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BACKGROUND: Human beings consume different chemical forms of iodine in their diet. These are transported by different mechanisms in the cell. The forms of iodine can be part of thyroid hormones, bind to lipids, be an antioxidant, or be an oxidant, depending on their chemical form. The excessive consumption of iodine has been associated with pancreatic damage and diabetes mellitus type 2, but the association between disease and the chemical form consumed in the diet is unknown. This research analyzes the effect of excessive iodine consumption as Lugol (molecular iodine/potassium iodide solution) and iodate on parameters of pancreatic function, thyroid and lipid profiles, antioxidant and oxidant status, the expression of IR/Akt/P-Akt/GLUT4, and transcription factors PPAR-γ and CEBP-ß. METHODS: Three groups of Wistar rats were treated with 300 µg/L of iodine in drinking water: (1) control, (2) KIO3, and (3) Lugol. RESULTS: Lugol and KIO3 consumption increased total iodine levels. Only KIO3 increased TSH levels. Both induced high serum glucose levels and increased oxidative stress and pancreatic alpha-amylase activity. Insulin levels and antioxidant status decreased significantly. PPAR-γ and C/EBP-ß mRNA expression increased. CONCLUSION: The pancreatic damage, hypertriglyceridemia, and oxidative stress were independent of the chemical form of iodine consumed. These effects depended on PPAR-γ, C/EBP-ß, GLUT-4, and IR.
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BACKGROUND: Epidemiological clinical reports have shown an association between iodine excess with diabetes mellitus type 2 and higher blood glucose. However, the relationship between iodine, the pancreas, adipose tissue, and glucose transport is unclear. The goal of this study was to analyze the effect of iodine concentrations (in Lugol solution) on glucose transport, insulin secretion, and its cytotoxic effects in mature 3T3-L1 adipocytes and pancreatic beta-TC-6 cells. METHODS: Fibroblast 3T3-L1, mature adipocytes, and pancreatic beta-TC-6 cells were treated with 1 to 1000 µM of Lugol (molecular iodine dissolved in potassium iodide) for 30 min to 24 h for an MTT proliferation assay. Then, glucose uptake was measured with the fluorescent analog 2-NBDG, insulin receptor, Akt protein, p-Akt (ser-473), PPAR-gamma, and Glut4 by immunoblot; furthermore, insulin, alpha-amylase, oxidative stress, and caspase-3 activation were measured by colorimetric methods and the expression of markers of the apoptotic pathway at the RNAm level by real-time PCR. RESULTS: Low concentrations of Lugol significantly induce insulin secretion and glucose uptake in pancreatic beta-TC-6 cells, and in adipose cells, iodine-induced glucose uptake depends on the serine-473 phosphorylation of Akt (p-Akt) and Glut4. Higher doses of Lugol lead to cell growth inhibition, oxidative stress, and cellular apoptosis dependent on PPAR-gamma, Bax mRNA expression, and caspase-3 activation in pancreatic beta-TC-6 cells. CONCLUSIONS: Iodine could influence glucose metabolism in mature adipocytes and insulin secretion in pancreatic beta cells, but excessive levels may cause cytotoxic damage to pancreatic beta cells.
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BACKGROUND AND STUDY AIMS: Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) is a complication associated with important morbidity, occasional mortality and high costs. Preventive strategies are suboptimal as PEP continues to affect 4% to 9% of patients. Spraying epinephrine on the papilla may decrease oedema and prevent PEP. This study aimed to compare rectal indomethacin plus epinephrine (EI) versus rectal indomethacin plus sterile water (WI) for the prevention of PEP. PATIENTS AND METHODS: This multicentre randomised controlled trial included patients aged >18 years with an indication for ERCP and naive major papilla. All patients received 100 mg of rectal indomethacin and 10 mL of sterile water or a 1:10 000 epinephrine dilution. Patients were asked about PEP symptoms via telephone 24 hours and 7 days after the procedure. The trial was stopped half way through after a new publication reported an increased incidence of PEP among patients receiving epinephrine. RESULTS: Of the 3602 patients deemed eligible, 3054 were excluded after screening. The remaining 548 patients were randomised to EI group (n=275) or WI group (n=273). The EI and WI groups had similar baseline characteristics. Patients in the EI group had a similar incidence of PEP to those in the WI group (3.6% (10/275) vs 5.12% (14/273), p=0.41). Pancreatic duct guidewire insertion was identified as a risk factor for PEP (OR 4.38, 95% CI (1.44 to 13.29), p=0.009). CONCLUSION: Spraying epinephrine on the papilla was no more effective than rectal indomethacin alone for the prevention of PEP. TRIAL REGISTRATION NUMBER: This study was registered with ClinicalTrials.gov (NCT02959112).
Assuntos
Colangiopancreatografia Retrógrada Endoscópica , Pancreatite , Administração Retal , Anti-Inflamatórios não Esteroides/uso terapêutico , Colangiopancreatografia Retrógrada Endoscópica/efeitos adversos , Epinefrina , Humanos , Pancreatite/etiologiaRESUMO
Abstract Pancreatic trauma is a rare but potentially lethal injury because often it is associated with other abdominal organ or vascular injuries. Usually, it has a late clinical presentation which in turn complicates the management and overall prognosis. Due to the overall low prevalence of pancreatic injuries, there has been a significant lack of consensus among trauma surgeons worldwide on how to appropriately and efficiently diagnose and manage them. The accurate diagnosis of these injuries is difficult due to its anatomical location and the fact that signs of pancreatic damage are usually of delayed presentation. The current surgical trend has been moving towards organ preservation in order to avoid complications secondary to exocrine and endocrine function loss and/or potential implicit post-operative complications including leaks and fistulas. The aim of this paper is to propose a management algorithm of patients with pancreatic injuries via an expert consensus. Most pancreatic injuries can be managed with a combination of hemostatic maneuvers, pancreatic packing, parenchymal wound suturing and closed surgical drainage. Distal pancreatectomies with the inevitable loss of significant amounts of healthy pancreatic tissue must be avoided. General principles of damage control surgery must be applied when necessary followed by definitive surgical management when and only when appropriate physiological stabilization has been achieved. It is our experience that viable un-injured pancreatic tissue should be left alone when possible in all types of pancreatic injuries accompanied by adequate closed surgical drainage with the aim of preserving primary organ function and decreasing short and long term morbidity.
