Surg Endosc DOI 10.1007/s00464-012-2593-9
and Other Interventional Techniques
Increase in gastroesophageal reflux disease symptoms and erosive esophagitis 1 year after laparoscopic sleeve gastrectomy among obese adults Chi-Ming Tai • Chih-Kun Huang • Yi-Chia Lee • Chi-Yang Chang • Ching-Tai Lee • Jaw-Town Lin
Received: 13 May 2012 / Accepted: 17 September 2012 Ó Springer Science+Business Media New York 2012
Abstract Background Although laparoscopic sleeve gastrectomy (LSG) is an effective treatment for morbid obesity, the effects of LSG on gastroesophageal reflux disease (GERD) are controversial. This study evaluated the changes of GERD symptoms and erosive esophagitis (EE) in severely obese patients who underwent LSG. Methods Forty-seven severely obese women and 19 severely obese men (mean age of 37.2 ± 12.7 years) who underwent LSG between August 2007 and November 2009 C.-M. Tai C.-K. Huang Bariatric and Metabolic International Surgery Center, E-Da Hospital, Kaohsiung, Taiwan, ROC e-mail:
[email protected] C.-M. Tai Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, ROC C.-M. Tai C.-Y. Chang C.-T. Lee Department of Internal Medicine, E-Da Hospital/I-Shou University, Kaohsiung, Taiwan, ROC C.-K. Huang Department of Surgery, E-Da Hospital/I-Shou University, Kaohsiung, Taiwan, ROC Y.-C. Lee Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan, ROC J.-T. Lin (&) School of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan, ROC e-mail:
[email protected] J.-T. Lin Department of Internal Medicine, E-Da Hospital, Kaohsiung, Taiwan, ROC
were enrolled. All patients completed the Reflux Disease Questionnaire and underwent esophagogastroduodenoscopy preoperatively and at least 1 year after LSG. Results The median follow-up period was 12 months (range, 12–21). After surgery, significant decreases were reported in mean body mass index (36.3 ± 4.1 vs. 25.8 ± 2.9 kg/m2), mean waist circumference (109.5 ± 12. 8 vs. 85.7 ± 9.5 cm), and prevalence of metabolic syndrome (54.5 vs. 7.6 %; P \ 0.001 for both). Conversely, a significant increase was observed in the prevalence of GERD symptoms (12.1 vs. 47 %) and EE (16.7 vs. 66.7 %) after LSG (P \ 0.001 for both). The prevalence of hiatal hernias also increased significantly (6.1 vs. 27.3 %; P \ 0.001) after LSG, and it was significantly higher in patients with than those without EE after LSG (9.1 vs. 36.4 %, respectively; P = 0.02). Conclusions Although LSG can achieve significant weight loss and improvement of comorbidities in severely obese patients, the prevalence and severity of GERD symptoms and EE increase after the operation. The occurrence of EE after LSG is related to the presence of a hiatal hernia after the operation. Keywords Gastroesophageal reflux disease Erosive esophagitis Hiatal hernia Laparoscopic sleeve gastrectomy Bariatric surgery Obesity
Gastroesophageal reflux disease (GERD), as defined by the presence of GERD symptoms or erosive esophagitis (EE), is a common disease [1]. Because obesity is a key risk factor for GERD, the increasing prevalence of obesity has coincided with an increasing prevalence of GERD [2]. The connection between obesity and GERD is thought to be mediated by an increase in intragastric pressure due to
123
Surg Endosc
external compression by surrounding adipose tissue, resultant frequent relaxation of the lower esophageal sphincter, and hence, the occurrence of acid reflux [3–6]. Weight reduction often is recommended for management of GERD among obese patients [7]. Bariatric surgery, including laparoscopic Roux-en-Y gastric bypass (LRYGB) and laparoscopic sleeve gastrectomy (LSG), has been proven to be effective in reducing weight and improving obesityrelated comorbidities in morbidly obese patients [7, 8]. Whereas LRYGB has been shown to consistently and effectively reduce both body weight and improve GERD symptoms [7, 9], the influence of LSG on GERD is less clear [10]. Specifically, although improvement of GERD symptoms following LSG has been reported in some studies [11, 12], others have shown a 9–34.6 % increase in the prevalence of GERD symptoms during the first year following LSG [13– 17]. In addition, endoscopic evaluations of changes in EE and gastric anatomy after LSG are scarce. In the present study, we evaluated changes in GERD symptoms and EE among severely obese patients who underwent LSG. As assessed endoscopically, changes in gastric anatomy following LSG and their association with EE also were investigated.
