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)

In a double-blind randomized study, 30 patients received somatostatin infusion during ERCP and 30 patients placebo with the aim of evaluating whether somatostatin can reduce the incidence of injection pancreatitis. S-amylase, U-amylase and S-lipase were evaluated before, during and after (up to 48 hours) ERCP. C-peptide was also determined as a marker of the function of the endocrine pancreas. While no statistically significant effect of somatostatin in terms of amylase and lipase was to be found, somatostatin did significantly decrease c-peptide levels in plasma, indicating that the peptide inhibited beta-cell secretion. About 40% of patients in the somatostatin group and about 50% in the placebo group showed signs of injection pancreatitis (elevated levels of enzymes) and in both groups there are patients with clinically apparent pancreatitis.
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PMID:Can somatostatin prevent injection pancreatitis after ERCP? 138 Apr 75

This study evaluates the effect of the long acting somatostatin analogue octreotide on biochemical and clinical parameters of endoscopic retrograde cholangiopancreatography (ERCP) induced pancreatitis. Altogether 245 patients were randomised to receive either octreotide or isotonic saline. Octreotide (100 micrograms) was administered intravenously five minutes before ERCP and subcutaneously 45 minutes after ERCP. There were no significant differences in the median serum amylase and lipase activities at baseline, eight, and 24 hours after ERCP. Five patients (2%) developed clinical pancreatitis--three in the octreotide and two in the placebo groups. Excluding patients who developed pancreatitis, 43 (18%) developed abdominal pain after ERCP--21 in the octreotide and 23 in the placebo groups. There were no significant differences in the median serum amylase and lipase values between the treatment groups. None of the 52 patients who had therapeutic interventions developed pancreatitis. This study suggests that octreotide may not protect against ERCP induced pancreatitis.
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PMID:Does the somatostatin analogue octreotide protect against ERCP induced pancreatitis? 138 99

An immunoactivation assay for determining pancreatic lipase mass concentration was clinically evaluated and compared with results obtained by measuring total amylase and pancreatic amylase activity. A group of 30 patients with pancreatitis was compared with a control group of 32 patients in which this disease was suspected but excluded. Both lipase mass concentration and pancreatic amylase activity exhibit good sensitivity (0.93 each) and specificity (0.94 and 0.97, respectively) at cutoff concentrations of 200 micrograms/L and 200 U/L, respectively. The median increase in lipase mass concentration (37.1 times the upper limit of the reference interval) in the pancreatitis group was higher than that for either total amylase or pancreatic amylase activity (5.94 and 14.5 times, respectively) but showed a similar time to peak value. We conclude that the lipase assay is the method of choice for diagnosing pancreatitis.
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PMID:Clinical evaluation of a pancreatic lipase mass concentration assay. 138 18

Severe necrotizing pancreatitis is accompanied by release of hemorrhagic ascites fluid (HAF), which is thought to be related to the occurrence and frequency of cardiocirculatory and pulmonary failure as a consequence of acute pancreatitis. The purpose of this study was to evaluate the role of HAF due to these systemic complications. Experiments were performed in 25 pigs (mean b.wt. 22 +/- 1 kg) under general anesthesia and mechanical ventilation. The animals received 50 ml/kg b.wt. i.p. of either physiologic saline solution (control CO, n = 9) or hemorrhagic ascites fluid (HAF, n = 16). HAF was obtained from 16 pigs with pancreatitis induced by intraductal infusion of bile salt. Eight animals in the HAF group were pretreated with indomethacin (10 mg/kg i.v. INDO/HAF). All animals were followed up for 6 h. Mean arterial pressure, cardiac output, and stroke volume fell significantly in the HAF (-25%, -27%, -27%) and in the INDO/HAF groups (-24%, -20%, -17%) as compared with controls (-6%, -6%, -6%). Also, left ventricular end-diastolic pressure (LVEDP) decreased by 52% and 48% in both HAF recipient groups, whereas LVEDP was unchanged in the control group. Myocardial contractility (Vmax) remained unaltered in all experimental groups. No significant differences in gas exchange and lung dry/wet weight ratio were observed. Lipase and PGI2 of the unpretreated HAF group rised to 203% and 198% in arterial blood at 6 h compared with unaltered levels in the control group. No increase of prostanoid concentrations was detected in the indomethacin-pretreated group, whereas lipase increase by a comparable extent as in the HAF group. We conclude that the early consequences of HAF are mainly characterized by systemic hypotension due to hypovolemia.
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PMID:Hemodynamic effects following intraperitoneal infusion of pancreatic ascites fluid. 141 Aug 1

A 44-year-old woman with C1q esterase inhibitor deficiency was seen in consultation for recurrent right upper quadrant abdominal discomfort, nausea, and vomiting. Each of these episodes was accompanied by concomitant peripheral edema. Initial diagnostic efforts were fruitless. In time, intermittent elevations in amylase and lipase developed, and a diagnosis of relapsing pancreatitis was made. We contend that the patient's recurrent acute pancreatitis is associated with her hereditary angioedema. Possible pathogenesis could involve intermittent intrapancreatic edema with partial ductal obstruction or loss of inhibition on the kallikrein-kinin system.
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PMID:Hereditary angioedema associated with pancreatitis. 143 59

