Search PubMed⌕ Search

Biomedical subjects

G W Falk

Publications and source records attributed to G W Falk.

At least 37 records · Page 2Linked to original sources
PubMed1999

Gastroesophageal reflux disease.

Gastroesophageal reflux disease is a common clinical problem. Transient lower esophageal sphincter relaxation is central to the pathogenesis. New studies have identified the importance of nitric oxide and cholinergic pathways in modulating transient lower esophageal sphincter relaxation. Provocative information suggests that infection with Helicobacter pylori may protect patients from developing complications of gastroesophageal reflux disease. Endoscopy may be used by clinicians to tailor therapy, but an empiric trial of a proton pump inhibitor may be an alternative diagnostic approach. Nocturnal acid breakthrough during proton pump inhibitor therapy has emerged as an important new treatment concept, although its clinical importance remains unproven. Studies continue to show that laparoscopic antireflux surgery is a cost-effective treatment option for patients requiring maintenance therapy with proton pump inhibitors. However, the minimally invasive nature of the operation should not alter the indications for antireflux surgery, especially for patients with atypical symptoms.

Journal Article↗
PubMed1999

The incidence of adenocarcinoma and dysplasia in Barrett's esophagus: report on the Cleveland Clinic Barrett's Esophagus Registry.

OBJECTIVE: The reported incidence of adenocarcinoma in Barrett's esophagus is variable. The aim of this study was to determine the incidence of dysplasia and adenocarcinoma in a population of patients with Barrett's esophagus followed prospectively and to compare these findings with other series. METHODS: All patients enrolled in the Cleveland Clinic Foundation's Barrett's esophagus registry from 1979 to 1995 were followed. Barrett's esophagus was defined as intestinal metaplasia anywhere in the tubular esophagus. The incidence of dysplasia and adenocarcinoma in these patients was recorded systematically. RESULTS: A total of 136 patients (91 male, 45 female) were followed in an endoscopic surveillance program for a mean of 4.2 yr and a total of 570 patient-years of follow-up. Thirty patients (22%) had short segment Barrett's esophagus. Two adenocarcinomas developed during follow-up, yielding an incidence of one per 285 patient-years of follow-up. Low grade dysplasia developed in 24 patients, whereas high grade dysplasia developed in four patients. CONCLUSIONS: Our study suggests that the incidence of adenocarcinoma in Barrett's esophagus is lower than initially thought. However, large multicenter studies are required to clarify the epidemiological and clinical factors related to the development of dysplasia and adenocarcinoma in Barrett's esophagus.

Adenocarcinoma↗
PubMed1998

The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease.

BACKGROUND & AIMS: The role of Helicobacter pylori in the pathogenesis of gastroesophageal reflux disease (GERD) is unknown. We determined the prevalence of cagA-positive (cagA+) H. pylori strains in patients with GERD or its complications compared with controls of similar age. METHODS: A total of 153 consecutive patients with GERD, Barrett's esophagus, and Barrett's esophagus complicated by dysplasia or adenocarcinoma were compared with 57 controls who underwent upper endoscopy for reasons other than GERD. H. pylori infection and CagA antibody status were determined by histology and enzyme-linked immunosorbent assay. RESULTS: H. pylori prevalence was lower (34%) in patients with GERD and its sequelae than in the control group (45.6%)(P = 0.15). Regardless of the group, increasing age was associated with higher prevalence of H. pylori (P = 0.003). When compared with controls (42.3%), the prevalence of cagA+ H. pylori strains decreased (P = 0.008) in patients with more severe complications of GERD (GERD, 36.7% [nonerosive GERD, 41.2%; erosive GERD, 30.8%]; Barrett's esophagus, 13.3%; and Barrett's with adenocarcinoma/dysplasia, 0%). CONCLUSIONS: Prevalence of H. pylori in patients with GERD and its sequelae was lower but not significantly different than that of a control group. However, patients carrying cagA+ strains of H. pylori may be protected against the complications of GERD, especially Barrett's esophagus and its associated dysplasia and adenocarcinoma.

Adult↗
PubMed1998

Inflammation and intestinal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection.

