Benign Lesions of the Esophagus and Cancer: Answers to 210 Questions

ISBN-13: 9783642730573 / Angielski / Miękka / 2012 / 847 str.

Robert Giuli; Richard W. McCallum

Opis

In an attempt to attain the best possible delimitation of all the problems posed today by benign diseases of the esophagus, 181 authors each agreed to answer one or more of 210 questions that had been drawn up on the subject. These questions, each one deliberately limited and difficult, mostly concerned reflux esophagitis: its natural history, the means of its diagnosis, all existing treatments, and its eventual degeneration. The authors approached are today's most reputed specialists in the fields of epidemiology, gastroenterology, endoscopy, pathology, and surgery of esophageal diseases. The authors were all assigned one or more questions in their own field, none of which was simple: all did their best to synthesize in their replies their own experience on the precise point under review and included all the most useful bibliographical references on the topic. The book is thus the result of an original, individual approach to try to pinpoint the heart of a problem. The 210 answers succeed one another in logical progression according to the different diagnostic and therapeutic stages, specifying, at each step, the degree of precision sought. Consequently, the reader has at his disposal an exceptional synthesis of facts and concepts. Opening the book at random he will find at once the detail he is looking for, the professional opinion he is lacking, or the development of a question he had perhaps not yet asked himself.

Spis treści

Statistical estimation of the prevalence and incidence of the degeneration of benign lesions.- Statistical estimation of the prevalence and incidence of the degeneration of benign lesions.- Infrequent but recognized associations.- Plummer Vinson Syndrome.- Myomas.- Diverticula.- What is the prognostic significance of esophageal papillomas?.- Can esophageal keratosis be considered as a precancerous lesion?.- What is the association between granular cell tumors of the esophagus and cancer?.- Isn’t treatment by repeated dilatations a factor of chronic mucosal irritation?.- Should the ineffectiveness of dilatations lead to suspect a cancer?.- What are the rules to follow in the surgical treatment of megaesophagus?.- What is the incidence of reflux in achalasia?.- Is it possible not to combine an antireflux procedure with the treatment of a megaesophagus?.- What is the influence of the treatment of a megaesophagus on the development of a peptic esophagitis or a stenosis?.- Are there pseudo-achalasias of neoplastic origin?.- Caustic Stenosis: anatomo-radiological correlations.- Can early calibration with an esophageal dilator prevent the anatomic development of granulation tissue?.- What is the incidence of dysplasia associated with the regeneration of the esophageal mucosa?.- What are the comparative late results of the different treatments?.- Is it really possible to follow a patient for several decades?.- Esophageal dysplasia.- How can esophageal dysplasia be demonstrated?.- Is “Asiatic” dysplasia specific?.- Do the endoscopic methods and the non-endoscopic methods have the same degree of reliability?.- How should dyplasias be followed?.- Do they require treatment?.- Should severe dysplasia associated with esophagitis be resected?.- Reflux esophagitis.- When must we consider reflux esophagitis?.- How can a normal esophago-gastric junction be defined?.- Can clinical reflux exist together with normal esophagus?.- Reflux can occur without hiatus hernia: misplacement of the cardia.- There seems to be a total independence between the LES tonus and the existence of a hiatal hernia.- Esophageal reflux can exist despite an elevated LES.- Physiopathology of peptic esophagitis (1).- Is stenosing esophagitis a different disease from esophagitis without stenosis?.- What is the endoscopic incidence of stenosis related to reflux?.- What is the endoscopic incidence of stenosis related to reflux and what is the incidence of recurrences of reflux stenosis?.- Is it possible to quantify reflux?.- What are the relations between gastroesophageal reflux and pharyngoesophageal dysphagia?.- What is an appropriate biopsy?.- What are the limitations of the histological interpretation of a biopsy taken from the area of esophagitis?.- In what proportion of cases are there poor quality biopsies?.- What is the role of a decrease in the peristalsis secondary to esophagitis linked disorders?.- Can the role of esophageal clearance disorders be defined?.