Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute fatty infiltration of the liver in pregnancy is characterised by microvacuolar fatty infiltration, without necrosis, occuring at the end of pregnancy. This syndrome, defined by Sheehan in 1940, remains rare. The authors were able to find 62 authentic cases in the french, english and german literature. The course is fatal in 75% of cases for the mother and 70% for the child. The gravity is related to hepatocellular failure, but also to extra-hepatic complications (renal failure, haemorrhagic syndrome, infectious complications, acute haemorrhagic and/or necrosing pancreatitis). When the course is favourable, the hepatic lesions disappear in a few weeks and there is no recurrence during subsequent pregnancies. The histological lesions of acute fatty infiltration of the liver in pregnancy are identical to those of fatty infiltration of the liver induced by cyclines and of Reye syndrome.
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PMID:[Acute fatty infiltration of the liver in pregnancy. One case (author's transl)]. 47 44

A review of 18 cases of Reye's syndrome autopsied at Indiana University Hospital since 1970 was done to document pancreatic lesions associated with the syndrome. A spectrum of inflammatory lesions was identified and grouped into four categories: group 1, no changes; group 2, minimal microscopic changes; group 3, moderate changes, ie, focal necrosis, exudates, or congestion; and group 4, severe acute pancreatitis. Patients in group 4 often had clinical or laboratory data suggesting the onset of pancreatitis after hospitalization. Acute pancreatitis is associated with Reye's syndrome, and patients should be monitored for its development. Hypotension, hypocalcemia, and glucose lability may herald the onset of acute pancreatitis in these patients.
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PMID:Pancreatitis and Reye's syndrome. 49 90

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

A five-year-old-girl with a history of recurrent hypoglycemia presented with acidosis, intractable vomiting, and abdominal tenderness; the diagnosis of acute pancreatitis was made by abdominal ultrasonography and supportive biochemical studies. Urinary organic acid analysis revealed metabolites suggestive of HMG-CoA lyase deficiency, and subsequent enzyme assays of lymphocytes and fibroblasts confirmed this diagnosis. Acute pancreatitis, an uncommon condition in childhood, is seen with increased frequency in patients with Reye syndrome, a metabolic disorder with which HMG-CoA lyase deficiency may be confused. The pathogenesis of pancreatitis in Reye syndrome or in HMG-CoA lyase deficiency has not been determined.
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PMID:A child with acute pancreatitis and recurrent hypoglycemia due to 3-hydroxy-3-methylglutaryl-CoA lyase deficiency. 648 80

Reye syndrome was observed in a 5 1/2-year-old girl after an appendectomy. It was accompanied by insulin-resistant hyperglycaemia. Central adaptation failure resulted in death on the fourth day of treatment. Post mortem and histological results showed phlegmonous pancreatitis of the excretory type, apart from the established manifestations of Reye syndrome (severe cerebral oedema, excessive hepatic steatosis, moderate fatty degeneration of renal tubuli). Neuropathology revealed exclusively signs of hypoxic damage. Pancreatitis, usually necrotising or haemorrhagic, is not infrequent in Reye's syndrome. Girls are predominantly affected and pancreatitis is associated with a tendency towards sometimes serious hyperglycaemia. The possibility of this complication should be considered in the treatment of Reye syndrome.
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PMID:[Reye's syndrome with pancreatitis and hypoxic brain damage]. 669 70

Three patients who died of a Reye's syndrome had biochemical or pathological evidence of pancreatitis. None of the 38 survivors had clinical or biochemical evidence of pancreatic dysfunction. The use of hypertonic glucose solutions and exogenous insulin may reverse the metabolic abnormalities seen in Reye's syndrome and may spare the pancreas, thereby preventing the development of pancreatitis. In addition, serum calcium and glucose concentrations appear to correlate with pancreatic function and may be of value in detecting the occurrence of pancreatitis. It is our impression that the development of pancreatitis protends a poor prognosis in patients with Reye's syndrome.
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PMID:Pancreatitis in patients with Reye's syndrome. 724 Jun 93