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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of probiotics (live viable microbial organisms) in the treatment of specific diseases has evolved into an extremely valuable option yet to be optimally used in clinical medicine. Probiotics have been shown to have immunomodulating properties and enhance the mucosal barrier. This review will briefly discuss the use of probiotics in inflammatory bowel disease, pancreatitis, liver transplantation, and various uses in diarrhea. When using probiotics, one must be cautious of the sometime overzealous claims that are commonly made when dealing with medical foods. As we begin to appreciate the degree of complexity that our indigenous microbial population has on health, it is only then that we can begin to understand the importance in disease. In the arena of probiotics, numerous fundamental questions remain unanswered.
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PMID:Probiotics: a practical review of their role in specific clinical scenarios. 1620 61

This review highlights areas of clinical research in gastroenterology and hepatology that were published during the last year and were summarized during the most recent American Gastroenterological Association Plenary Session. The topics include a comparison of the risk of recurrent bleeding in patients taking clopidogrel versus aspirin plus a proton pump inhibitor, the introduction of rifaximin for the treatment of traveler's diarrhea, and the results of an oral vaccine for cholera tested in a high endemic area where there is also a high prevalence of human immunodeficiency virus infection. In inflammatory bowel disease, the impact of a biomarker of inflammation, C-reactive protein, to the response to a new biologic therapy is identified as potentially important because it might facilitate the selection of patients for these treatments. Results of device, endoscopic, and surgical treatment of obesity are reviewed, including the evidence of significant impact of surgery-induced weight loss on comorbid diseases. In the field of cancer, colonoscopic screening results in more polyps detected, down-staging of cancers identified, and improved cancer survival. A new familial syndrome associated with a serrated adenoma/carcinoma phenotype and variability in microsatellite instability is described. A controlled study demonstrates that a urine-derived substance, ulinastatin, reduces the risk of post-endoscopic retrograde cholangiopancreatography pancreatitis. Hepatic stellate cells are involved in the fibrogenesis associated with nonalcoholic fatty liver disease. These areas of clinical research demonstrate the breadth of significant advances that will impact on the clinical practice of gastroenterology and hepatology.
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PMID:GIH clinical research update: 2004-2005. 1636 Oct 39

A clinically and pathologically distinct form of chronic pancreatitis is now widely recognized and has been designated variably as lymphoplasmacytic sclerosing pancreatitis, duct-destructive (duct-centric) pancreatitis or autoimmune pancreatitis. This entity is currently defined by a constellation of clinical and pathologic findings, including the lack of both conventional risk factors for pancreatitis, such as alcohol use and gallstones, and their hallmark pattern of injury, including calcifications and pseudocysts. Histologically, it is characterized by lymphoplasmacytic inflammation with abundant IgG4-positive plasma cells that exhibit an affinity for ducts as well as venules ("peri-venulitis," with or without frank vasculitis). Inflammation is often associated with sclerosis and expansion of periductal tissue. In some cases, fibroblastic activity is prominent and resembles "inflammatory pseudotumor" or is even misdiagnosed as "inflammatory myofibroblastic tumor." In what appears to be a distinct subset of this entity, intraepithelial granulocytic infiltrates may be seen. Well-developed examples are readily recognized; however, lesser ones may be difficult to distinguish from other forms of pancreatitis based on morphology alone. This type of pancreatitis is considered an autoimmune process. In about 15% to 20% of patients, the clinical stigmata of autoimmune conditions are present at the time of diagnosis, and in many others, discovered subsequently. The usual "lymphoplasmacytic sclerotic" type tends to be associated with Sjogren, whereas the "granulocytic" subset, with inflammatory bowel disease. Most patients present with a pancreatic head mass, often with an accompanying stricture of the distal common bile duct, which thus radiologically resembles "pancreas cancer." In fact, this entity accounts for more than a third of the cases of pseudotumoral pancreatitis (mass-forming inflammatory lesions that resemble carcinoma). Elevated serum IgG4 levels are characteristic and may be very helpful in the differential diagnosis from tumors and tumor-like lesions of the pancreas which seldom result in levels above 135 mg/dL. The mean age of the patients with this condition is in the mid-50s; the subset with granulocytic intraepithelial lesions seem to be younger (mid 40s). Despite the autoimmune association, males are afflicted as commonly as (if not more than) females. Following resection, emergence of new fibro-inflammatory lesions in the remaining pancreaticobiliary tree has been noted in some cases; however, the process typically responds to steroids. It is important to recognize the distinctive clinicopathologic features of this entity, so that it can be diagnosed accurately and managed appropriately.
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PMID:Diagnostic features and differential diagnosis of autoimmune pancreatitis. 1693 59