- What are the troubles of gastric emptying of solid food which most often causes an esophagitis? Disorders of the proximal tonus, Disorders of antrum motility.- What is the incidence of alkaline reflux in patients suffering from esophageal reflux?.- What is the underlying mechanism of the toxicity of biliary acids?.- There is no demonstrated correlation between the severity of esophagitis and the concentration of biliary salts in the reflux fluid.- Physiopathology of peptic esophagitis (2).- The physiology of the LES is now well-known.- The essential anatomical features of peptic stenosis are quite accurate.- The concordance between endoscopy and histology seems good in certain types of esophagitis.- A methodology and a precise histological technique actually often enable a good concordance between clinical symptoms, endoscopy and histological alterations.- Transit with Technetium-99 enables to detect motility disorders unnoticed by usual means.- Radioisotopes techniques do not seem to be able to replace pH measurement.- The increase of intra-parietal esophageal collagen could provide elements in the evaluation of motor disorders associated with esophagitis.- Does the determination of an acid reflux score enable a better classification of the disease in question?.- When are motility tests indicated for the choice of treatment?.- Non-surgical treatments.- Is the dilatation of tight esophageal stenosis a therapeutic procedure?.- What is the risk of declining results when a peptic stenosis is treated by dilatation?.- Medical treatments of peptic esophagitis.- Is esophageal reflux always symptomatic?.- Is the underlying mechanism of LES insufficiency known? Can there be some independence between the value of LES and the existence of a hiatal hernia?.- Can the natural history of reflux esophagitis be defined?.- What is the rate of gastric acid secretion in patients with esophagitis?.- What factors intervene in the genesis of esophageal mucosal lesions caused by reflux?.- Can the brief duration of action of antacids enable them to practically decrease nocturnal acidity?.- Is the use of antacids justified in biliary reflux?.- Is the antalgic effect of antacids on reflux pain linked with a neutralizing action? (Comparison with placebo).- What is the effectiveness of antacids on the healing of esophageal lesions?.- What is the effect of alginates on acid neutralization and on LES pressure?.- What is the action of sucralfate in the treatment of peptic esophagitis?.- Metoclopramide has an effect on LES pressure, esophageal contractions and gastric acid secretion.- Doesn’t metoclopramide allow a significant decrease in antacid consumption?.- Is the effect of metoclopramide on the healing of the lesions of esophagitis different from that of cimetidine?.- What effective dosage to propose for metoclopramide?.- Domperidone: is its effect different from that of metoclopramide?.- Domperidone: is its effect different from that of metoclopramide and does it have central side effects?.- Bethanechol: is its association to antacid therapy advantageous for the healing of esophagitis lesions?.- Does the eso-gastric prokinetic action of cisapride play a role in the treatment of esophagitis?.- What are the indications of pirenzepine?.- What are the effects of H2-receptor- antagonists on esophageal burns, on esophagitis lesions and on the evolution of peptic stenosis?.- Is healing of esophagitis lesions possible with this treatment? What is the optimal daily dosage? Is maintenance treatment necessary?.- Can Omeprazole allow healing of certain ulcerated esophagitis?.- Can Omeprazole be efficient in cases that do not heal under H2-receptor blockers?.- Do we know the effect of inhibitors in the synthesis of prostaglandins (indomethacin) in the treatment of esophagitis?.- Can peptic esophagitis be healed by prostaglandins?.- What are the comparative effects of the different treatments on LES pressure?.- Comparative effects of the treatments on esophageal motricity and esophageal clearance.- Comparative effects of the treatments on duodeno-gastric reflux.- Comparative effects of the treatments on the volume and the number of bouts of reflux.- Effects of the different treatments on the acidity of reflux.- What are the treatments that undoubtedly increase the pressure of LES?.- Can continuous administration of antacids be considered?.- After interruption of the treatment, is the risk of recurrence elevated, and what other factors could be implicated in the determinism of reflux to avoid an indefinite intake of antacids?.