Introduction
Achalasia after bariatric surgery is a rare pathological entity. Nonetheless, several cases have been described in literature. Per oral endoscopic myotomy has recently emerged as the ...preferred approach for the management of esophageal motility disorders.
Material and Methods
We report a video case of POEM performed in a female patient with prior multiple bariatric surgical procedures. In her past medical history, she underwent to laparoscopic lap band, sleeve gastrectomy, and Roux-Y-gastric bypass.
Results
POEM was carried out without complication. Myotomy was performed only for 1 cm below the cardias due to the presence of the gastro-jejunal anastomosis. Post-operative course was uneventful and oral diet was restarted after one day. At 2 months follow-up, the patient is asymptomatic with no weight regain.
Conclusion
We report the first case of POEM after three different bariatric surgical procedure. Fibrosis due to prior interventions did not hampered POEM procedure, and the shorter myotomy due to the presence of small gastric pouch did not reduced its efficacy.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Humans with obesity differ in their susceptibility to developing insulin resistance and type 2 diabetes (T2D). This variation may relate to the extent of adipose tissue (AT) inflammation that ...develops as their obesity progresses. The state of macrophage activation has a central role in determining the degree of AT inflammation and thus its dysfunction, and these states are driven by epigenomic alterations linked to gene expression. The underlying mechanisms that regulate these alterations, however, are poorly defined. Here we demonstrate that a co-repressor complex containing G protein pathway suppressor 2 (GPS2) crucially controls the macrophage epigenome during activation by metabolic stress. The study of AT from humans with and without obesity revealed correlations between reduced GPS2 expression in macrophages, elevated systemic and AT inflammation, and diabetic status. The causality of this relationship was confirmed by using macrophage-specific Gps2-knockout (KO) mice, in which inappropriate co-repressor complex function caused enhancer activation, pro-inflammatory gene expression and hypersensitivity toward metabolic-stress signals. By contrast, transplantation of GPS2-overexpressing bone marrow into two mouse models of obesity (ob/ob and diet-induced obesity) reduced inflammation and improved insulin sensitivity. Thus, our data reveal a potentially reversible disease mechanism that links co-repressor-dependent epigenomic alterations in macrophages to AT inflammation and the development of T2D.
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IJS, NUK, SBMB, UL, UM, UPUK
Introduction: The realization of an antireflux valve according to the Nissen technique during the operation of one-anastomosis gastric bypass (OAGB) may theoretically decrease the incidence of ...postoperative reflux in patients with hiatal hernia (HH). Material and Methods: In this retrospective study, we included all patients operated on between January 2015 and January 2019 for an OAGB associated with the creation of an antireflux Nissen valve (360-degree wrap). The patients included had type II or type III HH that had been diagnosed preoperatively or discovered intraoperatively. Results: Twenty-two patients were operated on during the period considered. The mean preoperative BMI was 40 ± 14 kg/m2. Five patients (22.7%) had a history of bariatric surgery. Typical symptoms of gastroesophageal reflux disease (GERD) were preoperatively present in four patients (18%), and HH was revealed preoperatively only in four patients; for all the other patients, the diagnosis of HH was made intraoperatively. The rate of early and/or late postoperative complications was 0%. The mean duration of follow-up was 23 ± 15 months. No dysphagia was reported during follow-up. Three patients presented with symptomatic GERD postoperatively, including one de novo. Mean BMI at the end of follow-up was 24 ± 3 kg/m2, and the % of total weight loss was 108 ± 30%. Conclusions: OAGB with a Nissen antireflux valve seems to be a safe and effective surgical technique and it could be an extra arrow in the surgeon’s quiver in the presence of HH in a patient scheduled for OAGB.
Obesity modifies T cell populations in adipose tissue, thereby contributing to adipose tissue inflammation and insulin resistance. Here, we show that Rab4b, a small GTPase governing endocytic ...trafficking, is pivotal in T cells for the development of these pathological events. Rab4b expression is decreased in adipose T cells from mice and patients with obesity. The specific depletion of Rab4b in T cells causes adipocyte hypertrophy and insulin resistance in chow-fed mice and worsens insulin resistance in obese mice. This phenotype is driven by an increase in adipose Th17 and a decrease in adipose Treg due to a cell-autonomous skew of differentiation toward Th17. The Th17/Treg imbalance initiates adipose tissue inflammation and reduces adipogenesis, leading to lipid deposition in liver and muscles. Therefore, we propose that the obesity-induced loss of Rab4b in adipose T cells may contribute to maladaptive white adipose tissue remodeling and insulin resistance by altering adipose T cell fate.
