Preface

The functional role of the esophagus is motility, which is the motion that advances liquid and solid foods from the mouth to the stomach; there is no secretion activity. The term esophagitis refers to all inflammations and irritative effects on the esophageal mucosa. Common causes include acid gastric reflux, side effects of some medications, bacterial or viral infections, ingestion of strong acid or alkali solutions or solid substances, and so on. The clinical appearance of esophagitis can be characterized by heartburn, dysphagia, odynophagia, cough, nausea, vomiting, chest pain, or sore throat. In general, esophagitis, if untreated, can cause esophageal ulcers followed by scarring and narrowing or neoplastic degeneration. Acid reflux leads to gastroesophageal reflux disease, which is a complex clinical condition with some mucosal esophageal lesions with increasing severity (Barrett's esophagus). Usually, infectious esophagitis, by bacteria, viruses, fungi, or parasites, can occur in patients with weakened immune systems. Eosinophilic esophagitis is based on the excessive response to some allergens (milk, eggs, peanuts, etc.). The expression "gastritis" is the more discussed and ambiguous diagnostic definition of gastric clinicopathological conditions. In the current medical language, there is confusion regarding the definition of this pathology because the term "gastritis" is currently used indifferently for symptoms in the upper gastrointestinal (GI) tract or for endoscopic aspects and histological characteristics that can be referred to as gastric mucosal phlogosis, erosion, hemorrhagic lesions, or injury. We must remember that inflammation of the gastric mucosa should not present symptoms in the upper GI tract. Clinical and instrumental exams provide data that are difficult to correlate with each other. The symptoms that can be referred to as esophagogastroduodenal tract are epigastric pain, heartburn, and dyspepsia; endoscopy can identify various mucosal characteristics such as hypertrophy, friability, atrophy, and hemorrhagic and erosive lesions. It is important to underline the poor correlations between endoscopic mucosal abnormalities and histological features of the same lesions. In fact, for example, gastric mucosa described endoscopically as normal should show histologically severe signs of inflammation. On the contrary, evident endoscopic damage by drugs (e.g., aspirin) might turn out to be mild phlogistic lesions upon histological examination. We can conclude that the term gastritis should be used in the case of presence of phlogistic characteristics in the histological exam. However, the endoscopic examination has a fundamental role in the clinical scenario of gastritis because the microscopic evaluation is made on the mucosal biopsy. Endoscopic mucosal biopsies concern mucosal abnormalities such as erosion, ulcers, polyps, hemorrhagic lesions, endoluminal protuberances, or in cases of suspicion of *Helicobacter pylori* infection. Furthermore, the identification of *H. pylori* in gastric pathology has given a central role to gastritis. Gastritis includes acute and chronic inflammations of the gastric mucosa. The classifications of gastritis are based on histological data. Unfortunately, also within the histological field, it should be difficult to present a classification of gastritis because there are various criteria that can be followed. First, histological features of inflammation subdivide acute and chronic gastritis. Second, more detailed

histological characteristics identify gastritis due to drugs, chemicals, infectious agents (viral, fungal, parasitic, bacterial), trauma, foreign bodies, tumors, autoimmune gastritis, vascular gastropathies, granulomatous gastritis, and so on. Finally, other histological features of the evolution and development of inflammation differentiate between chronic atrophic and hypertrophic gastritis (e.g., Sjogren's syndrome, Menetrier disease). In summary, gastritis is an inflammatory lesion of the gastric mucosa with various and numerous etiologic factors and histological features of inflammation; consequently, gastritis is a pathological state, but not a defined disease.

Peptic ulcers are based on acid peptic disorders, caused by the corrosive action of acid gastric juice on the vulnerable epithelium. This pathology can occur, through various clinical conditions, in the esophagus, stomach, and duodenum, or with ectopic gastric mucosa, in Meckel's diverticulum. Many peptic ulcers are due to the unregulated use of nonsteroidal anti-inflammatory drugs (NSAIDs) or infection with *H. pylori.* Additional factors include tobacco smoke and emotional stress, although the mechanisms are not clear. Ulcers may be defined as a pathological process of failure of the mucosal defense mechanism against the action of gastric acid and proteolytic enzymes, a secondary effect, in most cases, of NSAID drugs and *H. pylori* infection. Gastropathies are pathological conditions with the detriment of gastric mucosa without inflammation, which can be caused by an autoimmune reaction, drugs, infection, or chronic vascular congestive status, based on portal hypertension. Gastritis is inflammatory mucosal status due to damage from various agents such as drugs, autoimmune reactions, or infections. A particular kind of gastropathy is Menetrier disease, characterized by gastric mucosal hyperplasia, increased secretions, and loss of proteins. The clinical appearance of peptic ulcer disease is almost always abdominal pain. Epigastric pain, which may be diffuse or radiate to the back, is the characteristic symptom of the disease. Gastritis in most patients is asymptomatic. In Menetrier disease, in addition to epigastric pain, there is nausea, vomiting, loss of appetite, edema, weakness, and weight loss. The complications of peptic ulcer disease are hemorrhage, perforation, obstruction, and penetration. Hemorrhage occurs in 15% of cases and perforation occurs in 7% of cases. The penetrating ulcer erodes into the adjacent organs without perforation in the peritoneal cavity. Inflammation, edema, fibrosis, and scarring of the peptic ulcer cause outlet obstruction.

This book provides a comprehensive overview of esophagitis and gastritis and the many manifestations of these conditions. It begins with an introductory chapter that analyzes the complications of gastroduodenal ulcers. Section 2, "Esophagitis," discusses some topics of current clinical interest in the field of esophageal pathology. The first chapter in this section discusses the numerous infectious pathologies that can affect the esophagus. The second chapter in this section highlights the clinical characteristics of eosinophilic esophagitis. The third chapter examines extraesophageal manifestations and symptoms of esophageal disease. The section concludes with a chapter analyzing the innovative oral neuromuscular treatment of reflux caused by a hiatus hernia, as an aggravating factor in esophagitis.

The third section of the book, "Gastritis," includes several chapters on this wide and complex topic. The first chapter discusses the pathophysiology of *H. pylori*,

**V**

colonoscopy.

as well as its infiltration through the surface epithelium and the body's induction of the immune response. The next chapter in this section discusses gastrointestinal pathophysiological testing for upper GI functional disorders. The last two chapters present two classic themes of gastroenterology: gastroduodenal lesions associated with portal hypertension and the anesthetic involvement in gastroscopy and

> **Vincenzo Neri** Professor,

**Monjur Ahmed** Professor,

Pennsylvania, USA

Italy

University of Foggia,

Department of Medicine,

Department of Medical and Surgical Sciences,

Thomas Jefferson University Philadelphia,

as well as its infiltration through the surface epithelium and the body's induction of the immune response. The next chapter in this section discusses gastrointestinal pathophysiological testing for upper GI functional disorders. The last two chapters present two classic themes of gastroenterology: gastroduodenal lesions associated with portal hypertension and the anesthetic involvement in gastroscopy and colonoscopy.

> **Vincenzo Neri** Professor, Department of Medical and Surgical Sciences, University of Foggia, Italy

### **Monjur Ahmed**

Professor, Department of Medicine, Thomas Jefferson University Philadelphia, Pennsylvania, USA

Section 1 Preamble
