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Gastroesophageal reflux disease (GERD) is an extremely common chronic disorder associated with impaired quality of life and huge economic burden. Recently, an International Consensus Group developed a global definition of GERD (The Montreal Definition): a condition that develops when the reflux of stomach contents causes troublesome symptoms and/or complications. The traditional endoscopy-based classification of GERD patients into one of three groups - non-erosive reflux disease, erosive esophagitis, and Barrett's esophagus - is fraught with several limitations. Due to the lack of a gold standard, GERD is a symptom-based diagnosis, and hence symptom evaluation will remain the primary means by which treatment decisions are made for patients with suspected GERD. We propose that patients reporting the predominant GERD-like symptoms (GERS) in the primary care setting be classified based upon their response to an empiric trial of acid suppressive therapy: complete response to acid suppressive therapy, partial response to acid suppressive therapy, and no response to acid suppressive therapy. Given the limitations of objective medical testing, implementation of our proposed new symptom-based classification of patients with GERS would guide primary care physicians on when to refer patients to a gastroenterologist, which in turn could help in better resource utilization. Validation of this proposed classification by well-designed prospective multicenter studies is awaited.
Dis Esophagus 2009
PMID:Endoscopy of the esophagus in gastroesophageal reflux disease: are we losing sight of symptoms? Another perspective. 1919 51

The relationship between Helicobacter pylori eradication and reflux esophagitis is controversial. We analyzed the development of reflux esophagitis and the change in the grade of pre-existing reflux esophagitis after eradication. Enrolled were 559 Japanese patients who received eradication therapy for H. pylori. The grade of reflux esophagitis by endoscopy before and after therapy was evaluated retrospectively. No esophagitis was present before eradication in 526 patients. H. pylori was and was not eradicated in 429 and 97, respectively. Reflux esophagitis developed in 40 of the eradication group and in three of the treatment failure group, with prevalence higher with successful eradication (P = 0.04). Successful eradication and hiatus hernia were significant risk factors for reflux esophagitis development. Twenty-seven of 33 patients with pre-existing reflux esophagitis had successful eradication and six treatment failure. The reflux esophagitis grade worsened in two (Los Angeles classification from A to B) and improved in 14 patients after eradication. With treatment failure, reflux esophagitis worsened in none and improved in three patients. There showed no significant change in the grade of pre-existing reflux esophagitis after H. pylori eradication but the sample size was too small to evaluate the difference. In conclusion, the eradication of H. pylori increases the prevalence of reflux esophagitis, and hiatus hernia was a significant risk factor for the development of reflux esophagitis.
Dis Esophagus 2009
PMID:Influence of Helicobacter pylori eradication on reflux esophagitis in Japanese patients. 1919 52

Megaesophagus is the end-stage of achalasia cardiae. It is the result of peristaltic disorders and slow decompensation of the muscular layer of the esophagus. The aim of this article is to detail the diagnostic criteria and surgical management of megaesophagus. Criteria were acute bending of esophagus axis; lack of esophagus peristalsis, and no response to stimulation in the manometric test; and Los Angeles C/D esophagitis in the endoscopic examination. Between 1991 and 2004 seven patients (5 females, 2 males; age, 51-67 years; average age, 59 +/- 8 years) were treated. A bypass made from the pedunculated part of the jejunum connecting the part of esophagus above the narrowing with the praepyloric part of the stomach was made. Access was by an abdominal approach. A jejunum bypass was made in six patients with megaesophagus. A transhiatal esophageal resection was carried out, and in the second stage a supplementary esophagus was made from the right half of the colon on the ileocolic vessels in one patient who had experienced two earlier unsuccessful operations. Symptoms of dysphagia, recurrent inflammation of the respiratory tract, and pain subsided in all patients. Complications were not reported in the postoperative period. All patients survived. Subsequent radiographic and endoscopic examination showed very good outcome. The jejunum bypass gave very good results in the surgical treatment of megaesophagus.
Dis Esophagus 2009
PMID:Diagnostic criteria and surgical procedure for megaesophagus--a personal experience. 1920 50