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•Rab4b expression is decreased in adipose T cells of mice and patients with obesity•Mice with a deficiency of Rab4b in T cells develop insulin resistance•WAT expansion is impaired in mice with a deficiency of Rab4b in T cells•Mice with a deficiency of Rab4b in T cells exhibit altered Th17/Treg balance
Gilleron et al. show that Rab4b expression is decreased in adipose T cells during obesity in mice and humans. They reveal that Rab4b in T cells is critical for the control of adipose tissue remodeling and insulin sensitivity by regulating the adipose Th17/Treg balance.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Hypertrophic white adipose tissue (WAT) represents a maladaptive mechanism linked to the risk for developing type 2 diabetes in humans. However, the molecular events that predispose WAT to ...hypertrophy are poorly defined. Here, we demonstrate that adipocyte hypertrophy is triggered by loss of the corepressor GPS2 during obesity. Adipocyte-specific GPS2 deficiency in mice (GPS2 AKO) causes adipocyte hypertrophy, inflammation, and mitochondrial dysfunction during surplus energy. This phenotype is driven by HIF1A activation that orchestrates inadequate WAT remodeling and disrupts mitochondrial activity, which can be reversed by pharmacological or genetic HIF1A inhibition. Correlation analysis of gene expression in human adipose tissue reveals a negative relationship between GPS2 and HIF1A, adipocyte hypertrophy, and insulin resistance. We propose therefore that the obesity-associated loss of GPS2 in adipocytes predisposes for a maladaptive WAT expansion and a pro-diabetic status in mice and humans.
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•Adipose-specific GPS2 deficiency predisposes for adipocyte hypertrophy•Loss of GPS2 triggers transcriptional activation of HIF1A pathways•Deregulation of GPS2-HIF1A interplay provokes disrupted mitochondrial activity•GPS2 and HIF1A levels are negatively correlated in human adipose tissue
Drareni et al. identify a role for the transcriptional corepressor GPS2 in the regulation of adipocyte hypertrophy. They provide evidence that adipocyte-specific loss of GPS2 predisposes toward maladaptive adipose tissue expansion and pro-diabetic status through activation of HIF1A transcriptional activity.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Background and Aims
Endoscopy is effective in management of bariatric surgery (BS) adverse events (AEs) but a comprehensive evaluation of long-term results is lacking. Our aim is to assess the ...effectiveness of a standardized algorithm for the treatment of BS-AE.
Patients and Methods
We retrospectively analyzed 1020 consecutive patients treated in our center from 2012 to 2020, collecting data on demographics, type of BS, complications, and endoscopic treatment. Clinical success (CS) was evaluated considering referral delay, healing time, surgery, and complications type. Logistic regression was performed to identify variables of CS.
Results
In the study period, we treated 339 fistulae (33.2%), 324 leaks (31.8%), 198 post-sleeve gastrectomy twist/stenosis (19.4%), 95 post-RYGB stenosis (9.3 %), 37 collections (3.6%), 15 LAGB migrations (1.5%), 7 weight regains (0.7%), and 2 hemorrhages (0.2%). Main endoscopic treatments were as follows: pigtail-stent positioning under endoscopic view for both leaks (CS 86.1%) and fistulas (CS 77.2%), or under EUS-guidance for collections (CS 88.2%); dilations and/or stent positioning for sleeve twist/stenosis (CS 80.6%) and bypass stenosis (CS 81.5%). After a median (IQR) follow-up of 18.5 months (4.29–38.68), complications rate was 1.9%. We found a 1% increased risk of redo-surgery every 10 days of delay to the first endoscopic treatment. Endoscopically treated patients had a more frequent regular diet compared to re-operated patients.
Conclusions
Endoscopic treatment of BS-AEs following a standardized algorithm is safe and effective. Early endoscopic treatment is associated with an increased CS rate.
Graphical abstract
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Few data exist about the characteristics and management of enteric leaks after mini-gastric bypass (MGB).