A retrospective study is discussed, in which the disorder of pancreatic enzymes in hospitalized patients because of an acute infectious gastroenteritis is analyzed. Of 30 cases, 15 showed a raise in lipase levels, being over 1,000 IU in five of them. There was no associated raise in amylase levels. Patients with high lipase levels did not show more fever, leucocytosis nor disorders on the hepatic enzymes, in comparison with those patients with normal lipase levels. Mean age was slightly lower in patients with high lipase levels than in those with normal lipase. Chronic diseases are not a predisposing factor to suffer pancreatic complications in patients with gastroenteritis. There was no case with intense abdominal pain which would suggest a pancreatitis, and a raise in lipase did not modify the evolution of the gastroenteritis.
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PMID:[Pancreatic changes associated with acute gastroenteritis]. 147 Jul 20

The pathophysiology of pancreatic autodigestion is poorly understood. Pancreatitis affects all age groups, and the diagnosis is sometimes missed when serum amylase and lipase activities are not measured in the child with abdominal pain. Acute pancreatitis in children has become a more commonly seen condition and the causes have varied. Laboratory and radiological studies play an important role in determining the diagnosis and prognosis. Family history is important in the diagnosis of idiopathic hereditary pancreatitis. Most acute episodes resolve with supportive care, but the mortality in acute pancreatitis is currently about 15% (Hadorn et al., 1980). Endoscopic retrograde cholangiopancreatography or an endoscopic retrograde pancreatogram may be necessary to investigate relapses of pancreatitis. Chronic pancreatitis can be a life-threatening condition requiring lifetime medical management.
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PMID:Pancreatitis in children. 147 58

The theory of granulocyte embolization in the retinal arterioles in acute pancreatitis cannot account for several aspects of the ophthalmic complication. Therefore we studied retinal circulation by fluorescein angiography, light and transmission electron microscopy following the first six hours of acute experimental necrotizing pancreatitis. The studied period was characterized by high serum lipase and amylase concentrations, hypocalcemia, necrosis of the pancreatic tissue and preceded the development of hypovolemic shock. Ophthalmoscopy and fluorescein angiography revealed no pathologic alterations and no granulocyte aggregation was found. Our results suggest that granulocyte aggregation induced by pancreatic enzymes is not the reason for the ophthalmic circulatory disturbances in acute pancreatitis.
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PMID:Is retinopathy in pancreatitis caused by leukocyte emboli? 148 94

Acute pancreatitis is observed in patients with the acquired immunodeficiency syndrome (AIDS) (4-22%), and is reported with increasing frequency as a complication of therapy in human immunodeficiency virus-spectrum disease. The cause is multifactorial (virus, neoplasm, drugs), and the natural history generally mild and uncomplicated. 2',3'-Dideoxyinosine (ddI) is an experimental antiretroviral agent implicated as a cause of acute pancreatitis in a small number (0.9-2%) of patients. To better define this relationship, we conducted a retrospective analysis of a prospective clinical trial involving 51 homosexual males with AIDS treated with ddI (10-12 mg/kg/day) and reported on the incidence and natural history of pancreatitis. Clinical pancreatitis (symptoms, elevated serum amylase, and lipase and, in most cases, abnormal radiographic studies of the pancreas) was observed in 12 patients (23.5%). Asymptomatic elevations of amylase and lipase were identified in 10 additional patients (39.2%). The onset of pancreatitis was consistently delayed in both groups (overall mean 14.1 +/- 1.2 wk, 98% confidence interval). Ten of 12 symptomatic patients required hospitalization (mean length of stay, 9.4 days); two of 12 progressed to fulminant pancreatitis and died. Two patients with asymptomatic pancreatitis which occurred after starting ddI were rechallenged; severe symptomatic pancreatitis developed shortly after drug reinstitution. In each case, complete recovery followed discontinuation of the drug. We conclude that 1) The incidence (62.7%) and severity of pancreatitis in patients with AIDS receiving ddI therapy are significantly greater than expected, 2) the onset is predictably delayed about 14 wk, 3) ddI should be added to the list of drugs that cause acute pancreatitis, and 4) careful sequential monitoring of pancreatic function and early identification of potential "risk factors" for pancreatitis in AIDS patients treated with ddI may be essential in avoiding this serious complication.
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PMID:Acute pancreatitis as a common complication of 2',3'-dideoxyinosine therapy in the acquired immunodeficiency syndrome. 843 64

A 28 year old patient with a moderate attack of ulcerative colitis was treated with sulfasalazine. Ten days after, the patient was admitted with clinical and laboratory symptoms of acute pancreatitis (serum amylase 631 u., serum lipase 1080 u. urine amylase, 910 u.). Upon recovery, sulfasalazine was reintroduced at lower dosage (2 Gm/day), and the patient repeated the clinical and biological picture of acute pancreatitis (serum amylase of 710 and lipase 1010 u.) CAT scan showed pancreatic edema and ultrasonography demonstrated a normal gallbladder. The symptoms and laboratory abnormalities disappeared in three days after stopping sulfasalazine. The patient has been followed-up for one year without recurrence of pancreatitis on maintenance treatment with 1.5 Gm 5-Aminosalicylic acid.
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PMID:[Acute pancreatitis caused by salazopyrine. An unusual association]. 168 Mar 57


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