Outcomes of Bariatric Surgery in Patients with Inflammatory Bowel Disease.

BACKGROUND: Obesity has become prevalent in patients with inflammatory bowel disease (IBD). Bariatric surgery can be considered to be contraindicated in IBD patients. We aimed to evaluate feasibility, safety, and efficacy of bariatric surgery in IBD patients. METHODS: We retrospectively identified all morbidly obese patients with a known diagnosis of IBD, who underwent bariatric surgery between January 2005 and December 2012. Postoperative outcomes and status of IBD in patients on maintenance therapy for their disease were assessed. RESULTS: We identified 20 IBD patients including 13 ulcerative colitis (UC) and 7 Crohn's disease (CD) patients with a mean age of 54.0 ± 10.5 years, BMI of 50.1 ± 9.0 kg/m(2), and duration of IBD of 11.3 ± 5.2 years. Eleven patients were on medication for IBD at baseline. Bariatric procedures included sleeve gastrectomy (N = 9), gastric bypass (N = 7), gastric banding (N = 3), and one conversion of band to gastric bypass. There were no intraoperative complications, but two conversions to laparotomy due to adhesions. Mean BMI change and excess weight loss at 1 year was 14.3 ± 5.7 kg/m(2) and 58.9 ± 21.1 %, respectively. Seven early postoperative complications occurred including dehydration (N = 5), pulmonary embolism (N = 1), and wound infection (N = 1). During a mean follow-up of 34.6 ± 21.7 months, five patients developed complications including pancreatitis (N = 2), ventral hernia (N = 2), and marginal ulcer (N = 1). Nine out of ten eligible patients experienced improvement in their IBD status. CONCLUSIONS: Bariatric surgery is feasible and safe in morbidly obese patients suffering from IBD. In addition to being an effective weight loss procedure, bariatric surgery may help mitigate symptoms in this patient population.

The incidence of acute venous injury as a result of proximity penetrating trauma screened with colour flow duplex ultrasound.

INTRODUCTION: The incidence of acute deep venous thrombosis as a result of penetrating proximity extremity trauma (PPET) to the thigh has been demonstrated to be 16% in a single report. The purpose of the current study is to demonstrate the incidence and clinical significance of venous injury as a result of proximity trauma to the thigh in a large cohort screened with colour flow duplex (CFD) ultrasound and to identify factors predictive of defining a wound in proximity to a major vascular structure. PATIENTS AND METHODS: A prospective observational study was conducted from January 1st, 2010 to January 1st, 2012 on all patients presenting with penetrating extremity trauma. Data on injury location, mechanism, associated extremity and non-extremity injuries, use and results of CFD, as well as the admitting trauma surgeon were recorded and analysed. RESULTS: 220 thigh wounds with a normal physical examination were identified, of which 167 (75.9%) underwent CFD due to proximity. The incidence of acute venous injury was 4.8% (8/167). 37.5% (3/8) of these injuries resulted in morbidity. Injury mechanism and which attending physician was on call were predictive of a wound being defined as in proximity, whereas an injury with an associated fracture was a negative predictor. CONCLUSIONS: Occult venous injuries as a result of PPET occur in 4.8% of patients with thigh wounds in proximity to a major vascular structure. The designation of a wound as being in "proximity" was influenced by injury mechanism, associated fractures, and the judgement of the on-call attending. Colour flow duplex is a valuable tool with the ability to identify not only occult arterial injuries, but also venous injuries with the potential to cause significant morbidity as well.

Dehydroepiandrosterone stimulates phosphorylation of FoxO1 in vascular endothelial cells via phosphatidylinositol 3-kinase- and protein kinase A-dependent signaling pathways to regulate ET-1 synthesis and secretion.

