Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-one patients (1 to 18 1/2 years of age) with acute pancreatitis were evaluated. In over one third of cases, acute pancreatitis was one feature of a multisystem disease (Reye syndrome, sepsis, shock, hemolytic-uremic syndrome, viral infections). Other common causes included blunt trauma (15%), acquired or congenital structural defects (10%), metabolic diseases (10%), and drug toxicity (3%). In 25% of cases, no cause was identified. All conscious patients complained of abdominal pain, but the location, severity, and duration of pain were extremely variable. Vomiting was a common symptom. Ultrasonography was helpful in establishing the diagnosis and for assessment of complications such as pseudocyst formation. Endoscopic retrograde cholangiopancreatography was used to identify structural or anatomic lesions in patients with recurrent acute pancreatitis. Serum cationic trypsin(ogen) was superior to amylase in the early diagnosis of acute pancreatitis, and was more consistently elevated during the first 5 days in the hospital. Patients were managed conservatively with complete bowel rest, gastric decompression, intravenous fluid therapy, and pain relief. Pancreatic pseudocysts occurred in 10% of patients. There were 13 fatalities, all in patients with a severe multisystem disorder. Recurrences of acute pancreatitis were noted only in certain diagnostic groups: idiopathic pancreatitis, structural anomalies of the pancreaticobiliary tree, metabolic disorders, and (in a single patient) familial pancreatitis.
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PMID:Acute pancreatitis in childhood. 245 30

We employed a radioimmunoassay for human cationic trypsin to define the time course for alterations in the molecular forms of this enzyme in plasma from patients with pancreatitis. Six patients developed acute pancreatitis as a complication of a known disorder [three, Reye's syndrome; two, hemolytic uremic syndrome (HUS); one, choledochal cyst]. The immunoreactive forms of cationic trypsin were determined by gel filtration of each plasma sample followed by radioimmunoassay of the column fractions. Early in the course of the disease, predominantly free trypsinogen was released into the circulation in five patients. In the three patients with Reye's syndrome, subsequent plasma samples showed, in addition to free trypsinogen, increasing amounts of immunoreactive trypsin complexed to alpha 2-macroglobulin and alpha 1-protease inhibitor. In contrast, subsequent samples from the two patients with HUS contained little or no inhibitor-bound trypsin. The remaining patient had intermediate concentrations of cationic trypsin complexed to these two circulating protease inhibitors. Five patients died and postmortem studies showed a striking correlation between the histological severity of acute pancreatic inflammation and the amount of immunoreactive trypsin complexed to alpha 2-macroglobulin and alpha 1-protease inhibitor. This preliminary study suggests that measurement of alpha 2-macroglobulin or alpha 1-protease inhibitor-bound trypsin may be a useful method of monitoring the progression and severity of disease in patients with acute pancreatitis. Characterization of serial changes in the forms of circulating pancreatic proteases may enhance our understanding of time-dependent pathophysiologic events, possibly leading to improved forms of specific therapy.
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PMID:Serial alterations in the forms of immunoreactive pancreatic cationic trypsin in plasma from patients with acute pancreatitis. 258 Sep 62

The pathogenesis of the influenza and Sendai viruses is primarily determined by host cellular trypsin-type processing proteases that activate viral fusion activity and infectivity. We isolated three secretory trypsin-type proteases from rat lungs, such as tryptase Clara, mini-plasmin, and ectopic anionic trypsin, candidates for the processing proteases of viral envelope glycoproteins. These enzymes specifically cleave the precursor of fusion glycoprotein hemagglutinin (HA) of influenza virus at Arg(325) and the F(0) of Sendai virus at Arg(116) in the consensus cleavage motif, Gln(Glu)-X-Arg, resulting in the induction of infectivity of these viruses. These proteases show different localization in the airway and susceptibility for the processing of various subtypes of influenza virus HA, suggesting that these processing proteases determine the viral pathogenicity. Influenza virus readily infects and replicates in the airway epithelial cells but occasionally replicates in the central nervous system, particularly in children below 5-6 years of age and Reye's syndrome patients. We found an invasion by a non-neurovirulent influenza virus in cerebral capillaries with progressive brain edema of mice having impaired mitochondrial fatty acid metabolism congenitally or posteriorly in the newborn period. In the brain of these mice, mini-plasmin, which potentiates viral-multiplication in vivo and destroys the blood-brain barrier, accumulated with virus antigen in the brain capillaries but only a little in the control mice without impaired mitochondrial fatty acid metabolism.
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PMID:[Host cellular proteases trigger the infectivity of the influenza virus in the airway and brain]. 1284 72

The infectivity and pathogenicity of influenza virus are primarily determined by host cellular trypsin-type processing proteases which cleave the viral membrane fusion glycoprotein hemagglutinin (HA). Therefore the distribution of the processing protease is a major determinant of the infectious organ tropism. The common epidemic human influenza A virus is pneumotropic and the HA processing proteases tryptase Clara, mini-plasmin, tryptase TC30 and ectopic anionic trypsin have all been isolated from mammalian airways. However, the pneumotropic influenza virus occasionally causes severe brain edema, particularly in children presenting with Reye's syndrome treated with aspirin, or in children with influenza-associated encephalopathy without antipyretic treatment. We have observed that, after influenza virus infection, the accumulation of mini-plasmin in the cerebral capillaries in mice with a congenital or acquired abnormality of mitochondrial beta-oxidation mimicking the pathological findings of Reye's syndrome, causes an invasion and multiplication of the pneumotropic influenza virus at these same locations. From these findings, we hypothesize that the accumulated mini-plasmin modifies the brain capillaries from a non-permissive to a permissive state, thereby allowing multiplication of pneumotropic influenza virus. In addition, mini-plasmin proteolytically destroys the blood-brain barrier. These pathologic findings, consistent with encephalopathy in mice with a systemic impairment of beta-oxidation, may have implications for human influenza encephalopathy.
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PMID:Accumulation of mini-plasmin in the cerebral capillaries causes vascular invasion of the murine brain by a pneumotropic influenza A virus: implications for influenza-associated encephalopathy. 1525 80