The Experts below are selected from a list of 2646 Experts worldwide ranked by ideXlab platform
Qing He - One of the best experts on this subject based on the ideXlab platform.
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polyvinyl alcohol and gelatin sponge particle embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis
World Journal of Gastroenterology, 2005Co-Authors: Yongsong Guan, Xiangping Zhou, Xiaohua Zheng, Xiao Li, Qing HeAbstract:AIM: To assess the effectiveness of and complications associated with polyvinyl alcohol (PVA) and gelatin sponge particles embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis. METHODS: A 42-year-old man with splenic artery pseudo-aneurysm formation secondary to chronic Alcoholic Pancreatitis was admitted. We used PVA and gelatin sponge particles embolization of splenic artery pseudoaneurysm by superselective embolization techniques. RESULTS: The splenic artery pseudoaneurysm was successfully controlled with splenic embolization. The patient was discharged in 9 d with complete recovery. CONCLUSION: This case confirms that superselective transcatheter embolization by PVA and gelatin sponge particles may represent an effective treatment for pseudoaneurysm caused by chronic Alcoholic Pancreatitis in the absence of other therapeutic alternatives.
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polyvinyl alcohol and gelatin sponge particle embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis
World Journal of Gastroenterology, 2005Co-Authors: Yongsong Guan, Xiangping Zhou, Xiaohua Zheng, Xiao Li, Qing HeAbstract:AIM: To assess the effectiveness of and complications associated with polyvinyl alcohol (PVA) and gelatin sponge particles embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis. METHODS: A 42-year-old man with splenic artery pseudo-aneurysm formation secondary to chronic Alcoholic Pancreatitis was admitted. We used PVA and gelatin sponge particles embolization of splenic artery pseudoaneurysm by superselective embolization techniques. RESULTS: The splenic artery pseudoaneurysm was successfully controlled with splenic embolization. The patient was discharged in 9 d with complete recovery. CONCLUSION: This case confirms that superselective transcatheter embolization by PVA and gelatin sponge particles may represent an effective treatment for pseudoaneurysm caused by chronic Alcoholic Pancreatitis in the absence of other therapeutic alternatives.
Jeremy S Wilson - One of the best experts on this subject based on the ideXlab platform.
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CLINICAL RESEARCH ON Alcoholic LIVER AND PANCREATIC DISEASES Individual susceptibility to Alcoholic Pancreatitis
2015Co-Authors: Minoti V Apte, Romano C Pirola, Jeremy S WilsonAbstract:The observation that only a minority of heavy drinkers develop Pancreatitis has prompted an intensive search for a trigger factor/cofactor/susceptibility factor that may precipitate a clinical attack. Putative susceptibility factors examined so far include diet, smoking, amount and type of alcohol consumed, the pattern of drinking and lipid intolerance. In addition, a range of inherited factors have been assessed including blood group antigens, human leukocyte antigen serotypes, alpha-1-antitrypsin phenotypes and several genotypes. The latter group comprises mutations/polymorphisms in genes related to alcohol-metabolizing enzymes, detoxifying enzymes, pancreatic digestive enzymes, pancreatic enzyme inhibitors, cystic fibrosis and cytokines. Disappointingly, despite this concerted research effort, no clear association has been established between the above factors and Alcoholic Pancreatitis. Experimentally, the secretagogue cholecystokinin (CCK) has been investigated as a candidate ‘trigger ’ for Alcoholic Pancreatitis. However, the clinical rel-evance of CCK as a trigger factor has to be questioned, as it is difficult to envisage a situation in humans where abnormally high levels of CCK would be released into th
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mechanisms of Alcoholic Pancreatitis
Journal of Gastroenterology and Hepatology, 2010Co-Authors: Minoti V Apte, Romano C Pirola, Jeremy S WilsonAbstract:Alcoholic Pancreatitis is a major complication of alcohol abuse. The risk of developing Pancreatitis increases with increasing doses of alcohol, suggesting that alcohol exerts dose-related toxic effects on the pancreas. However, it is also clear that only a minority of Alcoholics develop the disease, indicating that an additional trigger may be required to initiate clinically evident pancreatic injury. It is now well established that alcohol is metabolized by the pancreas via both oxidative and non-oxidative metabolites. Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of Alcoholic chronic Pancreatitis. Efforts to identify clinically relevant factors that may explain the susceptibility of some Alcoholics to Pancreatitis have been underway for several years. An unequivocal, functionally characterized, association is yet to be identified in clinical studies, although in the experimental setting, endotoxin has been shown to trigger overt pancreatic injury and to promote disease progression in alcohol-fed animals. Thus, while the molecular effects of alcohol on the pancreas have been increasingly clarified in recent years, identification of predisposing or triggering factors remains a challenge.