Patients and methods Patients with a body mass index (BMI) C37 kg/m2 or a BMI C32 kg/m2 with obesity-related comorbidities were evaluated by a multidisciplinary team consisting of dietitians, endocrinologists, gastroenterologists, psychiatrists, and surgeons at the E-Da Hospital in Kaohsiung, Taiwan. According to the recommendations of the Asia-Pacific consensus, those who were unable to reduce their BMI via dieting, behavior modification, or pharmacologic therapy were considered for bariatric surgery [18]. The patients’ anthropometrics, age, sex, laboratory data, and comorbidities were recorded before surgery. Additionally, Reflux Disease Questionnaires (RDQs) were completed and esophagogastroduodenoscopy (EGD) was performed before surgery to assess GERD symptoms and EE, respectively. All patients were asked to undergo the same assessments at a minimum of 12 months following surgery. The study was approved by the ethical committee of E-Da Hospital. Surgical procedures for LSG All operations were performed by the same surgeon (Dr. C. K. Huang). LSG was performed using five ports. Beginning 4 cm proximal to the pylorus, the omentum was separated from the greater curvature by dividing the branches of the gastroepiploic vessels and the short gastric vessels just adjacent to the stomach serosa using a Harmonic scalpel (Ethicon Endosurgery, Cincinnati, OH). A 36-Fr bougie was
123
used to size the gastric tube before division of the stomach. With the bougie in situ, longitudinal division of the stomach was performed by consecutive applications of an endoscopic stapler (green and blue cartridges, EndoGIA 60-mm or Echelon gold cartridges, Ethicon Endosurgery) from 40 cm proximal to the pylorus to the gastroesophageal junction. A gastric tube was constructed. In selected cases, including those with excessive bleeding from the staple line or serosal tears, or any suspicion of inadequate closure, the staple line was oversewn with 3-0 Vicryl. The stomach was removed from the opening of the 15 mm trocar near the umbilicus. The enlarged fascial opening was closed with a 2-0 Vicryl suture. During the first postoperative day, each patient was started on small quantities of clear liquids. Demographic characteristics Anthropometric measurements including body weight, height, and waist circumference (WC) were obtained. BMI was calculated as the weight in kilograms divided by the square of height in meters (kg/m2). WC was measured at the midpoint between the lowest rib and the iliac crest with the subjects standing, after gentle expiration. As per current guidelines, the metabolic syndrome was defined by the presence of three or more of the following: (1) WC C90 cm for men or C80 cm for women; (2) serum triglyceride levels C150 mg/dL; (3) high-density lipoprotein cholesterol levels \40 mg/dL in males and \50 mg/dL in females; (4) blood pressure C130/85 mmHg or taking hypertensive medication; (5) and serum glucose levels C100 mg/dL or on antidiabetic medication [19]. Patients was categorized as current smokers or nonsmokers and alcohol drinkers ([20 g/day) or nondrinkers (B20 g/day). Evaluation of reflux symptoms The frequency and severity of GERD symptoms were assessed by the 12-item RDQ [20] and were scored on a 6-point scale (0–5). The items on the RDQ were divided into three dimensions—heartburn, regurgitation, and dyspepsia—with a score between 0 and 20 for each dimension and the sum of all three dimensions gave the total score. The GERD score was determined by the sum of the items within the heartburn and regurgitation dimensions. The presence of GERD symptoms were defined as typical heartburn and/or acid regurgitation occurring at least once per week during the past 3 months. Classification of EE All patients underwent endoscopy for preoperative evaluation. The esophagus, stomach, and duodenal bulb were carefully evaluated, and all endoscopic findings were recorded. Diagnosis and classification of esophagitis was
Surg Endosc
