Transarterial chemoembolization for HCC in patients with extensive liver transplantation waiting times.

The treatment of hepatocellular cancer (HCC) with transarterial chemoembolization (TACE) prior to orthotopic liver transplant (OLT) is of increasing importance due to the rise in HCC incidence and donor shortage. This single-center study examines 28 patients treated with TACE and 7 patients not treated with TACE, with HCC prior to OLT between 1999 and 2008. The overall 1- and 5-year survival of all transplanted patients with HCC was 94% (33 of 35) and 80% (28 of 35). There was no difference in survival (P = .99) between patients who underwent transplantation immediately (median 95 days) and patients who had significantly longer wait times (median 308 days) when treated with TACE. During extensive wait times for OLT, TACE can be used to keep patients with HCC on the waiting list by preventing tumor progression, with similar outcomes compared with those who underwent transplantation immediately.

Inguinal hernia is not a sign of colon cancer: results of a prospective screening trial.

BACKGROUND: It has been suggested that patients with an inguinal hernia harbour an increased risk for colorectal cancer. METHODS: In a prospective clinical trial, we compared the prevalence of colonic neoplasms in 100 cases with inguinal hernia and 100 controls without inguinal hernia. The number, size, histology type, and the location of all colorectal lesions found during a screening flexible sigmoidoscopy were recorded. RESULTS: Not a single case of colorectal cancer was detected in the patients with inguinal hernia pending surgical repair. In the asymptomatic control subjects, one Dukes A and one Dukes B1 colon cancer were detected. Polypectomy was performed in 15% and 17% of the case and control subjects, respectively. During a 5-year period following the initial screening procedure, none of the case or control subjects was diagnosed with colon cancer. CONCLUSIONS: The decision for or against performing an endoscopic procedure in a patient with inguinal hernia should be guided by the general principles of screening for colorectal cancer. The mere presence of an inguinal hernia does not automatically increase the risk of colorectal cancer.

There are no reliable symptoms for erosive oesophagitis and Barrett's oesophagus: endoscopic diagnosis is still essential.

AIMS: To evaluate the sensitivity and specificity of different symptoms in erosive reflux oesophagitis and Barrett's oesophagus. METHODS: The presence of reflux symptoms was compared between a case population of 306 patients with endoscopically determined erosive reflux oesophagitis, 235 patients with biopsy-proven Barrett's oesophagus and a control population of 198 subjects without reflux disease. RESULTS: Heartburn at any time and heartburn at night represented the only two symptoms to be simultaneously sensitive and specific. Symptoms that were induced by various foods, such as fat, tomato, chocolate, citrus or spices, tended to cluster in the same sub-group of patients. Similarly, heartburn induced by exercise, lying down or bending over tended to occur in the same sub-groups. The frequency of symptoms was influenced more by the presence of mucosal erosions than by the presence of Barrett's oesophagus. Reflux symptoms occurred more frequently in the presence rather than the absence of Barrett's oesophagus, and in long segment rather than short segment of Barrett's mucosa. CONCLUSIONS: Endoscopic inspection of the oesophageal mucosa remains the only certain method by which to reliably diagnose erosive reflux oesophagitis and Barrett's oesophagus.

Gastric surgery is not a risk for Barrett's esophagus or esophageal adenocarcinoma.