- What are the factors that play a role in the genesis of esophagitis and on which ones do antacids react?.- At what time must medical treatment give way to surgical indication in erythematous esophagitis.- Surgical indication in erosive esophagitis.- Surgical indication in Barrett’s esophagus.- Surgical indication in peptic esophagitis in children.- Surgical indication in stenosis.- When a peptic esophageal lesion is healed, is maintenance therapy nevertheless indicated?.- Is it necessary to consider standardizing the methods of evaluation in order to compare the different treatments?.- Conclusion.- Surgical treatment of peptic esophagitis.- What are the factors contributing to the continence of the cardia? Increase of the LES.- How does the length of the abdominal esophagus contribute to the continence of the cardia?.- How does intra-abdominal pressure contribute to the continence of the cardia?.- Anatomical procedures.- The Lortat-Jacob procedure.- The Belsey Mark IV procedure.- Cardiopexy with umbilical ligament.- What is the real function of a gastro-esophageal valve?.- What is a Nissen fundoplication?.- Effects of fundoplication on gastric emptying.- Results of the Nissen procedure.- Partial fundoplication.- What is the value of an intrathoracic fundoplication?.- The fixed retroesophageal valve.- The degradation of posterior fundoplication.- The Hill procedure.- The Toupet procedure.- What is the effect of an antireflux procedure on esophageal dyskinesis?.- When is it appropriate to add vagotomy to an antireflux procedure?.- Migration of the cardia and the posterior aspect of the stomach in large irreducible hiatal hernias.- How can a conservative procedure be considered in view of a stenosis on an irreducible cardia?.- The Collis-Nissen procedure.- The advantage of Collis-Nissen procedure via an abdominal or thoracic approach.- Results of Collis-Nissen operation.- The Collis-Belsey procedure.- Comparison of Collis-Nissen and Collis-Belsey procedures.- Are there still indications for cardioplasty?.- Total duodenal diversion.- Must duodenal diversion be reserved for alkaline reflux?.- From the clinical point of view, do peptidic hormones have an effect on LES?.- Surgical resection Evaluation of surgical results.- Gastric replacement.- Colon interposition.- Can a jejunal loop offer more resistance to acidity?.- The Thal procedure, combined with that of Nissen.- Why have so many antireflux procedures been devised? Can specific factors be defined in order to properly choose the procedure to offer?.- Is intra-operative manometry useful?.- What are the criteria for evaluation of the results of an operation for peptic esophagitis?.- The effects of the different procedures on the opening pressures of the LES.- A comparison of manometric and pH measurements in different continence procedures.- Is the measurement of LES always parallel to the functional results of an antireflux procedure?.- The role of incomplete LES relaxation in postoperative dysphagia.- Is it possible to quantify dysphagia to enable comparison between patients?.- Can the pharmacological improvement of gastric emptying improve the results of certain procedures?.- Can we specify the differences existing between endoscopic healing and histologic healing?.- Healing of esophagitis and intraparietal esophageal collagen.- Recurrences and technical pseudo-recurrences.- What follow-up period is required to assess the results of surgical treatment?.- Should the reported failure of a method be linked to its popularity?.- Recurrences with different techniques.- Mortality of reoperations.- Does the persistence of histologic signs suggest that other factors than acidity could occur?.- What is the incidence of gastric epithelium lying below a treated peptic stenosis?.- What value should be attributed to the persistence of radiological signs of reflux or persistent acid pH without clinical signs following anti-reflux surgery?.- Do radioactive methods enable a better approach to reflux by evaluating the esophageal clearance?.- Are the disorders of esophageal motility corrected by anti-reflux surgery?.- How does one interpret peptic stenosis occurring after antireflux surgery?.- Is the progression of the stenosis controlled permanently after treatment?.- Do the classifications of peptic stenosis allow a definition of the risk of degeneration?.- What is the respective incidence of peptic stenosis and columnar epithelium lined lower esophagus (Barrett’s esophagus)?.- Barrett’s esophagus (1).- What is the definition of Barrett’s esophagus?.