gastroesophageal reflux disease: nonpharmacological treatment
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GUIDELINES IN FOCUS
Rev Assoc Med Bras 2012; 58(1):18-24
Federação Brasileira de Gastroenterologia, Sociedade
Brasileira de Endoscopia Digestiva, Colégio Brasileiro de
Cirurgia Digestiva, Sociedade Brasileira de Pneumologia,
Associação Brasileira de Otorrinolaringologia e Cirurgia
Aloisio Carvalhaes, Angelo Paulo Ferrari Junior, Antonio
Frederico Magalhães, Ary Nasy, Celso Mirra Paula e
Silva, Claudio L. Hashimoto, Décio Chinzon, Edson Pedro
da Silva, Eduardo G.H. Moura, Eponina Maria Oliveira
Lemme, Farid Butros Iuan Nader, Fauze Maluf Filho,
Gerson R. de Souza Domingues, Igelmar Barreto, Isac
Jorge Filho, Ismael Maguilnik, Ivan CecconelloI, Jaime
Natan Eisig, Joaquim Padro P. de Moraes-Filho, Joffre
Rezende Filho, José Carlos Del Grande, José Luiz Pimenta
Modena, José Roberto Almeida, Lilian R.O. Aprile,
Luciana Camacho-Lobato, Luciana Dias Moretzohn,
Marcelo de Souza Cury, Marcio Matheus Tolentino, Marco
Aurélio Santo, Marcos Kleiner, Marcos Tulio Haddad,
Maria do Carmo Friche Passos, Olavo Mion, Osvaldo
Malafaia, Paulo Roberto Savassi Rocha, Rafael Stelmach,
Ricardo Aires Correa, Ricardo Correa Barbuti, Richard
Gursky, Rimon Sobhi Azzam, Roberto El Ibrahim, Rubens
Antonio Aissar Sallum, Roberto Oliveira Dantas, Schilioma
Zaterka, Sérgio Gabriel Silva de Barros, Tomas Navarro
Rodriguez, Ulysses G. Meneghelli, Wilson Modesto Polara,
Esophagus and Motility Group of the Discipline of Clinical
Gastroenterology of the Department of Gastroenterology of
FMUSP, Sociedade Brasileira de Motilidade Digestiva
May 20, 2009
CONFLICT OF INTEREST
Chinzon D received reimbursement for attending confe-
rences sponsored by Jansen and, also received speaker
and consulting fees sponsored by Jansen, AstraZeneca
and Medley. Lemme EMO received speaker fees sponsored
by AstraZeneca and received grants for research sponsored
by Nycomed. Moraes Filho JPP received reimbursement
for attending a symposium sponsored by AstraZeneca,
Gastroesophageal reflux disease: nonpharmacological treatment©2012 Elsevier Editora Ltda. All rights reserved.
Nycomed, and Medley; received speaker fees sponsored by
AstraZeneca and Nycomed; received financial support for
organizing educational activities sponsored by Nycomed,
Aché and AstraZeneca. Rezende Filho J received speaker
fees sponsored by Nycomed. Mion O received speaker fees
sponsored by AstraZeneca. Stelmach R received speaker
fees; financial support to organize teaching activities and
to perform research; and consulting fees sponsored by
AstraZeneca, Aché, Bayer Shering Plough, Boerhinger-
Inghelhein, Eurofarma, Glaxo-Smith Kline, Novartis and
Mantercorpe. Barbut RC received speaker fees; financial
support to organize teaching activities and to perform
research; and consulting fees sponsored by AstraZeneca,
Aché and Medley. Dantas RO received speaker fees
sponsored by AstraZeneca. Zaterka S received financial
support for teaching and consulting activities sponsored by
Jansen-Cilag. Navarro T received speaker fees; financial
support for teaching and consulting activities, and
performed research sponsored by AstraZeneca.
DESCRIPTION OF THE EVIDENCE COLLECTION METHOD
A search was performed in the EMBASE, SciELO / LILACS,
PubMed / Medline and Cochrane Library databases using the
following words: gastroesophageal reflux, gerd, heartburn,
nerd, gero, esophagus, esophagitis, extra-esophageal,
asthma, atypical symptoms, chest pain, cough, globus
sensations, hoarseness, otorhinolaryngology diseases, pain,
respiratory tract diseases, laryngitis, anti-ulcer agents,
enzyme inhibitors, proton pumps, lansoprazole, omeprazole,
proton pump inhibitors, rabeprazole, continuous, on-demand,
surgery, fundoplication, non acid*, alkaline, weakly acid*,
gas, stomach diseases, stomach/pathology, Helicobacter, Helicobacter infections, burimamide, cimetidine, ebrotidine,
etintidine, famotidine, lafutidine, loxtidine, metiamide,
mifentidine, nizatidine, oxmetidine, ranitidine, ranitidine
bismuth citrate, roxatidine acetate, tiotidine, zolantidine,
histamine H2 antagonists, benzamides, dopamine antagonists,
bromopride, domperidone metoclopramide, smoking, alcohol,
obesity, weight loss, caffeine, coffee, citrus, chocolate, spicy
food, head of bed elevation, late-evening meal, diet*, life
style, body mass index, alcoholic, postprandial period, beer,
wine, supine position, food*, eating, exercise, dietary fiber,
dietary fats, beds*, bedding and linens*.