BACKGROUND & AIMS: The contribution of duodeno-gastroesophageal reflux to the development of Barrett's esophagus has remained an interesting but controversial topic. The present study assessed the risk for Barrett's esophagus after partial gastrectomy. METHODS: The data of outpatients from a medicine and gastroenterology clinic who underwent upper gastrointestinal endoscopy for any reason were analyzed in a case-control study. A case population of 650 patients with short- segment and 366 patients with long-segment Barrett's esophagus was compared in a multivariate logistic regression to a control population of 3047 subjects without Barrett's esophagus or other types of gastroesophageal reflux disease. RESULTS: In the case population, 25 (4%) patients with short-segment and 15 (4%) patients with long-segment Barrett's esophagus presented with a history of gastric surgery compared with 162 (5%) patients in the control population, yielding an adjusted odds ratio of 0.89 with a 95% confidence interval of 0.54-1.46 for short-segment and an adjusted odds ratio of 0.71 (0.30-1.72) for long-segment Barrett's esophagus. Similar results were obtained in separate analyses of 64 patients with Billroth-1 gastrectomy, 105 patients with Billroth-2 gastrectomy, and 33 patients with vagotomy and pyloroplasty for both short- and long-segment Barrett's esophagus. Caucasian ethnicity, the presence of hiatus hernia, and alcohol consumption were all associated with elevated risks for Barrett's esophagus. CONCLUSIONS: Gastric surgery for benign peptic ulcer disease is not a risk factor for either short- or long-segment Barrett's esophagus. This lack of association between gastric surgery and Barrett's esophagus suggests that reflux of bile without acid is not sufficient to damage the esophageal mucosa.

Preventing death of Barrett's cancer: does frequent surveillance endoscopy do it?

Patients experiencing gastroesophageal reflux may be predisposed to developing Barrett's esophagus, which is thought to be a precursor for the development of esophageal cancer. Currently, endoscopic surveillance is recommended for patients with Barrett's esophagus in the hope that esophageal cancer may be detected or even prevented. However, the frequency of endoscopic evaluations is a matter of debate. This article will examine whether regular endoscopic surveillance can prevent death of Barrett's cancer. The issues that are evaluated include the death rate from esophageal cancer, the need to scope all patients with reflux, the need to perform surveillance on all patients with Barrett's esophagus, survival data for Barrett's patients, and the incidence of nonsymptomatic Barrett's cancer.

Reflux symptoms are associated with psychiatric disease.

AIMS: To evaluate the frequency of reflux symptoms in patients with a diagnosed psychiatric disorder and to assess potential risk factors for symptom occurrence. METHODS: The presence of reflux symptoms was compared between a case population of 94 psychiatric patients and a control population of 198 non-psychiatric patients. RESULTS: Heartburn, exercise-induced heartburn, cough and dysphagia were all reported significantly more frequently by subjects with psychiatric disorders than by control subjects. The presence of any psychiatric diagnosis exerted an increased risk for both heartburn (odds ratio, 2.71; 95% confidence interval, 1.01-7.30) and exercise-induced heartburn (3.34; 1.12-9.96). The type of psychiatric disorder, the type of psychotropic medication and the lifestyle did not influence the presence of reflux symptoms. CONCLUSIONS: Reflux symptoms occur more frequently in patients with than without a diagnosed psychiatric disorder. The reflux symptoms are not associated with any specific type of medication and may reflect a generally reduced threshold for or distorted perception of symptoms.

Temporal associations between coughing or wheezing and acid reflux in asthmatics.

BACKGROUND AND AIMS: The pulmonary symptoms of patients with lung disease may be ascribed to gastro-oesophageal reflux although a causal relationship between acid reflux and coughing or wheezing has not been proved. Does cough cause reflux or does reflux cause cough? The aim of this study was to evaluate 24 hour oesophageal pH tracings of asthmatics with gastro-oesophageal reflux to determine the temporal association between acid reflux and coughing or wheezing. METHODS: The oesophageal tracings of 128 asthmatics from the outpatient clinics who underwent oesophagogastroduodenoscopy, oesophageal manometry, and 24 hour oesophageal pH monitoring were analysed. Three possible temporal relationships between the occurrence of acid reflux and the occurrence of coughs or wheezes were evaluated: (1) pulmonary symptoms preceding reflux; (2) reflux preceding pulmonary symptoms; and (3) unrelated occurrence of both events. RESULTS: Of 128 asthmatics, 53 recorded five or more coughs and 19 recorded three or more wheezes during the 24 hour recording period. Mean acid contact time was similar in asthmatics with and without pulmonary symptoms (12.2 (1.2)% v 10.4 (0.6)%). Of all coughs and wheezes, 46% and 48%, respectively, were associated with acid reflux. For the individual asthmatic, the likelihood of reflux induced coughing increased as the number of coughs increased. CONCLUSIONS: Half of all coughs and wheezes in asthmatics are associated with acid reflux into the oesophagus. While an occasional coughing episode can lead to reflux, it is rather the reflux episode in the vast majority of instances that leads to cough.

