Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aims of initial diagnostic procedures leading to early treatment in an appropriate setting in acute pancreatitis are: initial diagnosis and differential diagnosis, assessment of etiology and assessment of prognosis. Etiology can be assessed with certainty only by endoscopic retrograde cholangiopancreaticography. This method allows us to differentiate between pancreatic duct abnormalities as seen in so-called alcoholic pancreatitis as an exacerbation of chronic pancreatitis and biliary causes of the disease. Contrast-guided computed tomography is useful for detecting necroses and their infection. As in other inflammatory diseases, the prognosis in acute pancreatitis seems to be determined by mediators leading to "whole body inflammation", confirmed by high concentrations of interleukin-8 as a major attractant of neutrophils, by interleukin-6 preceding high levels of CRP, as well as by leukocyte immigration into the pancreas. Besides these determinants of the course of acute pancreatitis the prognosis can be assessed by simple clinical means. A clinical score based on physical examination seems to be the best standard for assessing prognosis. Measurement of PMN-elastases and CRP may be additionally helpful.
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PMID:Diagnostic approach to acute pancreatitis: diagnosis, assessment of etiology and prognosis. 811 37

Pancreatitis is a common and potentially lethal necro-inflammatory disease with both acute and chronic manifestations. Current evidence suggests that the accumulated damage incurred during repeated bouts of acute pancreatitis (AP) can lead to chronic disease, which is associated with an increased risk of pancreatic cancer. While parathyroid hormone-related protein (PTHrP) exerts multiple effects in normal physiology and disease states, its function in pancreatitis has not been previously addressed. Here we show that PTHrP levels are transiently elevated in a mouse model of cerulein-induced AP. Treatment with alcohol, a risk factor for both AP and chronic pancreatitis (CP), also increases PTHrP levels. These effects of cerulein and ethanol are evident in isolated primary acinar and stellate cells, as well as in the immortalized acinar and stellate cell lines AR42J and irPSCc3, respectively. Ethanol sensitizes acinar and stellate cells to the PTHrP-modulating effects of cerulein. Treatment of acinar cells with PTHrP (1-36) increases expression of the inflammatory mediators interleukin-6 (IL-6) and intracellular adhesion protein (ICAM-1), suggesting a potential autocrine loop. PTHrP also increases apoptosis in AR42J cells. Stellate cells mediate the fibrogenic response associated with pancreatitis; PTHrP (1-36) increases procollagen I and fibronectin mRNA levels in both primary and immortalized stellate cells. The effects of cerulein and ethanol on levels of IL-6 and procollagen I are suppressed by the PTH1R antagonist, PTHrP (7-34). Together these studies identify PTHrP as a potential mediator of the inflammatory and fibrogenic responses associated with alcoholic pancreatitis.
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PMID:Role of parathyroid hormone-related protein in the pro-inflammatory and pro-fibrogenic response associated with acute pancreatitis. 2228 Aug