Printer Friendly

Analysis of weight changes after left gastric artery embolization in a cancer-naive population.

Obesity is an epidemic that affects more than a third of adults in the United States (1, 2). Despite advances in medical research and surgical techniques, obesity remains one of the largest drivers of chronic disease and healthcare costs in the United States (2, 3). In response to the growing obesity epidemic, left gastric artery (LGA) embolization has evolved as a promising procedure for weight loss therapy (4, 5). LGA embolization, also termed bariatric embolization when used for weight loss, decreases blood supply to the gastric fundus, which has the highest concentration of cells responsible for releasing ghrelin, a potent appetite-stimulating hormone (6). LGA embolization has been shown to suppress serum ghrelin levels and modulate weight in animal models (4, 5, 7). Promising results in animal models prompted investigators to retrospectively evaluate patients who underwent LGA embolization, an established procedure in interventional radiology for treatment of gastrointestinal (GI) bleeding. Early retrospective studies, though limited by small sample sizes and potential confounding factors, demonstrated significant weight loss as a nonintended side effect of LGA embolization and showed promise for reproducibility in humans. Results from clinical trials investigating the utility of LGA embolization to modulate weight have demonstrated promising results (4-6, 8-15). However, studies have been limited to small sample sizes and long-term data are lacking.

This retrospective cohort affords us a unique opportunity to assess a potential treatment population where weight loss is not intended and also to evaluate adverse events such as mucosal ulcers in the absence of strict standardized GI prophylaxis regimens implemented by current ongoing clinical trials. Drawing from the current literature on this topic, our hypothesis is that LGA embolization for GI bleeding will result in weight loss as an unintended side effect.


Patient selection

This single institution retrospective study was approved by the Institutional Review Board. Patients who underwent LGA embolization for treatment of acute gastrointestinal (GI) bleeding from 2001 to 2016 were identified through a search of the institutional database. Patients had to be at least 18 years of age and have no known cancer diagnoses at the time of procedure. All of the patients reviewed underwent LGA embolization in the inpatient or emergency setting. Twenty-one patients had documented pre- and postprocedure weights in their electronic medical record.

LGA embolization technique

While variations in technique existed depending on user preference, a generalized institutional approach to LGA embolization demonstrated the following technique: After sterile preparation of the right groin, the right common femoral artery was accessed with an 18-gauge needle. A Bentson wire was advanced into the aorta. The needle was exchanged for a 6 French (F) sheath and connected to a heparinized saline drip. A 5 F SOS catheter was advanced into the celiac artery. Selective catheterization was performed using a Progreat catheter and GT wire. The choice of embolic used depended on the type and location of the vascular lesion as well as user preference. The most common embolic agents used included gelfoam slurry followed by coil embolization and polyvinyl alcohol (PVA) particle embolization.

Outcome measures

Patients were assessed for any treatment-related adverse events. Primary adverse events were defined as the presence of gastric mucosal abnormalities ranging from superficial mucosal abnormalities to bleeding gastric ulcers on esophagogastroduodenoscopy. Medical records were evaluated for postprocedure complications, rebleeding events, or complaints of worsening abdominal pain within 30 days following the procedure. Height (m) and weight (kg) data were obtained through electronic medical records. Postprocedure weights were obtained based on availability in subsequent clinic notes. Changes in weight as well as changes in body mass index (BMI) as measured by weight in kilograms (kg) per height in meters squared (m2) were calculated.

Statistical analysis

Continuous variables were summarized using means ([+ or -]SD) or median (25%, 75%) and categorical variables using frequencies (percent). Pre and post BMI and weight were compared using a paired t-test. All tests were two-sided and conducted in SAS v9.4. A P value of 0.05 was considered statistically significant.


Patients ranged from 33-92 years of age. The median preprocedure weight and BMI of the patients evaluated in this study were 93.4 kg and 29.9 kg/[m.sup.2], respectively. Additional demographics and clinical characteristics of all patients are displayed in Table 1.

The method of arterial embolization included coils (n=6), gelfoam slurry (n=19), PVA particles ranging from 100-300 [micro]m, 300-500 [micro]m, and 500-700 [micro]m (n=5), and combination embolics (n=9). Additional data regarding embolization techniques are displayed in Table 2.