No association between gallstones and gastroesophageal reflux disease.

OBJECTIVES: Gallstones and hiatal hernia reportedly have been linked to similar dietary factors prevalent in western countries, and patients with cholelithiasis or previous cholecystectomy have been reported to have more duodenogastric reflux than healthy controls. Nonetheless, the contribution of duodenogastric reflux to the development of gastroesophageal reflux disease (GERD) remains controversial. The present study was aimed to assess the association between gallstone disease and GERD. METHODS: Outpatients from general medical clinics who underwent upper GI endoscopy and abdominal ultrasonography were recruited into a case-control study. A case population of 790 patients with various grades of GERD was compared to a control population of 407 patients without GERD. In a multivariate logistic regression, the presence of GERD served as the outcome variable, whereas the presence of gallstones, hiatal hernia, social habits, and demographic characteristics served as predictor variables. RESULTS: No associations were found between the presence of cholelithiasis or previous cholecystectomy and GERD or between the presence of cholelithiasis or previous cholecystectomy and hiatal hernia. The severity of GERD also remained unaffected by the presence of gallstones. The occurrence of GERD was influenced only by hiatal hernia (odds ratio [OR] = 3.15, 95% CI = 2.44-4.08), alcohol consumption (OR = 1.47, CI = 1.08-1.99), and not by cholelithiasis (OR = 1.02, CI = 0.68-1.51), or cholecystectomy (OR = 0.90, CI = 0.64-1.28). The frequency of GERD among hiatus hernia patients with gallstones (437/592 = 74%) was similar to the frequency of GERD among hiatus hernia patients without gallstones (168/220 = 76%, p = 0.516). CONCLUSIONS: Neither cholelithiasis nor cholecystectomy poses a risk for the occurrence of GERD or hiatal hernia. Gallstone disease does not seem to influence the integrity of the esophageal mucosa through GERD.

Comparing lansoprazole and omeprazole in onset of heartburn relief: results of a randomized, controlled trial in erosive esophagitis patients.

OBJECTIVE: This randomized, double-blind, multicenter study was conducted to confirm a previous finding that lansoprazole relieves heartburn faster than omeprazole in patients with erosive esophagitis. METHODS: A total of 3510 patients with erosive esophagitis and at least one episode of moderate to very severe daytime and/or nighttime heartburn during the 3 days immediately before the screening visit were randomized to lansoprazole 30 mg once daily or omeprazole 20 mg once daily for 8 wk. Patients recorded the presence and severity of daytime and nighttime heartburn in daily diaries. On treatment days 1-4, patients were telephoned to confirm the completion of their daily diary. The primary efficacy parameters were the percentage of heartburn-free days and heartburn-free nights, as well as the average severity of daytime and nighttime heartburn. RESULTS: During treatment day I and all evaluation time points including the entire 8-wk treatment period, significantly (p < 0.05) higher percentages of patients treated with lansoprazole than those treated with omeprazole did not experience a single episode of heartburn. Onset of heartburn relief was more rapid in lansoprazole-treated versus omeprazole-treated patients: on day 1, 33% versus 25% of lansoprazole- versus omeprazole-treated patients were heartburn-free. The percentages of heartburn-free days and heartburn-free nights were also significantly (p < 0.01) greater for patients treated with lansoprazole at all evaluation time points. Heartburn severity was significantly less among those treated with lansoprazole compared with omeprazole. Both treatments were safe and well tolerated. CONCLUSIONS: Over 8 wk, lansoprazole 30 mg once daily relieved heartburn symptoms faster and more effectively than omeprazole 20 mg once daily in patients with erosive esophagitis.

Risk factors of oesophagitis in arthritic patients.

