastic lesions in flat mucosa should be followed by a control endoscopy after 2-6 months, and if dysplasia is seen again, colectomy is recommended.

Adenocarcinoma, Mucinous↗

Abdominal actinomycosis: complication of endoscopic stenting in chronic pancreatitis?

Pancreatic endotherapy is frequently performed in patients with chronic pancreatitis and stenoses of the main pancreatic duct. In a patient with long-standing chronic pancreatitis and treatment with pancreatic stents, metastatic pancreatic head carcinoma was suspected because of infiltration of the neighboring organs and hepatic lesions. Ultrasound-guided aspiration of one liver lesion revealed grains typical for actinomycosis. In the light of this case, an extracted pancreatic stent was microbiologically investigated for actinomycetes in another patient who had a suspicious lesion of the pancreatic head. Microbiological examination of the extracted pancreatic stent revealed colonization by Actinomyces meyeri, Klebsiella oxytoca, and mixed cultures of anaerobic and saprophytic Gram-positive bacteria. In the following weeks, she developed a septic clinical picture with multiple abscesses of the liver. Actinomyces meyeri, Corynebacterium species, Candida and Enterococcae were cultivated in the aspirates. It seems possible, that treatment with pancreatic stents could have caused invasion of actinomycetes into the parenchyma of the pancreas, which was already harmed by the chronic inflammation, followed by the typical infiltrative growth and hematologic or biliary seeding into the liver.

Actinomycosis↗

Echo-enhanced color- and power-Doppler EUS for the discrimination between focal pancreatitis and pancreatic carcinoma.

BACKGROUND: EUS is a precise method for detection and staging of pancreatic tumors. However, differentiation between inflammatory pseudotumor and pancreatic carcinoma remains difficult. The aim of this study was to evaluate contrast-enhanced EUS as a method of differentiating inflammation and carcinoma based on perfusion characteristics. METHODS: Patients with solid pancreatic masses underwent EUS with a linear echoendoscope. Perfusion in the pancreatic tissue and the mass was assessed with native and contrast-enhanced EUS with power- and color-Doppler imaging. Examinations were evaluated by a blinded reader. A markedly hyperperfused lesion was considered an inflammatory pseudotumor whereas lesions that were hypoperfused compared with surrounding tissue were considered to be carcinoma. RESULTS: Fifteen of 23 patients had hypoperfusion within the mass and 8 patients had hyperperfused lesions. Of the 15 patients with hypoperfused masses, all had pancreatic adenocarcinoma; 1 of 8 patients with a hyperperfused lesion also had adenocarcinoma. The remaining 7 patients had focal inflammation. Sensitivity for differentiation of pancreatic carcinoma versus inflammatory changes was 94%, specificity 100%. CONCLUSION: Echo-enhanced power-Doppler EUS reliably differentiates pancreatic neoplasm and focal pancreatitis. The diagnostic accuracy of this technique is comparable to CT, magnetic resonance imaging, positron emission tomography, and ERCP.

Adenocarcinoma↗

Light-induced autofluorescence spectroscopy for the endoscopic detection of esophageal cancer.

BACKGROUND: Any innovative optical system that facilitates the early endoscopic detection of neoplastic change in the GI mucosa has the potential to greatly improve survival and quality of life for patients prone to have GI malignancies develop. The present article describes light-induced autofluorescence spectroscopy with violet-blue excitation light for in vivo diagnosis of cancerous tissue of the esophagus during routine endoscopy. METHODS: One hundred twenty-nine endogenous fluorescence spectra were obtained from normal mucosa and malignant lesions in 9 patients with squamous cell cancer and 4 with adenocarcinoma of the esophagus. Following spectrographic measurements, biopsy specimens were obtained for definitive classification of the spectra. A special light source capable of delivering either white or violet-blue light for excitation of tissue autofluorescence by means of an endoscope was used. Endogenous fluorescence spectra emitted by tissues were detected with a fiberoptic probe and analyzed with a spectrograph. RESULTS: Squamous cell cancer and adenocarcinoma of the esophagus exhibit specific changes in the emitted fluorescence spectra as compared with normal mucosa. Based on the results obtained in earlier studies, malignant and benign spectra were differentiated with the aid of a mathematical algorithm. By using this algorithm, a sensitivity of 97% and specificity of 95% were obtained for the diagnosis of esophageal carcinoma. CONCLUSIONS: Light-induced fluorescence spectroscopy is useful for the endoscopic detection of squamous cell cancer and adenocarcinoma of the esophagus. This spectroscopic study provides a basis for the design of a simplified autofluorescence imaging system for detection of esophageal neoplasms.