Dehydroepiandrosterone (DHEA) is an endogenous adrenal steroid hormone with controversial actions in humans. We previously reported that DHEA has opposing actions in endothelial cells to stimulate phosphatidylinositol (PI) 3-kinase/Akt/endothelial nitric-oxide synthase leading to increased production of nitric oxide while simultaneously stimulating MAPK-dependent secretion of the vasoconstrictor ET-1. In the present study we hypothesized that DHEA may stimulate PI 3-kinase-dependent phosphorylation of FoxO1 in endothelial cells to help regulate endothelial function. In bovine or human aortic endothelial cells (BAEC and HAEC), treatment with DHEA (100 nM) acutely enhanced phosphorylation of FoxO1. DHEA-stimulated phosphorylation of FoxO1 was inhibited by pretreatment of cells with wortmannin (PI 3-kinase inhibitor) or H89 (protein kinase A (PKA) inhibitor) but not ICI182780 (estrogen receptor blocker), or PD98059 (MEK (MAPK/extracellular signal-regulated kinase kinase) inhibitor). Small interfering RNA knockdown of PKA inhibited DHEA-stimulated phosphorylation of FoxO1. DHEA promoted nuclear exclusion of FoxO1 that was blocked by pretreatment of cells with wortmannin, H89, or by small interfering RNA knockdown of PKA. DHEA treatment of endothelial cells increased PKA activity and intracellular cAMP concentrations. Transfection of BAEC with a constitutively nuclear FoxO1 mutant transactivated a co-transfected ET-1 promoter luciferase reporter. Treatment of BAEC with DHEA inhibited transactivation of the ET-1 promoter reporter in cells overexpressing FoxO1. ET-1 promoter activity and secretion in response to DHEA treatment was augmented by PI 3-kinase blockade and inhibited by MAPK blockade. We conclude that DHEA stimulates phosphorylation of FoxO1 via PI 3-kinase- and PKA-dependent pathways in endothelial cells that negatively regulates ET-1 promoter activity and secretion. Balance between PI 3-kinase-dependent inhibition and MAPK-dependent stimulation of ET-1 secretion in response to DHEA may determine whether DHEA supplementation improves or worsens cardiovascular and metabolic function.

Minimally invasive repair of traumatic right-sided diaphragmatic hernia with delayed diagnosis.

BACKGROUND: Traumatic diaphragmatic hernias are a diagnostic and therapeutic challenge due to variable presentations. Early repair is important because of risks of incarceration and strangulation of abdominal contents along with respiratory and cardiovascular compromise. Minimally invasive techniques have been useful for diagnosis and treatment of diaphragmatic hernias in both blunt and penetrating trauma. METHOD: We present the case of a 54-year-old victim of a motor vehicle crash who presented with a delayed diagnosis of a right-sided traumatic diaphragmatic hernia. By using a 4-port technique and intracorporeal suturing, the hernia was repaired. This case highlights the difficulties associated with diagnosing diaphragmatic hernias and the role of minimally invasive techniques to repair them. CONCLUSION: Minimally invasive surgical techniques are being increasingly used to both diagnose and repair traumatic diaphragmatic injuries with excellent results.

Oral glucosamine for 6 weeks at standard doses does not cause or worsen insulin resistance or endothelial dysfunction in lean or obese subjects.

Glucosamine is a popular nutritional supplement used to treat osteoarthritis. Intravenous administration of glucosamine causes insulin resistance and endothelial dysfunction. However, rigorous clinical studies evaluating the safety of oral glucosamine with respect to metabolic and cardiovascular pathophysiology are lacking. Therefore, we conducted a randomized, placebo-controlled, double-blind, crossover trial of oral glucosamine at standard doses (500 mg p.o. t.i.d.) in lean (n = 20) and obese (n = 20) subjects. Glucosamine or placebo treatment for 6 weeks was followed by a 1-week washout and crossover to the other arm. At baseline, and after each treatment period, insulin sensitivity was assessed by hyperinsulinemic-isoglycemic glucose clamp (SI(Clamp)) and endothelial function evaluated by brachial artery blood flow (BAF; Doppler ultrasound) and forearm skeletal muscle microvascular recruitment (ultrasound with microbubble contrast) before and during steady-state hyperinsulinemia. Plasma glucosamine pharmacokinetics after oral dosing were determined in each subject using a high-performance liquid chromatography method. As expected, at baseline, obese subjects had insulin resistance and endothelial dysfunction when compared with lean subjects (SI(Clamp) [median {25th-75th percentile}] = 4.3 [2.9-5.3] vs. 7.3 [5.7-11.3], P < 0.0001; insulin-stimulated changes in BAF [% over basal] = 12 [-6 to 84] vs. 39 [2-108], P < 0.04). When compared with placebo, glucosamine did not cause insulin resistance or endothelial dysfunction in lean subjects or significantly worsen these findings in obese subjects. The half-life of plasma glucosamine after oral dosing was approximately 150 min, with no significant changes in steady-state glucosamine levels detectable after 6 weeks of therapy. We conclude that oral glucosamine at standard doses for 6 weeks does not cause or significantly worsen insulin resistance or endothelial dysfunction in lean or obese subjects.