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)

Inflammatory bowel disease, a chronic condition of the intestine, is associated with numerous extraintestinal manifestations, including pancreatitis. This study investigated the effect of octreotide administration on oxidative damage in a rat model of colitis induced by 2,4,6-trini-trobenzene sulfonic (TNBS) acid. Colonic and pancreatic malondialdehyde and glutathione levels are indicators of oxidative damage, and TNBS-induced colitis significantly increased the colonic and pancreatic malondialdehyde levels and decreased glutathione levels. Octreotide treatment was associated with decreased malondialdehyde levels and increased glutathione levels in the colonic and pancreatic tissue. The colonic mucosal structure was preserved and pancreatic inflammation decreased in rats treated with octreotide. Octreotide also significantly decreased nuclear factor-kB expression by immunohisto-chemistry in the colonic and pancreatic tissue compared with TNBS-induced colitis group. Octreotide appears to have protective effects against TNBS-induced colonic and pancreatic damage. These results imply the reduction in mucosal damage owing to the anti-inflammatory and antioxidant effects of octreotide.
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PMID:The effect of octreotide on pancreatic damage in TNBS-induced colitis. 1701 50

A 43-year-old man with chronic alcohol pancreatitis was admitted in our intensive care unit for an haemorrhagic shock. An abdominal CT-scan performed on admission showed bleeding from a vessel in a pancreatic pseudocyst. Initial treatment included intravenous fluids, transfusion, mechanical ventilation and vasopressive support. Percutaneous arterial embolization (PAE) of a bleeding right superior colon artery was performed with an initial good result. Nevertheless after initial clinical improvement, hypotension refractory to fluid management occurred. An abdominal CT-scan disclosed pneumatosis in right colon. A right hemicolectomy was performed. Histologic analysis confirmed ischemic colitis. The patient recovered and was discharged from the intensive care unit. Colitis necrosis after PAE for pancreatic pseudoaneurysm had never been described before. It should be suspected when haemodynamic instability occurs following PAE.
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PMID:[Colonic necrosis following a pancreatic pseudocyst embolization]. 1717 20

Scurfy mice which lacks functional Foxp3 transcription factor and CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells, spontaneously develop autoimmune responses against skin, lung, liver and tail. However, many organs/tissues are spared from autoimmune attack. Here, we demonstrate that scurfy mice contain dormant autoimmune T cells that induced new diseases such as sialoadenitis, dacryoadenitis, pancreatitis, gastritis, intestinal inflammation, colitis, and myositis in RAG-1 KO mice. Inflammation in as many as 12 organs/tissues was consistently induced in individual recipients with scurfy lymph node cells containing as few as 1.25 x 10(6) CD4(+) T cells. Moreover, transfer of the multiple organ autoimmune diseases could be suppressed by as little as 0.5 x 10(6) CD4(+)CD25(+) Treg cells, mediated by inhibiting autoimmune T-cell expansion. Our study provides evidence for the presence of a large repertoire of autoimmune lymphocytes against various organs/tissues in scurfy mice as well as Treg cells in B6 mice capable of suppressing the expansion of these autoimmune lymphocytes. Various conditions that control the expression of autoimmune T cells are discussed.
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PMID:Large functional repertoire of regulatory T-cell suppressible autoimmune T cells in scurfy mice. 1752 82

A 37-year-old male presented with intermittent abdominal pain and 9 kg weight loss within 3 weeks. Gastroscopy showed no pathological findings, coloscopy showed a colitis limited to the left flexure. Histology revealed a sustained infectious enterocolitis. A culture of the patient's stool was positive for CAMPYLOBACTER COLI. Because of the recurrent abdominal discomfort and weight loss the patient was admitted to the hospital. Ultrasound and multislice spiral computed tomography showed an acute oedematous pancreatitis. No other causes for the pancreatitis were found, the only remaining possibility was a CAMPYLOBACTER COLI-associated pancreatitis. Under symptomatic therapy the patient recovered definitively. An administration of antibiotics was not necessary.
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PMID:[Acute pancreatitis - association with a Campylobacter coli-infection]. 1787 59

Drug-induced pancreatitis injury due to celecoxib, a first generation Cox-2 inhibitor, has been rarely reported. We describe one case of severe pancreatitis after treatment with celecoxib for 3 months in a woman. No aetiology has been found for pancreatitis. The role of celecoxib in the etiology of colitis was considered probable. This report and a few other cases in the literature suggest to seek a pancreatitis in the event of pains abdominal when there is a catch of the cyclooxygenase-2 selective non-steroidal anti-inflammatory drug inhibitor.
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PMID:[Acute pancreatitis after treatment by celecoxib]. 1792 65