Following LGA embolization, median weight decreased from 93.4 kg to 77.1 kg and BMI decreased from 29.9 kg/m2 to 27.1 kg/m2 (n=21; P = 0.045) over a median time of 12 months (range, 2-72 months).

Pre- and postprocedure endoscopies were performed in 6 of the 39 patients. Of these patients, 2 had worsening ulcers following LGA embolization and 4 had stable or no abnormal findings. The majority of patients who did not have endoscopies were lost to follow-up or had no documentation of GI associated complications. One patient with a complex medical history requiring lifelong anticoagulation for multiple prosthetic heart valves was found to have complications with ischemic segment of jejunum requiring surgical intervention two days postprocedure. Given the site of ischemia, these findings are favored to represent thrombus related to holding anticoagulation rather than being related to LGA embolization. Another patient died within 60 days following the procedure from preexisting complex medical complications related to heart failure, again not directly related to LGA embolization.


Studying a retrospective cohort of patients for weight loss provides an opportunity to assess patients without confounding factors such as intrinsic motivation, diet modification or other weight loss strategies. Gunn et al. (16) reported on a small retrospective cohort (n=22) where they compared patients with LGA embolization for GI bleeding against those that had embolization elsewhere (extra-gastric) for GI bleeding. The group that received LGA embolization demonstrated significant nonintended weight loss (7.3% at 3 months) compared with the control group; however, this study was limited due to the inclusion of patients with a cancer diagnosis which introduces a significant confounding variable. A subsequent retrospective study was performed by Anton et al. (17), where they investigated patients with LGA embolization for GI bleeding in patients without cancer diagnoses (n=10). Their study also demonstrated significant weight loss (9.8% at one month and 11.7% at 4 months) compared with baseline weight.

Our study involves a retrospective cohort that does not include patients with a cancer diagnosis at the time of procedure. The patients in the study experienced a median 16.3 kg (17.4%) of unintended weight loss following LGA embolization for GI bleeding, over a median time interval of 12 months. Our cohort had an average BMI of 29.9 kg/[m.sup.2] which classifies them as overweight, whereas current clinical trials have been performed on morbidly obese individuals. This finding may provide insight into the effectiveness of LGA embolization on individuals who are not morbidly obese; however, clinical trials are needed to validate this claim.

Current clinical trials implement GI prophylaxis regimens both pre and post LGA embolization. While many of the patients received proton pump inhibitors on admission for GI bleeding, there was no rigorous standardized GI prophylaxis regimen before or after the procedure, as defined in clinical trials. Current clinical trials administer protracted dosing of sucralfate and proton-pump inhibitors to reduce the rate of gastric ulceration after LGA embolization (5). Our findings suggest that even in the absence of standardized preprocedure GI prophylaxis, the majority of patients appear to tolerate the procedure with minimal complications following LGA embolization. Of note, the authors do not advocate eliminating GI prophylaxis from clinical trials as the embolization techniques are quite different.

Our study has several limitations. Most notably, without a large sample size and low statistical power, our findings regarding association between weight change related to LGA embolization and various endpoints such as embolic type and follow-up time interval serve as observations, and true efficacy of this procedure cannot be inferred from this observation. Furthermore, the retrospective nature of this study introduces inevitable selection bias. Second, is an inability to determine whether the mechanism of weight loss was due to appetite suppression or other confounding factors such as weight loss due to illness, as is usually present in a hospitalized patient. Third, is lack of a control group which will make it difficult to assess the net effect of this LGA embolization. Fourth, is the non-standardized embolization technique with no consistent embolic endpoint.

In conclusion, our findings suggest that LGA embolization for GI bleeding results in weight loss as an unexpected side effect. This procedure appears to be well tolerated and may be a promising technique for modulating weight in obese adults. However, further larger and prospective studies are needed to confirm these preliminary findings.