BACKGROUND: The risk factors that precipitate the occurrence of oesophageal mucosal injury in patients on continuous nonsteroidal anti-inflammatory drug (NSAID) therapy are unknown. METHODS: Outpatients who regularly consumed NSAIDs for osteoarthritis were recruited from a rheumatology clinic into a prospective case-control study. All patients answered a structured interview and underwent upper gastrointestinal endoscopy. RESULTS: Of 450 eligible patients, 195 (43%) consented to be interviewed and undergo upper gastrointestinal endoscopy. Oesophagitis was diagnosed in 41 of these 195 patients (21%). The occurrence of gastric or duodenal ulcer in individual patients did not predict the concomitant damage of the oesophageal mucosa. Young age (odds ratio: 1.79 per decade of life; 95% confidence interval: 1.11-2.86) and hiatus hernia (odds ratio: 3.72; 95% confidence interval: 1.63-8.49) both increased the risk of developing oesophagitis. When questioned, all oesophagitis patients revealed at least one gastrointestinal symptom, heartburn being named most frequently (odds ratio: 4.78; 95% confidence interval: 2.04-11.17). The type of anti-inflammatory medication, the use of alcohol and the use of nicotine were not associated with any significant risk for erosive oesophagitis. CONCLUSIONS: Patients on chronic NSAID therapy for rheumatological disease suffer frequently from erosive oesophagitis. While the risk may be higher in patients with a pre-existing tendency for gastro-oesophageal reflux, any concomitant history of NSAID-induced peptic ulcer disease does not add to the risk. Erosive oesophagitis should be considered especially in patients on NSAIDs who complain of heartburn.

Is there a link between cervical inlet patch and Barrett's esophagus?

BACKGROUND: Heterotopic gastric-type mucosa occurs as a flat island or islands of red mucosa in the proximal third of the esophagus where it gives rise to the "cervical inlet patch" (CIP). The aim of the present study was to delineate the clinical epidemiology of the CIP, especially its possible relationship to Barrett's esophagus. METHODS: A case-control study compared 53 case subjects with CIP and 4882 control subjects without CIP. In a multivariate logistic regression, the presence of CIP was chosen as the outcome variable, whereas demographic characteristics, social habits, and presence of other endoscopic diagnoses served as predictor variables. RESULTS: The prevalence of CIP was 1.1%. Its presence was associated with hiatal hernia (odds ratio 2.26: 95% CI [1.12, 4.56]) gastric ulcer (2.93: 95% CI [1.34, 6.40]) and Barrett's esophagus (4.41: 95% CI [2.31, 8.41]). CONCLUSIONS: The coincidence of the cervical inlet patch and Barrett's esophagus could suggest a shared embryonic etiology.

Long-term nonsurgical management of Barrett's esophagus with high-grade dysplasia.

BACKGROUND & AIMS: Surgical resection of the esophagus is frequently recommended for Barrett's high-grade dysplasia (HGD) without cancer. METHODS: During a 20-year period, patients were diagnosed and observed through an organized surveillance program at the Hines Veterans Affairs Hospital. The program was supported by Hines VA and organized and managed by 2 endoscopists using preestablished endoscopic criteria. RESULTS: Barrett's esophagus was diagnosed in 1099 patients, and 36,251 esophageal mucosal specimens were reviewed. Seventy-nine of 1099 patients (7.2%) initially had HGD (34 prevalent) or subsequently developed HGD (45 incident) without evidence of cancer. Of the 75 HGD patients who remained without detectable cancer after the 1 year of intensive searching, 12 developed cancer (16%) during a mean 7.3-year surveillance period: 11 of the 12 who were compliant were considered cured with surgical or ablation therapy. Cancer did not develop in the remaining 63 HGD patients during the surveillance period. CONCLUSIONS: HGD without cancer in Barrett's esophagus follows a relatively benign course in the majority of patients. In the patients who eventually progress to cancer during regular surveillance, surgical resection is curative. Surveillance endoscopies with biopsy is a valid and safe follow-up strategy for Barrett's patients who have HGD without cancer.

