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  • 1
    Keywords: INHIBITOR ; Germany ; DISEASE ; RISK ; SITE ; GENE ; GENES ; PROTEIN ; ACTIVATION ; CLEAVAGE ; MUTATION ; genetics ; MUTATIONS ; Jun ; INDIVIDUALS ; heredity ; chronic pancreatitis ; RECOMBINANT ; pancreas ; VARIANT ; ENZYME ; pancreatic ; LOSSES ; odds ratio ; PROTECTS ; HEREDITARY PANCREATITIS ; HUMAN CATIONIC TRYPSINOGEN
    Abstract: Chronic pancreatitis is a common inflammatory disease of the pancreas. Mutations in the genes encoding cationic trypsinogen (PRSS1) 1 and the pancreatic secretory trypsin inhibitor (SPINK1) 2 are associated with chronic pancreatitis. Because increased proteolytic activity owing to mutated PRSS1 enhances the risk for chronic pancreatitis, mutations in the gene encoding anionic trypsinogen (PRSS2) may also predispose to disease. Here we analyzed PRSS2 in individuals with chronic pancreatitis and controls and found, to our surprise, that a variant of codon 191 (G191R) is overrepresented in control subjects: G191R was present in 220/6,459 (3.4%) controls but in only 32/2,466 (1.3%) affected individuals (odds ratio 0.37; P = 1.1 x 10(-8)). Upon activation by enterokinase or trypsin, purified recombinant G191R protein showed a complete loss of trypsin activity owing to the introduction of a new tryptic cleavage site that renders the enzyme hypersensitive to autocatalytic proteolysis. In conclusion, the G191R variant of PRSS2 mitigates intrapancreatic trypsin activity and thereby protects against chronic pancreatitis
    Type of Publication: Journal article published
    PubMed ID: 16699518
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  • 2
    Keywords: CELL ; DISEASE ; liver ; NEW-YORK ; GENE ; VARIANTS ; genetics ; DEGRADATION ; REPLICATION ; INDIVIDUALS ; HEALTHY ; heredity ; chronic pancreatitis ; pancreas ; VARIANT ; secretion ; PANCREATITIS ; ENZYME ; analysis ; USA ; LIVER-DISEASE ; HEREDITARY PANCREATITIS ; MISSENSE MUTATIONS ; FUNCTIONAL-ANALYSIS ; RATIO ; Replication studies ; CATIONIC TRYPSINOGEN GENE ; INHIBITOR GENE ; PRSS1 ; TROPICAL CALCIFIC PANCREATITIS
    Abstract: Chronic pancreatitis is a persistent inflammatory disease of the pancreas, in which the digestive protease trypsin has a fundamental pathogenetic role. Here we have analyzed the gene encoding the trypsin-degrading enzyme chymotrypsin C (CTRC) in German subjects with idiopathic or hereditary chronic pancreatitis. Two alterations in this gene, p.R254W and p.K247_R254del, were significantly overrepresented in the pancreatitis group, being present in 30 of 901 (3.3%) affected individuals but only 21 of 2,804 (0.7%) controls ( odds ratio (OR)=4.6; confidence interval (CI)=2.6 - 8.0; P=1.3x10(-7)). A replication study identified these two variants in 10 of 348 (2.9%) individuals with alcoholic chronic pancreatitis but only 3 of 432 ( 0.7%) subjects with alcoholic liver disease (OR=4.2; CI=1.2 - 15.5; P=0.02). CTRC variants were also found in 10 of 71 (14.1%) Indian subjects with tropical pancreatitis but only 1 of 84 (1.2%) healthy controls (OR=13.6; CI=1.7 - 109.2; P=0.0028). Functional analysis of the CTRC variants showed impaired activity and/or reduced secretion. The results indicate that loss-of-function alterations in CTRC predispose to pancreatitis by diminishing its protective trypsin-degrading activity
    Type of Publication: Journal article published
    PubMed ID: 18059268
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  • 3
