Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From a review of 2,000 autopsies of children, 16 cases of extensive necrosis and scarring fibrosis of the myocardium were found. These lesions involved mainly the left ventricle and spared the endocardium, the pericardium, and the coronary vessels. These necrotic of fibrotic heart lesions were found to be closely associated with various pancreatic diseases: cystic fibrosis (11 cases), pancreatic lipomatosis (2 cases), extensive small bowel resection (3 cases, 2 of which were associated with acute interstitial pancreatitis). To explain these unexpected associations, two hypotheses can be put forth: (1) The lack of absorption of some presently undetermined substances indispensable for the correct trophicity of the myocardium, and (2) the release in the blood of proteolytic enzymes with consecutive activation of phlogistic substances such as kinins.
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PMID:Multifocal myocardial necrosis and fibrosis in pancreatic diseases of children. 44 Aug 37

The influence of ribonuclease on the morphogenesis of experimental pancreatitis in the albino rats has been studied. The drug injected during edematous stage of pancreatitis caused some decrease of pancreatic enzymes level in the blood at hemorrhagic stage and its normalization at necrotic stage of pancreatitis. The development of hemorrhagic and necrotic stages of pancreatitis did not change under the influence of ribonuclease. The maturation of connective tissue of pseudocyst capsule was delayed and inflammatory infiltration of necrotic tissues and their elimination were increased under the influence of the drug. There were extensive tubular transformations of acini and early fibrosis and lipomatosis in the frontier zone. In the viable parts of pancreas moderate hypertrophy of exocrine pancreatocytes developed and chronic pancreatitis features appeared with use of ribonuclease.
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PMID:[Ribonuclease in the experimental therapy of pancreatitis]. 261 83

In order to evaluate the effects of chronic alcohol consumption on pancreas morphology we reviewed the autopsy data of 530 patients: 148 with liver alcoholic cirrhosis (group I), 39 with non alcoholic cirrhosis (group II), 47 autopsies of chronic alcohol drinkers without liver cirrhosis (group III) and 296 non alcoholic patients with normal liver, age and sex-matched with group I (group IV). In the control group (group IV) lipomatosis and intralobular fibrosis were common (57 percent and 40 percent) and increased with age. The prevalence of five elementary lesions (protein plug, dilatation of duct, epithelial atrophy, canalicular regression and perilobular fibrosis) and of one pathologic diagnosis (diffuse fibrosing pancreatitis) were higher in group I than in group IV. Duct lesions (protein plugs, canalicular regression and epithelial atrophy) were also significantly higher in drinkers without cirrhosis (group III) than in group IV. Chronic calcifying pancreatitis was rare (2 cases in group I). Thirty-six cases were classified as diffuse fibrosing pancreatitis. This constituted an homogeneous histopathologic group, significantly more frequent in the group of alcoholic cirrhosis, and was always discovered incidentally at autopsy. Because diffuse fibrosing pancreatitis might easily be confused with the morphological changes of chronic calcifying pancreatitis, we suggest to include this histopathologic entity into the Marseille's classification of pancreatitis.
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PMID:Diffuse fibrosis of the pancreas: a peculiar pattern of pancreatitis in alcoholic cirrhosis. 275 5

It has been substantiated that the use of a new synthetic drug tageflar analogous to L-enkephalin was accompanied by the depression in pancreatic enzyme activity in the blood of rats, acceleration of necrotic and lytic processes in irreversibly damaged exocrine pancreocytes in the course of experimental pancreatitis. The drug promoted microcirculation retention in the injury zone and acceleration of the arrangement and elimination of necrotic glandular tissue. The influence of tagaflar diminished the extent of perifocal necrobiotic zone and suppressed sclerotic processes and pancreatic lipomatosis.
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PMID:[Effect of tageflar, a synthetic analog of L-enkephalin, on the morphogenesis of experimental pancreatitis]. 367 99

In summary, in addition to an acute interstitial pancreatitis the organotin compound DBTC induced a pancreatic fibrosis in rats. The course of the pancreatic fibrosis was studied 2-36 weeks after single i.v. treatment of rats with 6 or 8 mg/kg DBTC. The pancreatic fibrosis induced by DBTC differs from other experimental models of acute pancreatitis. Extensive infiltration by mononuclear cells is present in fibrotic areas without pancreatic atrophy or lipomatosis. The presence of chronic inflammatory lesions characterized by the destruction of exocrine parenchyma and fibrosis and in the later stages the endocrine parenchyma, indicate a chronic pancreatitis. In completion of the experimental model of the DBTC-induced acute interstitial pancreatitis in rats, the described late fibrotic effects on rat pancreas may be used as an experimental model of chronic pancreatitis.
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PMID:The course of pancreatic fibrosis induced by dibutyltin dichloride (DBTC). 1041 68