We aimed to describe the incidence, presentation, and surgical management of enteric leaks in ...patients who underwent laparoscopic MGB for morbid obesity.
Private practice.
An 8-year, 9-month retrospective chart review was performed on patients who had enteric leak requiring reoperation after MGB at a single institution.
Thirty-five of 2321 patients were included. Ninety-seven percent had symptoms. Arterial hypertension and heavy smoking were predicting factors of leaks occurrence post-MGB (P<.01). Enteric leak was diagnosed by systematic upper gastrointestinal series in 4 pts (11.4%) and by computed tomography with oral water soluble contrast in 4 of 31 pts (13%). In the other 27 patients, diagnosis of the leak was made intraoperatively. Eleven patients (32%) had leak arising from the gastric stapler line (type 1), 4 (11%) from the gastrojejunal anastomosis (type 2), and 20 (57%) from undetermined origin. The most common presentation was intra-abdominal abscess in type 1 and leaks of undetermined origin and generalized peritonitis in type 2. One third of the patients who underwent reoperation developed well-drained chronic fistula into the irrigation-drainage system, with complete healing in all patients without any further procedure. The mean hospital stay was 19 days with no mortality reported.
Enteric leak leading to intra-abdominal sepsis post-MGB is rare (1.5%) An operative aggressive management based on clinical symptoms is the treatment of choice allowing no postoperative leak-related mortality and complete healing.
After a failed laparoscopic adjustable gastric band (LAGB), laparoscopic sleeve gastrectomy (LSG) has been proposed as revisional surgery. Those patients that receive a second restrictive procedure ...fall into a small subgroup of patients with more than one restrictive procedure (MRP). If also the second restrictive procedure fails, the correct surgical strategy is a challenge for the surgeon. Roux-en-Y gastric bypass (RYGB) may be an option but there is no evidence in the literature on whether the procedure is effective in treating failures after MRP. This study aims to evaluate the influence of the previous number of restrictive interventions (MRP vs single LSG) in the results of RYGB as revisional surgery. We have retrospectively analyzed patients who underwent conversion from laparoscopic sleeve gastrectomy (LSG), or from multiple restrictive procedures (MRP), to RYGB for weight regain (WR) or insufficient weight loss (IWL) between 2009 and 2019. The number of patients analyzed was 69 with conversion to RYGB after LSG and 44 after MRP. The reduction of excess weight (%TWL) at 3, 6, 12, 24 RYGB postoperative months was respectively of 11.03%, 16.39%, 21.43%, and 24.22% in the MRP group, and of 10.97%, 16.4%, 21.22%, and 22.71% in the LSG group. No significant difference was found in %TWL terms after RYGB for the MRP group and the LSG group with an overall %TWL, which was 11.00 ± 6.03, 16.40 ± 8.08, 21.30 ± 9.43, and 23.30 ± 9.91 respectively at 3, 6, 12, and 24 months. The linear regression model highlighted a positive relationship between the %EWL post-bypass at 24 months and the time elapsed only between the LSG and RYGB in the MRP group patients (
< 0.001). RYGB has proved to be a reliable technique with good results in terms of weight loss after failed bariatric surgery both in patients who previously underwent MRP and in those who underwent exclusively LSG. RYGB showed better results in patients who experienced WR than in those who had IWL from previous techniques.
In human type 2 diabetes, adipose tissue plays an important role in disturbing glucose homeostasis by secreting factors that affect the function of cells and tissues throughout the body, including ...insulin-producing pancreatic beta cells. We aimed here at studying the paracrine effect of stromal cells isolated from subcutaneous and omental adipose tissue on human beta cells. We developed an in vitro model wherein the functional human beta cell line EndoC-βH1 was treated with conditioned media from human adipose tissues. By using RNA-sequencing and western blotting, we determined that a conditioned medium derived from omental stromal cells stimulates several pathways, such as STAT, SMAD and RELA, in EndoC-βH1 cells. We also observed that upon treatment, the expression of beta cell markers decreased while dedifferentiation markers increased. Loss-of-function experiments that efficiently blocked specific signaling pathways did not reverse dedifferentiation, suggesting the implication of more than one pathway in this regulatory process. Taken together, we demonstrate that soluble factors derived from stromal cells isolated from human omental adipose tissue signal human beta cells and modulate their identity.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK