Introduction

The association between obesity and malignancies is identified epidemiologically. The increased risk of the esophageal, gastric, colorectal, liver, gallbladder, pancreas, kidney, endometrial, breast, prostate cancers, non-Hodgkin’s lymphoma, and multiple myeloma in obese patients have been studied so far [1,2,3,4]. Generally, it is adenocarcinoma, not squamous cell carcinoma, of the esophagus that has increased risk in obese patients [5]. Also, there is a correlation between increased body mass index (BMI) and two-threefold increased risk of gastric cardia adenocarcinoma (unclear for non-cardia adenocarcinoma) [1, 6, 7]. In colorectal cancers (CRC), the relative risk for cancer is.1.5 to 2 (comparing with normal population), when BMI ≥ 28–30 kg/m2 is present (More obvious in colon cancer and in men) [8]. Meanwhile, the increasing number of bariatric surgeries is reported; the effect of bariatric surgeries on different cancers is not well understood. Bariatric surgery reduces cancer risk along with weight reduction [5, 9, 10]. For example, gastric cancer in obese patients who underwent bariatric surgery is dramatically lower than obese patients not subjected to the surgery (24/100000 versus 306/100000) [10], and a 27% decrease in CRC risk is seen after obesity surgery [11], but the issue is not that simple for the following reasons: (1) gastro-intestinal (GI) cancer early symptoms like epigastric discomfort, weight loss, oral intolerance, nausea, and vomiting are quite similar to ordinary post-op symptoms [12,13,14]. (2) Anatomic alterations make it difficult to use diagnostic modalities. As a result, GI cancer diagnosis after bariatric surgery is challenging, and progressive tumors are frequent. One recent study showed more than a threefold increase in mortality rate in rectal cancer patients with prior obesity surgery [15]. The bariatric surgeon should keep in mind that, though not frequent, GI tract cancers may occur after bariatric surgery and diagnosis needs a high index of suspicion.

Methods

We performed a search in PubMed, Google scholar, Cochrane and science direct, using one or more of the key words including gastrointestinal neoplasms, GI cancer, cancer, GI neoplasm, gastric cancer, gastric neoplasm, gastric tumor, gastric carcinoma, gastric adenocarcinoma, esophageal cancer, esophageal neoplasm, esophageal tumor, esophageal carcinoma, esophageal adenocarcinoma, sleeve gastrectomy, laparoscopic sleeve gastrectomy, SG, SG, OAGB, one anastomosis gastric bypass, LMGB, laparoscopic minigastric bypass, LRYGB, Laparoscopic Roux-en-Y gastric bypass, RYGB, Roux-en-Y gastric bypass, Omega loop gastric bypass, SAGB, single anastomosis gastric bypass, jejuno-ileal bypass, JIB, SASI, single anastomosis sleeve-ileal bypass, SASJ, single anastomosis sleeve-jejunal bypass, SADI, single anastomosis duodeno-ileal bypass, obesity surgery, bariatric surgery, gastric bypass, vertical banded gastroplasty, VBG, gastric banding, gastric band, laparoscopic gastric banding LAGB, duodenal switch, biliopancreatic diversion, excluded stomach, gastric bypass remnant, bypassed stomach and gastric pouch to find all published articles on GI cancers following bariatric surgery.

We excluded non-English language articles and animal model studies and considered all articles published until 30 September 2018. Tumors existing before surgery or at the time of surgery were omitted. Five hundred ninety-three articles were found of which, 22 were duplicates. According to the title, 462 papers were excluded. For 109 articles, abstracts were read which yielded in 40 irrelevant and 6 inaccessible papers. Finally, 63 articles were studied completely and epidemiological, clinical, and pathological data, as well as treatment and prognosis data, were collected and references for each paper were considered to figure out any neglected article.