GASTROESOPHAGEAL REFLUX DISEASE: NONPHARMACOLOGICAL TREATMENT
19Rev Assoc Med Bras 2012; 58(1):18-24
A total of 5,000 publications were retrieved. Using the
filters: humans, randomized controlled trial, randomized
AND controlled AND trial, clinical AND trial, clinical trials,
random*, random allocation, therapeutic use, epidemiologic
methods, cohort studies, cohort AND stud*, prognos*, first
AND episode, cohort, we selected 73 studies to support
DEGREE OF RECOMMENDATION AND STRENGTH OF EVIDENCE
A: Experimental or observational studies of best consistency.B: Experimental or observational studies of lower consistency.C: Case reports (non-controlled studies).D: Opinion without critical evaluation, based on consensuses, physiological studies or animal models.
Due to high prevalence, variety of the clinical presenta-tion forms and economic impact, consequences of loss of quality of life and clinical-laboratory research costs, the implementation of international consensus meetings has been encouraged. On the other hand, the diagnosis and therapeutic management of gastroesophageal reflux dis-ease (GERD) has varied from center to center, which is an important factor in the search for scientific evidence on the issue, prompting the implementation of this Guideline, which seeks to answer four key clinical questions of the non-pharmacological treatment of GERD.
1. DOES THE NONPHARMACOLOGICAL TREATMENT PRODUCE RESULTS IN GERD?OBESITY
Body mass index (BMI) > 25 is a risk factor for erosive GERD1 (B). There is an association between reflux symp-toms and obesity (OR: 2.6)2 (B). BMI is associated with reflux (OR per 5 units: 1.9)3 (B). BMI > 25 is a risk fac-tor (OR: 1.41) for GERD4 (B). Obesity is associated with GERD5 (B). Weight decrease does not reduce the mani-festations of reflux6 (B). In patients with mean BMI of 42.5 kg/m2, there is no association with the prevalence of GERD7 (B). Obesity predisposes to gastroesophageal re-flux, and weight loss improves postprandial reflux and re-duces pH time < 48 (B).
Smoking is a risk factor for non-erosive GERD1 (B) and for reflux symptoms2 (B). Smokers have more reflux episodes than nonsmokers, but a 24-hour abstinence does not reduce the pH time < 49 (B).
24-hour smoking abstinence reduces the number of reflux episodes, but does not affect the total acid exposure10 (B). Individuals abstaining from smoking for 48 hours have in-creased esophageal acid exposure11 (B). Smoking is associ-ated with GERD5,12 (B).
Alcohol intake is a risk factor for erosive GERD1 (B). Frequent consumption of alcohol is a risk factor for re-flux symptoms2 (B). The habits of drinking wine or beer increase the risk of reflux (NNH 7 to 9)13 (B). Alcohol consumption is a risk factor for erosive GERD (OR: 2.42 to 2.85)4,5 (B).
Coffee consumption is associated with GERD (OR: 1.23)5(B).
The consumption of sweets and white bread is associated with symptoms of reflux2 (B). Fruit consumption has a protective effect on reflux symptoms2 (B). Protein intake is associated with erosive GERD, and fiber, with a lower risk of GERD14 (B). Excessive consumption of food and sweet food is associated with GERD5 (B). High-fat diet does not increase the number of reflux episodes, or acid esophageal exposure15 (B).
Working in an inclined position is a risk factor for non-erosive GERD1 (B). GERD episodes are triggered by pos-ture5 (B).
INCLINED HEAD OF THE BED Sleeping with a wedge-shaped support is associated with less acid exposure than in the horizontal position16 (B). Raising the head of the bed (28 cm) reduces the number of reflux episodes and pH time < 517 (B).
The later the night the meal is, the higher the rate of reflux episodes, especially in obese individuals and in those with erosive GERD18 (B). Going to bed immediately after din-ner is associated with increased risk of GERD, especially within a time period of less than 3 hours19 (B).
Physical activity seems to have a protective effect against GERD2 (B).
STRESS AND FATIGUE
GERD episodes are triggered by stress and fatigue11 (B). Stress is among the risk factors for GERD12 (B).
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20 Rev Assoc Med Bras 2012; 58(1):18-24
Although obesity (BMI > 25), smoking, alcohol consump-tion, coffee, sweets, proteins, excess food, inclined posture, stress and fatigue are associated with GERD, there is no consistent information to define that the resolution of these factors is followed by resolution or improvement of GERD. However, the elevation of the head of the bed and going to bed only after a minimum of three hours after the night meal are measures that reduce esophageal acid exposure.
2. WHAT ARE THE INDICATIONS OF SURGICAL TREATMENT OF GERD? HIATAL HERNIA
The laparoscopic Nissen fundoplication is equally effective in patients with GERD and paraesophageal hernia20 (B). There is improvement in abdominal pain, reflux, digestion score and quality of life score in patients with large para-esophageal hernias submitted to laparoscopic surgery21 (B). At the average follow-up period of 72 months, 93% of patients are free of GERD-related symptoms22 (B).