Melatonin (MT), an indole formed enzymatically from L-trytophan (Trp), was first discovered in the bovine pineal gland in 1958 by Lerner et al. Melatonin is the most versatile and ubiquitous hormonal molecule produced not only in the pineal gland but also in various other tissues of invertebrates and vertebrates, particularly in the gastrointestinal tract (GIT). This review focuses on the localization, production, metabolism and the functions of MT in GIT and the duodenal unit (liver, biliary routes and pancreas), where multi-step biosynthetic pathways of this indole, similar to those in pinealocytes, have been identified. These biosynthetic steps of MT, including two major rate limiting enzymes; arylalkylamine-N-acetyltransferase (AA-NAT) and hydroxyindole-O-methyltransferase (HIOMT), transforming L-tryptophan (Trp), originally identified in pinealocytes, have been also detected in entero-endocrine (EE) cells of GIT, where this indole appears to act in endocrine, paracrine and/or luminal pathway directly or through G-protein coupled MT receptors. Studies of the distribution of MT in GIT mucosa showed that this indole is generated in GIT in much larger amounts than it is produced in the pineal gland. Melatonin acts in GIT, partly locally in paracrine fashion and is partly released into portal circulation, to be taken up by the liver. It is then metabolized and excreted with the bile to small bowel and finally returns to liver through entero-hepatic circulation. The production of MT by the pineal gland shows circadian rhythm with high night-time surge, especially at younger age, followed by the fall during the day-light time. As a highly lipophylic substance, MT reaches all body cells within minutes, thus, serving as a convenient circadian timing signal. Following pinealectomy, the light/dark cycle of plasma MT levels disappears, while its day-time blood concentration is maintained mainly due to its release from the GIT. According to our experience, after oral application of Trp, the plasma MT increases in dose-dependent manner both in intact and pinealectomized animals and humans, indicating that GIT but not the pineal gland is a source of this indole. In GIT MT exhibits a wide spectrum of activities such as circadian entrainment, antioxidant and free radicals scavenging activity, Melatonin (MT), an indole formed enzymatically from L-trytophan (Trp), was first discovered in the bovine pineal gland in 1958 by Lerner et al. Melatonin is the most versatile and ubiquitous hormonal molecule produced not only in the pineal gland but also in various other tissues of invertebrates and vertebrates, particularly in the gastrointestinal tract (GIT). This review focuses on the localization, production, metabolism and the functions of MT in GIT and the duodenal unit (liver, biliary routes and pancreas), where multi-step biosynthetic pathways of this indole, similar to those in pinealocytes, have been identified. These biosynthetic steps of MT, including two major rate limiting enzymes; arylalkylamine-N-acetyltransferase (AA-NAT) and hydroxyindole-O-methyltransferase (HIOMT), transforming L-tryptophan (Trp), originally identified in pinealocytes, have been also detected in entero-endocrine (EE) cells of GIT, where this indole appears to act in endocrine, paracrine and/or luminal pathway directly or through G-protein coupled MT receptors. Studies of the distribution of MT in GIT mucosa showed that this indole is generated in GIT in much larger amounts than it is produced in the pineal gland. Melatonin acts in GIT, partly locally in paracrine fashion and is partly released into portal circulation, to be taken up by the liver. It is then metabolized and excreted with the bile to small bowel and finally returns to liver through entero-hepatic circulation. The production of MT by the pineal gland shows circadian rhythm with high night-time surge, especially at younger age, followed by the fall during the day-light time. As a highly lipophylic substance, MT reaches all body cells within minutes, thus, serving as a convenient circadian timing signal. Following pinealectomy, the light/dark cycle of plasma MT levels disappears, while its day-time blood concentration is maintained mainly due to its release from the GIT. According to our experience, after oral application of Trp, the plasma MT increases in dose-dependent manner both in intact and pinealectomized animals and humans, indicating that GIT but not the pineal gland is a source of this indole. In GIT MT exhibits a wide spectrum of activities such as circadian entrainment, antioxidant and free radicals scavenging activity, cytoprotective, anti-inflammatory and healing efficacy of various GIT lesions such as esophagitis, gastritis, peptic ulcer, pancreatitis and colitis. This review concentrates on the generation and pathophysiological implication of MT in GIT and related organs.
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PMID:Localization and biological activities of melatonin in intact and diseased gastrointestinal tract (GIT). 1792 38