Results

Jejunoileal Bypass

Historically, jejunoileal bypass (JIB) abandonment occurred early in the 1980s due to severe nutritional and metabolic complications. Nevertheless, clinicians still encounter post-JIB long-term complications [16]. According to our review, there are 4 reports of GI cancers following JIB (Supplementary Table 1). The earliest occurred eight years after JIB, whereas the latest lesion appeared 41 years after the surgery. Two of the cases were female and the mean age of patients was 56.6 years (44–63 years). Rectal bleeding happened in cecal and anal canal tumors but the transverse colon tumor exclusively had vague abdominal symptoms [16,17,18]. Interestingly, Burton et al. diagnosed the tumor using upper GI endoscopy [17]. Also, Voss et al. reported a squamous cell carcinoma of the upper anal canal, treated by open abdominoperineal resection followed by adjuvant radiation, but the tumors in Morris’s and Burton’s case reports were, adenocarcinomas of the cecum and transverse colon, orderly [16,17,18]. Moreover, the transverse colon adenocarcinoma passed away on post-op day 67 for severe pneumonia [16]. In addition to the malignancies mentioned above, McFarland et al. and Sylvan et al. reported polyp formation at the colon following JIB; none were malignant [19, 20].

Vertical Banded Gastroplasty

Vertical banded gastroplasty (VBG) is less frequent today so all eight articles noting gastric malignant neoplasms after VBG are of last decades (Supplementary Table 2). Three of the patients were male and all the patients were middle-aged, from 44 to 67 years (mean = 55.5 years) [21]. Except for Zirak et al.’s study in which they applied Silastic Ring-VBG, all patients had undergone VBG with mesh placement around the pouch [22]. Totally, cancer developed on an average 10.5 years after VBG (2–16.5 years). In the first study by Sweet et al. (1996), they presented pouch outlet obstruction caused by linitis plastica, though esophago-gastro-duodenoscopy (EGD) biopsies revealed no malignancy [23]. In three cases, the tumor’s location was in the pouch, one case in the pre-pyloric region extending to duodenum’s second part (D2), and two cases (including linitis plastica case) in the isolated gastric fundus. Allen and colleagues reported a case of esophagogastric junction (EGJ) cancer with a history of JIB converted to VBG for weight regain and impaired liver function [24]. The lesion in Melstrom’s report appeared in the distal esophagus. Generally, surgeons performed laparotomy for all patients (except for Melstrom’s case, which underwent chemo-radiotherapy and stenting). In Papakonstantinou et al.’s article, the patient underwent Whipple’s pancreaticoduodenectomy due to D2 involvement [21]. Investigations on pathology reports showed aggressive adenocarcinoma in five cases, but in one case (De Roover et al.), high-grade gastrointestinal stromal tumor (GIST) was the diagnosis [25]. In the early post-op period, one patient experienced anastomosis leak (Jain et al), managed conservatively [26]. The patient underwent Whipple’s procedure, passed away six months after the surgery for malnutrition and disseminated metastases. Also, Allen’s case died 15 months after the gastrectomy because of the tumor recurrence. The Melstrom’s patient died nearly two years after the VBG. The GIST patient had a recurrence at the liver and lung three years post-operation [27].

Laparoscopic Adjustable Gastric Banding

Once being one of the most prevalent bariatric surgeries, laparoscopic adjustable gastric banding (LAGB) is now declining globally, because of its complications like erosion and slippage. Our review showed there are eight cases (five females and three males) of GI malignancies following LAGB (Table 1). Only one of the patients underwent open surgery and surgeons used lap-band in most of the cases. The mean age of the patients was 53.9 years (37–66 years). Earliest and latest tumors presented six months and 10 years orderly (mean = 3.4 years). Two cases had lower esophageal cancer, one had EGJ cancer, and three had gastric cancer (one tumor located in the cardia and the other in the pouch just above the band and the last at the incisura angularis). Lower GI tract cancer happened in two patients: one of them was 2 cm above the anal verge and the other was at the recto-sigmoid junction, 18 cm from the anus. The aggressiveness of the tumors was worth noting: most of them were moderately or poorly differentiated adenocarcinomas and all except one had metastatic feature. Metastatic sites were the liver (three patients), vertebrae (one patient), abdominal wall (one patient), and retroperitoneal lymph nodes (one patient). We noticed peritoneal carcinomatosis and ascites in one patient. Four patients received palliative care and four of the patients passed away in the first two years after diagnosis.

