Upper Gastrointestinal Symptoms in Obese Patients and Their Outcomes After Bariatric Surgery

Marilia Carabotti; Carola Severi; Frida Leonetti; Francesco De Angelis; Olga Iorio; Enrico Corazziari; Gianfranco Silecchia


Expert Rev Gastroenterol Hepatol. 2013;7(2):115-126. 

In This Article

Upper GI Symptoms in Obese Patients

Heartburn & Regurgitation

Heartburn and regurgitation are the characteristic symptoms of the typical reflux syndrome, which can be diagnosed on a clinical basis without further diagnostic testing.[9] In the available literature, these two symptoms have often been considered together as GERD. In general, GERD is a common condition that develops when the reflux of stomach contents causes troublesome symptoms and/or complications. In the USA, 20–30% of the general population refers troublesome heartburn and regurgitation, with an annual cost for proton pump inhibitor (PPI) treatment of US$10 billion.[10] A strong correlation between obesity and GERD has been demonstrated.

The prevalence of GERD is higher in obese patients compared with normal weight controls, with an increased risk of 2.5 of developing symptoms and erosive esophagitis.[11] This is most likely related to increased esophageal acid exposure.[12] On the basis of the evidence of upper GI endoscopy and 24-h pH-metry, Fornari et al. showed that obese patients have higher prevalence of erosive disease and a lower frequency of nonerosive and functional heartburn with respect to a normal-weight control group.[13] In particular, concerning the risk of developing erosive esophagitis, Nam et al. observed a positive correlation between erosive esophagitis and each of the obesity indexes, including BMI, waist circumference, waist-to-hip ratio and abdominal visceral adipose tissue volume, but the multivariate analysis only indicates a correlation between abdominal visceral adipose tissue volume and erosive esophagitis.[14] Moreover, BMI seems to also play an important role in the development of GERD symptoms in normal-weight individuals; it has been noted that GERD symptoms occur more often in people who gain weight even if they remain in the range of normal weight.[15]

Increased esophageal exposure to gastric contents is the main pathogenic event occurring in GERD, whose genesis is multifactorial. Several pathophysiological mechanisms are involved ( Table 1 ): transient lower esophageal sphincter relaxation (TLESR), lower esophageal sphincter (LES) pressure, presence of hiatal hernia, esophageal factors such as poor esophageal clearance, altered esophageal motility, altered gastroesophageal pressure gradient and delayed gastric emptying. In morbidly obese patients, several of these mechanisms concur, thus increasing the risk of developing severe GERD.

Esophageal Factors

Increased TLESRs have been considered one of the most important mechanisms for GERD development: 55–80% of reflux episodes are TLESRs related.[16] Under physiological conditions, the LES relaxes for 3–10 s on swallowing to allow the bolus to enter the stomach. In GERD patients, TLESRs occur spontaneously, unrelated with swallowing and esophageal peristalsis, and can last longer (up to 45 s). Overweight and obese patients present a significantly higher rate of TLESRs during the first 2 h after meal ingestion in associated with acid reflux.[17]

Regarding LES pressure, contrasting data are reported. Iovino et al. found a decreased LES pressure in obese patients compared with controls (11.9 ± 5.3 vs 15.9 ± 2.7 mmHg, respectively; p < 0.05).[18] Suter et al. found that in a group of obese patients who were candidates for bariatric surgery, only 18% of morbidly obese patients had an hypotensive LES, with low LES pressure more likely to be associated with reflux symptoms than in those patients with normal sphincter pressure (52.6 vs 32.1%; p = 0.003).[19] On the contrary, Fornari et al. reported that GERD obese patients show higher LES pressure than nonobese controls (20.5 ± 10.6 vs 18.2 ± 10.6 mmHg; p = 0.049).[13] The reason for this discrepancy remains unclear, although it should be noted that, in general, LES pressure does not play an essential role in the genesis of reflux.