BACKGROUND & AIMS: Whether inflammation of the cardia indicates gastroesophageal reflux disease (GERD) and/or is a manifestation of pangastritis caused by Helicobacter pylori infection is unknown. The aim of this study was to evaluate the relationship between cardia inflammation, H. pylori infection, and cardia intestinal metaplasia in patients with and without GERD. METHODS: Patients with GERD were compared with controls undergoing endoscopy for a variety of other conditions. Endoscopic biopsy specimens from the distal esophagus and cardia, fundus, and antrum were evaluated for inflammation, H. pylori infection, and intestinal metaplasia. RESULTS: Neither the prevalence of H. pylori infection (controls, 48%; GERD, 41%) nor cardia inflammation (controls, 41%; GERD, 40%) differed between groups. All 11 controls and 22 of 23 patients with GERD (96%) and cardia inflammation had H. pylori infection. Esophagitis was more common among GERD patients (33%) than controls (7%; P = 0.01). Cardia intestinal metaplasia was more common among controls (22%) than GERD patients (3%; P = 0.01); all had cardia inflammation, 7 had H. pylori infection, and 6 had metaplasia elsewhere in the stomach. CONCLUSIONS: The prevalence of cardia inflammation is similar in patients with and without GERD and is associated with H. pylori infection (P < 0.001). Cardia intestinal metaplasia is associated with H. pylori-related cardia inflammation (P = 0.01) and intestinal metaplasia elsewhere in the stomach, indicating that it is distinct from Barrett's esophagus.

Adult↗
PubMed1998

Helicobacter pylori and gastroesophageal reflux disease: the bug may not be all bad.

Peptic ulcer disease and gastric cancer of the antrum and body have been declining in the 20th century. In contrast, a new group of diseases are increasingly rapidly in Western countries: gastroesophageal reflux disease, Barrett's esophagus, and adenocarcinoma of the distal esophagus. Recent studies suggest this phenomenon may be related to the simultaneous fall in the prevalence of Helicobacter pylori (H. pylori) colonization, especially by the virulent cagA + strains. H. pylori infection with the cagA+ strain is potentially protective against the spectrum of gastroesophageal reflux disease because it lowers intragastric acidity as the result of a pangastritis, frequently with multifocal gastric atrophy and possibly increased intragastric ammonia production. Assuming that some types of H. pylori strains are protective, our entire approach to the worldwide elimination of this organism, sometimes indiscriminately, will need critical reevaluation.

Adenocarcinoma↗
PubMed1997

Effect of pneumatic dilation on gastroesophageal reflux in achalasia.

The aims of this study were to assess the effect of pneumatic dilation on gastroesophageal reflux in achalasia, differentiate esophageal acid due to lactate from acid due to gastroesophageal reflux, and determine if chest pain and heartburn are reliable indicators of gastroesophageal reflux. Eight untreated achalasia patients underwent pre- and postdilation esophageal fluid/food residue lactate and pH analysis, esophageal manometry, 24-hr pH monitoring, and symptom assessment. All patients had a successful clinical outcome and a decrease in lower esophageal sphincter pressure from 29.1 +/- 12.7 to 14.7 +/- 3.8 mm Hg (mean +/- SD; P = 0.04). Abnormal acid exposure was present in two patients before and two patients after dilation. Postdilation acid exposure was mild. Lactate was detected before dilation in all patients. A lactate concentration >2 mmol/liter was associated with acidic residue and one abnormal 24-hr pH profile. There was no correlation between an abnormal 24-hr pH test and age, lower esophageal sphincter pressure, or duration of symptoms prior to treatment. Chest pain and heartburn were unrelated to drops in pH. Gastroesophageal reflux is rare in untreated achalasia and esophageal acidity may result from ingestion of acidic foods or production of lactate. Mild gastroesophageal reflux occurs after dilation but is of no clinical significance. Chest pain and heartburn are not indicators of acid reflux in achalasia.

Catheterization↗
PubMed1997

Surveillance of patients with Barrett's esophagus for dysplasia and cancer with balloon cytology.

BACKGROUND & AIMS: A less costly cancer surveillance method for Barrett's esophagus is desirable. The aim of this study was to compare nonendoscopic balloon cytology with biopsy and brush cytology for detecting dysplasia and carcinoma in patients with Barrett's esophagus. METHODS: Patients in a surveillance program underwent balloon cytology before endoscopy with biopsy and brush cytology. Results of cytology were compared with those of histology. RESULTS: Adequate columnar epithelium was obtained in 52 of 63 (83%) patients with balloon cytology and 59 of 61 (97%) with brush cytology. Balloon cytology obtained abnormal cells in 6 of 8 patients with adenocarcinoma, 2 of 2 patients with high-grade dysplasia, and 2 of 8 patients with low-grade dysplasia. Sensitivity of balloon cytology for high-grade dysplasia or carcinoma was 80% but only 25% for low-grade dysplasia. No patients without dysplasia or carcinoma had abnormal cells. Brush cytology was abnormal in all 11 patients with high-grade dysplasia or carcinoma but only 2 of 9 patients with low-grade dysplasia (sensitivity, 22%). Two of 39 patients without dysplasia had abnormal cells (specificity, 95%). Balloon cytology cost was sixfold less than endoscopy with biopsy. CONCLUSIONS: Balloon cytology detected 80% of patients with high-grade dysplasia or carcinoma when sampling was adequate. Brush cytology data suggest that a more abrasive balloon may improve balloon cytology sensitivity. The potential cost savings of balloon cytology compared with endoscopic cancer surveillance in Barrett's esophagus support further studies of this technique.