Table 1 Reported cases of GI cancers following laparoscopic adjustable gastric banding (LAGB)
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Laparoscopic Sleeve Gastrectomy (SG)

Up to now, there are only four cases of GI cancers after SG according to our review (Table 2). Scheepers et al. [36] reported the only lower esophageal cancer after SG and all the other three cancers were in the stomach. All the cases were female and the mean age at diagnosis was 51.7 years (44–57 years). The average BMI before SG was 49.6. Tumors appeared 2.2 years after SG on average: one 4 months, one 9 months, and two of the tumors diagnosed four  years post-operation. Pre-op EGD was not done in the tumors diagnosed at four months and nine months after the surgery, and they could be present at the time of SG. Three of the patients were smokers and also three had obstructive sleep apnea prior to the surgery. One patient was a pancreas transplant case (immunocompromised). One case has had gastric pacemaker implantation and one case had balloon placement before the SG. Moreover, three cases had dysphagia and food intolerance and one patient had nonspecific abdominal and back pain. Pathology showed two poorly differentiated adenocarcinoma (all four were adenocarcinoma) and two cases had invaded the adjacent structures (T4). The patient with lower esophageal adenocarcinoma underwent definite chemoradiotherapy (Table 1). Kuper et al. reported a case of pancreatic cancer (aside from nesidioblastosis and other endocrine tumors), after SG. The patient was a 52-year-old male with a history of splenectomy, renal cell carcinoma, and asymptomatic pelvic vein thrombosis who underwent SG and then acute pancreatitis repeatedly after the surgery. Investigations identified a tumor in the head of the pancreas and elevated carbohydrate antigen 19–9 (CA19_9), three months post-operation. The patient underwent pylorus-preserving pancreaticoduodenectomy using the gastric sleeve. Pathology report revealed a ductal adenocarcinoma (T3N0M0). There was local recurrence with hepatic metastases nine months after the Whipple’s procedure (Kuper) [37].

Table 2 Reported cases of GI cancers following laparoscopic sleeve gastrectomy (SG)
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Roux en-Y Gastric Bypass (RYGB)

Our review showed 29 cases (19 female-10 male) of GI cancer after RYGB (Table 3). The average age at the diagnosis was 57.2 years (45–70 years). The mean time between the surgery and cancer diagnosis was 7.9 years (2 months to 28 years). In three patients, RYGB was a redo surgery (VBG: two cases—LAGB: one case). Four patients (13%) were asymptomatic. The most frequent symptom was abdominal pain which occurred in 16 patients (55%), followed by dysphagia, and excessive weight loss (each 17%). Tumor location was the gastric remnant in most cases: one in the fundus, two in the body, and 11 patients in the antrum and pyloric regions. In three patients, the location was the pouch, four in the EGJ and three patients in the distal esophagus, duodenum in two patients, head of the pancreas in two patients, and left colon in one patient. In 20 patients, pathology was adenocarcinoma and nine had different pathologies: Diffuse large B cell lymphoma of gastric remnant in two patients, mucosa-associated lymphoid tissue tumor in one (remnant), GIST of remnant in one, neuroendocrine tumor of duodenum’s first part (D1) in one, Krukenberg tumor in one (remnant), and high-grade dysplasia of distal esophagus in one patient. Two patients had linitis plastic: one invaded both the pouch and the remnant and in the other, only pouch infiltration occurred. Five patients had even local or distant metastases at the time of surgery. In four patients, no surgery was done and definite chemo (radio) therapy started while palliative surgery was performed in three patients. Surgeons performed laparotomy in three cases and Ivor-Lewis surgery in three other patients. As a result of periampullary lesions, three patients underwent pancreaticoduodenectomy. Six patients passed away afterwards.

Table 3 Reported cases of GI cancers following Roux en-y gastric bypass (RYGB)
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One Anastomosis Gastric Bypass (OAGB)

As our review shows, there is only one report of GI cancer after OAGB (Wu et al. 2013): a 51-year-old female with symptoms of melena and abdominal pain and a poorly differentiated adenocarcinoma, located at the excluded stomach’ pylorus. Consequently, the resection included the distal two-thirds of the bypassed gastric remnant and surgeons stapled the duodenal stump, performed lymph node dissection, and re-anastomosed the gastric pouch and remnant’s fundus. Finally, they constructed a new Billroth II gastrojejunostomy between the proximal gastric remnant and the jejunum. Consequently, the patient received adjuvant chemotherapy [55]. It is clear that 3 other cases considered as “vertical gastric bypass with loop gastrojejunostomy”, and Mason’s bypass are not categorized as OAGB (Table 4).