Reduced symptoms and need for antisecretory therapy in veterans 3 years after Helicobacter pylori eradication with ranitidine bismuth citrate/amoxicillin/clarithromycin.

OBJECTIVE: The most effective combination therapy to eradicate Helicobacter pylori has not yet been found. The perfect combination would be effective, relatively free of side effects, and easy to comply with. We studied a 14-day course of three medications taken twice daily by H. pylori-infected patients who were enrolled in the outpatient Veterans Affairs (VA) clinics. The two major objectives were 1) to determine the effectiveness of the combination therapy and 2) to determine the compliance of patients in a VA population. METHODS: Fifty-two male patients were identified with H. pylori infection by positive CLO (Rapid Urease Test) test, positive Giemsa stain, or positive serology. Active infection was confirmed by a positive 13C urea breath test (UBT). Patients were treated for 14 days with open-label triple-combination therapy of ranitidine bismuth citrate (RBC; 400 mg b.i.d.), amoxicillin (1000 mg b.i.d.), and clarithromycin (500 mg b.i.d.). Successful eradication of H. pylori was confirmed by repeat UBT at 6-8 wk after the final dose of therapy. RESULTS: Of the 52 enrolled patients, 49 (94.2%) met the criteria for successful completion of the study (per protocol analysis based on compliance with at least 80% of medication and performance of both UBTs). Of the three patients who did not successfully complete, one was cured (after 6 days of treatment), and two remained infected (after 3 days and 9 days of treatment). Of the 49 completed patients, 45 (91.8%) were cured, and four remained infected. Overall, regardless of compliance (intent-to-treat analysis), 46 of the 52 (88.4%) patients had documented cure of H. pylori infection as determined by the posttreatment UBT. By 3 yr after H. pylori eradication, two of 15 (13.3%) patients who were not on baseline medications had developed the need for antisecretory therapy, but 18 of 31 (58.1%) who were on baseline medications were able to stop therapy. Thus, at 3 yr, successful H. pylori eradication decreased the need for antisecretory therapy from 67.4% of the H. pylori-infected population to 43% of the H. pylori-eradicated population. The effect of H. pylori eradication in improving symptoms at 3 yr was statistically significant in both the ulcer population and the nonulcer population. Adverse events were mild, and included diarrhea (26 patients), bad taste in mouth (24 patients), nausea/upset stomach (nine patients), and headache (two patients). The diarrhea was self-limiting in 25 of the 26 patients. Only two patients discontinued medication because of adverse events. CONCLUSION: The RBC/amoxicillin/clarithromycin combination was, in our VA population, an easily complied with, highly effective, and safe triple therapy with a 90% H. pylori eradication rate. Successful eradication of H. pylori leads to a dramatic decrease in upper-gut symptoms and decreased need for antisecretory therapy.

Risk factors for erosive reflux esophagitis: a case-control study.

OBJECTIVES: It is presently not fully understood which risk factors contribute to the occurrence of reflux esophagitis and how such factors might influence the severity of the disease. The aim of this study was to delineate the clinical epidemiology of erosive reflux esophagitis. METHODS: Outpatients from a medicine and gastroenterology clinic who underwent upper GI endoscopy were recruited into a case-control study. A total of 1,533 patients with and 3,428 patients without endoscopically diagnosed reflux esophagitis were categorized as case and control subjects, respectively. Using multivariate logistic regressions for statistical analysis, the presence of esophageal erosions, ulcers or strictures, served as three separate outcome variables. Demographic characteristics, intake of nonsteroidal anti-inflammatory drugs (NSAIDs), consumption of alcohol and cigarettes, and the presence of hiatus hernia or peptic ulcer served as predictor variables. RESULTS: Erosive reflux esophagitis tended to occur more frequently in Caucasian male patients. Hiatus hernia was associated with a strong risk for developing esophageal erosions, ulcers, and strictures. Although statistical significance was demonstrated only for esophageal erosions, in all grades of reflux esophagitis alike, gastric and duodenal ulcer exerted a protective influence. Consumption of NSAIDs increased the risk for esophageal ulcers only. Smoking and alcohol were not associated with an increased risk of developing any type of erosive reflux esophagitis. CONCLUSIONS: The results stress the critical role played by hiatus hernia in all grades of erosive reflux esophagitis. NSAIDs may act through a mechanism of topically induced esophageal injury. Our data also suggest that the presence of either gastric or duodenal ulcer exerts a protective influence against the development of reflux disease.

