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Cytokines acute pancreatitis

D4. DeBeaux, A. C., Ross, J. A., and Maingay, J. P., Proinllammatory cytokine release by peripheral blood mononuclear cells from patients with acute pancreatitis. Br. J. Surg. 83, 1071-1075... [Pg.72]

M8. McKay, J., Gallagher, G., Imrie, C. W., and Baxter, J. N., Increased monocyte cytokine production in association with systemic complications in acute pancreatitis. Br. J. Surg. 83, 919—923 (1996). [Pg.77]

Simovic, M. O., Bonham, M. J., Abu-Zidan, F. M., and Windsor, J. A., Anti-inflammatory cytokine response and clinical outcome in acute pancreatitis. Crit. Care. Med. 27, 2662-2665... [Pg.80]

Stoelben, E., Nagel, M., Ockert, D., Scheibenbogen, C., Klein, B., and Saeger, H. D., Clinical significance of cytokines IL-6, IL-8 and C-reactive protein in serum of patients with acute pancreatitis. Chirurg 67,1231 (1996). [Pg.80]

This volume continues our objective of expanding the intellectual horizon of clinical chemistry. Included are chapters on Clinical Applications of Cytokine Assays Diagnosis and Treatment of Acute Pancreatitis Mitochondrial Mutations and Mitochondrial Diseases Pathobiochemistry of Nephrotic Syndrome Total Antioxidant Capacity Autoantibodies to dsDNA, Ro/SSA, and LaSSB in Systemic Lupus Erythematosis and Lymphoid Malignancies and Immunosuppressive Analysis. The meld of analytical, anatomical, subcellular, and molecular sciences represented by these subjects will continue to evolve and expand. Clinical chemistry is a vibrant and vital profession. Future volumes, their editors, and their contributors will undoubtedly be an important part of the practice and science of clinical chemistry. [Pg.379]

Acute pancreatitis occnrs from antodigestion of the acinar cells by inappropriate activation of the pancreatic enzymes (especially trypsinogen) within the ceU, leading to ceUnlar injnry mediated by proinflammatory cytokines. [Pg.176]

Denham W, Fink G, Yang J, Ulrich P, Tracey K, Norman J. Small molecule inhibition of tumor necrosis factor gene processing during acute pancreatitis prevents cytokine cascade progression and attenuates pancreatitis severity. Am Surg 1997 63(12) 1045-9 discussion 9-50. [Pg.646]

Laboratory testresults vary depending on the severity of the inflammatory process, whether damage is confined to the pancreas or involves contiguous organs, and the time course from the onset of the acute attack (see Table 39-3). Serum concentrations of prointlammatory cytokines such as tumor necrosis factor-a and interleukin-6 are markers of disease severity, but elevations are not specific for pancreatitis and the tests are not widely available. ... [Pg.725]

Riche FD, Cholley BO, Laisne MJC, et al. Inflammatory cytokines, C reactive protein, and procalcitonin as early predictors of necrosis infection in acute necrotizing pancreatitis. Surgery 2003 133 257-262. [Pg.735]


See other pages where Cytokines acute pancreatitis is mentioned: [Pg.1188]    [Pg.50]    [Pg.51]    [Pg.58]    [Pg.72]    [Pg.78]    [Pg.659]    [Pg.17]    [Pg.38]    [Pg.39]    [Pg.377]    [Pg.324]    [Pg.625]    [Pg.55]    [Pg.34]    [Pg.173]    [Pg.510]    [Pg.551]    [Pg.174]    [Pg.173]    [Pg.49]    [Pg.250]    [Pg.3222]   
See also in sourсe #XX -- [ Pg.50 , Pg.58 , Pg.59 , Pg.60 ]




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Pancreatitis, acute

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