Table 4 Reported cases of GI cancers following one anastomosis gastric bypass (OAGB) and its older versions
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Biliopancreatic Diversion (BPD)

Fernandez et al. reported a case of a 42-year-old female with a history of BPD six years ago, presented with nonspecific abdominal pain, fatigue and highly elevated carcinoembryonic antigen (CEA), CA19-9, and mild anemia. Subsequently, investigations revealed a moderately differentiated adenocarcinoma of the right colon with invasion to the BPD alimentary limb (Table 5). The patient underwent right hemicolectomy and resection of the infiltrated alimentary limb with the reconstruction of BPD. There were bi-lobar unresectable liver metastases, so adjuvant chemotherapy initiated. However, the patient died eight months after the operation [60]. Adami et al. reported seven cases of colorectal cancer after BPD in 1898 patients for a 26-year follow-up period. Three of seven patients were female and the average age at the time of cancer was 56.4 years (43–66 years). The mean time from BPD was 13 years (6–27 years). Only one case was in the right colon and the rest were left colon cancers. Accordingly, the surgery team performed right hemicolectomy and left hemicolectomy for patients and two patients underwent a second surgery for resection of the liver and lung metastases. Two patients died during the follow-up period and the rest were free of the tumor [61]. Another report by Fernandez et al. was about a metastatic carcinoid tumor in a 58-year-old female with morbid obesity and diabetes mellitus, presented with periodic severe diarrhea three years after BPD. There was an incidental finding of two nodules in the liver’s left lobe. Fine needle aspiration of nodules resulted in a metastatic neoplastic lesion of unknown origin. The nodules resected by laparotomy but the primary tumor was uncertain. Afterwards, lab tests showed a carcinoid tumor, so an octroscan was done which located the primary lesion in the pancreas and new hot spots in the liver, i.e., new metastases to the liver, in about 1 month after the surgery. Lastly, somatostatin analogs started with excellent response and the patient was alive at the time of publication [59].

Table 5 Reported cases of GI cancers following biliopancreatic diversion (BPD)
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Discussion

In contrast to numerous bariatric surgeries performed, just a few cases of GI cancers are post-obesity operations. This is probably due to a decrease in risk factors, firstly elevated BMI. Also, pre-operative investigations appear to play an essential role [25].

Colorectal Cancer as a Complication of JIB

Regional and systemic etiologies (notably enteroglucagon) may play a role for GI cancers after JIB. Anatomic changes following JIB alters bowel transit time, increases bile flow to the distal small bowel and colon (10 times increase in bile flow to the colon), and changes gut flora. Also, fat, carbohydrate, and protein intake changes dramatically [19]. Silverman et al. studied microbial flora of patients who underwent JIB, but the result did not support a carcinogenic role for gut flora [20]. Compensatory mechanisms after JIB are studied well in rat bowel and similar changes may be present in man. Bristol et al. reported a 17% increase in colorectal length, a 29% increase in wet weight, and an 86% increase in cecal weight. Also, crypts were 25% deeper in the distal third of the colon. Crypt cell proliferation rates (CCPR) more than doubled in the middle third of the colorectum and trebled in the distal third, following JIB [62]. Moreover, hyperplasia of sialomucin cells occurs in man after JIB [63]. In one animal model study, considering CRC, nearly 75% of the tumors happened in the distal half of the colorectum, 28% were malignant, and most were polypoid, while, in the small bowel, most of the tumors occurred in the proximal duodenum or upper jejunum, all were sessile and 60% were malignant [62]. Sylvan et al. propose long-term colonoscopic follow-up after JIB [20].

Esophagogastric Cancers and VBG

According to Mason, several factors may be responsible for esophagogastric carcinoma after VBG: (1) Barrett’s esophagus as a result of chronic reflux gastritis. Barret’s metaplasia is present in about 28% of redo VBGs has done for severe reflux [64]. (2) Too large pouch has impaired motility and results in chronic irritation of the outlet mucosa and (3) mucosal irritation and ischemia caused by the mesh surrounding the outlet [21, 65]. Negri et al. reported mucosal hyperplasia and metaplasia at the outlet of the VBG [21]. Generally, underlying stomach carcinoma should be suspected in any late gastric outlet stenosis in a VBG patient [26]. Surveillance EGD after VBG is controversial; however, De Roover et al. recommend endoscopic surveillance for patients symptomatic for gastro-esophageal reflux disease (GERD) and also after 15 years following VBG [66, 67].