Walking and chewing reduce postprandial acid reflux.

BACKGROUND: Gastro-oesophageal reflux is worse after meals, and antacids are usually consumed after dietary indiscretion. AIM: To investigate whether walking or gum chewing affect meal-induced gastro-oesophageal reflux. METHODS: The study population comprised 12 case subjects with gastro-oesophageal reflux disease and 24 healthy controls. Each subject was studied using pH-metry for 5 h on 3 separate days. After baseline recording of pH for 1 h, all subjects were fed a standard breakfast over a 20-min period. On one of the days, oesophageal pH was recorded after the 20-min eating period for an additional 4 h in the sitting position. On another day, postprandial oesophageal pH was recorded for the first hour whilst walking, and for 3 subsequent hours whilst sitting. During a third day, oesophageal pH was recorded for the first postprandial hour whilst gum-chewing, followed by 3 h of sitting. RESULTS: Food intake promoted gastro-oesophageal reflux in case subjects with GERD as well as in healthy controls, although postprandial reflux was more pronounced amongst the refluxers than amongst the controls. Chewing gum for 1 h after the meal reduced the acid contact time in both groups, with a more profound effect in refluxers than in controls. Whilst the beneficial effect of 1-h of gum-chewing lasted for up to 3 h in both groups, the beneficial effect of 1-h of walking was apparent only in refluxers, only to a mild degree, and only for a short duration. CONCLUSIONS: Chewing gum after a meal helps to reduce postprandial oesophageal acid exposure.

Gastroesophageal reflux disease and asthma.

Gastroesophageal reflux (GER) and asthma occur together frequently. The relationship has been recognized for more than 2,000 years but has not been appreciated until recently. Attempts to determine the number of asthmatics that currently have GER (prevalence) have shown a higher-than-expected prevalence. Of the approximately 200 published studies on the relationship between GER and asthma, the true prevalence of GER in asthmatics, however, can be estimated from fewer than 20 of the studies. These studies, which comprise highly selected referred populations, are unlikely to reflect the overall population of patients with asthma. Nevertheless, the estimated prevalence of GER in asthmatics is between 60-80% in adults and 50-60% in children. No attempts have been made to determine the incidence of GER in asthmatics. To identify asthmatics who develop GER over time would be a formidable task, requiring decades of close follow-up of asthmatics who do not now have GER. Despite the lack of data on the incidence of GER, data on the prevalence raise an important issue: If the prevalence of GER in adult asthmatics is similar to the prevalence of GER in child asthmatics, what is the true incidence of GER? There are two potential answers: (1) all of the child asthmatics with GER grow up to become the adult asthmatics with GER (GER incidence = 0%); and (2) some child asthmatics with GER outgrow either the GER or the asthma; some adults with asthma develop GER while others with GER develop asthma (low, medium, or high incidence depending on the numbers). It is not unreasonable to suspect that some child asthmatics with GER become adult asthmatics with GER, and that children with GER who apparently "outgrow" their asthma surface later as adults with both asthma and GER. Because most children leave their pediatricians after adolescence, the information required to demonstrate continued asthma or GER is lost. As a result, the medical community sees two completely different populations, each with very similar conditions: childhood asthma with GER and adult asthma with GER. If the high prevalence of GER in asthmatics is clinically relevant, it should be readily explainable. We suggest that the GER/asthma relationship consists of a self-propagating situation whereby reflux aggravates asthma, which in turn induces further reflux. In the early course of the disease, asthma may not be apparent, as aspiration-induced pulmonary symptoms may occur very infrequently-perhaps once or twice a year. With time, however, aspiration may become more frequent, and the pulmonary tree may become hypersensitive. The individual may be diagnosed as having asthma. The pulmonary tree becomes increasingly hypersensitive, to a variety of stimuli. In such a scenario, the initial contribution of acid aspiration is no longer apparent, as the primary focus is on the asthma. In any individual patient, the emphasis may be placed on the GER if reflux symptoms predominate or on asthma if pulmonary symptoms predominate. The result is confusion over whether a patient with GER has asthma or whether a patient with asthma has GER. The unending debate about whether GER is a cause of the asthma or a result of the asthma becomes the focus of attention. At such a point, the question of whether GER exists in asthmatics or whether pulmonary symptoms exist in refluxers is irrelevant. For the individual patient, gastric contents refluxed into the pulmonary tree is an undesirable event, whether cause or effect, and it is up to the physician to determine how such events can be stopped.