Hiatal hernia is a risk factor for erosive GERD1 (B). A hia-tal hernia < 3 cm is a risk factor for non-erosive GERD, and a hiatal hernia > 3 cm, for erosive GERD and Barrett’s esophagus23 (B). The size of hiatal hernia, low pressures in the lower esophageal sphincter, esophageal acid expo-sure and number of reflux episodes are associated with esophagitis severity24 (B). Hiatal hernias > 2 cm are asso-ciated with Barrett’s esophagus and erosive GERD25 (B). The presence of hiatal hernia is associated with more se-vere esophagitis and predisposes patients with non-erosive GERD to more severe histological alterations26 (B). Patients with hiatal hernias have a high incidence of pathological reflux, regardless of the low pressure in the lower eso- phageal sphincter. Patients with pathologic reflux have esophageal propulsion failure and/or mechanical defects of the cardia associated with hiatal hernia27 (B).
Recurrence after fundoplication (Nissen or Toupet) is higher in large hernias (grades 3 and 4)28 (B). The perma-nent migration of the esophagogastric junction has more relevance in GERD prognosis than in sliding hiatal hernia, with reduction of the junction. Hiatal insufficiency and concentric hiatal hernia are determinant factors of irre-versible cardia incontinence29 (B). In patients with GERD and hiatal hernia (31% erosive GERD and 75% lower sphincter dysfunction), reduction, crural closure, and Nis-sen fundoplication result in symptom improvement, at a
14-month follow-up30 (B). In patients with GERD (com-plicated or not), the presence of hiatal hernia determines significant increase in the PPI dose to achieve intraesopha-geal acid suppression31 (B).
Considering that:The presence of the permanent migration of esopha-
gogastric junction and size of hiatal hernia (> 2 cm) are factors of worst prognosis for GERD;
The presence of hiatal hernia requires higher doses of PPIs;
The result of the laparoscopic fundoplication is ad-equate, including for paraesophageal hernia.
Hiatal hernias associated with GERD, especially those > 2 cm and fixed, should be treated surgically.
The Nissen fundoplication has good results in patients with normal esophageal motility, and the Toupet tech-nique, in patients with esophageal dysmotility32 (B). There is no difference in postoperative symptoms in pa-tients with or without esophageal dysmotility submitted to fundoplication (Nissen or Toupet)33 (A). The type of fundoplication should not be determined by the pres-ence of dysmotility, as the postoperative dysphagia is not related to it34 (A). Preoperative dysmotility reflects a more severe disease, does not affect the postoperative outcomes, does not improve fundoplication and may oc-cur after surgery35 (B).
Considering that:The preoperative dysmotility reflects a more severe
disease, does not affect the postoperative outcomes, does not improve with fundoplication and may occur after sur-gery; no surgical treatment should be indicated using the parameter of esophageal dysmotility.
From the perspective of the National Health System, lapa-roscopic fundoplication is more cost-effective over eight years than PPI36 (B). Over five years, the cost of PPI is low-er than the open surgery for GERD37 (B). Apparently, the Nissen fundoplication is more cost-effective in the treat-ment of GERD than treatment with PPI38 (B).
RECOMMENDATION Apparently, the laparoscopic Nissen fundoplication, from the perspective of the National Health System, is more cost effective than PPI therapy over eight years. However, this is not the case with open surgery.
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3. WHEN SHOULD CLINICAL TREATMENT BE INDICATED VERSUS SURGICAL TREATMENT? In patients with GERD (erosive and non-erosive), antire-flux surgery, compared to drug treatment with a PPI re-duces the pH time < 4.0 and improves the VAS symptom score, the GERSS score, and scores of heartburn and re-gurgitation39 (A).
In patients with chronic erosive GERD, the Nissen surgery, compared to the use of PPIs, improves symptom scores, including the digestive score, and reduces the pH time < 4.040 (A).
In patients with chronic erosive reflux disease, Nissen surgery compared to PPI increases the degree of patient satisfaction (NNT 5)41 (A).
In patients with erosive reflux disease, antireflux sur-gery (Nissen or Toupet) compared to omeprazole 20 mg daily reduces the risk of treatment failure over 5 years. There is a greater number of treatment failures over five years with clinical treatment of omeprazole 40 mg or 60 mg compared to surgery (Nissen or Toupet). Surgery reduces the risk of treatment failure by 11.6% (95% CI: 0.6-22.6) - NNT: 9. However, symptom scores (GSRS) and quality of life scores (PGWB) were similar in the two com-pared forms of treatment42 (A).
In patients with chronic erosive reflux disease, antire-flux surgery (Nissen or Toupet) in comparison to omepra-zole 20 mg reduces treatment failure, and, maintained for seven years, reduces dysphagia (NNT 38) and hiatal hernia (NNT 2)43 (A).
In patients with chronic GERD (reflux symptoms + esophagitis + previous treatment > 3 months), treatment with esomeprazole 20 mg or 40 mg is equivalent to lapa-roscopic surgery (Nissen), with 93% and 90% of patients remaining in symptom remission, respectively 44 (A).
There is a greater number of therapeutic failures in three years with the clinical treatment of omeprazole 40 mg or 60 mg, when compared to surgery (Nissen or Toupet). Surgery reduces the risk of treatment failure by 12.9% (95% CI: 1.9-23.9) - NNT: 8. However, symptom scores (GSR) and quality of life (PGWB) were similar in the two forms of treatment45 (A).
SYMPTOMS, ESOPHAGITIS AND PHIn patients with GERD not submitted to surgery, at a fol-low-up of 17 to 22 years, symptoms improved in 70% and worsened in 20%. Of these patients, 66% developed ero-sive GERD and/or pH changes, and 10% Barrett’s esopha-gus46 (B).