GI Cancers after LAGB

As a whole, probable mechanisms in pathogenesis of esophagogastric carcinoma after LAGB are (1) prolonged contact of exogenous carcinogen containing food in the gastric pouch, (2) increased intraluminal pressure, (3) erosion and ischemia caused by the band (incidence:1.6%) (4) Helicobacter pylori (H.pylori) infection and (5) increased GERD after LAGB [28, 29, 31, 33,34,35, 68]. As LAGB augments lower esophageal sphincter, it may relieve GERD symptoms especially, in the early post-op period, as reported by some studies. However, Forsell et al. (in 326 patients who had undergone LAGB) found GERD is the most common complication requiring re-operation [69]. Consequently, all LAGB candidates should have an exact EGD and if Barret’s esophagus is found or the patient is high risk for gastrointestinal cancer or has GERD symptoms, then, it is wise to change the plan to RYGB rather than LAGB [31, 32].

GI Cancers Following SG

SG has become the most prevalent bariatric surgery, done worldwide, and available literature show only 4 cases of upper GI cancer after this surgery [1, 9, 12, 36]; hence, SG is probably the safest bariatric surgery in terms of GI tract cancers, though it should be investigated in complementary studies [12]. As our review shows, all post SG cancers are adenocarcinomas at the distal esophagus or the sleeve. Kant and colleagues stated that unlike RYGB, there is no increase in mucosal biomarkers of CRC at 6 months following SG [70]. One of the scenarios frequently seen during SG is facing a GIST. Yuval et al. stated in their cohort that the incidence of GIST in SG (1%) is much higher than that of previous reports, but was nearly comparable with the incidence of incidental GISTs found in RYGB patients. All GISTs were near the lesser curvature. Also, tumors were more prevalent in lower BMI and older patients. As a rule, the surgeon should check the entire stomach before resection and all GISTs should be removed. Also, all liver and peritoneal surfaces should be examined for metastases. Finally, they reported the presence of a GIST on the lesser curvature may change the surgical plan from SG to RYGB or even abort the procedure [71, 72]. One of the technical challenges after SG is conducting an esophagectomy to treat esophageal or proximal gastric cancers. The gastroepiploic arch is usually damaged or detached from the stomach so conduit creation, using the sleeve, is rarely possible and colon interposition should be considered [5]. Lastly, two of the cancers after SG happened four months and nine months post-op and EGD was not done before the surgery in these patients. This fact may necessitate pre-op EGD in SG patients.