- The various degrees of differentiation toward gastric or intestinal epithelium seem to predispose to dysplasia and cancer.- Is the initial anomaly definitely congenital in certain cases?.- Experimental Barrett’s esophagus leads to conclude that this lesion is almost constantly acquired.- “Diffuse” Barrett’s esophagus.- Are there specific radiologic signs in Barrett’s esophagus?.- Is post-prandial pH measurement an adequate method of diagnosis?.- What is the importance of the difference of esophageal potentials after manometry in the diagnosis of Barrett’s esophagus?.- Are the histochemical and immuno-cyto-chemical criteria useful?.- How long does it take for Barrett’s esophagus to develop?.- Can the pathogenesis of this lesion be defined?.- Barrett’s esophagus (2).- Classifications of Barrett’s esophagus.- Can motility studies be of use in the classification of these lesions?.- How should one interpret the histologic changes observed during the endoscopic surveillance of these patients ?.- What is the role of alkaline reflux in the development of complications?.- Are clinical symptoms of reflux a necessary indication for antireflux surgery in Barrett’s esophagus?.- Can the ectopic epithelium regress after antireflux surgery?.- Can esophageal mucosa return to a malpighian configuration?.- What is the outcome of esophageal fibrosis after correction of reflux?.- Malignant degeneration of benign lesions (1).- Experimental cancers of the esophagus.- What are the histologic criteria of developing carcinoma in biopsies of benign lesions?.- What is the value of retrograde biopsies?.- Malignant degeneration of benign lesions (2).- Degeneration of megaesophagus. Is there a particular symptomatology?.- Malignant change in megaesophagus: has it a specific clinical picture?.- Is the incidence of this degeneration known?.- Verrucous cancers of the esophagus.- Degeneration of caustic stenosis.- What are the indications of conservative surgery in caustic stenosis?.- Degeneration in peptic esophagitis.- Must the risks of degeneration be taken into consideration in the choice of treatment for a caustic or peptic stenosis in an infant or a child?.- Degeneration of Barrett’s esophagus.- Can the delay in this degeneration be defined?.- What are the means of early detection of malignant degeneration?.- Does the symptomatology of cancer differ when occurring in Barrett’s esophagus?.- How to differentiate cancers of the cardia from those occurring in Barrett’s esophagus?.- May squamous cell carcinoma occur in Barrett’s mucosa?.- Malignant degeneration of benign lesions (3).- The incidence of cancer in Barrett’s esophagus vary according to series.- Is their prevalence in patients with Barrett’s esophagus overestimated?.- How can the risk of degeneration be distinguished from the associated epidemiologic risk?.- Must scleroderma, a factor of Barrett’s esophagus, be considered as a precancerous lesion?.- Does aperistalsis, in certain cases, lead to abandon a Nissen type procedure on behalf of a direct resection?.- Does the presence of an associated stenosis modify the principle of the operation proposed?.- Is it logical to treat a Barrett’s type lesion by a simple antireflux operation?.- What should be the approach to surveillance of these patients?.- Symposium on the anatomic pathology of esophageal neoplasia.- to the classification of esophageal neoplasms.- What are the morphologic features of usual squamous cell carcinoma?.- Superficial squamous cell carcinoma.- What is known about precursor and squamous cell carcinoma? Are there different nomenclatures in different parts of the world for these lesions?.- Are there animal models in non-human primates of precursor lesions and squamous cell carcinoma of the esophagus?.- What are the morphologic predictors of behavior of squamous cell carcinoma of the esophagus? The OESO malignancy index and histologic staging.- The role of the pathology panel in the OESO study.- What are the general morphologic features of Barrett’s esophagus and the carcinomas arising in it? Can Barrett’s carcinoma be differentiated from carcinoma of the gastric cardia?.- What is the status of our understanding of the morphologic predictors of cancer risk in patients with Barrett’s mucosa? How do histochemistry and immunohistochemistry help in the prediction of this risk?.- Unusual and rare epithelial tumors of the esophagus.- Stromal and lymphoid tumors of the esophagus.- Current state of the various surveys and therapeutic trials conducted by the group OESO.- General conclusions and future outlook.- Conclusions of the Congress.