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The Pathophysiology of Gastroesophageal Refiux Disease

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The Pathophysiology of Gastroesophageal Refiux Disease REVIEW ARTICLE The Pathophysiology of Gastroesophageal Refiux Disease Bradley Jimmy Waleleng, Marcellus Simadibrata, Ari Fahrial Syam * Division of Gastroentero-hepatology, Department of Internal Medicine Faculty of Medicine, University of Sam Ratulangie, Prof. Dr. RD Kandou Hospital, Manado ** Division of Gastroenterology, Department of Internal Medicine, Faculty of Medicine University of Indonesia/Dr. Cipto Mangunkusumo General National Hospital, Jakarta ABSTRACT The incidence of Gastroesophageal Reflux Disease (GERD), especially in Indonesia, is increas- ing with the change of community life-style. Also, the doctors’ perception in understanding clinical manifestation of GERD is alike in addition to the development of diagnostic facilities such as endoscopy in Indonesia. The GERD incidence in Indonesia is as high as the incidence in developed countries. Esophageal reflux develops in physiological condition, which may be found in normal individual. GERD development is caused by anatomical and physiological disorders such as hereditary or acquired factor; and other factors that may be categorized into offensive factors such as gastric acid, pepsin, bile acid, trypsin and disturbance in defensive factors such as hypotensive Lower Esophageal Sphinc- ter (LES), Transient Lower Esophageal Sphincter Relaxations (TLESR), hiatal hernia, disrupted saliva production, esophageal peristaltic disorder; as well as other factors such as genetic, diet, or certain drugs. Imbalance of such factors may cause pathological repeated esophageal refiux which may damage esophageal mucosa and lead to GERD development including all of complications. Keywords: esophageal refiux, GERD, LES INTRODUCTION 13.4-16.3% patients with GERD in Taiwan, Malaysia Gastroesophageal Reflux Disease (GERD) is and Japan. At the Faculty of Medicine, Cipto Man- a condition of gastric content refiux into the esophagus gunkusumo hospital, Syam AF et al, reported that there and causes clinical manifestations.1 This disease is was increased GERD prevalence from 5.7% in 1997 a consequence of various physiological and into 25.18% in 2002 (approximately 13.13%).3,4 anatomical disorders which may have important Heartburn and acid regurgitation are reported role of anti-refiux mechanism in the stomach and once weekly by 20% of Americans, and the annual esophagus. Basically, gastrointestinal reflux is prevalence is more than 59%. Traditionally, refiux a physiological process which normally occurs for treatment is aimed to deal with aggressive substance approximately one hour daily in normal individual. of gastric acid. However, we found other factors which Such refiux may not occur continuously due to ana- have important roles in GERD development and tomical barriers, i.e. lower esophageal sphincter (LES), esophageal mucosa damage.5 diaphragm crural and phrenoesophageal ligament.2 Noxious substances that may damage esopha- The incidence of GERD is high in Western geal mucosa include gastric-derived substances, i.e. countries and recently, the experts are getting more gastric acid and pepsin and duodenal-derived curios about GERD. It is reported that there are substances, i.e. conjugated and unconjugated bile acid as well as trypsin. Injury induced by such substances Correspondence: BJ Waleleng may cross esophagogastric junction and moisten Division of Gastroentero-hepatology esophageal mucosa. To prevent such condition, LES Department of Internal Medicine Prof. Dr. RD Kandou Hospital together with diaphragm crural have a major role Jl. Raya Tanawangko Manado, Indonesia in protecting structures from noxious substances of E-mail: [email protected] gastroduodenal refiux. Gastroesophageal Munction may 84 The Indonesian Journal of Gastroenterology, Hepatology, and The Pathophysiology of Gastroesophageal Reflux Disease be pass due to transient lower esophageal relaxations that esophagitis, including the Barrett’s esophagus, (TLESR), hypotensive LES (HLES), or by other cause increases with frequency and contact duration associated with hiatal hernia.5 The mucosa is exposed of esophagus and the refiuxate at pH < 4.5,8,9 It is to noxious gastroduodenal substance, therefore interesting that GERD may occur even when esophagus lumen is protected by esophageal clearance the patient’s gastric acid production does not increase. mechanism through peristaltic and acid neutraliza- This is found by Hirschowitz et al, who reveal that tion process which is also part of defense mechanism stimulation of basal pentagastrin gastric acid secretion and epithelial cell recovery. Hence, it is important in and pepsin is similar in GERD patients and normal preventing mucosa damage.5 Normally, there is control