Concerning hiatal hernia, it has been reported that obese subjects are more likely to have esophagogastric junction (EGJ) disruption that leads to hernia development.[20] Indeed, hiatal hernia is more prevalent in overweight subjects[21] and has been reported in 26–52.6% of obese patients who were candidates for bariatric surgery.[19,22] This anatomical modification is associated with GERD being found in 68.2% of the patients with esophagitis compared with 11.4% of patients without esophagitis (p < 0.001).[21]

Other factors that may contribute to the increased risk of GERD in obese patients are esophageal motility disorders. In a study carried out in obese patients who were candidates for bariatric surgery,[23] abnormal manometric findings were found in 41% of patients: nonspecific esophageal motility disorders (23%), nutcracker esophagus (11%), isolated hypertensive LES pressure (3%), isolated hypotensive LES pressure (3%), diffuse esophageal spasm (1%) and achalasia (1%). Similarly, Suter et al. reported abnormal motility findings in 25.6% of obese patients.[19] Nevertheless, no significant relationship has been found between upper GI symptoms and esophageal emptying in obese patients[24] and motor alterations are rarely associated with upper GI symptoms. This discrepancy between frequently altered manometric findings and the lack of GI symptoms is likely to be ascribed to an autonomic nervous system dysfunction reported in obese patients.[25,26]

Gastric Factors

A strong correlation between increased gastric basal pressure and GERD in obese patients has been reported. Pandolfino et al. observed a positive correlation between BMI and waist circumference with intragastric pressure and gastroesophageal pressure gradients.[20] Previously, Mercer et al. also confirmed that obese patients have an elevated gastroesophageal pressure gradient, presumably caused by the increased intra-abdominal pressure resulting from the mechanical burden of excess fat.[27] In addition, both increased gastric basal pressure and overeating may contribute to increased TLESRs, the most important factor in the pathogenesis of GERD in obese and nonobese patients.

The latest advocated physiopathological mechanism involved is gastric emptying, even if data are contrasting. Maddox et al.[24] observed delayed gastric emptying for both solids and liquids in obese patients compared with control subjects, whereas other authors observed a accelerated gastric emptying[28] or even normal emptying.[29] The observed discrepancy may be related to the complex mechanisms of appetite and satiation that influence gastric emptying.[30] Gastric motility and digestion are critically involved in the interaction between food intake and its processing. Regardless, both of the patterns of gastric emptying may facilitate the development of obesity. Rapid emptying would reduce the negative feedback satiety signal produced by the presence of nutrients inside the stomach and thus precipitate a feeling of hunger and thus shorten the interval between consecutive meals. On the other hand, a delay in emptying may be a consequence of high-fat diets, a sedentary lifestyle and increased gastric distension associated with obesity, increased intra-abdominal pressure or a contributing factor in the pathogenesis of obesity resulting from the inactivation of GI satiety signals, resulting in an increase in food intake.[31]

Other Upper GI Symptoms

Beyond heartburn and regurgitation, the other upper GI symptoms to be considered are esophageal-related chest pain, functional dysphagia, globus, nausea and vomiting, bloating, postprandial fullness, early satiation and pain or burning localized to the epigastrium. The latter symptoms, similar to GERD, are often combined to define dyspepsia that is further divided into two subtypes: the postprandial distress (fullness/satiation) and epigastric pain dyspepsia syndrome.[32]

Before bariatric surgery, the prevalence of chest pain is 11%, dysphagia 10% and globus 8%. Epigastric pain and postprandial distress syndromes are present in 28 and 11% of patients, respectively.[8] In a population-based study, nausea, vomiting, early satiety, upper abdominal pain and bloating are, respectively, present in 10.6, 4.0, 9.0, 19.8 and 23.4% of obese patients, compared with 7.9, 1.2, 6.5, 3.5 and 11.4% of normal-weight control subjects.[33] Similarly, Talley et al., using a validated questionnaire in an Australian cohort found that bloating and upper abdominal pain are referred in 34.3 and 26.2%, respectively, of obese patients compared with 29.1 and 20.6% of normal-weight subjects.[34] The same group also found in a birth cohort in Dunedin that obesity is significantly and positively associated with pain and nausea/vomiting cluster (odds ratio: 2.04; 95% CI: 1.12–2.91; p = 0.04), whereas no significant association is found with early satiety and abdominal pain.[35] This is not surprising because early satiety is associated with an impaired gastric accommodation response to a meal, which then reduces food ingestion that would protect against obesity. A further positive relationship is reported between BMI and vomiting frequency (p = 0.02), upper abdominal pain (p = 0.03) and bloating (p = 0.02).[35] In the pathogenesis of vomiting, it is likely that an important role is played by the large meal more often consumed by obese patients, which may provoke a rapid gastric distention, increasing the risk of developing this symptom.[36]

All of these functional GI symptoms are likely to be ascribed to an alteration in gastric emptying, gastric capacity and accommodation, even if only few data are available in obese people. Concerning gastric capacity, available evidences suggest that obese patients tend to have a higher gastric capacity or enlarged antrum,[37] but it is not clear whether the increased gastric capacity is the cause or the effect of obesity. Kim et al. did not find any difference in gastric accommodation between asymptomatic obese and control subjects.[38]

Last but not least is the consideration that psychological behavior and eating disorders that frequently present in obese patients may deeply influence GI symptoms.[39,40] Among eating disorders, binge eating is also common in obese patients and may contribute to the development of upper GI symptoms, in the sense that often these patients eat to the point of abdominal discomfort.

Possible Pathophysiological Mechanisms Involved

Role of Inflammation. The visceral adipose tissue is actually recognized as an endocrine organ producing various proinflammatory cytokines, such as TNF-α, IL-6, IL-1, leptin and several chemokines. These cytokines may act systemically to alter both esophageal muscle activity and contractility,[41] as well as gastric acid secretion through gastrin output.[42] In parallel to the increase in proinflammatory cytokines, there is a decrease in release of the potent anti-inflammatory adiponectin.[6] Kato et al. investigated the role of adiponectin on the pathogenesis of erosive esophagitis, showing that low serum adiponectin levels were associated with an increased risk of erosive esophagitis in men.[43] The same protective effect of adiponectin was observed by Rubenstein et al., who found an association between high levels of adiponectin and a decreased risk of Barrett's esophagus in patients with GERD.[44]

Gender Factors. Both gender and lifestyle factors may play an important role in GI disorders observed in obese patients, similar to that in the normal-weight subjects. The association between obesity and GERD in women has been strengthened and is likely to be ascribed to the relatively high estrogen concentration that may cause more frequent TLESRs.[45] Piretta et al., in a 24-h pH-metry study on GERD patients, underlined an association of GERD with being overweight and obesity solely in female patients, strengthening a possible role of sexual hormones.[46]

In summary, it can then be stated that beyond GERD, other chronic GI symptoms are remarkably common in obese patients, which are most likely related to the alteration of GI motility. The exact alterations responsible for GI dysmotility, however, require further mechanistic studies.

Upper GI Symptoms After Bariatric Surgery

In the treatment of obesity, many nonsurgical therapies are included, such as behavior therapy, diet (low-fat diets, low energy density diets, low-carbohydrate diets, very low-calorie diets) and exercise; unfortunately, weight loss levels of <10% below baseline are achieved. In the field of treatment of obesity, pharmacotherapy is also included, and because all medications inherently have more risks than diet and exercise, medications should only be used when the benefits justify the risk. Current medications for the treatment of obesity can be divided into two broad categories: those that act primarily on the CNS to reduce food intake and those that act primarily outside the brain. The drugs approved by the US FDA for the treatment of obesity are pancreatic lipase inhibitor (orlistat), norepinephrine–serotonin reuptake inhibitor (sibutramine) and noradrenergic drugs (diethylpropion, phentermine, benzphetamine and phendimetrazine). However, given the limited efficacy of dietetic and pharmacological treatments, surgical treatment has become increasingly popular.