GI Cancers Following LRYB

According to the published literature, it seems that bariatric surgery, especially LRYGB, causes a real decrease in esophageal and gastric cancers [10, 24, 73,74,75]. The incidence of gastric cancer is 306/100000/year in obese patients while it reduces to 24/100000/year in patients who underwent the surgery [10]. The probable causes of this reduction in GI cancers may be as follows: (1) LRYGB is a potent antireflux surgery and is an excellent remedy for Barret’s metaplasia (one study reported 57% regression of Barret’s esophagus and 100% resolution of symptoms in the study group, underwent LRYGB after 2 years [40, 45, 74]); (2) the lack of food content (carcinogens) in the excluded stomach [38, 73, 76]; (3) minimal or no acid production in the small gastric pouch [48, 74]; (4) minimal or no bile reflux into the pouch or distal esophagus; (5) lower bacteria concentration in the gastric content [77]. So, GI cancer following LRYGB is rare, but it may happen after the surgery and the patient must be completely attentive prior to the operation. Unfortunately, most of the gastric tumors occur in the remnant; thus, the clinical symptoms are vague and conventional EGD cannot diagnose them easily [10, 51, 53]. Pathogenesis and etiology of these tumors are not well understood but these factors may play a role in pathogenesis: (1) chronic bile reflux into the gastric remnant: duodenal reflux happens in the remnant of 36–68% of LRYGB patients [6, 39, 52]. Also, 97% of patients have superficial and 94% have pan gastritis at the excluded stomach [52]. (2) Intestinal metaplasia at the remnant: approximately, it occurs in 6.5–19% of patients who underwent LRYGB [6, 52, 54]. (3) H. pylori infection: in one study, 20% of cases were seropositive for H. pylori and in another study, a high proportion of patients were H. pylori positive. So, H. pylori screening is essential for all patients and we should treat any infection before the operation [6, 52]. Interestingly, pepsinogen I, pepsinogen II, and gastrin anti-Helicobacter pylori antibodies have some relations to atrophic gastritis and may be useful for prediction of neoplastic changes of gastric mucosa in LRYGB patients and also for cancer surveillance after the surgery [39]. As noted before, investigation of the gastric remnant is very difficult and most of the tumors are diagnosed in late stages. Unfortunately, conventional EGD is possible, only in cases with very short Roux limb [39, 46]. As a result, various diagnostic modalities have been proposed for investigation of the gastric remnant and duodenum after LRYGB: (1) insertion of a gastrostomy tube in the remnant and also placement of a radio-opaque marker around the gastrostomy site enabling performance of contrast study, (2) the use of a pediatric colonoscope or a long retrograde endoscope, (3) double-balloon endoscopy (DBE), (4) virtual computed tomography (CT) scan. Also, positron emission tomography-CT (PET-CT) has a sensitivity of 94% in the diagnosis of excluded stomach tumors (5) introducing a trocar in the remnant laparoscopically and performing endoscopy through the trocar [7, 41, 44, 49, 52, 56]. Hereon, Inoe stated that LRYGB is a safe remedy for obesity even in areas with high incidence of gastric cancer [77]. Braghetto et al. declared that resection of the excluded stomach does not increase morbidity after LRYGB. In general, they recommended routine resection of the gastric remnant in high-risk situations including (1) high-risk populations such as Asia, Latin-America, Eastern Europe, and some areas of Western Europe; (2) pathologies found in screening EGD, especially adenomatous polyps, dysplasia, intestinal metaplasia, and Menetrier’s disease; (3) a family history of gastric cancer, hereditary non-polyposis colon cancer (HNPCC), and the Li-Fraumeni syndrome; (4) bile reflux and bacterial overgrowth [6, 39]. In contrast, Ghanem and colleagues propose SG instead of LRYGB in high-risk patients [78]. In terms of EGJ and distal esophagus cancers following LRYGB, some considerable points are present according to the existing literature; first, both minimally invasive transhiatal esophagectomy and Ivor Lewis surgeries are feasible. Second, all patients should have a mechanical bowel preparation prior to the surgery. Third, computed tomography angiography (CTA) of the mesenteric vessels is compulsory before the surgery. Even if CTA of mesenteric vessels is normal, the surgeon should start the dissection from the remnant to evaluate its blood supply sufficiency. Fourth, pyloroplasty is controversial and some protocols do not recommend this manipulation. And last but not the least, the part of the alimentary limb between the resected pouch and jejunojejunal anastomosis should not be resected because aside from the absorptive role, it can be used for feeding jejunostomy placement [5, 14, 43, 47, 50, 74]. As noted before, 2 cases of gastric lymphoma are reported post-LRYGB. Basically H. pylori eradication is the mainstay of treatment if the patient has the infection. Close follow-up and EGD with biopsies is vital up to 3 years which is difficult for excluded stomach lymphoma. In such cases, adding local radiotherapy may help overcome this problem [4]. According to our review, except for 1 tubulovillous adenoma with atypia which occurred 8 years after LRYGB near the gastrojejunal anastomosis [13], no case of small bowel cancer is reported following LRYGB. Although there are rare reports about increased colorectal epithelial cell proliferation and Crypt fission associated with Roux-en-y gastric bypass [8.78], no case of CRC following LRYGB is reported currently.