Fig. 1 Endoscopic findings from obese patients who underwent laparoscopic sleeve gastrectomy (LSG). A case 1: normal appearance of hiatus before LSG. B Erosive esophagitis, hiatal hernia, and incompetent hiatus occurred after LSG. Operative scar can be found
above hiatus (arrow). C case 2: Dilated upper sleeve at upper portion of the tubulized stomach (arrow). D case 3: Tubulized stomach without stricture. E case 4: Fluid accumulated above the stricture of the midstomach
based on the Los Angeles (LA) classification [21]. According to this system, esophagitis was classified as grade A (one or more mucosal breaks below 5 mm in length that do not extend between the tops of two mucosal folds), grade B (one or more mucosal breaks[5 mm in length that do not extend between the tops of two mucosal folds), grade C (one or more continuous mucosal breaks between the tops of two or more mucosal folds involving \75 % of the esophageal circumference), and grade D (one or more mucosal breaks that involve at least 75 % of the esophageal circumference). A hiatal hernia was diagnosed in the presence of a diaphragmatic indentation that was at least 2 cm distal to the Z-line and the proximal margins of the gastric mucosal folds [22]. Infection with Helicobacter pylori was confirmed by a positive Campylobacter-like organism (CLO) test, which was performed during endoscopy.
performed by single endoscopist (Dr. C. M. Tai). Assessments of EE and hiatal hernias following LSG were performed as described above. Although the stomach will ideally be in a tubular shape following LSG, different degrees of a narrowed lumen can be found at middle portion of stomach in most patients. However, we only recorded the severe stricture of the midstomach when the lumen was not visible after air inflation. Postoperative scarring above the hiatus and dilated upper sleeve also were recorded (Fig. 1A–E).
Endoscopic evaluation after LSG The preoperative endoscopy was performed by three experienced and similarly trained endoscopists (Drs. C. M. Tai, C. Y. Chang, and C. T. Lee), and all postoperative endoscopy was
Statistical analysis Descriptive results regarding categorical variables were given as percentages (%) of subjects affected. Normally distributed continuous variables were presented as the mean ± standard deviation (SD), whereas those variables without a normal distribution were presented as the median (interquartile range, IQR). Changes in clinical characteristics, RDQ scores, and EE grade were compared pre- and postoperatively. Categorical variables were compared using the McNemar test, whereas continuous variables were compared using a paired t test or Wilcoxon signed-
123
Surg Endosc
rank test, as appropriate. Following LSG, patients were divided into two groups according to the presence of EE. Characteristics of these two groups were compared by using chi-squared test and Student’s t test, as appropriate. P \ 0.05 was taken to indicate statistical significance. All analyses were performed using SPSS version 12.0 software (SPSS Inc., Chicago, IL) for Windows.
Results Patient demographics Between August 2007 and November 2009, a total of 96 obese patients underwent LSG at our hospital. Because of the learning curve of the surgeon, the first 10 cases were not enrolled in the present study. Of the remaining 86 patients originally enrolled, 20 patients were subsequently excluded. Reasons for exclusion included conversion to LRYGB because of severe acid reflux caused by stricture of the midstomach following LSG (n = 2), loss to follow up (n = 8), and refusal to undergo follow-up EGD (n = 10). Accordingly, 66 patients (76.7 % of original sample) were finally evaluated in the present study, 19 (28.8 %) of whom were men. The mean ± SD age of patients was 37.2 ± 12.7 years, and mean BMI was 36.3 ± 4.1 kg/m2. Median time to follow-up EGD was 12 months (range, 12–21). Ten (15.2 %) patients reported taking proton pump inhibitors (PPIs) to relieve GERD symptoms and four (6.1 %) patients had received EGD because of GERD symptoms within the year following LSG. All patients received the scheduled follow-up EGD 1 year after EGD.
Table 1 Clinical characteristics of 66 obese patients at baseline and 1 year following LSG Pre-LSG Age (year), mean (SD) Male sex, n (%)
Change of GERD symptoms after LSG The prevalence of GERD symptoms increased significantly from 8 (12.1 %) to 31 (47 %) after LSG (P \ 0.001; Table 2). Of the eight patients with preoperative GERD symptoms, five (62.5 %) continued to experience GERD symptoms, whereas three (37.5 %) became asymptomatic after surgery. Of the 58 patients who were asymptomatic before surgery, 26 (44.8 %) developed GERD symptoms after LSG, whereas 32 (55.2 %) patients remained asymptomatic. Following LSG, the median (IQR) score for
123
19 (28.8)
P
38.4 (12.7) \0.001 19 (28.8)
–
BMI (kg/m2), mean (SD)
36.3 (4.1)
25.8 (2.9)
\0.001
Waist circumference (cm), mean (SD)
109.5 (12.8)
85.7 (9.5)
\0.001
5 (7.6)
\0.001
Metabolic syndrome, n (%)
36 (54.5)
WC C90 cm for men or C80 cm for women
66 (100)
40 (60.6) \0.001 0 (0)
\0.001
Triglyceride C150 mg/dL
25 (37.9)
HDL-C\40 mg/dL in men or \50 mg/dL in women
39 (59.1)
19 (28.8) \0.001
Hypertension or BP C130/ 85 mmHg
44 (66.7)
17 (25.8) \0.001
Diabetes or fasting glucose C100 mg/dL
21 (31.8)
4 (6.1)
\0.001
LSG laparoscopic sleeve gastrectomy, BMI body mass index, WC waist circumference, BP blood pressure, HDL-C high-density lipoprotein cholesterol
the GERD dimension of the RDQ also increased significantly from 0 (0–0.5) to 4.5 (0–13.3; P \ 0.001; Table 2). Change of EE after LSG Before surgery, only 11 patients (16.7 %) were found to have EE, and all cases were grade A according to the LA classification. After LSG, 44 patients (66.7 %) had EE, Table 2 GERD symptoms and EE among 66 obese patients at baseline and 1 year following LSG
Change of clinical characteristics after LSG Following LSG, a significant decrease in both BMI (36.3 ± 4.1 vs. 25.8 ± 2.9 kg/m2, P \ 0.001) and waist circumference (109.5 ± 12.8 vs. 85.7 ± 9.5 cm, P \ 0.001) was achieved. As outlined in Table 1, the prevalence of the metabolic syndrome and its components also was reduced (54.5 vs. 7.6 %, P \ 0.001) after LSG.
37.2 (12.7)
Post-LSG
GERD symptoms, n (%)
Pre-LSG
Post-LSG
P
8 (12.1)
31 (47.0)
\0.001
RDQ score, median (IQR) Total score
0 (0–1.3)
7 (0–18.3) \0.001
Heartburn dimension
0 (0–0)
0 (0–6)
\0.001
Dyspepsia dimension
0 (0–0)
0 (0–5)
\0.001
2 (0–8)
\0.001
Regurgitation dimension
0 (0–0) 0 (0–0.5) 11 (16.7)
4.5 (0–13.3) \0.001 44 (66.7) \0.001
No EE
55 (83.3)
22 (33.3)
Grade A
11 (16.7)
24 (36.4)
Grade B
0
16 (24.2)
Grade C
0
GERD dimension Erosive esophagitis, n (%)
4 (6.1) 18 (27.3)
\0.001
0
8 (12.1)
\0.001
0
4 (6.1)
Hiatal hernia, n (%)
4 (6.1)
Dilated upper sleeve, n (%) Stricture of mid-stomach, n (%)
0.047
GERD gastroesophageal reflux disease, EE erosive esophagitis, LSG laparoscopic sleeve gastrectomy, RDQ Reflux Disease Questionnaires, IQR interquartile range
Surg Endosc Table 3 Distribution of EE according to grade among 66 obese patients at baseline and 1 year following LSG Grade of EE before LSG
No EE A Total
Table 4 Comparisons between patients with or without EE after LSG
Grade of EE after LSG No EE
A
B
C
Total
20
19
13
3
55
2
5
3
1
11
22
24
16
4
66
LSG laparoscopic sleeve gastrectomy, EE erosive esophagitis
including 24 (36.4 %) with grade A, 16 (24.2 %) with grade B, and 4 (6.1 %) with grade C (Table 2). Among the 11 patients with grade A EE at baseline, the condition resolved in 2 patients (18.2 %) following LSG, persisted at grade A in 5 patients (45.4 %), and progressed to grade B in 3 patients (27.3 %) and grade C in one patient (9.1 %). Among the 55 patients without EE at baseline, 35 patients (63.6 %) developed de novo EE after LSG at grades A (n = 19), B (n = 13), and C (n = 3), whereas the remaining 20 patients (36.4 %) remained asymptomatic (Table 3). The prevalence of hiatal hernias also increased significantly from 6.1 to 27.3 % after LSG (P \ 0.001; Table 2). The 4 patients with hiatal hernia before surgery continued to have hiatal hernia, whereas 14 patients (27.3 %) developed a hiatal hernia after surgery. Postoperatively, eight (12.1 %) and four patients (6.1 %) developed a dilated upper sleeve and stricture of the midstomach, respectively. Factors associated with EE after LSG The clinical characteristics and endoscopic findings of the 44 patients with and the 22 patients without EE after LSG are compared in Table 4. Male sex and the presence of GERD symptoms after LSG were associated with the presence of EE after LSG. Also, the prevalence of hiatal hernias was significantly higher in patients with than those without EE after LSG (9.1 vs. 36.4 %, respectively; P = 0.02).