Recent research suggests that allergy may be the key factor in the etiology of eosinophilic esophagitis (EE); however, historically, the condition was hypothesized as related to reflux injury to the esophageal mucosa. We studied this hypothesis by comparing markers of inflammation and cellular proliferation in EE and reflux esophagitis. Lower esophageal biopsies of adult patients with EE (n = 10), reflux esophagitis (n = 8), and normal controls (n = 13) were assessed quantitatively for the expression of the cyclooxygenase-2 (COX-2) enzyme, cellular proliferation, and oncogenic resistance to apoptosis using monoclonal antibodies for COX-2, Ki-67, and Bcl-2, respectively. Normal esophageal epithelium demonstrated weak diffuse uptake of COX-2 stain in the basal layer. No COX-2 expression was demonstrated in the EE group, significantly less than the control and reflux groups (P < 0.01 and P < 0.001, respectively). Cellular proliferation measured by Ki-67 expression was higher in EE and reflux compared with control (P < 0.001 and P < 0.01). Ki-67 expression, and thus degree of hyperplasia, appeared greater in EE than reflux, but was not statistically significant (P = 0.228). The degree of apoptosis was similar in all study groups. EE and reflux esophagitis are proliferative conditions expressing Ki-67 in higher concentrations than control. Mucosal proliferation in reflux esophagitis is COX-2 dependent. This novel research in EE has demonstrated downregulation of COX-2 expression compared with reflux esophagitis and control. We hypothesize that the allergy-related cytokine IL-13 known to inhibit COX-2 expression and found in high concentrations in EE as responsible for this. The pathogenesis of EE is likely dependent on allergy rather than reflux injury to the esophagus.
Dis Esophagus 2009
PMID:Is the etiology of eosinophilic esophagitis in adults a response to allergy or reflux injury? Study of cellular proliferation markers. 1920 51

In some populations, Helicobacter pylori eradication is associated with development of erosive esophagitis. The aim of this study was to evaluate the contribution of salivary bicarbonate and glycoprotein secretion to the pathogenesis of erosive esophagitis developing after H. pylori eradication. Gastroscopy and saliva collection were performed at recruitment and 12 months after completion of eradication therapy. Eighty-eight patients with duodenal ulcer were recruited to the study. Erosive esophagitis was found in 13 patients (grade A, 8 patients; grade B, 4 patients; grade C, 1 patient). Among the 74 subjects who completed the study, erosive esophagitis was detected in 21 patients (grade A, 15 patients; grade B, 6 patients); they all were successfully eradicated. Bicarbonate and glycoprotein secretion was not found to differ significantly between the subjects with and without erosive esophagitis both before and 1 year after H. pylori eradication. However, it was lower in H. pylori-infected (baseline) than in H. pylori-noninfected erosive esophagitis subjects (1 year after successful eradication) (bicarbonate 2.34 [1.29-3.40)]vs. 3.64 [2.70-4.58]micromol/min and glycoprotein 0.23 [0.15-0.31]vs. 0.35 [0.28-0.43] mg/min, P= 0.04 and P= 0.04, respectively). We conclude that changes in salivary bicarbonate and glycoprotein secretion related to H. pylori eradication do not promote the development of erosive esophagitis in duodenal ulcer patients.
Dis Esophagus 2009
PMID:Association of erosive esophagitis with Helicobacter pylori eradication: a role of salivary bicarbonate and glycoprotein secretion. 1922 37

Gastroesophageal reflux disease (GERD) is a major risk factor for the development of esophageal adenocarcinoma (ACE). Many molecular alterations occur in esophageal carcinogenesis, yet the exact mechanism of ACE development remains unknown. This study aims to determine p53 protein and Ki-67 expression in esophageal mucosa of patients with GERD and study the correlation between these markers and the progression from normal squamous epithelium to esophagitis, columnar epithelium with or without intestinal metaplasia and ACE. We analyzed p53 protein and Ki-67 expression in biopsies of 200 patients with GERD and 35 patients with ACE. Those biopsies were classified into five groups: (i) G1 normal squamous epithelium (58); (ii) G2 esophagitis (80); (iii) G3 columnar epitheliums without intestinal metaplasia (30); (iv) G4, columnar epitheliums with intestinal metaplasia (32); and (v) G5 ACEs (35). p53 protein overexpression was found in 7% (4) of G1, 37.5% (30) of G2, 30% (9) of G3, 62.5% (20) of G4, and 71.4% (25) of G5 (p < 0.001). Ki-67 index increased according to the severity of histopathological diagnoses. Ki67 index was 21.3 +/- 19.5% in G1, 38.8 +/- 24.9% in G2, 37.7 +/- 26.3% in G3, 52.8 +/- 24.6% in G4, and 57.1 +/- 25.1% in G5 (P < 0.001). Linear correlation between p53/Ki67 expression and the multistep progression from squamous epithelium to ACE was observed (P < 0.001 and P < 0.05). Our results indicate that overexpression of p53 and increased Ki-67 could be associated with the development and progression to ACE in patients with GERD.
Dis Esophagus 2009
PMID:P53 and Ki-67 overexpression in gastroesophageal reflux disease--Barrett's esophagus and adenocarcinoma sequence. 1930 8