Adenocarcinoma↗
PubMed1997

H pylori 1997: testing and treatment options.

Although the discovery of Helicobacter pylori infection in peptic ulcer disease is revolutionizing ulcer diagnosis and treatment, the role of universal empiric therapy for infected patients with dyspepsia or peptic ulcers is not fully elucidated. This article reviews current thinking on the diagnosis of H pylori infection in 1997.

Breath Tests↗
PubMed1997

Advances in the treatment of esophageal carcinoma.

Recent changes in the epidemiology of esophageal carcinoma now recognize adenocarcinoma as the predominant histologic cell type. Barrett's esophagus and dysplasia in this epithelium identify patients who are at risk of developing invasive adenocarcinoma. This neoplasm is not a single entity with a consistently poor prognosis, and disease stage is important for determining therapy. These findings offer the potential for further development of therapeutic regimens. Endoscopic esophageal ultrasound is an accurate and reproducible staging tool. It allows the physician to determine clinical stage and modify treatment. T2 N0 M0 or lesser stage tumors have acceptable surgical cure rates, and patients should undergo immediate resection. Patients with more advanced T3 or N1 tumors have a potential for cure but do poorly with surgery alone. These patients should be considered for multimodality therapy. Palliative therapy should be given to patients with hematogenous metastatic disease. Treatment stratification by stage proves that esophageal carcinoma is not a uniformly fatal disease without hope for cure.

Adenocarcinoma↗
PubMed1996

Barrett's esophagus and adenocarcinoma. The need for a consensus conference.

The fear of cancer has evoked calls for intensive surveillance programs in Barrett's esophagus. Two evolving issues are fueling this fire: (a) the rising risk of adenocarcinoma of the esophagus over the past 20 years and (b) the coincidental increase in the recognized prevalence of Barrett's esophagus in the general population. However, these sobering statistics must be carefully weighed against the lack of adverse effects on survival and the cost of an extensive surveillance program for adenocarcinoma in Barrett's esophagus, the latter estimated at between $(300) and $(1,500) million per year. Barrett's esophagus and its associated cancer risk represent a crisis in gastroenterology. A consensus conference of leading basic and clinical scientists is needed in this area.

Adenocarcinoma↗
PubMed1995

Observer variation and reproducibility of endoscopic ultrasonography.

To investigate interobserver variation and reproducibility of endosonographic findings, both experienced and inexperienced endosonographers evaluated depth of tumor invasion (T stage) and presence of lymph node metastasis (N stage) in 50 patients with nonobstructing esophageal carcinoma. Results were compared with the findings by surgical pathology of the resected specimens. The kappa statistic (kappa) was used to assess interobserver and intraobserver agreement and consistency of accurate interpretation (reproducibility) for the two groups. Agreement between the experienced endosonographers was excellent (kappa = > .75) for T1 and T4 lesions, good (kappa = .61) for T3 lesions, but only poor (kappa = > .46) for T2 lesions. The overall agreement between the experienced endosonographers was equally good for both T and N stages. Agreement between the inexperienced endosonographers was poor for all T stages but was good for lymph node metastasis (kappa = .52). For experienced endosonographers, endosonographic reproducibility of histologically confirmed T4 lesions was excellent, followed closely by T3 and T2 lesions; T1 tumors were frequently interpreted differently by the same endosonographer. Reproducibility of N stage determinations was excellent for N0 lymph nodes and good for N1 nodes. Thus, for experienced endosonographers, interobserver agreement was excellent for all T stages except T2, whereas reproducibility of determination of depth of tumor invasion was good to excellent for T2, T3, and T4 lesions but poor for T1 lesions. As yet poorly defined operator and machine-dependent factors that cause misinterpretation of T1 and T2 tumors will require additional study.

Endoscopy↗
PubMed1995

Endosonographic evaluation of the patient with achalasia: appearance of the esophagus using the echoendoscope.