At 12 months of follow-up, GERD treatment with medication and surgery (Nissen) is effective. However, surgery offers additional benefit to patients who had par-tial improvement with medication at a mean follow-up of 6.9 years41 (A).
At 18 months, regression from dysplasia to Barrett’s esophagus obtained with Nissen fundoplication (93.8%) is higher than that obtained with PPI (63.2%)47 (B).
The quality of life is higher in patients submitted to surgery compared to those undergoing medical treatment, at 12 months of follow-up48 (B).
The laparoscopic Nissen fundoplication leads to lower esophageal acid exposure in three months and better qual-ity of life after 12 months, when compared to clinical treat-ment40 (A).
Patients with Barrett’s esophagus have a 33% regression after antireflux surgery. The regression is more significant the longer the time after surgery49 (B).
Laparoscopic surgery improves the quality of life of pa-tients whose symptoms are adequately controlled with PPIs50 (B).
In patients with GERD submitted to surgery after a fol-low-up of 5.9 years, 37% were using medications (PPIs, H2 blockers or antacids), of which 17% had never stopped and 83% resumed after 2.5 years due to return of symp-toms. The pH-metry was abnormal in 32%51 (B).
Comparing the response to surgical treatment of GERD, after 43 months, 66% had symptom improvement, which was lower in patients with non-erosive GERD52 (B).
After five years, there was no difference in symptom improvement, adverse effects, or quality of life scores among patients with erosive and non-erosive GERD who underwent laparoscopic Nissen fundoplication53 (B).
There was no difference in response rates among pa-tients undergoing surgery for GERD with open or laparo-scopic techniques, and this was higher in patients under-going clinical treatment54 (B).
In two years, 14.5% of medically treated patients de-veloped Barrett’s esophagus compared with no patients submitted to surgery55 (B).
Heartburn and esophagitis are effectively treated by medical and surgical therapy. Only surgery improved re-gurgitation, dysphagia and esophageal motility56 (B).
At 10.9 years of follow-up, the Nissen fundoplication produces 84% symptom resolution, 89% esophagitis reso-lution and 5% use of medication, while the clinical treat-ment produces, respectively, 53%, 45%, and 21%57 (B).
Laparoscopic fundoplication produces the same re-sults in patients with erosive or nonerosive GERD, with symptom improvement and reduction in PPI use58 (B).
Patients with Barrett’s esophagus have a 33% regres-sion after antireflux surgery. The regression is more sig-nificant the longer the time after surgery49 (B).
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LOWER ESOPHAGEAL SPHINCTER PRESSURE
In patients with erosive GERD treated with PPI, the rate of recurrence at 12 months was 7.7% when they had normal pressure of the lower esophageal sphincter (> 8 mmHg), 38.1% in those with sphincter dysfunction and preserved motility and 79.5% in those with sphinc-ter dysfunction and dysmotility59 (B).
In five years of follow-up, patients with inadequate response to PPIs can benefit from laparoscopic fundo-plication, especially regarding the improvement of the quality of life60 (B).
During one year of follow-up, antireflux surgery obtained better results than medical treatment in rela-tion to the symptoms of heartburn (19% versus 43%), regurgitation (8% versus 30%), increase in the need for PPIs (19% versus 74%), quality of life score (4 ± 0.6 versus 21 ± 1.4); and patient satisfaction (21.6% versus 5.9%)61 (B).
The success rate of Nissen fundoplication is 75.3%, and is associated with 77.1% of patients who responded to medical treatment and 56.0% who did not respond62 (B).
In two years of follow-up of patients with erosive GERD and stenosis, antireflux surgery reduces the number of dilations by a factor of 10, reduces the dysphagia score in 50%, and 91.9% of patients were satisfied63 (B).
In a 10-year follow-up of patients that underwent Nissen fundoplication, the persistence or presence of symptoms was 32 %, and 68% were asymptomatic. The quality of life remained high, although 80% had to un-dergo a new fundoplication procedure64 (B).
NON-ACID GERD In patients on acid suppression, episodes of acid re- flux are not associated with symptoms, but with mixed reflux episodes (liquid-gas)65 (B).
When compared to healthy patients, the number of reflux events in 24 hours after fundoplication is signifi-cantly lower. Most reflux episodes after surgery are non-acid66 (B).
Most preoperative patients had a positive symptom index, and 14 months after surgery, these patients were asymptomatic or had improved greatly67 (B).
Most patients undergoing prolonged PPI use, with persistent symptoms and a positive symptom index, have non-acid reflux, including patients with atypical symptoms68 (B).
In patients with GERD refractory to medical therapy, where gastric acid production is small (< 1 mEq/hour), about 50% have esophageal pH < 4.0 for more than 1.7% of the time69 (B).
Patients refractory to acid suppression, with typical or atypical symptoms, have non-acid reflux most of the time, and may benefit from surgical treatment.
In a two-year follow-up of patients with erosive GERD and stenosis, antireflux surgery shows a 10-fold reduction in the number of dilations, reduces the score of dysphagia in 50%, and 91.9% of patients are satisfied.
Considering that:Low pressures in the lower esophageal sphincter are
related to the severity of esophagitis, and in patients with erosive GERD treated with PPIs for 12 months, the recur-rence rate, when there is lower sphincter dysfunction with pressure < 8 mmHg, whether or not associated with dys-motility, is respectively 38.1% and 79.5%. Surgical treat-ment should be considered in these patients.