    Keywords: Germany ; CLASSIFICATION ; DISEASE ; liver ; RISK ; GENE ; METABOLISM ; ACCUMULATION ; PATIENT ; FREQUENCY ; polymorphism ; SUSCEPTIBILITY ; VARIANTS ; FREQUENCIES ; NO ; DIFFERENCE ; genetics ; HETEROZYGOSITY ; PATHOGENESIS ; GENOTYPES ; HEREDITARY ; LENGTH ; adenocarcinoma ; pathology ; DIABETES-MELLITUS ; PREVALENCE ; heredity ; chronic pancreatitis ; MELLITUS ; pancreas ; VARIANT ; INCREASE ; PANCREATITIS ; HEREDITARY HEMOCHROMATOSIS ; IRON ; analysis ; methods ; pancreatic ; pancreatic adenocarcinoma ; GENOTYPE ; USA ; RISK-FACTOR ; FRAGMENT ; Diabetes Mellitus ; genetic analysis ; CHRONIC-PANCREATITIS ; acute pancreatitis ; ALCOHOLIC LIVER-DISEASE ; C282Y ; CYS282TYR MUTATION ; CYSTIC-FIBROSIS GENE ; H63D MUTATIONS ; hemochromatosis ; HFE ; IRON-OVERLOAD ; melting ; NONALCOHOLIC STEATOHEPATITIS
    Abstract: Purpose: The homozygous p.C282Y variant of the HFE gene is a major risk factor for hereditary hemochromatosis, a disorder of iron metabolism resulting in progressive iron accumulation in a variety of organs including the pancreas. Heterozygosity of p.C282Y and p.H63D may increase susceptibility to chronic liver and pancreatic disease. This study determines the frequencies of p.C282Y and p.H63D alterations in patients with chronic pancreatitis and pancreatic adenocarcinoma. Methods: In total, 958 patients (349 with alcoholic pancreatitis, 343 with idiopathic pancreatitis, 64 with familial chronic pancreatitis, 34 with acute pancreatitis, and 168 with pancreatic adenocarcinoma) were enrolled and compared with 681 healthy and 100 alcoholic controls. Furthermore, 45 parent-offspring trios were included for segregation analysis. Genotyping of p.C282Y and p.H63D was performed by restriction fragment length polymorphism or melting curve analyses. Results: No significant differences were found in heterozygosity for p.C282Y and p.H63D when patients with alcoholic (8.0/21.5%), idiopathic (7.3/24.5%), or familial (9.8/ 23.0%) pancreatitis, or pancreatic adenocarcinoma (5.4/28.6%) were compared with healthy (6.2/24.8%) and alcoholic (7.0/25.0%) controls. Neither genotype was associated with the presence of secondary diabetes mellitus in patients with chronic pancreatitis. Conclusion: Although hemochromatosis is associated with pancreatic pathology, the p.C282Y and p.H63D variants do not play a significant role in the pathogenesis of chronic pancreatitis or pancreatic adenocarcinoma
    Type of Publication: Journal article published
    PubMed ID: 17666895
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  • 4
    Publication Date: 2009-11-18
    Description: The main role of carbohydrates in the human body is to provide energy. Carbohydrates should always be infused with PN (parenteral nutrition) in combination with amino acids and lipid emulsions to improve nitrogen balance. Glucose should be provided as a standard carbohydrate for PN, whereas the use of xylite is not generally recommended. Fructose solutions should not be used for PN. Approximately 60% of non-protein energy should be supplied as glucose with an intake of 3.0-3.5 g/kg body weight/day (2.1-2.4 mg/kg body weight/min). In patients with a high risk of hyperglycaemia (critically ill, diabetes, sepsis, or steroid therapy) an lower initial carbohydrate infusion rate of 1-2 g/kg body weight/day is recommended to achieve normoglycaemia. One should aim at reaching a blood glucose level of 80-110 mg/dL, and at least a glucose level 〈145 mg/dL should be achieved to reduce morbidity and mortality. Hyperglycaemia may require addition of an insulin infusion or a reduction (2.0-3.0 g/kg body weight/day) or even a temporary i〈TextGroup〉 nte 〈/TextGroup〉rruption of glucose infusion. Close monitoring of blood glucose levels is highly important.
    Description: Die wichtigste Rolle der Kohlenhydratzufuhr bei parenteraler Ernährung (PE) ist die Bereitstellung von Energie. Bei jeder PE sollten Kohlenhydrate infundiert werden, zur Verbesserung der Stickstoffbilanz möglichst gemeinsam mit Aminosäuren und Fettemulsionen. Während Glukose als Standardkohlenhydratlösung eingesetzt wird, kann der Zuckeraustauschstoff Xylit nicht generell empfohlen werden. Fruktoselösungen sollten keine Verwendung in der PE finden. In der Regel sollten etwa 60% der Nichteiweiß-Energie als Kohlenhydrate zugeführt werden mit einer Zufuhrrate von 3,0-3,5 g/kg KG/Tag (2,1-2,4 mg/kg KG/min). Patienten mit einem hohem Hyperglykämierisiko (kritisch Kranke, Diabetes, Sepsis, Steroidtherapie) sollten eine niedrigere initiale Kohlenhydratzufuhrrate von 1-2 g/kg KG/Tag erhalten. Die Einhaltung einer Normoglykämie ist anzustreben. Der Zielbereich für die Blutglukosespiegel ist 80-110 mg/dl, aber zumindest sollten Werte unter 145 mg/dl erreicht werden um Morbidität und Mortalität zu verminderen. Eine Hyperglykämie kann eine Insulingabe und eine Reduktion der Kohlenhydratzufuhr mit der PE auf 2-3 g/kg KG/Tag oder auch eine zeitweilige Unterbrechung der Kohlenhydratinfusion erfordern. Engmaschige Blutzuckerkontrollen sind unbedingt erforderlich.
    Keywords: glucose ; fructose ; non-protein calories ; hyperglycaemia ; insulin ; Glukose ; Fruktose ; Nicht-Eiweiß-Kalorien ; Hyperglykämie ; Insulin ; ddc: 610
    Language: English
    Type: article
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  • 5
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  67. Jahrestagung der Norddeutschen Gesellschaft für Kinder- und Jugendmedizin (NDGKJ); 20180413-20180414; Bremen; DOC18ndgkj25 /20180412/
    Publication Date: 2018-04-13
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 6
    ISSN: 1432-1041
    Keywords: Key Words HIV infection ; Ketotifen; nutritional status ; Tumor Necrosis Factor alpha ; Tumor Necrosis Factor Receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: Tumor necrosis factor alpha (TNF-α) is involved in the genesis of HIV-associated malnutrition. We performed an open-label trial on the effects of ketotifen, an in vitro inhibitor of TNF-α release from peripheral blood mononuclear cells (PBMCs), on the nutritional status and TNF-α release of HIV-infected subjects. Patients: Six HIV-infected subjects received oral ketotifen 4 mg per day for 84 days and were followed up for an additional 70-day period. Body composition was measured by bioelectrical impedance analysis. TNF-α plasma levels, TNF-α release from PBMCs, and plasma concentration of soluble TNF receptors were measured repeatedly during the study and control period. Results: During ketotifen intake, TNF-α release from stimulated PBMCs significantly decreased (68 vs 155 pg ml−1), but not TNF-α and soluble TNF receptor plasma concentrations. Subjects gained weight (+ 2.7 kg), whereas weight loss was observed after cessation of treatment (−1.6 kg). Conclusion: Ketotifen inhibits TNF-α release from stimulated PBMCs and might thus be useful in the management of HIV-associated malnutrition.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Mutations within the NOD2/CARD15 gene have recently been shown to be associated with Crohn's disease.Aims : To investigate the clinical impact of the three common NOD2/CARD15 mutations in patients with Crohn's disease.Methods : We investigated the prevalence of the three common NOD2/CARD15 mutations (Arg702Trp, Gly908Arg, 3020insC) in 180 patients with Crohn's disease, 70 patients with ulcerative colitis and 97 controls. In patients with Crohn's disease, prevalence of NOD2/CARD15 mutations were correlated to clinical and demographical parameters.Results : In Crohn's disease patients, 35.6% carried at least one mutant allele of NOD2/CARD15 mutations compared with 14.3% of patients with ulcerative colitis (P = 0.006) and to 15.5% of controls (P = 0.0001). Genotype phenotype analyses revealed that NOD2/CARD15 mutations determined younger age at disease diagnosis (P = 0.03), ileal disease location (P = 0.01) and ileocecal resections (P = 0.0002). Interestingly, reoperation with resection of the anastomosis was significantly more frequent in patients with NOD2/CARD15 mutations (P = 0.01).Conclusions : Our investigations support the current hypothesis that NOD2/CARD15 mutations are associated with a phenotype of Crohn's disease with younger age at diagnosis, ileal involvement, ileocecal resections and a high risk of postoperative relapse and reoperation. NOD2/CARD15 mutations might therefore be used to identify high risk patients for relapse prevention strategies.