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new insights into Alcoholic Pancreatitis and pancreatic cancer
Journal of Gastroenterology and Hepatology, 2009Co-Authors: Minoti V Apte, Romano C Pirola, Jeremy S WilsonAbstract:Pancreatitis and pancreatic cancer represent two major diseases of the exocrine pancreas. Pancreatitis exhibits both acute and chronic manifestations. The commonest causes of acute Pancreatitis are gallstones and alcohol abuse; the latter is also the predominant cause of chronic Pancreatitis. Recent evidence indicates that endotoxinemia, which occurs in Alcoholics due to increased gut permeability, may trigger overt necroinflammation of the pancreas in Alcoholics and one that may also play a critical role in progression to chronic Pancreatitis (acinar atrophy and fibrosis) via activation of pancreatic stellate cells (PSCs). Chronic Pancreatitis is a major risk factor for the development of pancreatic cancer, which is the fourth leading cause of cancer-related deaths in humans. Increasing attention has been paid in recent years to the role of the stroma in pancreatic cancer progression. It is now well established that PSCs play a key role in the production of cancer stroma and that they interact closely with cancer cells to create a tumor facilitatory environment that stimulates local tumor growth and distant metastasis. This review summarizes recent advances in our understanding of the pathogenesis of Alcoholic Pancreatitis and pancreatic cancer, with particular reference to the central role played by PSCs in both diseases. An improved knowledge of PSC biology has the potential to provide an insight into pathways that may be therapeutically targeted to inhibit PSC activation, thereby inhibiting the development of fibrosis in chronic Pancreatitis and interrupting stellate cell-cancer cell interactions so as to retard cancer progression.
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pancreas Alcoholic Pancreatitis it s the alcohol stupid
Nature Reviews Gastroenterology & Hepatology, 2009Co-Authors: Minoti V Apte, Romano C Pirola, Jeremy S WilsonAbstract:The management of Alcoholic Pancreatitis is mostly reactive; little is done to prevent disease progression. It is time for physicians to pay attention to the root cause of the condition—that is, alcohol—rather than just responding to its effects. This article discusses an important paper that describes the first prospective, randomized, controlled, clinical trial to investigate the effect of brief interventions for alcohol abuse on the progression of Alcoholic Pancreatitis.
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bacterial endotoxin a trigger factor for Alcoholic Pancreatitis evidence from a novel physiologically relevant animal model
Gastroenterology, 2007Co-Authors: Alain Vonlaufen, Romano C Pirola, Jeremy S Wilson, Balu Daniel, Rakesh K Kumar, Minoti V ApteAbstract:Background & Aims: This study examined the possible role of endotoxinemia (from increased gut permeability) as an additional trigger factor for overt pancreatic disease and as a promoter of chronic pancreatic injury in Alcoholics by using a rat model of chronic alcohol feeding and in vitro experiments with cultured pancreatic stellate cells (PSCs), the key mediators of pancreatic fibrosis. Methods: In the in vivo model, Sprague-Dawley rats fed isocaloric Lieber-DeCarli liquid diets ± alcohol for 10 weeks were challenged with a single dose or 3 repeated doses of the endotoxin lipopolysaccharide (LPS) and the pancreas was examined. In the in vitro studies, rat PSCs were assessed for activation on exposure to LPS ± ethanol. The expression of LPS receptors TLR4 and CD14 also was assessed in rat and human PSCs. Results: In the in vivo model, single or repeated LPS challenge resulted in significantly greater pancreatic injury in alcohol-fed rats compared with rats fed the control diet without alcohol. Notably, repeated LPS injections caused pancreatic fibrosis in alcohol-fed rats, but not in rats fed the control diet. In the in vitro studies, PSCs were activated by LPS. Alcohol + LPS exerted a synergistic effect on PSC activation. Importantly, both rat and human PSCs expressed TLR4 and CD14. Conclusions: This study describes, for the first time, a clinically relevant animal model of alcohol-related pancreatic injury and provides strong in vivo and in vitro evidence that suggests that LPS is a trigger factor in the initiation and progression of Alcoholic Pancreatitis.
Yongsong Guan - One of the best experts on this subject based on the ideXlab platform.