There is evidence of estimated surgery benefit, with treatment failure reduction of 12% (NNT 8), when com-pared to medical treatment, and rates are maintained in the long term (7 years). But there is also evidence of equiv-alence for medical treatment with PPIs and laparoscopic surgery (Nissen), with 93% and 90% of patients remaining in symptom remission for 3 years, respectively.
In the long term, surgery reduces the risk of esophagitis by 44% (NNT: 2), and of Barrett’s esophagus and dysplasia, when compared to PPI therapy. In seven years of follow-up, surgery may benefit patients with GERD (erosive or non-erosive) who had partial response to PPIs, especially in relation to quality of life. However, after 2.5 years, 37% of patients may be using PPIs, and, additionally, in 10 years, many (80%) may require reoperation. Laparoscopic surgery enhances patient’s quality of life, even in those whose symptoms are adequately controlled with PPIs.
4. AMONG PATIENTS WITH SURGICAL INDICATION, WHICH TECHNIQUE HAS THE BEST RESULT: TOTAL (NISSEN) OR PARTIAL FUNDOPLICATION (TOUPET)?There is no difference after one year regarding the presence of symptoms of heartburn, regurgitation or other symptoms related to reflux in patients who underwent Nissen versus Toupet surgeries. However, the Nissen surgery increas-es the risk of dysphagia of any degree by 18.7% (95% CI: 6.0-31.4) – NNH: 5, and chest pain at meals by 17.1% (95% CI: 5.7-28.5) – NNH: 6. There is no difference regarding post-operative symptoms related to esophageal motility33 (A).
After two postoperative years, patient satisfaction is equivalent between those submitted to the Nissen or Tou-pet laparoscopic techniques. However, the Nissen sur-gery increases the risk of dysphagia by 11.0% (95% CI: 1.7-20.3) – NNH: 934 (A).
There is no difference between Nissen and Toupet sur-geries, regarding the severity of symptoms in the one-year postoperative period70 (A).
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In patients treated by Nissen surgery versus Toupet, there was no difference related to heartburn or acid regurgi-tation control. There was also no difference in the prevalence of dysphagia between the two surgical techniques71 (A).
Patients who underwent the Nissen or Toupet tech-niques are equally satisfied and reflux control is equivalent. However, the Nissen surgery increases the risk of dyspha-gia, not correlated to differences in esophageal motility, in 19.0% (95% CI: 8.1-29.9) – NNH: 572 (A).
There was no difference regarding symptom recur-rence, dysphagia, or reflux control in the three-year post-operative period of Nissen versus Toupet techniques73 (A).
There is no difference between the Nissen and Toupet sur-gical techniques in relation to therapeutic response; how-ever, the Nissen technique may produce more dysphagia, with NNH of 5 to 9, not correlated with motility.
REFERENCES1. Kim N, Lee SW, Cho SI, Park CG, Yang CH, Kim HS, et al. The prevalence of
and risk factors for erosive oesophagitis and non-erosive reflux disease: a na-tionwide multicentre prospective study in Korea. Aliment Pharmacol Ther. 2008;27:173-85.
2. Nocon M, Labenz J, Willich SN. Lifestyle factors and symptoms of gas-trooesophageal reflux: a population-based study. Aliment Pharmacol Ther. 2006;23:169-74.
3. Nandurkar S, Locke GR 3rd, Fett S, Zinsmeister AR, Cameron AJ, Talley NJ. Relationship between body mass index, diet, exercise and gastro-oesophageal reflux symptoms in a community. Aliment Pharmacol Ther. 2004;20:497-505.
4. Rosaida MS, Goh KL. Gastro-oesophageal reflux disease, reflux oesophagitis and nonerosive reflux disease in a multiracial Asian population: a prospec-tive, endoscopy based study. Eur J Gastroenterol Hepatol. 2004;16:495-501.
5. Wang JH, Luo JY, Dong L, Gong J, Tong M. Epidemiology of gastroesopha-geal reflux disease: a general population-based study in Xi’an of Northwest China. World J Gastroenterol. 2004;10:1647-51.
6. Kjellin A, Ramel S, Rossner S, Thor K. Gastroesophageal reflux in obese patients is not reduced by weight reduction. Scand J Gastroenterol. 1996; 31:1047-51.
7. Lundell L, Ruth M, Sandberg N, Bove-Nielsen M. Does massive obesity promote abnormal gastroesophageal reflux? Dig Dis Sci. 1995;40:1632-5.
8. Mathus-Vliegen EM, Tygat GN. Gastrooesophageal reflux in obese subjects: influence of overweight, weight loss and chronic gastric balloon distension. Scand J Gastroenterol. 2002;37:1246-52.
9. Schindlbeck NE, Heinrich C, Dendorfer A, Pace F, Muller-Lissner SA. Influ-ence of smoking and esophageal intubation on esophageal pH-metry. Gas-troenterology. 1987;92:1994-7.
10. Waring JP, Eastwood TF, Austin JM, Sanowski RA. The immediate effects of cessation of cigarette smoking on gastroesophageal reflux. Am J Gastroen-terol. 1989;84:1076-8.
11. Kadakia SC, Kikendall JW, Maydonovitch C, Johnson LF. Effect of cigarette smoking on gastroesophageal reflux measured by 24-h ambulatory esopha-geal pH monitoring. Am J Gastroenterol. 1995;90:1785-90.