The best long-term results in weight loss and resolution of comorbidity are achieved with bariatric surgery. Bariatric surgery should be carried out in specialized medical institutions to limit the increased risk of postoperative morbidity and mortality in patients.[47] To gain access to surgery, patients must complete an extensive screening process, including consultation with a surgeon, psychological evaluation, nutrition consultation, chest roentgenography, electrocardiography, pulmonary function testing, polysomnography and an esophagogastroduodenoscopy. This last procedure is recommended by the European Association for Endoscopy Surgery to detect and treat any upper GI lesions that may cause postoperative complications or influence the decision of which type of bariatric surgery should be performed.[48] Helicobacter pylori evaluation and eradication is recommended in all patients who are candidates for major metabolic/bariatric surgery,[49] even if it has been observed that BMI may affect its eradication.[50] Weight loss operations are classified as malabsorptive, restrictive and mixed. Malabsorptive interventions include biliopancreatic diversion (Scopinaro procedure) and its variation, the so-called duodenal switch, whereas the most popular restrictive procedures are laparoscopic adjustable gastric banding (LAGB) and laparoscopic sleeve gastrectomy (LSG). Among mixed procedures, the most popular is the Roux-en-Y gastric bypass (RNYGB).

Bariatric surgery dramatically alters anatomical and physiological characteristics of the upper GI tract, influencing GI symptom outcomes. Nevertheless, available data, mainly concerning GERD, are most likely conflicting because of the different methods used for its diagnosis (questionnaire, pH-metry, manometry, esophagogastroduodenoscopy, PPI treatment), the different pattern of outcomes and follow-up time. In this context, our attention has been focused on the three most utilized interventions: RNYGB, LAGB and LSG.

ROUX-en-Y Gastric Bypass. RNYGB, which accounts for 70% of bariatric surgery in the USA, is both restrictive and partially malabsorptive (mixed procedure) (Figure 1). The stomach is stapled to create a small (≤30 ml) upper gastric pouch, then the small intestine is divided at the mid-jejunum, and the distal portion (roux/limb) is anastomosed to the gastric pouch. The distal portion of the stomach and proximal small intestine (biliopancreatic limb) are anastomosed end-to-side further down at the jejunum,[51] the length of the alimentary limb influencing the malabsorptive effect of the procedure. Considering this new anatomical assessment, it is easily understandable how presurgical GI symptoms may be modified. In fact, the small size of the gastric pouch and the diversion of bile lead to a remarkable reduction of the gastric content that can reflux into the esophagus. Indeed, several authors have reported that after RNYGB, there is an improvement in GERD ( Table 2 ).[52–57] After 6 months from surgery, in >70% of the patients, GERD was no longer present, even if a relative increase is observed in further follow-up.[55] Similar observations were reported by Ortega et al., who analyzed separately the prevalence of heartburn and regurgitation.[57] After 3 months postsurgery, heartburn disappeared in 92% of the patients and reoccurred in 21% of the patients after 1 year. In turn, regurgitation disappeared in 75% of the patients 3 months after surgery, and its prevalence further decreased prolonging the follow-up (84% after 1 year). Of note, Madalosso et al. further extended the analysis to the presence of atypical GERD symptoms, and found that chest pain, combined with troublesome heartburn as the chief complaint, is reported in the preoperative evaluation by 3.5% of the patients and disappeared postoperatively.[54] Concerning extraesophageal symptoms, chronic cough and laryngeal symptoms are present in 19% of the patients, and all but one of the patients deny these symptoms post-RNYGB (p = 0.0003). It is important to note that the improvement of GERD symptoms was accompanied by the reduction of PPI prescription,[54] improvement in esophageal acid exposure[54,55,57] and erosive esophagitis.[56] For these reasons, conversion to RNYGB is considered both an effective treatment for intractable reflux symptoms following restrictive procedure,[58] and after failure of LAGB or vertical banded gastroplasty.[59] It is also considered to be the best type of bariatric intervention in patients who present GERD symptoms independent of the presence of erosive esophagitis at the presurgical work-up.[60]

Figure 1.