Discussion In the present study, we evaluated changes in GERD symptoms, as assessed by RDQ, and EE, as assessed by EGD, in severely obese patients after at least 1 year following LSG. Our results indicated an increased prevalence and severity of GERD symptoms and EE after LSG. After LSG, we also reported an increased prevalence of hiatal hernias, which was associated with increased EE. Prior studies have shown that the prevalence of GERD symptoms can increase by 9–34.6 % during the first year
Without EE (n = 22)
With EE (n = 44)
P
Age (years), mean (SD)
38.4 (14.8)
Male sex, n (%)
1 (4.5)
36.6 (11.6)
0.591
18 (40.9)
0.002
BMI (pre-LSG) (kg/m2), mean (SD)
36.7 (4.4)
36.1 (4)
0.555
BMI (post-LSG) (kg/m2), mean (SD)
26 (3.1)
25.7 (2.7)
0.692
Waist circumference (preLSG) (cm), mean (SD)
108.7 (14.4)
109.8 (12)
0.744
Waist circumference(postLSG) (cm), mean (SD)
86.6 (10)
85.2 (9.3)
0.578
Metabolic syndrome (preLSG), n (%)
11 (50)
Metabolic syndrome (postLSG), n (%)
0
Alcohol consumption, n (%) Smoking, n (%)
25 (56.8)
0.6
5 (11.4)
0.16
2 (9.1) 2 (9.1)
10 (22.7) 13 (29.5)
0.176 0.062
GERD symptoms (pre-LSG), n (%)
4 (18.2)
4 (9.1)
0.286
GERD symptoms (post-LSG), n (%)
5 (22.7)
26 (59.1)
0.005
EE (pre-LSG), n (%)
2 (9.1)
9 (20.5)
0.243
Hiatal hernia (pre-LSG), n (%)
0
4 (9.1)
0.293
H. pylori positive, n (%)
7 (31.8)
11(25)
0.558
EGD findings (post-LSG), n (%) Hiatal hernia 2 (9.1)
16 (36.4)
0.021
Dilated upper sleeve
1 (4.5)
7 (15.9)
0.252
Stricture of mid-stomach
1 (4.5)
3 (6.8)
1
BMI body mass index, GERD gastroesophageal reflux disease, LSG laparoscopic sleeve gastrectomy, EE erosive esophagitis, EGD esophagogastroduodenoscopy
following LSG [13–17]. In the current study, the prevalence of GERD symptoms increased by 34.9 % (from 12.1 to 47 %) 1 year after LSG. Although our results show a greater increase in GERD symptoms, the comparison of these values between different studies is made difficult for two reasons. First, the patient-enrollment criteria are different. For example, patients with preoperative GERD symptoms were excluded from LSG in some studies but not others. However, the influence of preoperative GERD symptoms on the occurrence of GERD symptoms after LSG remains controversial. Second, different definitions of GERD symptoms are utilized in different studies. Rather than defining the presence of GERD symptoms by the regular use of PPIs [13]. We used the definition of typical heartburn and/or acid regurgitation occurring at least once per week. Indeed, the prevalence of GERD symptoms may be underestimated by using the former definition because not all patients with GERD symptoms take PPIs. In fact,
123
Surg Endosc
only 10 of 31 patients (32.3 %) who met our criteria of GERD symptoms in this study ever took PPIs for relief of symptoms. Little information regarding the prevalence of EE after LSG is available. Braghetto et al. [14] reported that 26 of 167 patients (15.5 %) developed de novo EE within 1 to 2 months after LSG. Applying the same definition of EE, we found that 66.7 % of patients had EE 1 year after LSG. Twenty of 55 patients (36.4 %) developed de novo EE, whereas 4 of 11 patients (36.4 %) with preoperative EE showed worsened EE following surgery. Because of the more consistent definition of EE, this result might be more reliable than those from GERD symptom-based studies. By using standardized assessments, our study confirmed the increase of GERD symptoms and EE after LSG. Although the underlying mechanisms contributing to the occurrence of GERD after LSG are not clear, the involvement of the lower esophageal sphincter (LES) might play an important role. LSG involves the resection at the angle of His and partial