12. Stanghellini V. Relationship between upper gastrointestinal symptoms and lifestyle, psychosocial factors and comorbidity in the general population: results from the Domestic/International Gastroenterology Surveillance Study (DIGEST). Scand J Gastroenterol Suppl. 1999;231:29-37.
13. Pehl C, Wendl B, Pfeiffer A. White wine and beer induce gastro-oesophageal reflux in patients with reflux disease. Aliment Pharmacol Ther. 2006;23:1581-6.
14. El-Serag HB, Satia JA, Rabeneck L. Dietary intake and the risk of gas-trooesophageal reflux disease: a cross sectional study in volunteers. Gut. 2005;54:11-7.
15. Penagini R, Mangano M, Bianchi PA. Effect of increasing the fat content but not the energy load of a meal on gastrooesophageal reflux and lower oesopha-geal sphincter motor function. Gut. 1998;42:330-3.
16. Hamilton JW, Boisen RJ, Yamamoto DT, Wagner JL, Reichelderfer M. Sleep-ing on a wedge diminishes exposure of the esophagus to refluxed acid. Dig Dis Sci. 1988;33:518-22.
17. Stanciu C, Bennett JR. Effects of posture on gastro-oesophageal reflux. Di-gestion. 1977;15:104-9.
18. Piesman M, Hwang I, Maydonovitch C, Wong RK. Nocturnal reflux episodes following the administration of a standardized meal. Does timing matter? Am J Gastroenterol. 2007;102:2128-34.
19. Fujiwara Y, Machida A, Watanabe Y, Shiba M, Tominaga K, Watanabe T, et al. Association between dinner-to-bed time and gastro-esophageal reflux disease. Am J Gastroenterol. 2005;100:2633-6.
20. Mark LA, Okrainec A, Ferri LE, Feldman LS, Mayrand S, Fried GM. Com-parison of patient-centered outcomes after laparoscopic Nissen fundoplica-tion for gastroesophageal reflux disease or paraesophageal hernia. Surg En-dosc. 2008;22:343-7.
21. Parameswaran R, Ali A, Velmurugan S, Adjepong SE, Sigurdsson A. laparo-scopic repair of large paraesophageal hiatus hernia: quality of life and dura-bility. Surg Endosc. 2006;20:1221-4.
22. Maziak DE, Todd TR, Pearson FG. Massive hiatus hernia: evaluation and surgical management. J Thorac Cardiovasc Surg. 1998;115:53-60.
23. Sgouros SN, Mpakos D, Rodias M, Vassiliades K, Karakoidas C, Andrikopoulos E, et al. Prevalence and axial length of hiatus hernia in pa-tients, with nonerosive reflux disease: a prospective study. J Clin Gastroen-terol. 2007;41:814-8.
24. Jones MP, Sloan SS, Rabine JC, Ebert CC, Huang CF, Kahrilas PJ. Hiatal her-nia size is the dominant determinant of esophagitis presence and severity in gastroesophageal reflux disease. Am J Gastroenterol. 2001; 96:1711-7.
25. Cameron AJ. Barrett’s esophagus: prevalence and size of hiatal hernia. Am J Gastroenterol. 1999;94:2054-9.
26. Gatopoulou A, Mimidis K, Giatromanolaki A, Papadopoulos V, Polychronidis A, Lyratzopoulos N, et al. Impact of hiatal hernia on histological pattern of non-erosive reflux disease. BMC Gastroenterol. 2005;5:2.
27. Xenos ES. The role of esophageal motility and hiatal hernia in esophageal exposure to acid. Surg Endosc. 2002;16:914-20.
28. Endzinas Z, Jonciauskiene J, Mickevicius A, Kiudelis M. Hiatal hernia recur-rence after laparoscopic fundoplication. Medicina (Kaunas). 2007;43:27-31.
29. Mattioli S, D’Ovidio F, Di Simone MP, Bassi F, Brusori S, Pilotti V, et al. Clini-cal and surgical relevance of the progressive phases of intrathoracic migra-tion of the gastroesophageal junction in gastroesophageal reflux disease. J Thorac Cardiovasc Surg. 1998;116:267-75.
30. Fuller CB, Hagen JA, DeMeester TR, Peters JH, Ritter M, Bremmer CG. The role of fundoplication in the treatment of type II paraesophageal hernia. Thorac Cardiovasc Surg. 1996;111:655-61.
31. Frazzoni M, De Micheli E, Grisendi A, Savarino V. Hiatal hernia is the key factor determining the lansoprazole dosage required for effective intra-oe-sophageal acid suppression. Aliment Pharmacol Ther. 2002;16:881-6.
32. Livingston CD, Jones HL Jr, Askew RE Jr, Victor BE, Askew RE Sr. Lapa-roscopic hiatal hernia repair in patients with poor esophageal motility or paraesophageal herniation. Am Surg. 2001;67:987-91.
33. Booth MI, Stratford J, Jones L, Dehn TC. Randomized clinical trial of lapa-roscopic total (Nissen) versus posterior partial (Toupet) fundoplication for gastrooesophageal reflux disease based on preoperative oesophageal ma-nometry. Br J Surg. 2008;95:57-63.
34. Strate U, Emmermann A, Fibbe C, Layer P, Zornig C. Laparoscopic fundopli-cation: Nissen versus Toupet two-year outcome of a prospective randomized study of 200 patients regarding preoperative esophageal motility. Surg En-dosc. 2008;22:21-30.