Adenocarcinoma↗

Fluorescence induced with 5-aminolevulinic acid for the endoscopic detection and follow-up of esophageal lesions.

BACKGROUND: The aim of this study was to investigate the use of orally administered 5-aminolevulinic acid (ALA) for in vivo photodynamic diagnosis and follow-up of premalignant and malignant esophageal lesions. METHODS: Twenty-two patients with known or treated malignant and precancerous esophageal lesions were sensitized with orally administered ALA (15 mg/kg). Six patients had Barrett's esophagus, with or without severe dysplasia, 5 squamous cell cancer or early-stage (uT1N0M0) adenocarcinoma, 1 advanced-stage (uT3N1) adenocarcinoma, and 1 patient a lesion with an appearance that suggested esophageal cancer. Nine patients underwent photodynamic diagnosis for follow-up after treatment of esophageal cancer with curative intent; 6 had no macroscopically visible lesion and 3 a barely visible lesion under standard (white-light) endoscopy. Photodynamic diagnosis was conducted 6 to 7 hours after oral administration of ALA by using a special light source capable of delivering either white or violet-blue light. Red fluorescence was detected with a charged coupled device camera attached to a fiberoptic endoscope. Corresponding endoscopic, fluorescence, and microscopic findings were compared. RESULTS: By using histology as the reference standard (n = 86 biopsies), 85% of the biopsy sites with premalignant or malignant histopathology exhibited red fluorescence, whereas only 25% were detected with white-light endoscopy. CONCLUSION: ALA-induced fluorescence might be useful for the early endoscopic detection of malignant esophageal lesions and follow-up after treatment of such lesions with curative intent.

Administration, Oral↗

Faecal elastase-1: lyophilization of stool samples prevents false low results in diarrhoea.

BACKGROUND: In patients with diarrhoea, faecal elastase-1 is used to detect exocrine pancreatic insufficiency. Diarrhoea is defined as >85% stool water content. METHODS: We analysed elastase-1 in 519 stool samples from 310 patients unprocessed as well as after lyophilization in a standard laboratory lyophilizator. Stool water content was calculated by weight difference before and after lyophilization. RESULTS: 151 stool samples were classified as 'diarrhoea' (mean stool water content 88.8%); all others had a mean water content of 75.4%. In the 'diarrhoea' samples, elastase-1 levels were considerably higher after lyophilization--with a calculated normal water content of 75% (606 +/- 359 microg/g, mean +/- s)--compared to measurement when unprocessed (279 +/- 151 microg/g; P < 0.0001). In 16 of the 151 cases (11%), the abnormally low elastase-1 level below 200 microg/g found in unprocessed stools proved normal (>200 microg/g) after lyophilization and correction for stool water content. CONCLUSION: Diarrhoea can result in falsely decreased elastase-1 levels in a number of patients with non-pancreatogenic diarrhoea. Lyophilization is a simple measure by which to determine elastase-1 independently of stool water content. Lyophilization of stool samples can therefore help to prevent wrong positive elastase-1 test results.

Adolescent↗

Influence of bacterial lipopolysaccharide on healing of chronic experimental ulcer in rat.