ROUX-en-Y gastric bypass.

However, after RNYGB patients may complain of dysphagia ( Table 3 ), which is most likely not related to GERD symptoms, but rather with the impaired emptying of the gastric pouch.[52,54,57] Of the three available studies with manometric data,[53,55,57] just one observed an alteration of esophageal motility with a decrease in esophageal body amplitude and ineffective esophageal peristalsis in 20% of patients,[53] which, however, was not associated to dysphagia or chest pain. When dysphagia was associated with pain, nausea and vomiting, a marginal ulcer of the gastrojejunal anastomosis occurred.[61] After RNYGB, the prevalence of gastric symptoms, such as postprandial fullness, early satiation, pain or epigastric burning, is lacking, most likely becuase of the exclusion of the stomach from the continuity of the digestive tract.

A clinical problem that arises after RNYGB is the malabsorption of minerals and nutrients leading to deficiencies of iron, calcium, folate, vitamin B12, due to the exclusion of the duodenum and the first part of the jejunum.[51] Furthermore, rarely intense and life-threatening cases of hypoglycemia have been described postsurgery,[62] which are most likely caused by hyperfunction of the pancreatic β-cell. In addition, after RNYGB, dumping syndrome may occur: this is a complex of neurohormone-mediated symptoms that include facial flushing, lightheadedness, palpitations, fatigue and diarrhea due to the rapid transit of the bolus in the alimentary limb that is observed in gastric surgery with different types of alimentary tract reconstruction.[62]

Laparoscopic Adjustable Gastric Banding. Described for the first time in 1993, LABG (Figure 2) is a safe and a reversible procedure where the surgeon creates a small gastric pouch (20–25 ml) by positioning a silicone ring around the upper portion of the stomach. The prosthesis is connected with a subcutaneous port, allowing the adjustability of the band. Despite good results in terms of weight loss and quality of life in patients,[63,64] several complications have been reported, such as pouch dilatation and slipping, band migration, band leakage, infection and obstruction. The effects of LAGB on upper GI symptoms, esophagogastric physiology and motility have been widely studied. Data on GERD are controversial, as several authors have reported an improvement, whereas others show a worsening of symptoms following LAGB ( Table 4 ).[55,64–72] In the studies reporting an improvement of GERD after surgery, GERD disappeared in approximately 70% of the patients, independent of the follow-up time. A lack of improvement in GERD must be considered abnormal and is likely to be representative of a LAGB that is simply too tight. Alternatively, persistent or more severe reflux, particularly with volume or nocturnal symptoms, suggests a band-related complication.[63] de Jong et al. stated that LAGB decreases GERD if there is no pouch formation during the follow-up, owing to the clear relationship found between pouch formation and reflux symptoms, pathological reflux, reflux esophagitis and the use of acid-reducing drugs.[73] It is likely that the same weight loss achieved by LAGB may in some way influence the improvement of GERD symptoms, but available data do not confirm this hypothesis.[64,74] Moreover, improvement of GERD was associated with a reduction of the need for antisecretory drugs from 27.5% (16–38.5%) presurgery to 9.5% (3.1–19.2%) postsurgery.[75] Nevertheless, it has to be kept in mind that even if GERD symptoms improve, acid esophageal exposure may worsen with abnormal 24-h pH rising from 16.7% presurgery to 36.4% postsurgery.[55] A scarce improvement of GERD after LAGB has instead been reported by Suter et al.[69] (i.e., in only 39% of the patients) and also by other studies that highlight either a worsening or newly developed GERD after surgery, mainly characterized by a prevalent worsening of regurgitation rather than heartburn ( Table 4 ).[71,72]

Figure 2.

Adjustable gastric banding.

