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Esophagus, Stomach, and Duodenum Part I

Selected Readings in General Surgery Cover ImageVol. 44, No. 5, 2018

  • Esophageal Perforation
  • Esophageal Diverticula
  • Esophageal Motility Disorders
  • Gastroesophageal Reflux
  • Barrett Esophagus
  • Benign Esophageal Neoplasia
  • Esophageal Cancer
  • Miscellaneous Esophageal Conditions

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Featured Commentary

The online formats of SRGS include access to What You Should Know (WYSK): commentaries on articles published recently in top medical journals. These commentaries, written by practicing surgeons and other medical experts, focus on the strengths and weaknesses of the research, as well as on the articles' contributions in advancing the field of surgery.

Below is a sample of one of the commentaries published in the current edition of WYSK.


Jirapinyo P, Thompson AC, Kröner PT, Chan WW, Thompson CC. Metabolic Effect of Foregut Exclusion Demonstrated by the Impact of Gastrogastric Fistula on Recurrence of Diabetes. J Am Coll Surg. 2018 Mar;226(3):259–266.

Commentary by: Raul Rosenthal, MD, FACS

In this study, a cohort of 126 severely obese subjects that underwent gastric bypass (GBP) was divided into two groups. The first group comprised 42 patients with gastrogastric fistula (GGF) formation; the second group comprised 82 matched controls without GGF. Forty-eight percent (n=20) of patients in the first group with GGF had experienced recurrence of diabetes mellitus (DM) when compared to only 13 percent in the control group. Of the 20 patients with GGF and recurrent DM, 13 underwent closure of the GGF that resulted in a higher and faster remission of DM when compared to those patients with recurrent DM, but that did not undergo closure of GGF. The authors concluded that the new formation of GGF resulting in a significantly higher incidence of recurrent DM and its closure in a higher rate of remission. These observations support the so-called “foregut theory” proposed by Rubino et al. as the most likely mechanism of action of metabolic effect after GBP.

Before we analyze the above-mentioned results, it is imperative that we acknowledge the concept of a “theory,” as a model that accurately explains a large number of observations. As surgeons and scientists, we collect data after experiments and/or surgical procedures and we use those to explain why phenomena happen. The benefit of a theory is that it might help us predict behavior and future events. However, these theories are not everlasting or verified; they also are disprovable and open to reform if there is new evidence that does not support the theory. This makes science evolve and constantly change.1

The observations made in this study could be seen either way, as disproving or supporting the foregut theory. As stated by the authors, there are two theories that have been postulated to explain metabolic effects of GBP. On the one hand, we have the foregut theory postulating that bypassing the duodenum prevents the stimulus and secretion of “unknown” inhibitory factors that will in turn result in insulin resistance and DM.2,3 On the other hand, we have the hindgut theory that accelerating transit time and exposure of undigested food to the distal small bowel will stimulate the L-cells of the intestine this in turn will increase the secretion of GLP-1, which will stimulate the B-cells of the pancreas and increase insulin secretion and remission of DM.4 So we can disprove the foregut theory and support the hindgut theory by stating that the formation or closure of a GGF will result in deceleration/acceleration of transit time and decreased/increased stimuli to the L-cells and GLP-1, resulting in recurrence or remission of metabolic syndrome. Unfortunately, in this study, no hormonal levels were obtained to support one or disprove the other theory.

Additionally, the authors fail to mention that one of the conclusions of the Surgical Treatment and Medications Potentially Eradicate Diabetes Efficiently (STAMPEDE) trial is that at five years follow-up, sleeve gastrectomy (SG) was equally efficient as GBP when it came to remission of DM and normalization of HBA1c. The fact that SG neither bypasses the duodenum/foregut theory nor accelerates the transit time/ hindgut theory disproves both theories as a potential pathophysiological explanation for remission of DM.5

Finally, the small number of cases and short follow-up in this study, plus the additional factors mentioned that were not addressed that might influence disease remission, such as simultaneous weight loss, hormonal changes, and microbiota changes, do not allow us to conclude that the foregut theory resulted in the recurrence or remission of DM.6,7

I take this opportunity to commend the authors for their efforts, and I thank the editors for giving me the privilege of commenting on this excellent work.

References

  1. Hawking S. A brief history of time. Bantam Books. 1988.
  2. Kwon Y, Abdemur A, Lo Menzo E, Park S, Szomstein S, Rosenthal RJ.The foregut theory as a possible mechanism of action for the remission of type 2 diabetes in low body mass index patients undergoing subtotal gastrectomy for gastric cancer. Surg Obes Relat Dis. 2014 Mar-Apr;10(2):235-42.
  3. Rubino F, Schauer PR, Kaplan LM, et al. Metabolic surgery to treat type 2 diabetes: clinical outcomes and mechanisms of action. Annu Rev Med 2010;61:393e411.
  4. Meek CL, Lewis HB, Reimann F, et al. The effect of bariatric surgery on gastrointestinal and pancreatic peptide hormones. Peptides. 2016;77:28e37.
  5. Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes 5-year outcomes. N Engl J Med 2017;376:641e651. Free Full Text
  6. Aron-Wisnewsky J, Doré J, Clement K. The importance of the gut microbiota after bariatric surgery. Nat Rev Gastroenterol Hepatol 2012;9:590e598. Free Full Text
  7. Li JV, Ashrafian H, Bueter M, et al. Metabolic surgery profoundly influences gut microbial-host metabolic cross-talk. Gut. 2011;60:1214e1223. Free Full Text
Recommended Reading

The editor has carefully selected a group of current, classic, and seminal articles for further study in certain formats of SRGS. The citations below are linked to their abstract on PubMed; free full-text is available where indicated.

Clermont M, Falk GW. Clinical Guidelines Update on the Diagnosis and Management of Barrett's Esophagus. Dig Dis Sci. 2018 Aug;63(8):2122-2128.

A review of updated guidelines for management of Barrett’s esophagus is presented in this article. Challenging issues such as approaches to surveillance in high-risk patients are clearly presented.

Saxena P, Khashab MA. Endoscopic Management of Esophageal Perforations: Who, When, and How? Curr Treat Options Gastroenterol. 2017;15(1):35-45.

This article provides a useful review of endoscopic approaches for management of esophageal perforations. Newer techniques such as endoscopic suturing and use of clips are presented.

Schlottmann F, Neto RML, Herbella FAM, Patti MG. Esophageal Achalasia: Pathophysiology, Clinical Presentation, and Diagnostic Evaluation. Am Surg. 2018;84(4):467-472.

Schlottman and coauthors provide a valuable review of the factors leading to development of achalasia and current methods of management.