subjects. Therefore, esophageal disturbance due a balance between aggressive factors and defense to acid exposure in GERD case may be identi›ed by mechanism.5,6 When the protection mechanism fails, ambulatory pH monitoring, which shows that the most it may cause GERD complication including frequent cause is esophageal barrier failure and poor esophagitis, stricture, or Barrett’s esophagus,5,7 or even esophageal clearance.5 A small number of patients with esophageal carcinoma.7 In some individuals, genetic Zollinger-Ellison syndrome and acid hypersecretion factor may also have a role as predisposition factor that cause increased gastroesophageal refiux.5 Frequen- of GERD.5 cy and duration of acid exposure on esophageal are not always reliable in predicting the severity of esophageal 3ATHOPHYSIOLOGY mucosa injury. Other factors may also play a role Gastroduodenal Factors including duodenogastroesophageal refiux, mechanism Gastric substances that most frequently cause of esophageal lumen clearance and epithelial recovery 5 injury are gastric acid produced by parietal cells and and protection. Pepsin, bile acid, trypsin and hyper- pepsin produced by gastric chief cells. In endos- osmolar diet increase the sensitivity of esophageal 6 copy, usually gastric substances may be mixed with mucosa to acid-induced injury. Locke et al, found that duodenal substances which contain bile acid and 72% of 2,118 participants who had body mass index of 2 trypsin. Therefore, when there is a refiux of gastric con- > 30 kg/m , family history of heartburn, or symptoms tent into esophagus, it is a combination of gastric and of esophageal or gastric disorder, smoking history, duodenal substances which contribute to pathogenesis alcohol consumption more than 7 times weekly and of GERD.5 Other gastric factor contributes to such obvious psychosomatic symptoms are associated with 9 pathogenesis is Helicobacter pylori, which has a role frequent heartburn. in acid secretion.5 Duodenal Substances Gastric Substances Duodenogastric reflux is a condition with Experimental findings and clinical evidences regurgitation of duodenal content (bile acid and support the important role of gastric acid and pepsin pancreas secretion) into the stomach. This condition in GERD. An experimental animal study demonstrates normally occurs especially after meal (post pran- 8 that the gastric acid itself may cause esophageal dial) and at night. If the duodenogastric refiux reach mucosa injury in a very low pH (pH 1-2).5 Acid refiux esophagus, it is referred as duodenal gastroesopha- may become pathological when the esophagus is geal refiux or it may be mentioned as bile refiux or exposed to acid condition (pH < 4) for more than 5.8% alkaline refiux (because of esophageal pH that > 7). of 24 hours pH-metry.7 Combination of acid and slight The high esophageal pH is also infiuenced by saliva concentrated pepsin will cause esophageal injury, bicarbonate.8 Bile acid and pancreatic enzymes may either macroscopic or microscopic.5,8,9 At pH 2, migrate from duodenum to gastric pylorus and cause pepsin disrupts the histological integrity of mucosa a mixture with gastric secretion. The role of duodenal barriers which increases the permeability of hydrogen content, especially bile acid and trypsin the pancreatic ion and produces bleeding. In contrast, esophageal enzyme in the development of esophageal mucosa contact with pepsin at pH 7.5 followed by solution injury is still controversial.5 Some studies propose contact at pH 2 without any pepsin demonstrate that the esophageal mucosa damage is depend on minimal mucosa disruption or permeability change. conjugation state of bile acid. Conjugated bile acid Hence, pepsin may produce mucosa injury depend on may bring damage at acid pH, while unconjugated pH with maximal enzyme activity at pH 3.6 In acid form may cause damage at alkaline pH. Little has been condition (pH < 4), pepsin may produce esophageal known of how bile acid may cause esophageal mucosa damage due to proteolytic characteristic and it is injury. The proposed mechanism is cell damage due to inactive at pH > 4.5,8 Several studies that measure dissolved lipid membrane of the mucosa and intra distal esophageal to acid exposure demonstrate that mucosa damage after bile acid infiux into the cells.5,8 there is a correlation between heartburn symptom and Trypsin, akin to pepsin, bring damage through prote- exposure of refiux substance at pH < 4. It is also found olysis mechanism and it frequently causes damage at Volume 8, Number 3, December 2007 85 Bradley Jimmy Waleleng, Marcellus Simadibrata, Ari Fahrial Syam pH 5-8.5,8 It seems that gastric acid itself only cause Gastric Emptying least mucosa damage. However, when it is combined The loose of gastric cardia is a main factor with pepsin or conjugated bile acid, it will cause in GERD development. Prolonged distention of a
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