After LAGB, different esophageal motility disorders affecting LES pressure and length have been reported,[73] as well as impairment of LES relaxation[65,66] and impaired esophageal peristalsis.[66] However, clinical data assessing the prevalence of dysphagia before and after are scarce ( Table 3 ).[66] Cruiziat et al. studied 22 LAGB patients with esophageal symptoms (dysphagia, vomiting and regurgitations) and found normal manometric data in only two patients.[76] The main alterations observed were functional EGJ obstruction (15 patients), followed by achalasia (three patients) and hypotensive peristalsis (two patients). Pseudoachalasia and esophageal dysmotility are usually reversed on removal of the gastric band.[77] Esophageal dysfunction over the long term has been studied by means of radiological technique by Naef et al., who found esophageal dysmotility in 68.8% of patients, with evident esophageal dilatation in 25.5%.[78] Furthermore, Klaus et al. showed that patients with postoperative GERD, with respect to patients whose symptoms improve or disappear after surgery, have a significantly poorer esophageal body motility (20.8 vs 12.8% defective propagations; p = 0.007), with worsening of scores for dysphagia (0.4 vs 0.9) and regurgitation (0.6 vs 1.4).[67] Two other studies[69,79] underlined the role of manometry in diagnosing weak esophageal body motility, which can lead to a dilated esophagus that is often combined with pouch dilation and achalasia-like symptoms. These data support the utility of a presurgical manometry that could be predictive of symptoms after implantation. Nevertheless, controversial data are available concerning the relevance of the presurgery manometry to advise whether esophageal motility disorders could influence outcome of surgery. Lew et al. showed that preoperative esophageal manometry does not predict GERD outcomes after LAGB, even if postoperative emesis was more common in patients with abnormal manometry findings.[80] However, the positive correlation between esophageal dysmotility and obesity, and the frequent absence of symptoms in esophageal motor disorders[23] suggest that esophageal manometry should be performed before a LAGB/restrictive procedure.

To summarize, most of the studies seem to indicate that GERD improves after LABG, whereas the most troublesome symptoms reported by patients after this procedure are consequential to the inability to consume certain food, probably due to the restriction imposed by LABG.[63] Currently, it is still not possible to identify any factors that could predict resolution or development of GERD symptoms after LABG. The most likely prevalent factor to keep in mind is the time interval from surgery[81] related to the progressive reduction of esophageal clearance in the long-term follow-up, leading to stasis of ingested food and refluxate of acid material, with increasing rates of heartburn, regurgitation and dysphagia, especially when the proximal pouch is dilated. In the long-term follow-up, the appearance of GERD symptoms and dysphagia most likely suggest overfilling of the band or band-related complications. Data on other GI symptoms are lacking after LAGB; satiety and early satiation are most likely associated with a short delay in bolus transit into the infraband stomach.[82]

Laparoscopic Sleeve Gastrectomy. LSG consists of removing the entire gastric greater curvature, leaving a narrow tube of stomach with reduced final capacity of about 100 ml (Figure 3). In recent years, LSG has been more frequently performed as a definitive surgery because of its limited invasiveness, safety and favorable metabolic effects determining restoration of insulin secretion, and improvement in insulin sensitivity independent of previous weight loss.[83] Compared with LABG, GI physiology is more dramatically changed after LSG because the removal of gastric fundus and body leads to important alterations of motility and acid secretion.[84] For instance, gastric fundus and corpus removal strongly reduces acid load after LSG,[84] and this aspect may have important therapeutic implications, in that a widespread use of PPI may be needless.

Figure 3.

Sleeve gastrectomy.

Until now, available studies on the effects of LSG have mainly investigated GERD, and the prevalence of symptoms after surgery is still a debate, as declared by the Second International Consensus Summit for Sleeve Gastrectomy, which reported a prevalence of postoperative GERD ranging from 0 to 83%.[85] It has been stated that this bias may arise from the different definitions and methodologies used between studies for GERD diagnosis,[86] as well as from the different surgical procedures used, in particular, the different positions of the stapler at the angle of His.[87] That further studies are needed to more clearly define the effect of LSG on GERD. Anatomical LSG-related modifications lead to a new balance between exacerbating and protective factors for GERD, the latter mainly being represented by the supposed reduced acid load[84] and possible faster gastric emptying.