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polyvinyl alcohol and gelatin sponge particle embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis
World Journal of Gastroenterology, 2005Co-Authors: Yongsong Guan, Xiangping Zhou, Xiaohua Zheng, Xiao Li, Qing HeAbstract:AIM: To assess the effectiveness of and complications associated with polyvinyl alcohol (PVA) and gelatin sponge particles embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis. METHODS: A 42-year-old man with splenic artery pseudo-aneurysm formation secondary to chronic Alcoholic Pancreatitis was admitted. We used PVA and gelatin sponge particles embolization of splenic artery pseudoaneurysm by superselective embolization techniques. RESULTS: The splenic artery pseudoaneurysm was successfully controlled with splenic embolization. The patient was discharged in 9 d with complete recovery. CONCLUSION: This case confirms that superselective transcatheter embolization by PVA and gelatin sponge particles may represent an effective treatment for pseudoaneurysm caused by chronic Alcoholic Pancreatitis in the absence of other therapeutic alternatives.
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polyvinyl alcohol and gelatin sponge particle embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis
World Journal of Gastroenterology, 2005Co-Authors: Yongsong Guan, Xiangping Zhou, Xiaohua Zheng, Xiao Li, Qing HeAbstract:AIM: To assess the effectiveness of and complications associated with polyvinyl alcohol (PVA) and gelatin sponge particles embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis. METHODS: A 42-year-old man with splenic artery pseudo-aneurysm formation secondary to chronic Alcoholic Pancreatitis was admitted. We used PVA and gelatin sponge particles embolization of splenic artery pseudoaneurysm by superselective embolization techniques. RESULTS: The splenic artery pseudoaneurysm was successfully controlled with splenic embolization. The patient was discharged in 9 d with complete recovery. CONCLUSION: This case confirms that superselective transcatheter embolization by PVA and gelatin sponge particles may represent an effective treatment for pseudoaneurysm caused by chronic Alcoholic Pancreatitis in the absence of other therapeutic alternatives.
Minoti V Apte - One of the best experts on this subject based on the ideXlab platform.
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CLINICAL RESEARCH ON Alcoholic LIVER AND PANCREATIC DISEASES Individual susceptibility to Alcoholic Pancreatitis
2015Co-Authors: Minoti V Apte, Romano C Pirola, Jeremy S WilsonAbstract:The observation that only a minority of heavy drinkers develop Pancreatitis has prompted an intensive search for a trigger factor/cofactor/susceptibility factor that may precipitate a clinical attack. Putative susceptibility factors examined so far include diet, smoking, amount and type of alcohol consumed, the pattern of drinking and lipid intolerance. In addition, a range of inherited factors have been assessed including blood group antigens, human leukocyte antigen serotypes, alpha-1-antitrypsin phenotypes and several genotypes. The latter group comprises mutations/polymorphisms in genes related to alcohol-metabolizing enzymes, detoxifying enzymes, pancreatic digestive enzymes, pancreatic enzyme inhibitors, cystic fibrosis and cytokines. Disappointingly, despite this concerted research effort, no clear association has been established between the above factors and Alcoholic Pancreatitis. Experimentally, the secretagogue cholecystokinin (CCK) has been investigated as a candidate ‘trigger ’ for Alcoholic Pancreatitis. However, the clinical rel-evance of CCK as a trigger factor has to be questioned, as it is difficult to envisage a situation in humans where abnormally high levels of CCK would be released into th
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Alcoholic Pancreatitis a tale of spirits and bacteria
World Journal of Gastrointestinal Pathophysiology, 2014Co-Authors: Alain Vonlaufen, Minoti V Apte, Laurent Spahr, Jeanlouis FrossardAbstract:Alcohol is a major cause of chronic Pancreatitis. About 5% of Alcoholics will ever suffer from Pancreatitis, suggesting that additional co-factors are required to trigger an overt disease. Experimental work has implicated lipopolysaccharide, from gut-derived bacteria, as a potential co-factor of Alcoholic Pancreatitis. This review discusses the effects of alcohol on the gut flora, the gut barrier, the liver-and the pancreas and proposes potential interventional strategies. A better understanding of the interaction between the gut, the liver and the pancreas may provide valuable insight into the pathophysiology of Alcoholic Pancreatitis.
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mechanisms of Alcoholic Pancreatitis
Journal of Gastroenterology and Hepatology, 2010Co-Authors: Minoti V Apte, Romano C Pirola, Jeremy S WilsonAbstract:Alcoholic Pancreatitis is a major complication of alcohol abuse. The risk of developing Pancreatitis increases with increasing doses of alcohol, suggesting that alcohol exerts dose-related toxic effects on the pancreas. However, it is also clear that only a minority of Alcoholics develop the disease, indicating that an additional trigger may be required to initiate clinically evident pancreatic injury. It is now well established that alcohol is metabolized by the pancreas via both oxidative and non-oxidative metabolites. Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of Alcoholic chronic Pancreatitis. Efforts to identify clinically relevant factors that may explain the susceptibility of some Alcoholics to Pancreatitis have been underway for several years. An unequivocal, functionally characterized, association is yet to be identified in clinical studies, although in the experimental setting, endotoxin has been shown to trigger overt pancreatic injury and to promote disease progression in alcohol-fed animals. Thus, while the molecular effects of alcohol on the pancreas have been increasingly clarified in recent years, identification of predisposing or triggering factors remains a challenge.