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In patients with gastrointestinal malignancies, i.e. cancers of the stomach, colon, liver, biliary tract or pancreas, progressive undernutrition can be regularly observed during the course of illness. Undernutrition significantly affects the patients’ quality of life, morbidity and survival.Pathogenetically, two different causes are relevant in the development of undernutrition in patients with gastrointestinal cancer. One cause is reduced nutritional intake. This condition is referred to as anorexia and can be worsened by the side effects of cancer therapy. The other cause is the release of endogenous transmitters and/or other products of the tumour leading to the cachexia syndrome, which is characterized by loss of body weight, negative nitrogen balance and fatigue. Cancer anorexia and cancer cachexia may have synergistic negative effects in affecting the patients’ status.In this review, current nutritional support strategies with respect to different clinically relevant situations are described. An algorithm of the treatment strategies, including dietetic counselling, oral supplements, enteral and parenteral nutritional support is given. One focus is the approach of nutrition-focused patient care, which shows promising results. In addition, the possibilities of pharmacological intervention are discussed.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1440
    Keywords: Malnutrition ; HIV-infection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Study objective: To determine forms of malnutrition and basal metabolism at different stages of immunological impairment in clinically stable patients infected with Human Immunodeficiency Virus (HIV).Design: Cross sectional study.Setting: 53 outpatients with HIV-infection classified according to the Walter Reed staging system (WR1 to WR6).Measurements and main results: 87% of the patients showed some evidence of malnutrition. Reduced body weight was found in 53%, 68% and 25% had decreases in fat and body cell mass, 17% had visceral protein deficiency, whereas extracellular mass and serum triglyceride concentrations were increased in 58% and 30%, respectively. Reduced serum albumin and transferrin closely paralleled immunological depression, whereas alterations in body composition were manifest early during HIV-infection (WR3) and remained unchanged during the transition to the Acquired Immune Deficiency Syndrome itself. Resting metabolic rate increased from WR1 to WR3; it remained within the expected range during later stages (WR4-WR6), but was not appropriately reduced in response to the loss in body cell mass.Conclusions: HIV-infected patients display both, calorie and protein malnutrition. Immunological depression was independent of loss of body mass, but was closely associated to decreases in serum albumin values. Nutritional assessment and intervention should therefore be performed at an early stage of HIV-infection.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Enterale Ernährung middot; Sondenkost ; Parenterale Ernährung ; Immunonutrition ; Sepsis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zum Thema Die künstliche Ernährung in der Intensivmedizin ist als eine “Ersatzmaßnahme” bei unzureichender bzw. nicht durchführbarer oraler Kostzufuhr zu verstehen. Sie erlaubt eine Sicherstellung der Substratzufuhr bei passagerer oder auch dauerhafter Unterbrechung der oralen Ernährungszufuhr durch Beatmung und Sedierung oder durch Erkrankungen, die mit Bewusstseinsstörung, Schluckbeschwerden oder Malabsorption einhergehen. Gerade im Bereich der Intensivmedizin nimmt die künstliche Ernährung eine prognostisch wichtige, in ihrer vollen Bedeutung nicht immer beachtete Stellung ein, die durch Zufuhr immunmodulatorischer Zusätze auch primärtherapeutische Bedeutung erlangen könnte. Bei der künstlichen Ernährung wird zwischen enteraler und par-enteraler Ernährung unterschieden. Der vorliegende Beitrag gibt einen Überblick über die Chancen und Probleme beider Formen der künstlichen Ernährung im Bereich der internistischen Intensivmedizin.
    Type of Medium: Electronic Resource
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