sectioning of the sling fibers, which may impair the function of the LES after LSG. Indeed, Braghetto et al. [23] reported that a decrease in LES pressure was found in 17 of 20 patients after LSG. In addition, by using multislice computed tomography to evaluate anatomical changes after LSG, Baumann et al. [24] reported that 10 of 27 patients had migration of the proximal sleeve above the level of the hiatus after LSG, indicative of a hiatal herniation of the sleeve. In the present study, 14 of 62 (22.6 %) patients without a hiatal hernia at baseline developed the condition following LSG. As illustrated in Fig. 1B, the migration of the upper sleeve also could be verified by the presence of an operative scar above the hiatus in 12 of the 14 patients with de novo hiatal hernia after LSG. Other anatomical changes related to GERD after LSG include dilated upper sleeve and narrowing of the midstomach. For instance, by using upper gastrointestinal barium swallow studies, Keidar et al. [25] reported a dilated upper stomach and a relative narrowing of the midstomach in patients with severe gastroesophageal dysmotility and reflux after LSG. The authors suggested that these anatomical changes might impair upper stomach emptying into the antrum and could predispose patients to postoperative GERD. In the present study, stricture of the midstomach and a dilated upper sleeve were identified in four and eight patients, respectively. Additionally, all of these patients had EE and/or GERD symptoms. In addition to negatively affecting patients’ quality of life, GERD is associated with Barrett’s esophagus and even esophageal adenocarcinoma [26, 27]. Because of the high incidence of postoperative GERD, it is important to evaluate this complication after LSG. Although with the prevalence of postoperative GERD symptoms increased in parallel with the prevalence of EE after LSG, 40.1 % of
123
patients without postoperative GERD symptoms still had postoperative EE. Thus, in addition to a follow-up GERD questionnaire, we recommended that a follow-up EGD should be performed for all patients following LSG. In addition, although about it remains uncertain whether preoperative EE or hiatal hernias are associated with postoperative GERD, it is recommended that patients with EE or hiatal hernias should not undergo LSG [28]. The fact that 4 of 4 patients with a hiatal hernia and 9 of 11 patients with EE at baseline had EE after LSG supports this recommendation. The novelty of the present study includes the use of both a standardized questionnaire and endoscopic criteria to evaluate changes in GERD symptoms and EE in patients undergoing LSG. In addition, we waited until at least 1 year following LSG, when the weight reduction and resolution of metabolic comorbidities had stabilized, before the follow-up assessment. However, our study has some limitations. First, 18 of 86 patients (20.1 %) were not enrolled in this study due to a loss to follow-up or refusal to participate in follow-up testing. It is possible that patients with postoperative GERD symptoms were more likely to receive follow-up EGD. However, only four patients underwent EGD because of GERD symptoms within the 12 months after LSG. This suggests that most patients underwent postoperative RQD and EGD at the scheduled follow-up, which might minimize the selection bias. Second, this study involved only a 1 year follow-up. Himpens et al. [29] reported a biphasic change of GERD symptoms after LSG in a 6 year follow-up study. Specifically, they reported that the prevalence of GERD symptoms at 1 year was 22 %, decreased to 3 % after 3 years, and rebounded to 26 % after 6 years. A longer follow-up period is required to elucidate the serial changes in GERD after LSG. Third, although we confirmed that anatomical changes were associated with GERD after LSG, some patients without the above-mentioned anatomical changes still developed EE meanwhile other patients had improvement of GERD after LSG. Further studies including manometry, pH measurements, and motility are necessary to elucidate other possible mechanisms contributing to the occurrence of GERD after LSG.