Drug-induced esophagitis is being recognized increasingly in the past few years. Since 1970 more than 650 cases have been reported worldwide caused by 30 or more medications. We have reviewed these cases with a view to classifying this disease based on underlying pathological mechanism. Drug-induced esophageal injury tends to occur at the anatomical site of narrowing, with the middle third behind the left atrium predominating (75.6%). The disease is broadly classified into two groups. The first group being transient and self-limiting as exemplified by the tetracycline group induced injury (65.8%). The second is the persistent esophagitis group, often with stricture, with two distinct entities: (i) patients on nonsteroidal anti-inflammatory agents whose injury is aggravated by gastroesophageal reflux (21.8%) (reflux aggravated); and (ii) patients with potasium chloride and quinidine sulphate induced injury (12.4%) (persistent drug injury). Severe esophageal injury has been reported in some women taking biphosphonates as treatment for postmenopausal osteoporosis. Endoscopic findings in such patients with esophageal injury generally suggested a chemical esophagitis, with erosions or ulcerations and exudative inflammation accompanied by thickening of the esophageal wall. Most cases of medication-induced esophageal injury heal without intervention within a few days. Thus, the most important aspect of therapy is to make the correct diagnosis and then to avoid reinjury with the drug. When possible, potentially caustic oral medications should be discontinued.
Dis Esophagus 2009
PMID:Drug-induced esophagitis. 1939 45

Combined modality treatment for esophageal carcinoma seems to improve survival over surgery alone. Different combinations of cytotoxic drugs have been studied to improve antitumor efficacy and limit the toxicity of chemoradiotherapy (CRT) with inconsistent results. We present a prospective study of neoadjuvant CRT with or without paclitaxel in chemotherapy schedule. One hundred seven patients (93 males, 14 females), median age 59 years (range 44-76), with operable esophageal cancer were enrolled. They received the following neoadjuvant therapy: Carboplatin, area under curve (AUC) = 6, intravenously on days 1 and 22, 5-fluorouracil (5-FU), 200 mg/m(2)/day, continuous infusion on days 1 to 42, radiation therapy 45 grays/25fractions/5 weeks beginning on day 1. Forty-four patients (41%) were furthermore non-randomly assigned to paclitaxel 200 mg/m(2)/3 h intravenously on days 1 and 22. Nutritional support from the beginning of the treatment was offered to all patients. Surgery was done within 4-8 weeks after completion of CRT, if feasible. All patients were evaluated for grade 3 plus 4 toxicities: leukopenia (28%), neutropenia (30%), anemia (6%), thrombocytopenia (31%), febrile neutropenia (6%), esophagitis (24%), nausea and vomiting (7%), pneumotoxicity (8%). Seventy-eight patients (73%) had surgery and 63 of them were completely resected. Twenty-two patients (20%) achieved pathological complete remission, and additional 20 (19%) had node-negative and esophageal wall-positive residual disease. There were 10 surgery-related deaths, mostly due to pulmonary insufficiency. Twenty-nine patients were not resected, 15 for early progression, 14 for medical reasons or patient refusal. After a median follow-up of 52 months (range 27-80), median survival of 18.0 months and 1-, 2-, 3- and 5-year survival of 56.7, 37.5, 27.0 and 21% was observed in the whole group of 107 patients. Addition of paclitaxel to carboplatin and continual infusion of FU significantly increased hematologic and non-hematologic toxicity, but treatment results as overall survival or time to progression did not differ significantly in groups with and without paclitaxel. Patients achieving pathological complete remission or nodes negativity after neoadjuvant therapy had favorable survival prognosis, whereas long-term prognosis of node positive patients was poor. Distant metastases prevailed as a cause of the treatment failure. Factors significant for survival prognosis in multivariate analysis were postoperative node negativity, performance status, and grade of dysphagia. Addition of paclitaxel to carboplatin and continual FU significantly increased hematologic and non-hematologic toxicity without influencing efficacy of the treatment. This study confirmed improved prognosis of patients after achieving negativity of nodes. Distant metastases prevailed as cause of the treatment failure. Prospectively, it is important to look for a therapeutic combination with better systemic effect.
Dis Esophagus 2010 Feb
PMID:Prospective non-randomized study of preoperative concurrent platinum plus 5-fluorouracil-based chemoradiotherapy with or without paclitaxel in esophageal cancer patients: long-term follow-up. 1951 90