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 35-year-old female received right hemicolectomy for a poorly differentiated adenocarcinoma of the ascending colon with lymph node metastasis (1/28) in February 1997. CEA was 1.68 ng/microl prior to colectomy. Adjuvant chemotherapy with weekly 5-FU and leucovorin intravenously was started following surgery and discontinued after 17 doses in May 1997. She received bilateral salpingo-ophorecctomy for metastatic cancer in August 1999. Intravenous chemotherapy was resumed with weekly 5-FU and leucovorin intravenously in August 1999. CEA was 93.8 ng/microl in November 1999. Intravenous chemotherapy was discontinued after 20 doses and oral chemotherapy with futraful and leucovorin was started in January 2000. CEA was found to be 240.3 ng/microl in December 1999 and then elevated to 1521.3 ng/microl in June 2001, which was 10 months after resection of metastatic ovarian cancer. No metastatic lesions could be detected, however, with image studies. The CEA decreased to 396.6 ng/microl three months later. Futraful was switched to uracil-tegafur (UFUR) in September 2001. The CEA for the patient ranged from 68.5 to 298.9 ng/microl for the following 5 years without aggressive chemotherapy. No evidence of recurrence could be demonstrated by imaging studies. The patient is not a smoker and denied exposure to a smoking environment. She was also not known to have persistent infections, inflammatory bowel disease, pancreatitis, cirrhosis of the liver, or any benign tumors. The current case suggested that: (i) elevation of CEA is not necessarily well correlated with presence of metastatic colon cancer; (ii) some patients may live with elevated CEA for years without evidence of recurrence or metastasis; (iii) aggressive chemotherapy may not be necessary in patients with only elevated CEA.
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PMID:Unusual elevation of CEA in a patient with history of colon cancer. 1706 Apr 6

A 7-year-old, male, castrated, Labrador Retriever with a history of pancreatitis and inflammatory bowel disease presented for vomiting and anorexia. Serum biochemistry findings were indicative of cholestasis, hepatocellular insult, and decreased hepatic function. Ultrasound examination showed sediment and gas within the gallbladder, and a diagnosis of emphysematous cholecystitis was made. Emergency gallbladder resection was performed. Cytologic examination of bile fluid collected at surgery showed a mixed population of bacteria (bactibilia) together with fungal organisms consistent with Cyniclomyces guttulatus (previously known as Saccharomycopsis guttulatus). Similar fungal organisms were seen on a fecal smear. Bacteria cultured were normal gastrointestinal flora, supporting ascending infection; the fungal organisms were interpreted as incidental. Histopathology of the gallbladder indicated active (suppurative) and chronic (lymphocytic) cholecystitis and sections of liver tissue had evidence of chronic liver disease. A positive liver culture indicated concurrent bacterial hepatitis or cholangiohepatitis. Despite supportive care, the dog continued to decline and was euthanized 30 days later. Necropsy results confirmed end stage liver disease, but an initiating cause was not found. This case highlights the role of bactibilia in the development of acute cholecystitis and the unique cytologic appearance of C guttulatus as an incidental finding in bile fluid.
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PMID:Gallbladder aspirate from a dog. 1712 57

This review summarises clinical pharmacological aspects of thiopurines in the treatment of chronic inflammatory bowel disease (IBD). Current knowledge of pharmacogenetically guided dosing is discussed for individualisation of thiopurine therapy, particularly to avoid severe adverse effects. Both azathioprine and mercaptopurine are pro-drugs that undergo extensive metabolism. The catabolic enzyme thiopurine S-methyltransferase (TPMT) is polymorphically expressed, and currently 23 genetic variants have been described. On the basis of an excellent phenotype-genotype correlation for TPMT, genotyping has become a safe and reliable tool for determination of a patient's individual phenotype. Thiopurine-related adverse drug reactions are frequent, ranging from 5% up to 40%, in both a dose-dependent and -independent manner. IBD patients with low TPMT activity are at high risk of developing severe haematotoxicity if pharmacogenetically guided dosing is not performed. Based on several cost-benefit analyses, assessment of TPMT activity is recommended prior to thiopurine therapy in patients with IBD. The underlying mechanisms of azathioprine/mercaptopurine-related hepatotoxicity, pancreatitis and azathioprine intolerance are still unknown. Although the therapeutic response appears to be related to 6-thioguanine nucleotide (6-TGN) concentrations above a threshold of 230-260 pmol per 8 x 10(8) red blood cells, at present therapeutic drug monitoring of 6-TGN can be recommended only to estimate patients' compliance.Drug-drug interactions between azathioprine/mercaptopurine and aminosalicylates, diuretics, NSAIDs, warfarin and infliximab are discussed. The concomitant use of allopurinol without dosage adjustment of azathioprine/mercaptopurine leads to clinically relevant severe haematotoxicity due to elevated thiopurine levels. Several studies indicate that thiopurine therapy in IBD during pregnancy is safe. Thus, azathioprine/mercaptopurine should not be withdrawn in strictly indicated cases of pregnant IBD patients. However, breastfeeding is contraindicated during azathioprine/mercaptopurine therapy. Use of azathioprine/mercaptopurine for induction and maintenance of remission in corticosteroid-dependent or corticosteroid-refractory IBD, particularly Crohn's disease, is evidence based. To improve response rates in thiopurine therapy of IBD, comprehensive analyses including metabolic patterns and genome-wide profiling in patients with azathioprine/mercaptopurine treatment are required to identify novel candidate genes.
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PMID:Thiopurine treatment in inflammatory bowel disease: clinical pharmacology and implication of pharmacogenetically guided dosing. 1771 77