BACKGROUND AND STUDY AIMS: Endoscopic ultrasonography (EUS) provides high-resolution images of the esophageal wall and adjacent structures. The purpose of this study was to evaluate the usefulness of EUS using the echoendoscope in the evaluation of patients with achalasia. PATIENTS AND METHODS: Seventeen patients with achalasia underwent esophagogastroduodenoscopy (EGD), esophageal manometery, and EUS. The esophageal wall thickness was measured endosonographically in four quadrants at the gastroesophageal junction (GEJ) and at 1 cm intervals proximally. Of the 17 patients evaluated, five had a tortuous esophagus (Group A) and 12 had a relatively straight esophagus (Group B). Six patients without esophageal symptoms served as controls (Group C). RESULTS: There was no significant difference in the mean esophageal wall thickness measured at the GEJ between the groups (4.0 mm, 3.3 mm, and 2.9 mm for Groups A, B, and C, respectively). Esophageal wall thickness was significantly greater in Group A than Group C when measured 2, 3, and 4 cm above the GEJ (4.2 mm vs. 2.8 mm; 4.1 mm vs. 2.4 mm; 4.0 mm vs. 2.4 mm, respectively) (p < .05). When measured 2 cm above the GEJ, the esophageal wall in Group A patients was significantly thicker (4.2 mm) than in patients in either Group B (3.2 mm) or Group C (2.8 mm) (p < 0.05). CONCLUSIONS: The appearance of esophageal wall thickening was common in patients with achalasia. Positioning of the echoendoscope in some patients with an irregularly-shaped, tortuous esophagus may result in tangential imaging and the production of artifacts simulating submucosal lesions. The production of such imaging artifacts suggests that caution must be exercise when EUS with the echoendoscope is used to evaluate patients with achalasia and a tortuous esophagus. Based on the present level of knowledge, EUS is not recommended in the routine evaluation of patients with achalasia.

Esophageal Achalasia↗
PubMed1994

Barrett's esophagus.

Barrett's esophagus is a complication of gastroesophageal reflux disease that is diagnosed with increasing frequency in connection with the increased utilization of upper endoscopy. It remains unclear why some patients with gastroesophageal reflux disease develop Barrett's esophagus while others do not. The association of Barrett's esophagus and adenocarcinoma is well established; if not for this fact, Barrett's esophagus would be of little clinical importance. Endoscopic surveillance with a rigorous biopsy protocol for the detection of dysplasia or early adenocarcinoma is indicated in any patient with Barrett's esophagus who is a candidate for surgery. New therapeutic strategies, including profound acid suppression with proton pump inhibitors, laser ablation of Barrett's epithelium, and photodynamic therapy, are currently under evaluation for the treatment of Barrett's esophagus.

Adenocarcinoma↗
PubMed1994

p53 immunoreactivity in Barrett's metaplasia, dysplasia, and carcinoma.

Barrett's esophagus is a metaplastic condition with an unpredictable potential for neoplasia. Mutations of the tumor-suppressor gene p53 have been implicated in the evolution of some carcinomas. These mutations frequently result in intranuclear protein accumulation, which can be detected immunohistochemically. This study was undertaken to determine whether p53 immunoreactivity in Barrett's esophagus is a marker of neoplasia and, if so, when it occurs in the metaplasia-dysplasia-carcinoma sequence. Twenty-eight esophageal resection specimens were studied. Barrett's mucosa was present in each specimen, low-grade dysplasia in 27, high-grade dysplasia in 26, intramucosal cancer in 18, and submucosal cancer in 5. Immunohistochemical staining with the monoclonal antibody Pab1801 was used to detect the intranuclear protein product of mutated p53. No p53 immunoreactivity was seen in specimens of Barrett's mucosa or low-grade dysplasia. p53 immunoreactivity was found only in specimens of high-grade dysplasia, intramucosal cancer, and submucosal cancer. Sixty-nine percent (18/26) of these specimens exhibited mutated p53; 18 of 26 specimens of high-grade dysplasia (69%), 12 of 18 intramucosal cancer specimens (67%), and two of five submucosal cancer specimens (40%) expressed mutated p53. When p53 staining was observed, the spectrum of neoplastic changes (high-grade dysplasia, intramucosal cancer, submucosal cancer) within the specimen was positive. We conclude that (1) p53 immunoreactivity in Barrett's esophagus is a frequent, but not inclusive, marker for high-grade dysplasia, intramucosal cancer, and submucosal cancer and (2) immunoreactivity occurs late in the metaplasia-dysplasia-carcinoma sequence, during the transition to high-grade dysplasia.

Adenocarcinoma↗
PubMed1994

Anticardiolipin antibody-associated cerebral infarction in cirrhosis: clearance of anticardiolipin antibody after liver transplantation.

We report a 47-yr-old woman with a 30-yr history of cryptogenic cirrhosis who sustained a cerebral infarction shortly before undergoing liver transplantation. Anticardiolipin antibody titers were positive prior to transplantation (IgG = 24 GPL; IgM > 80 MPL; IgA < 10 APL). After liver transplantation, however, the titers dropped to normal (< 10 PL units). This report suggests that cirrhotic patients with high anticardiolipin antibody titers may be at risk for thrombotic events, and that this tendency may be reversed by liver transplantation or post-transplant immunosuppressive agents.

Antibodies, Anticardiolipin↗