BACKGROUND: Lipopolysaccharides (LPS) are major components of the outer membrane of Gram-negative bacteria, which play a central role as potent endotoxins in the pathogenesis of the Gram-negative septicaemia. Although it is well known that large amounts of endotoxin may produce haemorrhagic lesions in the stomach, the effect of LPS on ulcer healing has not been fully clarified. The aim of the present study was to examine the effect of parenteral injection of LPS at different doses on the course of ulcer healing in rats. METHODS: Gastric ulcers were induced in Wistar rats by serosal application of an acetic acid area. After ulcer induction, vehicle (saline) or E. coli-LPS was injected at various doses (0.1, 1 and 5 mg/kg i.p.) for 7 days. The animals were sacrificed on day 8 after ulcer induction and the following parameters were analysed; ulcer area (planimetry), gastric blood flow (GBF) (H2 gas clearance method), gastric secretion, plasma levels of proinflammatory cytokines such as IL-1beta and TNFalpha, mucosal gene expression for cyclooxygenases (COX-1/-2), apoptosis-related proteins (Bax, Bcl-2), TNFalpha, IL-1beta and vascular endothelial growth factor (VEGF). RESULTS: Daily parenteral challenge with LPS resulted in a dose-dependent delay in ulcer healing with maximum observed at a dose of 5 mg/kg (12.14 +/- 1.2 mm2 versus 5.18 +/- 0.8 mm2 in the control group). The impairment of ulcer healing in LPS-treated rats was associated with a significant decrease in GBF, increased mRNA expression for IL-1beta, TNFalpha, the rise in plasma IL-1beta and TNFalpha levels, an overexpression of COX-2 and VEGF and imbalance in the ratio between pro-apoptotic Bax and antiapoptotic Bcl-2. The daily administration of 50 mg/kg pentoxifylline by itself failed to accelerate the ulcer healing but attenuated the deleterious effects of LPS on this healing. CONCLUSIONS: 1) Bacterial endotoxin impairs ulcer healing through the decrease in gastric mucosal blood flow, increased expression and release of proinflammatory cytokines IL-1beta and TNFalpha, the imbalance between pro- and anti-apoptotic members of Bcl-2 family via downregulation of antiapoptotic bcl-2, and 2) endotoxin leads to upregulation of genes for VEGF and COX-2, which fail to accelerate the ulcer healing.

Animals↗

Release of mast cell tryptase from human colorectal mucosa in inflammatory bowel disease.

BACKGROUND: Histologic detection of mast cells cannot adequately reflect their function and state of activation, since degranulated mast cells may escape from histologic assessment. To better define the role of mast cells in inflammatory bowel disease, the spontaneous secretion of mast cell tryptase, a highly mast cell specific protease, was measured from colorectal samples. METHODS: After detection of the initial basal tryptase release, gut mucosal samples were incubated in a modified Hanks/RPM1 medium using a mucosa oxygenation system. Spontaneous tryptase secretion from 153 viable samples of 22 controls, 30 patients with Crohn disease (CD) and 19 with ulcerative colitis (UC) was followed over 4 h. Tryptase was measured by radioimmunoassay. RESULTS: The rates of the initial basal tryptase release revealed that mast cell activation occurs during active inflammation in CD and UC. While the time course of tryptase release was similar in all three groups, spontaneous tryptase secretion (over 4 h) was found to be significantly enhanced and prolonged only in UC (P < 0.01 compared to controls), but not in CD. CONCLUSIONS: This study provides clear evidence from viable endoscopic colorectal samples that mast cell mediators were secreted during active inflammation in CD and UC. However, the extent of mast cell involvement and activation differs considerably between CD and UC. Significantly increased rates of tryptase secretion were found both in non-inflamed and inflamed tissue of UC, indicating that mast cell involvement is a typical feature of UC.

Adult↗

Risperidone-induced cholestatic hepatitis.