Available studies ( Table 5 )[81,88–94] comparing the prevalence of GERD before and after LGS almost indicate that GERD is not modified by this procedure. LSG modifies the anatomy of EGJ, converting it into a straight tubular segment, and acts at different levels by facilitating GERD-triggering mechanisms. In this regard, Braghetto et al. found an incompetent LES in 85% of patients after LSG and stated that the partial sectioning of the sling fibers during LSG may affect LES pressure.[87] On the contrary, Petersen et al. reported that LSG could restore a normal LES pressure in patients with previously hypotensive LES, independent of weight loss.[95]

Certainly, as for LABG, prevalence of GERD symptoms may change during time. Himpens et al., in a prospective study based on PPI use, showed that GERD appear de novo in 21.8 and 3.1% of patients, respectively, after 1 and 3 years postsurgery.[81] In their opinion, during LSG, the angle of His is usually blunted and consequently there is an early GERD appearance that regresses after 3 years, most likely because of restoration of the angle. However, after a 6-year follow-up[89] a second peak of GERD can appear and may be linked with the appearance of a neofundus. In fact, a sleeved stomach may dilate over time allowing patients to consume larger volumes of food with subsequent weight regain. Himpens et al. speculated that neofundus formation can be caused by leaving too much fundus at the time of operation.[89] If the surgeon, for safety reasons, decides to staple away from the left crus, they can end up with a sleeve tube with a conical rather than a cylindrical shape.

Besides LES function, gastric emptying and intra-abdominal pressure may also contribute to the genesis of GERD symptoms. LSG implies the resection of the gastric pacemaker[96] and leads to a greater intraluminal pressure and a smaller volume of the 'pouch' that becomes ten-times less distensible.[97] The consequent alterations in gastric emptying or compliance may contribute to the genesis of dyspepsia-like symptoms, the occurrence of which after LSG has been poorly analyzed. Few studies have evaluated gastric emptying by scintigraphic study. In two different studies,[91,92] Melissas et al. evaluated gastric emptying for solid food before and after surgery, and showed that gastric emptying was faster in both the short (6 months) and the long term (24 months) after LSG. Similar results for liquid and solid emptying have been obtained by Braghetto et al., who compared LSG patients and controls, with accelerated emptying in the former.[96]

Gastric motor activity is under the influence of ghrelin, which dramatically decreases after surgery.[98] Ghrelin is a hormone with multiple effects produced by endocrine cells in the oxyntic mucosa of the stomach. Ghrelin has orexigenic effects (increased secretion of growth hormone, food intake and weight gain), but it has an important role in stimulating gastric motility and gastric acid secretion.[99] Concerning gastric motility, ghrelin improves gastric emptying and induces inhibition of gastric accommodation;[100] in healthy volunteers, it has been shown that administration of ghrelin induces a premature Phase III activity and a prolonged increase in proximal gastric tone.[101] Furthermore, ghrelin stimulates acid secretion, inducing an increase in histamine level and in vagal nerve activation.[100] The reduction of ghrelin levels after LSG may then further alter gastric motility, affecting clinical GI outcomes. Indeed, in a recent clinical study, it has been observed that the most prevalent symptoms after LSG are postprandial fullness and early satiation rather than GERD, configuring a postprandial distress syndrome-like dyspepsia.[102] These aspects, as well as atypical GERD-related symptoms such as chest pain, dysphagia, hoarseness and cough, have scarcely been analyzed after LSG.

Finally, symptoms suggestive of dumping syndrome after LSG are lacking, even if data on faster gastric emptying may promote it. In a prospective clinical study by Tzovaras et al., conducted to evaluate its potential presence, incidence and severity by clinical provocation of signs and symptoms using an oral glucose challenge before and 6 weeks after the operation, the authors found that 29% of subjects experienced definite dumping or other symptoms suggestive of dumping syndrome.[103]