Conclusions Although LSG can achieve significant weight loss and improvement of comorbidities in severely obese patients, the prevalence and severity of GERD symptoms and EE increase after the operation. Because of a high incidence of GERD after LSG, we recommend that both a follow-up GERD questionnaire and EGD are necessary for the assessment of this complication after operation.
Surg Endosc Acknowledgments This study was supported by a Project of the E-Da Hospital, Grant Number EDAHP100031. Disclosures Chi-Ming Tai, Chih-Kun Huang, Yi-Chia Lee, ChiYang Chang, Ching-Tai Lee, and Jaw-Town Lin have no conflict of interest or financial ties to disclose.
References 1. Dent J, El-Serag HB, Wallander MA, Johansson S (2005) Epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut 54:710–717 2. Hampel H, Abraham NS, El-Serag HB (2005) Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications. Ann Intern Med 143:199–211 3. Wong BC, Kinoshita Y (2006) Systematic review on epidemiology of gastroesophageal reflux disease in Asia. Clin Gastroenterol Hepatol 4:398–407 4. El-Serag H (2008) Role of obesity in GORD-related disorders. Gut 57:281–284 5. Lee YC, Yen AM, Tai JJ, Chang SH, Lin JT, Chiu HM, Wang HP, Wu MS, Chen TH (2009) The effect of metabolic risk factors on the natural course of gastro-oesophageal reflux disease. Gut 58:174–181 6. Tai CM, Lee YC, Tu HP, Huang CK, Wu MT, Chang CY, Lee CT, Wu MS, Lin JT, Wang WM (2010) The relationship between visceral adiposity and the risk of erosive esophagitis in severely obese Chinese patients. Obesity (Silver Spring) 18:2165–2169 7. De Groot NL, Burgerhart JS, Van De Meeberg PC, de Vries DR, Smout AJ, Siersema PD (2009) Systematic review: the effects of conservative and surgical treatment for obesity on gastrooesophageal reflux disease. Aliment Pharmacol Ther 30:1091– 1102 8. Deitel M, Gagner M, Erickson AL, Crosby RD (2011) Third International Summit: current status of sleeve gastrectomy. Surg Obes Relat Dis 7:749–759 9. Tai CM, Lee YC, Wu MS, Chang CY, Lee CT, Huang CK, Kuo HC, Lin JT (2009) The effect of Roux-en-Y gastric bypass on gastroesophageal reflux disease in morbidly obese Chinese patients. Obes Surg 19:565–570 10. Chiu S, Birch DW, Shi X, Sharma AM, Karmali S (2011) Effect of sleeve gastrectomy on gastroesophageal reflux disease: a systematic review. Surg Obes Relat Dis 7:510–515 11. Cottam D, Qureshi FG, Mattar SG, Sharma S, Holover S, Bonanomi G, Ramanathan R, Schauer P (2006) Laparoscopic sleeve gastrectomy as an initial weight-loss procedure for high-risk patients with morbid obesity. Surg Endosc 20:859–863 12. Moon Han S, Kim WW, Oh JH (2005) Results of laparoscopic sleeve gastrectomy (LSG) at 1 year in morbidly obese Korean patients. Obes Surg 15:1469–1475 13. Himpens J, Dapri G, Cadiere GB (2006) A prospective randomized study between laparoscopic gastric banding and laparoscopic isolated sleeve gastrectomy: results after 1 and 3 years. Obes Surg 16:1450–1456 14. Braghetto I, Csendes A, Korn O, Valladares H, Gonzalez P, Henriquez A (2010) Gastroesophageal reflux disease after sleeve gastrectomy. Surg Laparosc Endosc Percutan Tech 20:148–153