Risperidone, a widely used atypical and potent neuroleptic drug, is assumed to induce fewer hepatic side-effects than phenothiazine anti-psychotics. Recently, we observed a case of risperidone-induced cholestatic hepatotoxicity. A 37-year-old male developed a rapid increase in liver enzymes and cholestatic parameters after starting treatment with risperidone for paranoid psychosis. Work-up for other potential aetiologies was negative. The results of a percutaneous liver biopsy were consistent with drug-induced liver injury and cholestasis. Over the course of one month after the discontinuance of all anti-psychotic agents, the liver function test results returned to near-normal values. This observation supports the need to monitor cholestatic parameters in addition to liver function enzymes during initiation and the first weeks of risperidone intake.

Adult↗

IgA anti-tissue transglutaminase: setting the stage for coeliac disease screening.

Coeliac disease is triggered in genetically predisposed individuals by the ingestion of wheat and related cereals. Affected persons raise an intestinal mucosal T-cell response against the gluten fraction of these cereals. Furthermore, they produce characteristic circulating IgA antibodies to a self-antigen present in the extracellular matrix that can be detected on tissue sections. The positive predictive value of these endomysial, reticular or umbilical cord antibodies for coeliac disease comes close to 100%. Recently, the enzyme tissue transglutaminase was identified as the main, if not sole, endomysial autoantigen in coeliac disease. Enzyme-linked immunosorbent assay tests with tissue transglutaminase from guinea pig or the recombinant human enzyme have been established that allow a standardized and quantitative determination of IgA anti-tissue transglutaminase titres. While the published assay variants report high positive and negative predictive values for coeliac disease, they were applied to preselected patients from mostly single centres. Therefore, validation and in part cross-validation of a standardized assay based on guinea pig tissue transglutaminase in 38 European and non-European centres is timely. With a sensitivity of 90% and specificity of 96% relative to local diagnostic standards the assay performed well. Considering further improvement by the use of recombinant human tissue transglutaminase as the antigen and central re-evaluation of the local standards for confirmation of coeliac disease, this enzyme-linked immunosorbent assay promises to become the primary tool for non-invasive diagnosis, therapy control and screening of coeliac disease. However, with an estimated prevalence of 1:100-1:200 of mostly atypical and subclinical coeliacs in Western populations, we are confronted with the question of how far mass screening is ethically feasible and cost effective.

Autoantibodies↗

Immunoglobulin E and eosinophilic cationic protein in segmental lavage fluid of the small and large bowel identify patients with food allergy.

OBJECTIVE: Members of the general population often assume that they suffer from food allergy, but the true prevalence is low. Testing for the diagnosis of food-related hypersensitivity entails laborious procedures, including GI endoscopy. Our objective was to develop an endoscopic screening approach for food allergy. METHODS: Endoscopically guided segmental lavage was performed in 11 patients with GI allergy and in 20 controls during lower GI endoscopy of the terminal ileum, the coecum, and the rectosigmoid. Eosinophilic cationic protein (ECP) and protein were measured in native lavage fluid, and immunoglobulin E (IgE) was also measured after a 10-fold lavage concentration. RESULTS: IgE/protein in lavage fluid from the coecum (0.055 +/- 0.068 U/mg vs 0.003 +/- 0.012 U/mg; p = 0.001) and the rectosigmoid (0.134 +/- 0.170 U/mg vs 0.019 +/- 0.042 U/mg; p < 0.05) was significantly elevated in patients with GI allergy. ECP/protein was significantly elevated at the terminal ileum (22.95 +/- 37.67 microg/mg vs 7.09 +/- 7.68 microg/mg; p < 0.05) and the rectosigmoid (23.66 +/- 19.43 microg/mg vs 11.97 +/- 16.39 microg/mg; p < 0.05). The combined use of GI lavage IgE and ECP as a diagnostic test for food allergy resulted in a sensitivity of 91% and a specificity of 80%. CONCLUSIONS: In endoscopically guided segmental lavage fluid, IgE and ECP/protein are increased in patients with food allergy. These measurements seem to offer an attractive diagnostic tool and may serve as a screening method.

Adult↗