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review of literature on clinical pancreatology - The Pancreapedia

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Associati<strong>on</strong> with liver diseaseAlthough chr<strong>on</strong>ic pancreatitis and liver cirrhosis are comm<strong>on</strong> sequelae <str<strong>on</strong>g>of</str<strong>on</strong>g> excess alcoholc<strong>on</strong>sumpti<strong>on</strong>, the two c<strong>on</strong>diti<strong>on</strong>s are rarely associated. It was studied the prevalence <str<strong>on</strong>g>of</str<strong>on</strong>g>simultaneous liver cirrhosis and chr<strong>on</strong>ic pancreatitis by post-mortem autopsy data from 620individuals with a history <str<strong>on</strong>g>of</str<strong>on</strong>g> excess alcohol c<strong>on</strong>sumpti<strong>on</strong> and 100 n<strong>on</strong>-alcoholics (c<strong>on</strong>trols).<strong>The</strong> individuals were classified into groups based <strong>on</strong> macroscopic observati<strong>on</strong>s <str<strong>on</strong>g>of</str<strong>on</strong>g> pancreas(no injury, acute pancreatitis, fibrosis and chr<strong>on</strong>ic pancreatitis) and liver (no injury, moderatesteatosis, severe steatosis, and cirrhosis). <strong>The</strong> same classificati<strong>on</strong> system was used forhistological data, which was used to c<strong>on</strong>firm and correlate macroscopic results. Out <str<strong>on</strong>g>of</str<strong>on</strong>g> the183 patients with liver cirrhosis, 33 (18 %) had chr<strong>on</strong>ic pancreatitis and 93 (51 %) pancreaticfibrosis. Out <str<strong>on</strong>g>of</str<strong>on</strong>g> the 230 patients with severe steatosis, 37 (16 %) had chr<strong>on</strong>ic pancreatitis and97 (42 %) were found to have a pancreatic fibrosis. Thirty-three (39 %) with chr<strong>on</strong>icpancreatitis also showed liver cirrhosis and 37 (44 %) severe steatosis. Thirty-eight percent<str<strong>on</strong>g>of</str<strong>on</strong>g> the patients with a pancreatic fibrosis were found to have also liver cirrhosis and in another40 percent severe steatosis. Thirty-five patients showed neither hepatic nor pancreatic injury.It was found no chr<strong>on</strong>ic pancreatitis or liver cirrhosis in the c<strong>on</strong>trol group (n=100). It wasc<strong>on</strong>cluded that c<strong>on</strong>trary to comm<strong>on</strong> believe there is a close associati<strong>on</strong> between pancreaticand hepatic injury in patients with increased alcohol c<strong>on</strong>sumpti<strong>on</strong>, and the degree <str<strong>on</strong>g>of</str<strong>on</strong>g> organdamage between the two organs correlate [261].Alcohol-induced chr<strong>on</strong>ic pancreatitisChr<strong>on</strong>ic pancreatitis is a progressive inflammatory c<strong>on</strong>diti<strong>on</strong> characterized by repeatedattacks <str<strong>on</strong>g>of</str<strong>on</strong>g> abdominal pain, and the destructi<strong>on</strong> and fibrosis <str<strong>on</strong>g>of</str<strong>on</strong>g> the pancreatic parenchymawhich causes to reduced exocrine and endocrine functi<strong>on</strong>s. Alcohol is the most comm<strong>on</strong>cause <str<strong>on</strong>g>of</str<strong>on</strong>g> chr<strong>on</strong>ic pancreatitis. Although abstinence is usually c<strong>on</strong>sidered a prerequisite forsuccessful treatment <str<strong>on</strong>g>of</str<strong>on</strong>g> alcoholic chr<strong>on</strong>ic pancreatitis, <strong>on</strong>e <str<strong>on</strong>g>of</str<strong>on</strong>g>ten encounter patients who haverepeated attacks from the compensated stage through the transiti<strong>on</strong>al stage. In alcoholicchr<strong>on</strong>ic pancreatitis, c<strong>on</strong>tinued alcohol c<strong>on</strong>sumpti<strong>on</strong> causes changes in the digestivehorm<strong>on</strong>es and vagal nerve functi<strong>on</strong> that induce the pancreatic acinar cells to oversecreteprotein, increasing the protein c<strong>on</strong>centrati<strong>on</strong> and viscosity <str<strong>on</strong>g>of</str<strong>on</strong>g> the pancreatic juice. Thisinduces protein sedimentati<strong>on</strong> from the pancreatic juice and formati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> protein plugs withinthe pancreatic duct, triggering repeated attacks <str<strong>on</strong>g>of</str<strong>on</strong>g> acute pancreatitis. <strong>The</strong> treatment <str<strong>on</strong>g>of</str<strong>on</strong>g>alcoholic chr<strong>on</strong>ic pancreatitis includes alleviati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> symptoms, particularly abdominal pain,eliminati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> trigger factors, preventi<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> recurrence and disease progressi<strong>on</strong>, adjuvanttherapies for pancreatic exocrine and endocrine failure. Recently, the main c<strong>on</strong>stituentproteins in these protein plugs have been identified, enabling trials <str<strong>on</strong>g>of</str<strong>on</strong>g> several therapies, suchas the administrati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> secretin formulati<strong>on</strong>s and endoscopic removal. Bromhexinehydrochloride, a br<strong>on</strong>chial mucolytic, has an affinity for the pancreatic acinar cells, inducingthem to secrete pancreatic juice <str<strong>on</strong>g>of</str<strong>on</strong>g> low viscosity. In <strong>on</strong>e <str<strong>on</strong>g>review</str<strong>on</strong>g>, it was summarized the mostrecent thoughts about alcoholic chr<strong>on</strong>ic pancreatitis, and the new treatments, and inparticular, it was presented our findings c<strong>on</strong>cerning the efficacy <str<strong>on</strong>g>of</str<strong>on</strong>g> bromhexine hydrochloridein the treatment <str<strong>on</strong>g>of</str<strong>on</strong>g> this disease [262].Seventy percent <str<strong>on</strong>g>of</str<strong>on</strong>g> pancreatitis cases are c<strong>on</strong>sidered to be induced by alcohol in Finland.Half <str<strong>on</strong>g>of</str<strong>on</strong>g> those fallen ill with alcohol-induced acute pancreatitis will have relapses. Aprospective follow-up study showed that the level <str<strong>on</strong>g>of</str<strong>on</strong>g> dependence <strong>on</strong> alcohol c<strong>on</strong>stitutes themost important risk factor. C<strong>on</strong>tinued drinking was shown to be a dose-resp<strong>on</strong>sive risk factorfor relapse; abstinence provided for a complete protecti<strong>on</strong> against renewed pancreatitis. In arandomized study, a semi-annual meeting with a healthcare pr<str<strong>on</strong>g>of</str<strong>on</strong>g>essi<strong>on</strong>al specialized insubstance abuse problems significantly reduced new episodes <str<strong>on</strong>g>of</str<strong>on</strong>g> acute pancreatitis. It is thus

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