15. Lakdawala MA, Bhasker A, Mulchandani D, Goel S, Jain S (2010) Comparison between the results of laparoscopic sleeve gastrectomy and laparoscopic Roux-en-Y gastric bypass in the Indian population: a retrospective 1 year study. Obes Surg 20:1–6 16. Carter PR, LeBlanc KA, Hausmann MG, Kleinpeter KP, deBarros SN, Jones SM (2011) Association between gastroesophageal reflux disease and laparoscopic sleeve gastrectomy. Surg Obes Relat Dis 7:569–572 17. Howard DD, Caban AM, Cendan JC, Ben-David K (2011) Gastroesophageal reflux after sleeve gastrectomy in morbidly obese patients. Surg Obes Relat Dis 7:709–713 18. Lee WJ, Wang W (2005) Bariatric surgery: Asia-Pacific perspective. Obes Surg 15:751–757 19. Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC Jr (2009) Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 120:1640–1645 20. Shaw MJ, Talley NJ, Beebe TJ, Rockwood T, Carlsson R, Adlis S, Fendrick AM, Jones R, Dent J, Bytzer P (2001) Initial validation of a diagnostic questionnaire for gastroesophageal reflux disease. Am J Gastroenterol 96:52–57 21. Lundell LR, Dent J, Bennett JR, Blum AL, Armstrong D, Galmiche JP, Johnson F, Hongo M, Richter JE, Spechler SJ, Tytgat GN, Wallin L (1999) Endoscopic assessment of oesophagitis: clinical and functional correlates and further validation of the Los Angeles classification. Gut 45:172–180 22. Johnson DA, Younes Z, Hogan WJ (2000) Endoscopic assessment of hiatal hernia repair. Gastrointest Endosc 52:650–659 23. Braghetto I, Lanzarini E, Korn O, Valladares H, Molina JC, Henriquez A (2010) Manometric changes of the lower esophageal sphincter after sleeve gastrectomy in obese patients. Obes Surg 20:357–362 24. Baumann T, Grueneberger J, Pache G, Kuesters S, Marjanovic G, Kulemann B, Holzner P, Karcz-Socha I, Suesslin D, Hopt UT, Langer M, Karcz WK (2011) Three-dimensional stomach analysis with computed tomography after laparoscopic sleeve gastrectomy: sleeve dilation and thoracic migration. Surg Endosc 25:2323–2329 25. Keidar A, Appelbaum L, Schweiger C, Elazary R, Baltasar A (2010) Dilated upper sleeve can be associated with severe postoperative gastroesophageal dysmotility and reflux. Obes Surg 20:140–147 26. Fox M, Forgacs I (2006) Gastro-oesophageal reflux disease. BMJ 332:88–93 27. Belhocine K, Galmiche JP (2009) Epidemiology of the complications of gastroesophageal reflux disease. Dig Dis 27:7–13 28. Gagner M, Deitel M, Kalberer TL, Erickson AL, Crosby RD (2009) The Second International Consensus Summit for Sleeve Gastrectomy, March 19–21, 2009. Surg Obes Relat Dis 5:476–485 29. Himpens J, Dobbeleir J, Peeters G (2010) Long-term results of laparoscopic sleeve gastrectomy for obesity. Ann Surg 252: 319–324
123