Conflict of interest disclosure

Dr Akinwande is supported by an institutional (Washington University School of Medicine) and departmental (Mallinckrodt Institute of Radiology) grant. Siemens Healthcare, Merit Medical, BTG, Clear Guide Medical, and NIH NIH/NIBIB R01EB017615 provide grant support for Dr. Weiss. Other authors have nothing to disclose.


(1.) Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999-2000. JAMA 2002; 288:1723-1727. [CrossRef]

(2.) Mitchell NS, Catenacci VA, Wyatt HR, Hill JO. Obesity: overview of an epidemic. Psychiatr Clin North Am 2011; 34:717-732. [CrossRef]

(3.) Cawley J, Meyerhoefer C. The medical care costs of obesity: an instrumental variables approach. J Health Econ 2012; 31:219-230. [CrossRef]

(4.) Paxton BE, Kim CY, Alley CL, et al. Bariatric embolization for suppression of the hunger hormone ghrelin in a porcine model. Radiology 2013; 266:471-479. [CrossRef]

(5.) Weiss CR, Gunn AJ, Kim CY, Paxton BE, Kraitchman DL, Arepally A. Bariatric embolization of the gastric arteries for the treatment of obesity. J Vasc Interv Radiol 2015; 26:613-624. [CrossRef]

(6.) Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 1999; 402:656-660. [CrossRef]

(7.) Paxton BE, Alley CL, Crow JH, et al. Histopathologic and immunohistochemical sequelae of bariatric embolization in a porcine model J Vasc Interv Radiol 2014; 25:455-461. [CrossRef]

(8.) Arepally A, Barnett BP, Montgomery E, Patel TH. Catheter-directed gastric artery chemical embolization for modulation of systemic ghrelin levels in a porcine model: initial experience. Radiology 2007; 244:138-143. [CrossRef]

(9.) Arepally A, Barnett B P, Patel TH, et al. Catheter-directed gastric artery chemical embolization suppresses systemic ghrelin levels in porcine model. Radiology 2008; 249:127-133. [CrossRef]

(10.) Bawudun D, Xing Y, Liu WY, et al. Ghrelin suppression and fat loss after left gastric artery embolization in canine model. Cardiovasc Interv Radiol 2012; 35:1460-1466. [CrossRef]

(11.) Diana M, Pop R, Beaujeux R, et al. Embolization of arterial gastric supply in obesity (EMBARGO): an endovascular approach in the management of morbid obesity. proof of the concept in the porcine model. Obes Surg 2015; 25:550-558. [CrossRef]

(12.) Kipshidze N, Archvadze A, Bertog S, Leon MB, Sievert H. Endovascular bariatrics: first in humans study of gastric artery embolization for weight loss. JACC Cardiovasc Interv 2015; 8:1641-1644. [CrossRef]

(13.) Pasciak AS, Bourgeois AC, Paxton BE, et al. Bariatric radioembolization: a pilot study on technical feasibility and safety in a porcine model. J Vasc Interv Radiol JVIR 2016; 27:1509-1517. [CrossRef]

(14.) Syed MI, Morar K, Shaikh A, et al. Gastric artery embolization trial for the lessening of appetite nonsurgically (GET LEAN): six-month preliminary data. J Vasc Interv Radiol JVIR 2016; 27:1502-1508. [CrossRef]

(15.) Weiss CR, Akinwande O, Paudel K, et al. Clinical safety of bariatric arterial embolization: preliminary results of the BEAT obesity trial. Radiology 2017; 283:598-608. [CrossRef]

(16.) Gunn AJ, Oklu R. A preliminary observation of weight loss following left gastric artery embolization in humans. J Obes 2014; 2014:185349.

(17.) Anton K, Rahman T, Bhanushali A, Nadal L, Pierce G, Patel AA. Weight loss following left gastric artery embolization in a human population without malignancy: a retrospective review. Obes Weight Loss Ther 2015; 5.