Why do the published data fail to clarify the relationship between gastroesophageal reflux and asthma?

The relationship between gastroesophageal reflux (GER) and asthma has troubled physicians for centuries and has been a source of debate among pulmonologists, allergists, and gastroenterologists for decades. Attempting to tie together the pieces of the puzzle, numerous investigators have struggled to show that in patients with asthma, GER symptoms occur too frequently, gastric acid dwells for too long in the esophageal lumen, and refluxed gastric acid injures the esophageal mucosa more than expected. Unfortunately, all of the work done by these fine investigators has failed to demonstrate a "cause and effect" relationship. Although they have succeeded in convincing us that GER occurs more frequently in asthmatics than in nonasthmatics, they still must continue until we all know how to predict which patients have gastroesophageal-induced or gastroesophageal-exacerbated asthma.

Defining GERD.

"It is not the death of GERD that I seek, but that it turns from its evil ways and follows the path of righteousness." The reflux world is fully aware of what GERD is and what GERD does. What the world does not know, however, is the answer to the most important yet least asked question surrounding GERD's raison-d'etre: Why is GERD here and why do we have it? What GERD is: abnormal gastric reflux into the esophagus that causes any type of mischief. What GERD does: causes discomfort and/or pain with or without destroying the mucosa; causes stricture or stenosis, preventing food from being swallowed; sets the stage for the development of esophageal adenocarcinoma; invades the surrounding lands to harass the peaceful oropharyngeal, laryngeal and broncho-pulmonary territories; reminds us that we are not only human, but that we are dust and ashes. Why GERD is here: We propose three separate and distinct etiologies of GERD, and we offer the following three hypotheses to explain why, after 1.5 million years of standing erect, we have evolved into a species (specifically Homosapiens sapiens) that is destined to live with the scourge of GERD. Hypothesis 1: congenital. The antireflux barrier, comprising the smooth-muscled lower esophageal sphincter, the skeletal-muscled right crural diaphragm and the phreno-esophageal ligament does not completely develop due to a developmental anomaly or incomplete gestation. Hypothesis 2: acute trauma: The antireflux barrier in adults suffering acute traumatic injury to the abdomen or chest is permanently disrupted by unexpected forces, such as motor vehicle accidents (with steering wheel crush impact), blows to the abdomen (from activities such as boxing, etc.), heavy lifting or moving (e.g., pianos, refrigerators) or stress positions (e.g., hand stands on parallel gym bars). The trauma creates a hiatal hernia that renders the antireflux mechanism useless and incapable of preventing GERD. Hypothesis 3: chronic trauma: The antireflux barrier in children and adults is gradually weakened over time as a result of chronic straining to defecate and straining in an unphysiologic position, both of which stem from our modern day habits of eating a low-fiber diet and living on the high-seated toilet. We suggest that the chronic traumatic hiatal hernia is (a) the cause of more than 90 percent of the GERD that stalks the Western world; (b) is a direct result of abandoning the popular and worldwide practice of squatting to socialize, eat and defecate; and (c) is our just reward for adopting the "civilized" high sitting position on chairs and modern toilets.