-
new insights into Alcoholic Pancreatitis and pancreatic cancer
Journal of Gastroenterology and Hepatology, 2009Co-Authors: Minoti V Apte, Romano C Pirola, Jeremy S WilsonAbstract:Pancreatitis and pancreatic cancer represent two major diseases of the exocrine pancreas. Pancreatitis exhibits both acute and chronic manifestations. The commonest causes of acute Pancreatitis are gallstones and alcohol abuse; the latter is also the predominant cause of chronic Pancreatitis. Recent evidence indicates that endotoxinemia, which occurs in Alcoholics due to increased gut permeability, may trigger overt necroinflammation of the pancreas in Alcoholics and one that may also play a critical role in progression to chronic Pancreatitis (acinar atrophy and fibrosis) via activation of pancreatic stellate cells (PSCs). Chronic Pancreatitis is a major risk factor for the development of pancreatic cancer, which is the fourth leading cause of cancer-related deaths in humans. Increasing attention has been paid in recent years to the role of the stroma in pancreatic cancer progression. It is now well established that PSCs play a key role in the production of cancer stroma and that they interact closely with cancer cells to create a tumor facilitatory environment that stimulates local tumor growth and distant metastasis. This review summarizes recent advances in our understanding of the pathogenesis of Alcoholic Pancreatitis and pancreatic cancer, with particular reference to the central role played by PSCs in both diseases. An improved knowledge of PSC biology has the potential to provide an insight into pathways that may be therapeutically targeted to inhibit PSC activation, thereby inhibiting the development of fibrosis in chronic Pancreatitis and interrupting stellate cell-cancer cell interactions so as to retard cancer progression.
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pancreas Alcoholic Pancreatitis it s the alcohol stupid
Nature Reviews Gastroenterology & Hepatology, 2009Co-Authors: Minoti V Apte, Romano C Pirola, Jeremy S WilsonAbstract:The management of Alcoholic Pancreatitis is mostly reactive; little is done to prevent disease progression. It is time for physicians to pay attention to the root cause of the condition—that is, alcohol—rather than just responding to its effects. This article discusses an important paper that describes the first prospective, randomized, controlled, clinical trial to investigate the effect of brief interventions for alcohol abuse on the progression of Alcoholic Pancreatitis.
Xiaohua Zheng - One of the best experts on this subject based on the ideXlab platform.
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polyvinyl alcohol and gelatin sponge particle embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis
World Journal of Gastroenterology, 2005Co-Authors: Yongsong Guan, Xiangping Zhou, Xiaohua Zheng, Xiao Li, Qing HeAbstract:AIM: To assess the effectiveness of and complications associated with polyvinyl alcohol (PVA) and gelatin sponge particles embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis. METHODS: A 42-year-old man with splenic artery pseudo-aneurysm formation secondary to chronic Alcoholic Pancreatitis was admitted. We used PVA and gelatin sponge particles embolization of splenic artery pseudoaneurysm by superselective embolization techniques. RESULTS: The splenic artery pseudoaneurysm was successfully controlled with splenic embolization. The patient was discharged in 9 d with complete recovery. CONCLUSION: This case confirms that superselective transcatheter embolization by PVA and gelatin sponge particles may represent an effective treatment for pseudoaneurysm caused by chronic Alcoholic Pancreatitis in the absence of other therapeutic alternatives.
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polyvinyl alcohol and gelatin sponge particle embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis
World Journal of Gastroenterology, 2005Co-Authors: Yongsong Guan, Xiangping Zhou, Xiaohua Zheng, Xiao Li, Qing HeAbstract:AIM: To assess the effectiveness of and complications associated with polyvinyl alcohol (PVA) and gelatin sponge particles embolization of splenic artery pseudoaneurysm complicating chronic Alcoholic Pancreatitis. METHODS: A 42-year-old man with splenic artery pseudo-aneurysm formation secondary to chronic Alcoholic Pancreatitis was admitted. We used PVA and gelatin sponge particles embolization of splenic artery pseudoaneurysm by superselective embolization techniques. RESULTS: The splenic artery pseudoaneurysm was successfully controlled with splenic embolization. The patient was discharged in 9 d with complete recovery. CONCLUSION: This case confirms that superselective transcatheter embolization by PVA and gelatin sponge particles may represent an effective treatment for pseudoaneurysm caused by chronic Alcoholic Pancreatitis in the absence of other therapeutic alternatives.