Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The therapeutic effects of loxiglumide on human acute pancreatitis was investigated in 104 Japanese institutes from October 1992 to March 1994. Acute pancreatitis was diagnosed by the Japanese Criteria of Acute Pancreatitis. Soon after the diagnosis was made, one of three doses of loxiglumide (100, 300 and 500 mg/day) were injected intravenously twice a day for 14 days. The efficacy of the treatment was evaluated by clinical signs, physical signs, and biochemical findings. 189 patients were included in this trial. The clinical signs, such as abdominal pain, disappeared in 20% of the patients on the 1st day after treatment, and the rate of improvements increased thereafter. Physical signs also improved. Serum amylase levels returned to normal within 3 days after treatment, and serum lipase showed almost the same changes as serum amylase levels, but serum lipase levels in the high-dose group (500 mg/day) returned to normal more quickly compared with the other two doses. It is concluded that the cholecystokinin A receptor antagonist, loxiglumide, may become a useful drug in the treatment of acute pancreatitis in man, although more detailed investigations are needed.
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PMID:Clinical evaluation of cholecystokinin-A- receptor antagonist (loxiglumide) for the treatment of acute pancreatitis. A preliminary clinical trial. Study Group of Loxiglumide in Japan. 1002 38

The objectives of this review are to summarize, analyse and discuss the roles played by the CCK receptor subtypes and their agonists on pancreatic enzyme secretion, pancreas growth and regeneration, define the receptors specific target cells and evaluate the role of gastrin in pancreatic pathologies including cancer. In rodents, it is clear that the CCKARs present on pancreatic acinar cells play a major role in enzyme secretion. In large mammals, CCK does not seem to be the final mediator of enzyme release. In rat, gastrin and its CCKBR seem responsible for foetal pancreas growth while after birth, CCK was shown to be the most potent trophic factor via occupation of its CCKAR. In pig and human, no one has yet established a direct link between CCK, gastrin and pancreas growth. In rodent's pancreas, the CCKAR were observed on acinar cells as well as on islet's alpha and beta cells; in six other species, the CCKAR were present only on alpha and beta cells with the CCKBR always present on delta cells. The CCKBRs were overexpressed in acute pancreatitis and in metaplastic pancreas following duct ligation. In pancreatic cancer cells, a gastrin autocrine loop involving the CCKBR was suggested. The presence of both CCKR-subtypes and gastrin was observed in many pancreatic tumors; however, their role in cancer growth remains controversial.
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PMID:What are the pancreatic target cells for gastrin and its CCKB receptor? Is this a couple for cancerous cells? 1544 15