David J. Kim [iD]

Hari S. Raman [iD]

Amber Salter [iD]

Raja Ramaswamy [iD]

Andrew J. Gunn [iD]

Clifford R. Weiss [iD]

Olaguoke Akinwande [iD]

From the Division of Interventional Radiology (D.J.K., H.S.R., R.R., O.A. [??] Mallinckrodt Institute of Radiology and Biostatistics and Department of Neurology (A.S.), Washington University School of Medicine in St. Louis, St. Louis, MO, USA; Division of Interventional Radiology A.J.G.), University of Alabama at Birmingham, Birmingham, AL, USA; Division of Interventional Radiology (C.R.W.), Department of Radiology, The Johns Hopkins University School of Medicine, Baltimore, USA.

Received 16 October 2017; revision requested 20 November 2017; last revision received 15 January 2018; accepted 30 January 2018.

DOI 10.5152/dir.2018.17412

You may cite this article as: Kim DJ, Raman HS, Salter A, Ramaswamy R, Gunn AJ, Weiss CR, Akinwande O. Analysis of weight changes after left gastric artery embolization in a cancer-naive population. Diagn Interv Radiol 2018; 24:94-97.

Main points

* Left gastric artery embolization was evaluated retrospectively for unintended weight loss.

* Left gastric artery embolization results in unintended weight loss.

* Left gastric artery embolization appears to be well tolerated in patients.
Table 1. Patient characteristics

                                 All LGA embolization patients

Age (years), median (range)      57 (41-92)
Age (years), mean (SD)           60.5 (14.7)
Gender, n (%)
  Male                           27 (69.2)
  Female                         12 (30.8)
Race, n (%)
  Caucasian                      30 (76.9)
  African American                9 (23.1)
Follow-up time intervals, n (%)
   1-3 months
   4-6 months
   7-12 months
  12-24 months
  24+ months

                                 LGA embolization patients
                                 with pre- and postprocedure
                                 weights (n=21)

Age (years), median (range)      57 (33-92)
Age (years), mean (SD)           56.3 (15.6)
Gender, n (%)
  Male                           12 (57.1)
  Female                          9 (42.9)
Race, n (%)
  Caucasian                      17 (81.0)
  African American                4 (18.2)
Follow-up time intervals, n (%)
   1-3 months                     4 (19.1)
   4-6 months                     3 (14.3)
   7-12 months                    4 (19.1)
  12-24 months                    5 (23.8)
  24+ months                      5 (23.8)

LGA, left gastric artery; SD, standard deviation.

Table 2. Embolization techniques

                              All LGA embolization
                              patients (n=39)

Embolic used, n (%)
  Coil                         6 (15.4)
  Gelfoam                     19 (48.7)
  PVA                          5 (12.8)
  PVA + coils                  3 (7.7)
  Gelfoam + coils              6 (15.4)
Embolic status, n (%)
  Permanent                   19 (48.7)
  Temporary                   20 (51.3)
Vessels embolized, n (%)
  LGA                         34 (87.1)
  LGA + splenic artery         3 (7.7)
  LGA + right gastroepiploic   1 (2.6)
  LGA + phrenic artery         1 (2.6)

                              LGA embolization patients with pre-
                              and postprocedure weights (n=21)

Embolic used, n (%)
  Coil                         4 (19.1)
  Gelfoam                     11 (52.4)
  PVA                          0 (0.0)
  PVA + coils                  2 (9.5)
  Gelfoam + coils              4 (19.5)
Embolic status, n (%)
  Permanent                   10 (47.6)
  Temporary                   11 (52.4)
Vessels embolized, n (%)
  LGA                         18 (85.7)
  LGA + splenic artery         2 (9.5)
  LGA + right gastroepiploic   1 (4.8)
  LGA + phrenic artery         0 (0.0)

LGA, left gastric artery; PVA, polyvinyl alcohol.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2018 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Kim, David J.; Raman, Hari S.; Salter, Amber; Ramaswamy, Raja; Gunn, Andrew J.; Weiss, Clifford R.;
Publication:Diagnostic and Interventional Radiology
Article Type:Report
Geographic Code:1USA
Date:Mar 1, 2018
Previous Article:Adrenal venous sampling: the learning curve of a single interventionalist with 282 consecutive procedures.
Next Article:N-butyl cyanoacrylate embolotherapy: techniques, complications, and management.

Terms of use | Privacy policy | Copyright © 2021 Farlex, Inc. | Feedback | For webmasters |