Pancreatic lipomatosis is characterized as massive lipid infiltration of the pancreatic tissue. Although its etiology is ill defined; obesity, diabetes mellitus, chronic pancreatitis, hereditary pancreatitis, and conditions that cause pancreatic ductal obstruction, for example tumors and stones, are related to its pathogenesis. Recently, with the increased use of computerized tomography and magnetic resonance imaging, it has become possible to observe the fat replacement of the pancreas. Herein, we report a 60-year-old man complaining of abdominal pain and weight loss. Preoperative work-up revealed a locally advanced (Stage III) pancreatic adenocarcinoma. Multimodal treatment was carried out and a 100% complete response was detected after neoadjuvant therapy. The patient underwent a standard pancreaticoduodenectomy, without complications. The tissue pathology revealed lipomatosis of the pancreas. He was disease-free and symptom-free at 1 year follow-up. To our knowledge, this is the first report in the literature of pancreatic head carcinoma with total fat replacement of the pancreas after neoadjuvant chemoradiotherapy.
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PMID:Fat replacement of the malignant pancreatic tissue after neoadjuvant therapy. 2009 Oct 80

For good performance in clinical and forensic toxicology, it is important to be aware of the signs and symptoms related to xenobiotic exposure since they will assist clinicians to reach a useful and rapid diagnosis. This manuscript highlights and critically analyses clinical and forensic imaging related to ethanol abuse. Here, signs that may lead to suspected ethanol abuse, but that are not necessarily related to liver disease are thoroughly discussed regarding its underlying mechanisms. This includes flushing and disulfiram reactions, urticaria, palmar erythema, spider telangiectasias, porphyria cutanea tarda, "paper money skin", psoriasis, rhinophyma, Dupuytren's contracture, multiple symmetrical lipomatosis (lipomatosis Lanois-Bensaude, Madelung's disease), pancreatitis-related signs, black hairy tongue, gout, nail changes, fetal alcohol syndrome, seborrheic dermatitis, sialosis and cancer.
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PMID:Clinical and forensic signs related to ethanol abuse: a mechanistic approach. 2427 40

Isolated granulomatous noncaseating pancreatitis is a rare condition exceptionally described in human population. We demonstrate a case of the a 71-years-old female patient suffering from recent diabetes mellitus, generalized atherosclerosis and hypertension who died due to pulmonary embolism and terminal bronchopneumonia. Lipomatosis of pancreatic tissue was observed during the postmortem examination. Histological examination of pancreatic tissue discovered multiple small noncaseating epithelioid cell and giant cell granulomas, partly replacing the islets of Langerhans. To our knowledge, our case represents the first description of noninfectious granulomatous pancreatitis associated with acute manifested insulin-dependent diabetes mellitus.
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PMID:Granulomatous pancreatitis in a patient with acute manifested insulin-dependent diabetes mellitus. 2471 51

Genetic diseases associated with defects in primary cilia are classified as ciliopathies. Pancreatic lesions and ductal cysts are found in patients with ciliopathic polycystic kidney diseases suggesting a close connection between pancreatic defects and primary cilia. Here we investigate the role of two genes whose deletion is known to cause primary cilium defects, namely Hnf6 and Lkb1, in pancreatic ductal homeostasis. We find that mice with postnatal duct-specific deletion of Hnf6 or Lkb1 show duct dilations. Cells lining dilated ducts present shorter cilia with swollen tips, suggesting defective intraciliary transport. This is associated with signs of chronic pancreatitis, namely acinar-to-ductal metaplasia, acinar proliferation and apoptosis, presence of inflammatory infiltrates, fibrosis and lipomatosis. Our data reveal a tight association between ductal ciliary defects and pancreatitis with perturbed acinar homeostasis and differentiation. Such injuries can account for the increased risk to develop pancreatic cancer in Peutz-Jeghers patients who carry LKB1 loss-of-function mutations.
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PMID:Chronic pancreatitis and lipomatosis are associated with defective function of ciliary genes in pancreatic ductal cells. 2815 92

Mitochondrial disorders (MIDs) due to respiratory-chain defects or nonrespiratory chain defects are usually multisystem conditions [mitochondrial multiorgan disorder syndrome (MIMODS)] affecting the central nervous system (CNS), peripheral nervous system, eyes, ears, endocrine organs, heart, kidneys, bone marrow, lungs, arteries, and also the intestinal tract. Frequent gastrointestinal (GI) manifestations of MIDs include poor appetite, gastroesophageal sphincter dysfunction, constipation, dysphagia, vomiting, gastroparesis, GI pseudo-obstruction, diarrhea, or pancreatitis and hepatopathy. Rare GI manifestations of MIDs include dry mouth, paradontosis, tracheoesophageal fistula, stenosis of the duodeno-jejunal junction, atresia or imperforate anus, liver cysts, pancreas lipomatosis, pancreatic cysts, congenital stenosis or obstruction of the GI tract, recurrent bowel perforations with intra-abdominal abscesses, postprandial abdominal pain, diverticulosis, or pneumatosis coli. Diagnosing GI involvement in MIDs is not at variance from diagnosing GI disorders due to other causes. Treatment of mitochondrial GI disease includes noninvasive or invasive measures. Therapy is usually symptomatic. Only for myo-neuro-gastro-intestinal encephalopathy is a causal therapy with autologous stem-cell transplantation available. It is concluded that GI manifestations of MIDs are more widespread than so far anticipated and that they must be recognized as early as possible to initiate appropriate diagnostic work-up and avoid any mitochondrion-toxic treatment.
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PMID:Gastrointestinal manifestations of mitochondrial disorders: a systematic review. 2828 66


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