Resumen El trauma pancreático es un tipo de trauma poco común potencialmente fatal que está asociado con lesiones de órganos abdominales o vasculares. Usualmente, los signos clínicos son tardíos aumentado el riesgo de complicaciones respecto al manejo y al pronóstico general. Debido a la baja prevalencia de la lesión del trauma, no existe consenso entre los cirujanos alrededor del mundo sobre cómo se debe diagnosticar y tratar adecuadamente este desafío quirúrgico. La precisión en el diagnóstico es difícil por la localización anatómica y las manifestaciones clínicas tardías. El abordaje quirúrgico ha ido cambiando de dirección hacia la preservación del órgano para evitar complicaciones secundarias asociada a la perdida de la función exocrina y endocrina, o de potenciales complicaciones postquirúrgicas incluyendo las dehiscencias y fistulas. El objetivo de este artículo es proponer un algoritmo de manejo del trauma pancreático a través de un consenso de expertos. Las lesiones del páncreas pueden ser manejadas con una combinación de maniobras hemostáticas, empaquetamiento pancreático, sutura de la herida y drenaje quirúrgico cerrado. La pancreatectomía distal con la perdida de tejido vital pancreático debe ser evitadas. Los principios generales de la cirugía de control de daños deben ser aplicados cuando sea necesario para un manejo quirúrgico definitivo cuando y solo cuando la estabilización fisiológica haya sido lograda. En nuestra experiencia, el tejido pancreático sano debe preservarse cuando el trauma se asocia de un manejo mediante un drenaje quirúrgico cerrado con el objetivo de preservar la función primaria del órgano y disminuir a corto y largo tiempo las morbilidades.
Assuntos
Humanos , Pâncreas/lesões , Pâncreas/cirurgiaRESUMO
Pancreatic trauma is a rare but potentially lethal injury because often it is associated with other abdominal organ or vascular injuries. Usually, it has a late clinical presentation which in turn complicates the management and overall prognosis. Due to the overall low prevalence of pancreatic injuries, there has been a significant lack of consensus among trauma surgeons worldwide on how to appropriately and efficiently diagnose and manage them. The accurate diagnosis of these injuries is difficult due to its anatomical location and the fact that signs of pancreatic damage are usually of delayed presentation. The current surgical trend has been moving towards organ preservation in order to avoid complications secondary to exocrine and endocrine function loss and/or potential implicit post-operative complications including leaks and fistulas. The aim of this paper is to propose a management algorithm of patients with pancreatic injuries via an expert consensus. Most pancreatic injuries can be managed with a combination of hemostatic maneuvers, pancreatic packing, parenchymal wound suturing and closed surgical drainage. Distal pancreatectomies with the inevitable loss of significant amounts of healthy pancreatic tissue must be avoided. General principles of damage control surgery must be applied when necessary followed by definitive surgical management when and only when appropriate physiological stabilization has been achieved. It is our experience that viable un-injured pancreatic tissue should be left alone when possible in all types of pancreatic injuries accompanied by adequate closed surgical drainage with the aim of preserving primary organ function and decreasing short and long term morbidity.
El trauma pancreático es un tipo de trauma poco común potencialmente fatal que está asociado con lesiones de órganos abdominales o vasculares. Usualmente, los signos clínicos son tardíos aumentado el riesgo de complicaciones respecto al manejo y al pronóstico general. Debido a la baja prevalencia de la lesión del trauma, no existe consenso entre los cirujanos alrededor del mundo sobre cómo se debe diagnosticar y tratar adecuadamente este desafío quirúrgico. La precisión en el diagnóstico es difícil por la localización anatómica y las manifestaciones clínicas tardías. El abordaje quirúrgico ha ido cambiando de dirección hacia la preservación del órgano para evitar complicaciones secundarias asociada a la perdida de la función exocrina y endocrina, o de potenciales complicaciones postquirúrgicas incluyendo las dehiscencias y fistulas. El objetivo de este artículo es proponer un algoritmo de manejo del trauma pancreático a través de un consenso de expertos. Las lesiones del páncreas pueden ser manejadas con una combinación de maniobras hemostáticas, empaquetamiento pancreático, sutura de la herida y drenaje quirúrgico cerrado. La pancreatectomía distal con la perdida de tejido vital pancreático debe ser evitadas. Los principios generales de la cirugía de control de daños deben ser aplicados cuando sea necesario para un manejo quirúrgico definitivo cuando y solo cuando la estabilización fisiológica haya sido lograda. En nuestra experiencia, el tejido pancreático sano debe preservarse cuando el trauma se asocia de un manejo mediante un drenaje quirúrgico cerrado con el objetivo de preservar la función primaria del órgano y disminuir a corto y largo tiempo las morbilidades.