35. Fibbe C, Layer P, Keller J, Strate U, Emmermann A, Zornig C. Esopha-geal motility in reflux disease before and after fundoplication: a pro-spective, randomized, clinical, and manometric study. Gastroenterology. 2001;121:5-14.
36. Cookson R, Flood C, Koo B, Mahon D, Rhodes M. Short-term cost effective-ness and long-term cost analysis comparing laparoscopic Nissen fundoplica-tion with proton-pump inhibitor maintenance for gastro-oesophageal reflux disease. Br J Surg. 2005;92:700-6.
37. Myrvold HE, Lundell L, Miettinen P, Pedersen SA, Liedman B, Hatlebakk J, et al. The cost of long term therapy for gastrooesophageal reflux disease: a randomized trial comparing omeprazole and open antireflux sur-gery. Gut. 2001;49:488-94.
38. Van Den Boom G, Go PM, Hameeteman W, Dallemagne B, Ament AJ. Cost effectiveness of medical versus surgical treatment in patients with severe or refractory gastroesophageal reflux disease in the Netherlands. Scand J Gas-troenterol. 1996;31:1-9.
39. Anvari M, Allen C, Marshall J, Armstrong D, Goeree R, Ungar W, et al. A randomized controlled trial of laparoscopic nissen fundoplication versus proton pump inhibitors for treatment of patients with chronic gastroesopha-geal reflux disease: One-year follow-up. Surg Innov. 2006;13:238-49.
40. Mahon D, Rhodes M, Decadt B, Hindmarsh A, Lowndes R, Beckingham I, et al. Randomized clinical trial of laparoscopic Nissen fun-doplication compared with proton-pump inhibitors for treatment of chronic gastro-oesophageal reflux. Br J Surg. 2005;92:695-9.
41. Mehta S, Bennett J, Mahon D, Rhodes M. Prospective trial of laparoscop-ic Nissen fundoplication versus proton pump inhibitor therapy for gas-troesophageal reflux disease: Seven-year follow-up. J Gastrointest Surg. 2006;10:1312-6.
42. Lundell L, Miettinen P, Myrvold HE, Pedersen SA, Liedman B, Hatlebakk JG, et al. Continued (5-year) follow up of a randomized clinical study comparing antireflux surgery and omeprazole in gastroesophageal re-flux disease. J Am Coll Surg. 2001;192:172-9.
43. Lundell L, Miettinen P, Myrvold HE, Hatlebakk JG, Wallin L, Malm A, et al. Seven-year follow-up of a randomized clinical trial comparing proton-pump inhibition with surgical therapy for reflux oesophagitis. Br J Surg. 2007;94:198-203.
GUIDELINES IN FOCUS
24 Rev Assoc Med Bras 2012; 58(1):18-24
44. Lundell L, Attwood S, Ell C, Fiocca R, Galmiche JP, Hatlebakk J, et al. Comparing laparoscopic antireflux surgery with esomeprazole in the management of patients with chronic gastro-oesophageal reflux disease: a 3-year interim analysis of the LOTUS trial. Gut. 2008;57:1207-13.
45. Lundell L, Miettinen P, Myrvold HE, Pedersen SA, Thor K, Lamm M, et al. Long-term management of gastrooesophageal reflux disease with ome-prazole or open antireflux surgery: results of a prospective, randomized clinical trial. The Nordic GORD Study Group. Eur J Gastroenterol Hepatol. 2000;12:879-87.
46. Isolauri J, Luostarinen M, Isolauri E, Reinikainen P, Viljakka M, Keyriläinen O. Natural course of gastroesophageal reflux disease: 17-22 year follow-up of 60 patients. Am J Gastroenterol. 1997; 92:37-41.
47. Rossi M, Barreca M, de Bortoli N, Renzi C, Santi S, Gennai A, et al. Efficacy of Nissen fundoplication versus medical therapy in the regression of low-grade dysplasia in patients with Barrett esophagus: a prospective study. Ann Surg. 2006;243: 58-63.
48. Ciovica R, Gadenstätter M, Klingler A, Lechner W, Riedl O, Schwab GP. Quality of life in GERD patients: medical treatment versus antireflux sur-gery. J Gastrointest Surg. 2006;10:934-9.
49. Gurski RR, Peters JH, Hagen JA, DeMeester SR, Bremner CG, Chandrasoma PT, et al. Barrett’s esophagus can and does regress after antire-flux surgery: a study of prevalence and predictive features. J Am Coll Surg. 2003;196:706-12.
50. Gillies RS, Stratford JM, Booth MI, Dehn TC. Does laparoscopic antireflux surgery improve quality of life in patients whose gastro-oesophageal reflux disease is well controlled with medical therapy? Eur J Gastroenterol Hepatol. 2008;20: 430-5.
51. Wijnhoven BP, Lally CJ, Kelly JJ, Myers JC, Watson DI. Use of antireflux medication after antireflux surgery. J Gastrointest Surg. 2008;12:510-7.
52. Thibault R, Coron E, Sébille V, Sacher-Huvelin S, Bruley des Varannes S, Gournay J, et al. Antireflux surgery for non-erosive and erosive reflux disease in community practice. Aliment Pharmacol Ther. 2006;24:621-32.
53. Kamolz T, Granderath FA, Schweiger UM, Pointner R. Laparoscopic Nissen fundoplication in patients with nonerosive reflux disease. Long-term quali-ty-of-life assessment and surgical outcome. Surg Endosc. 2005;19:494-500.