OAGB and GI Cancers

In one study conducted by Mahawar et al., regarding objections to OAGB, 50.9% of respondents stated that OAGB will result in an increase in the risk of gastric cancer while 45.4% was apprehensive about esophageal cancer risk increase after OAGB [79]. There is only one case of cancer reported in an Asian patient, 9 years after OAGB, located in the gastric remnant [55]. The impact of acid reflux on Barret’s esophagus and esophageal cancer is clear, but whether bile reflux induces esophageal cancer is controversial [80,81,82]. Bruzzi et al. reported a strong association between chronic biliary reflux, Barret’s metaplasia, and esophageal carcinoma in obese patients that have not undergone bariatric surgery [80]. In contrast, Carbajo’s study concluded there is no significant clinical association between bile reflux and increased esophageal cancer risk [81]. Some studies have reported few cases of gastroesophageal cancer, 20–30 years after Billroth II gastrectomy, but the situation is quite different for OAGB because there is a long narrow pouch and also biliary and pancreatic content dilution occurs at 1.5 m (at least) from the ligament of Treitz [82]. Also, no increase in esophagogastric cancer risk is seen after Mason’s loop gastric bypass, which has some similarities to OAGB [57, 83]. Babor et al. recommend regular endoscopies for cancer surveillance, starting 20 years after Mason’s loop gastric bypass [58]. Though, there is not enough evidence for GI cancer screening following OAGB, every OAGB patient, suffering from unusual complaints, is at risk for upper GI malignancies and proper investigation is crucial [55].

Colorectal Cancer After BPD

Theoretically, anatomic changes that happen after BPD may make large bowel prone to malignancies because increased contact with food carcinogens and biliary content along with an alteration in microflora may occur [59]. Adami and colleagues stated that only a substantial increase in CRC take place after BPD, which is related to the years passed after BPD, and age and gender are not major determinants [60, 61].

Carcinoid Tumors and Bariatric Surgery

A global increase in carcinoid tumors has transpired recently, due to environmental factors, diet alterations, and longer life expectancy [84]. Furthermore, multiple reports have stated that compared with the general population, carcinoid tumors have a higher incidence in obese patients [84, 85]. Also, malignant gastric carcinoid tumors are more prevalent in obese patients [86]. The increased incidence of these tumors may be due to hormonal changes that happen in obese people. Moreover, screening pre-op EGD results in a more precise diagnosis of the asymptomatic tumors [87]. Also, it is shown that hypergastrinemia occurs after SG in the animal model. Hypergastrinemia plays a major role in type 1 gastric carcinoid tumor pathogenesis; hence, we should be aware of probable increased carcinoid tumor risk after SG [87]. Moreover, intraoperative recognition of a gastric remnant carcinoid tumor, during gastric bypass, mandates excluded stomach resection [88]. Another issue is increased prevalence of appendix carcinoid tumors (ACT), in obese patients, and, when faced intraoperatively, seems challenging. Ordinarily, they are more frequent in female, young, and high-BMI bariatric surgery candidates [3]. Crea and colleagues recommend routine appendectomy or, at least, investigation of appendix during each obesity surgery. In addition, they stated that it neither causes additional complications nor increases the operation time significantly. If appendectomy is necessary and the patient is scheduled to undergo LAGB, then according to Crea, we should change the surgery plan. As a rule, simple appendectomy is sufficient for tumors less than 2 cm in diameter that have not involved mesoappendix or serosa, but if the tumor is greater than 2 cm or has involved mesoappendix or serosa, whether grossly or histopathologically, then right hemicolectomy is essential as the adjuvant surgery [3].

Finally, although hundreds of thousands of bariatric surgeries are done up to now, only these few cases are present as post-op GI malignancies, so there is not conclusive evidence about the correlation of obesity surgery and GI cancers, the epidemiologic features of the subjects and their clinical and paraclinical presentations. As a result, complementary studied are still demanded.

Conclusion

Bariatric surgery reduces the risk of obesity-related malignancies. Generally, GI cancers are rare following bariatric surgery but they may occur at any time after the operation. Unfortunately, their presentations are nonspecific and are mistaken with expectable symptoms arising in the post-op period. Also, anatomic alterations make investigations quite harder in these patients. As a result, most tumors appear in advanced stages and have a poor prognosis. All clinicians who deal with these patients should keep in mind that unusual complaints after bariatric surgery may be due to tumors and proper workup should be done. Finally, there is growing evidence in favor of pre-op screening EGD. This modality makes the bariatric team capable of early diagnosis of precancerous and malignant lesions and helps to make the best decision both in bariatric and oncosurgical aspects.