Barrett's esophagus (BE) appears to be more common in Western than in Asian countries. BE is a complication of gastroesophageal reflux disease (GERD). Anatomical abnormalities of the esophagogastric junction (EGJ) are an important factor in the pathogenesis of GERD. We aimed to determine the prevalence of BE in Turkey, which is geographically located between Europe and Asia, and to investigate the frequency of BE according to the degree of anatomical disruption in the EGJ. This prospective study was performed on 1000 consecutive patients referred for endoscopy for any clinical indication. All patients underwent a structured interview that assessed major symptoms of GERD (regurgitation and heartburn). BE was diagnosed when specialized intestinal metaplasia was detected histologically in the esophageal biopsy specimens. Endoscopically assessed integrity of the EGJ was classified as one of three types, as follows: 1 Normal EGJ. The endoscope shaft was gripped tightly by the cardia in retroflexed endoscopy, or it was gripped less tightly but the cardia was seen to open and close with respiration. 2 Widened EGJ. The cardia was open during all phases of respiration in retroflexed endoscopy, but there was no endoscopic evidence of hiatal hernia (HH) on the antegrade view. 3 HH. The axial length from the EGJ to the diaphragmatic hiatus was at least 2 cm. BE was found in 12 patients (1.2%). Normal EGJ was seen in 90.7% of patients, widened EGJ in 4.3%, and HH in 5%. Patients with widened EGJ had a significantly higher incidence of major reflux symptoms and erosive esophagitis compared with those with normal EGJ (P= 0.001). BE was found in 14% of patients with HH and in 0.5% of patients with a normal EGJ (P= 0.001). None of the patients with widened EGJ had BE. In terms of BE frequency, these patients did not differ significantly from those with normal EGJ (P= 0.793) but did differ significantly from those with HH (P= 0.014). The prevalence of BE was 1.2% in a Turkish population undergoing endoscopy for any reason. In terms of EGJ integrity, comparison of the groups showed that even in the absence of HH, patients with widening of the EGJ had an increased prevalence of major reflux symptoms and erosive esophagitis. However, histologically confirmed BE was not seen among patients with widened EGJ.
Dis Esophagus 2009
PMID:Barrett's esophagus and endoscopically assessed esophagogastric junction integrity in 1000 consecutive Turkish patients undergoing endoscopy: a prospective study. 1951 92

Gastroesophageal reflux (GER) with laryngopharyngeal reflux plays a significant role in voice disorders. A significant proportion of patients attending ear, nose, and throat clinics with voice disorders may have gastroesophageal reflux disease (GERD). There is no controlled study of the effect of voice therapy on GERD. We assessed the effect of voice therapy in patients with dysphonia and GERD. Thirty-two patients with dysphonia and GERD underwent indirect laryngoscopy and voice analysis. Esophageal and laryngeal symptoms were assessed using the reflux symptom index (RSI). At endoscopy, esophagitis was graded according to Los Angeles classification. Patients were randomized to receive either voice therapy and omeprazole (20 mg bid) (n=16, mean [SD] age 36.1 [9.6] y; 5 men; Gp A) or omeprazole alone (n=16, age 31.8 [11.7] y; 9 men; Gp B). During voice analysis, jitter, shimmer, harmonic-to-noise ratio (HNR) and normalized noise energy (NNE) were assessed using the Dr. Speech software (version 4 1998; Tigers DRS, Inc). Hoarseness and breathiness of voice were assessed using a perceptual rating scale of 0-3. Parameters were reassessed after 6 weeks, and analyzed using parametric or nonparametric tests as applicable. In Group A, 9 patients had Grade A, 3 had Grade B, and 1 had Grade C esophagitis; 3 had normal study. In Group B, 8 patients had Grade A, 2 had Grade B esophagitis, and 6 had normal study. Baseline findings: median RSI scores were comparable (Group A 20.0 [range 14-27], Group B 19.0 [15-24]). Median rating was 2.0 for hoarseness and breathiness for both groups. Values in Groups A and B for jitter 0.5 (0.6) versus 0.5 (0.8), shimmer 3.1 (2.5) versus 2.8 (2.0), HNR 23.0 (5.6) versus 23.1 (4.2), and NNE -7.3 (3.2) versus -7.2 (3.4) were similar. Post-therapy values for Groups A and B: RSI scores were 9.0 (5-13; P<0.01 as compared with baseline) and 13.0 (10-17; P<0.01), respectively. Ratings for hoarseness and breathiness were 0.5 (P<0.01) and 1.0 (P<0.01) and 2.0. Values for jitter were 0.2 (0.0; P=0.02) versus 0.4 (0.7), shimmer 1.3 (0.7; P<0.01) versus 2.3 (1.2), HNR 26.7 (2.3; P<0.01) versus 23.7 (3.2), and NNE -12.3 (3.0, P<0.01) versus -9.2 (3.4; P<0.01). Improvement in the voice therapy group was significantly better than in patients who received omeprazole alone. Dysphonia is a significant problem in GER. Treatment for GER improves dysphonia, but in addition, voice therapy enhances the improvement.
Dis Esophagus 2010 Jan
PMID:Effectiveness of voice therapy in reflux-related voice disorders. 1954 11


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