54. Ellis SG, Fisher L, Dushman-Ellis S, Pettinger M, King SB 3rd, Roubin GS, et al. Comparison of coronary angioplasty with medical treat-ment for single- and double-vessel coronary disease with left anterior de-scending coronary involvement: long-term outcome based on an Emory-CASS registry study. Am Heart J. 1989;118:208-20.
55. Wetscher GJ, Gadenstaetter M, Klingler PJ, Weiss H, Obrist P, Wykypiel H, et al. Efficacy of medical therapy and antireflux surgery to prevent Bar-rett’s metaplasia in patients with gastroesophageal reflux disease. Ann Surg. 2001;234:627-32.
56. Wetscher GJ, Glaser K, Gadenstaetter M, Profanter C, Hinder RA. The ef-fect of medical therapy and antireflux surgery on dysphagia in patients with gastroesophageal reflux disease without esophageal stricture. Am J Surg. 1999;177:189-92.
57. Isolauri J, Luostarinen M, Viljakka M, Isolauri E, Keyriläinen O, Karvonen AL. Long-term comparison of antireflux surgery versus conservative therapy for reflux esophagitis. Ann Surg. 1997;225:295-9.
58. Desai KM, Frisella MM, Soper NJ. Clinical outcomes after laparoscopic antireflux surgery in patients with and without preoperative endoscopic es-ophagitis. J Gastrointest Surg. 2003;7:44-51.
59. Klaus A, Gadenstaetter M, Mühlmann G, Kirchmayr W, Profanter C, Achem SR, et al. Selection of patients with gastroesophageal reflux disease for antire-flux surgery based on esophageal manometry. Dig Dis Sci. 2003;48:1719-22.
60. Anvari M, Allen C. Surgical outcome in gastro-esophageal reflux disease patients with inadequate response to proton pump inhibitors. Surg Endosc. 2003;17:1029-35.
61. Fernando HC, Schauer PR, Rosenblatt M, Wald A, Buenaventura P, Ikra-muddin S, et al. Quality of life after antireflux surgery compared with non-operative management for severe gastroesophageal reflux disease. J Am Coll Surg. 2002;194:23-7.
62. Morgenthal CB, Lin E, Shane MD, Hunter JG, Smith CD. Who will fail lapa-roscopic Nissen fundoplication? Preoperative prediction of long-term out-comes. Surg Endosc. 2007;21:1978-84.
63. Klingler PJ, Hinder RA, Cina RA, DeVault KR, Floch NR, Branton SA, et al. Laparoscopic antireflux surgery for the treatment of esophageal strictures refractory to medical therapy. Am J Gastroenterol. 1999;94:632-6.
64. Pidoto RR, Fama F, Giacobbe G, Gioffre’ Florio MA, Cogliandolo A. Qual-ity of life and predictors of long-term outcome in patients undergoing open Nissen fundoplication for chronic gastroesophageal reflux. Am J Surg. 2006;191:470-8.
65. Tutuian R, Vela MF, Hill EG, Mainie I, Agrawal A, Castell DO. Characteris-tics of symptomatic reflux episodes on Acid suppressive therapy. Am J Gas-troenterol. 2008;103:1090-6.
66. Roman S, Poncet G, Serraj I, Zerbib F, Boulez J, Mion F. Characterization of reflux events after fundoplication using combined impedance-pH recording. Br J Surg. 2007;94:48-52.
67. Mainie I, Tutuian R, Agrawal A, Adams D, Castell DO. Combined multi-channel intraluminal impedance-pH monitoring to select patients with per-sistent gastrooesophageal reflux for laparoscopic Nissen fundoplication. Br J Surg. 2006;93: 1483-7.
68. Mainie I, Tutuian R, Shay S, Vela M, Zhang X, Sifrim D, et al. Acid and non-acid reflux in patients with persistent symptoms despite acid suppressive therapy: a multicentre study using combined ambulatory impedance-pH monitoring. Gut. 2006;55:1398-402.
69. Ahlawat SK, Mohi-Ud-Din R, Williams DC, Maher KA, Benjamin SB. A prospective study of gastric acid analysis and esophageal acid exposure in patients with gastroesophageal reflux refractory to medical therapy. Dig Dis Sci. 2005;50:2019-24.
70. Guérin E, Bétroune K, Closset J, Mehdi A, Lefèbvre JC, Houben JJ, et al. Nis-sen versus Toupet fundoplication: results of a randomized and multicenter trial. Surg Endosc. 2007;21:1985-90.
71. Hagedorn C, Lönroth H, Rydberg L, Ruth M, Lundell L. Long-term efficacy of total (Nissen-Rossetti) and posterior partial (Toupet) fundoplication: re-sults of a randomized clinical trial. J Gastrointest Surg. 2002;6:540-5.
72. Zornig C, Strate U, Fibbe C, Emmermann A, Layer P. Nissen vs Toupet lapa-roscopic fundoplication. Surg Endosc. 2002;16:758-66.
73. Lundell L, Abrahamsson H, Ruth M, Rydberg L, Lönroth H, Olbe L. Long-term results of a prospective randomized comparison of total fundic wrap (Nissen-Rossetti) or semifundoplication (Toupet) for gastro-oesophageal reflux. Br J Surg. 1996;83:830-5.