We report a case of autoimmune pancreatitis (AIP) with cholangiography and histopathology showing features characteristic of primary sclerosing cholangitis (PSC) and colitis. A 55-year-old previously-healthy man was diagnosed with anti-nuclear antibody (ANA)-positive AIP according to the finding of serum biochemistry, abdominal US (ultrasonography), CT (computed tomography) and ERCP (endoscopic retrograde cholangiopancreatography). However, bead-like strictures of intrahepatic bile ducts were also found and liver tissue showed onion skin-like periductal fibrosis but no anti-IgG4-positive cells. In addition, colon fiberscopy showed a pancolitis similar to ulcerative colitis indicating that, in this case, there may be an association with PSC. Here, we report a rare case of IgG4-negative AIP with sclerosing cholangitis and colitis with many clinical features that support an association with PSC.
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PMID:IgG4-negative autoimmune pancreatitis with sclerosing cholangitis and colitis: possible association with primary sclerosing cholangitis? 1848 May 79

After the discovery of melatonin in the pineal gland by Lerner and co-workers in 1958, melatonin was also detected in the retina and the human appendix. Later, melatonin was confirmed immunohistologically in all segments of the gastrointestinal tract (GIT), in the guts of bovine embryos and in the GIT of low vertebrates. Melatonin was also confirmed in the pancreas and the hepatobiliary system. Melatonin is produced in the enteroendocrine cells of the GIT mucosa. The concentrations of melatonin in the GIT are 10-100x higher than in the plasma and the total amount of melatonin in the GIT is around 400x higher than the amount of melatonin in the pineal gland. Similar to pineal melatonin, GIT melatonin is a multifunctional compound which exhibits some general as well as some specific effects, depending on the organ and the location of GIT tissue. In the GIT, melatonin exhibits endocrine, paracrine, autocrine and luminal actions. Generally, the episodic secretion of melatonin from the GIT is related to the intake and digestion of food and to the prevention of tissue damage caused by hydrochloric acid and digestive enzymes. Some actions, such as the scavenging of hydroxyl free radicals, immunoenhancement and antioxidant effects are of general nature, whereas others, such as an increase of mucosal blood flow, the reduction of peristalsis and the regulation of fecal water content, are specific to the tubular GIT. Generally, melatonin actions oppose those of serotonin. Laboratory and clinical studies indicate that the utilization of melatonin can prevent or treat pathological conditions such as esophageal and gastric ulcers, pancreatitis, colitis, irritable bowel disease, and colon cancer.
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PMID:Thirty four years since the discovery of gastrointestinal melatonin. 1881 27

Gastrointestinal complications are common in patients undergoing various forms of cancer treatment, including chemotherapy, radiation therapy, and molecular-targeted therapies. Many of these complications are life-threatening and require prompt diagnosis and treatment. Complications of oncologic therapy can occur in the esophagus (esophagitis, strictures, bacterial, viral and fungal infections), upper gastrointestinal tract (mucositis, bleeding, nausea and vomiting), colon (diarrhea, graft-versus-host disease, colitis and constipation), liver (drug hepatotoxicity and graft-versus-host disease), and pancreas (pancreatitis). Treatment of the different gastrointestinal complications should be tailored to the individual patient and based on the underlying pathophysiology of the complication.
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PMID:Gastrointestinal complications of oncologic therapy. 1894 34

Recent studies have demonstrated that cytokine levels and inflammation can be regulated by specifically augmenting cholinergic signaling via the efferent vagus nerve and the alpha7 subunit-containing nicotinic acetylcholine receptor (alpha7nAChR). Cholinergic modalities, acting through vagus nerve- and/or alpha7nAChR-mediated mechanisms have been shown to suppress excessive inflammation in several experimental models of disease, including endotoxemic shock, sepsis, ischemia-reperfusion injury, hemorrhagic shock, colitis, postoperative ileus and pancreatitis. These studies have advanced the current understanding of the mechanisms regulating inflammation. They have also provided a rationale for exploring new possibilities to treat excessive, disease-underlying inflammation by applying selective cholinergic modalities in preclinical and clinical settings. An overview of this research is presented here.
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PMID:Cholinergic modulation of inflammation. 1907 59


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