The gastrointestinal tract is the preferred route for nutritional support in hospitalized patients. Patients with a functioning gastrointestinal tract, including those with pancreatitis or inflammatory bowel disease and those receiving chemotherapy, should be fed enterally. Parenteral nutrition (PN) should be limited to patients with gastrointestinal failure, including those with short gut syndrome, high-output fistula, prolonged ileus, or bowel obstruction. PN is associated with numerous complications, most notably increased risk of serious infection. Emerging data suggest that immunologic complications of PN may result from hyperglycemia and use of n-6 polyunsaturated fatty acids. Safety may be improved with a low-calorie formula and ensuring tight glycemic control with an insulin protocol. A lipid emulsion containing fish oil, olive oil, or both should replace soybean-containing emulsions. Supplemental glutamine, 0.2 g/kg/d to 0.5 g/kg/d, has been shown to reduce the risk of infection and to improve glycemic control.
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PMID:Maximizing efficacy from parenteral nutrition in critical care: appropriate patient populations, supplemental parenteral nutrition, glucose control, parenteral glutamine, and alternative fat sources. 1788 85

Although turmeric (Curcuma longa; an Indian spice) has been described in Ayurveda, as a treatment for inflammatory diseases and is referred by different names in different cultures, the active principle called curcumin or diferuloylmethane, a yellow pigment present in turmeric (curry powder) has been shown to exhibit numerous activities. Extensive research over the last half century has revealed several important functions of curcumin. It binds to a variety of proteins and inhibits the activity of various kinases. By modulating the activation of various transcription factors, curcumin regulates the expression of inflammatory enzymes, cytokines, adhesion molecules, and cell survival proteins. Curcumin also downregulates cyclin D1, cyclin E and MDM2; and upregulates p21, p27, and p53. Various preclinical cell culture and animal studies suggest that curcumin has potential as an antiproliferative, anti-invasive, and antiangiogenic agent; as a mediator of chemoresistance and radioresistance; as a chemopreventive agent; and as a therapeutic agent in wound healing, diabetes, Alzheimer disease, Parkinson disease, cardiovascular disease, pulmonary disease, and arthritis. Pilot phase I clinical trials have shown curcumin to be safe even when consumed at a daily dose of 12g for 3 months. Other clinical trials suggest a potential therapeutic role for curcumin in diseases such as familial adenomatous polyposis, inflammatory bowel disease, ulcerative colitis, colon cancer, pancreatic cancer, hypercholesteremia, atherosclerosis, pancreatitis, psoriasis, chronic anterior uveitis and arthritis. Thus, curcumin, a spice once relegated to the kitchen shelf, has moved into the clinic and may prove to be "Curecumin".
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PMID:Curcumin as "Curecumin": from kitchen to clinic. 1790 May 36

At a workshop on primary sclerosing cholangitis (PSC) held during Digestive Disease Week - Japan 2003, 388 PSC cases in Japan were analyzed. Two peaks in the age distribution were also observed in this survey. Jaundice and itching, major symptoms in PSC patients included in the diagnostic criteria, were observed in only 28% and 16%, respectively. Alkaline phosphatase levels were less than twofold of the upper limit of the normal range in 35%. In this regard, the diagnostic criteria in 2003 from the Mayo Clinic, including cholestatic symptoms and two- to threefold increases in serum alkaline phosphatase, should be modified in Japan. Inflammatory bowel diseases were complicated in 37%, and autoimmune pancreatitis (AIP) in 7.2%. PSC cases with inflammatory bowel diseases were younger than the average, creating the firstpeak in age distribution, and have similar characteristics compared to patients with PSC in foreign countries. In addition, even after the exclusion of cases of sclerosing cholangitis complicated with AIP, the second peak in the age distribution was clearly evident. Recently, a concept of immunoglobulin G4-related sclerosing cholangitis has been postulated, which has a similar pathogenesis to AIP but without apparent pancreatic lesions. PSC patients without apparent involvement of the pancreas may be present in older patients and seem to be specific to Japan.
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PMID:Characteristics of primary sclerosing cholangitis in Japan. 1793 Dec 5


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