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)

At least two chemotherapeutic agents, prednisone and L-asparaginase, have been demonstrated to produce pancreatic injury. Early diagnosis of pancreatitis is frequently not possible, as symptoms are vague, physical findings may be minimal, and laboratory studies are frequently inconclusive until the injury is severe. Abdominal echography, as a monitor of pancreatic size, has proven to be helpful in the diagnosis of subclinical and early pancreatic injury of 14 of 19 selected children receiving prednisone and/or L-asparaginase therapy for acute leukemia or non-Hodgkin's lymphoma at the M.D. Anderson Hospital and Tumor Institute. Employment of this new diagnostic method permits prompt withdrawal of the causative agent(s), thus preventing further insult.
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PMID:Early detection of chemotherapy-related pancreatic enlargement in children using abdominal sonography: a preliminary report. 99 Oct 74

Pancreatitis is seldom seen as a severe complication of renal transplantation. In a review on 1321 renal transplants, 23 cases with 12 deaths are reported (Johnson and Nabseth, 1970). Single case reports may be added. In our departments pancreatitis has proved to be a fairly frequent complication. It developed in 10 (7 percent) of 147 patients with renal transplantation one week to seven and a half years after transplantation (patients with primary hyperparathyroidism excluded). Three of the eight acute cases had haemorrhagic pancreatitis, in two of them leading to death. Two patients had chronic calcifying pancreatitis. Pancreatitis was complicated in one case by abscess formation and in two by severe haemorrhage into a pseudo-cyst. In two patients the diagnosis was made at necropsy only and death was probably not related to the acute pancreatitis. The exact pathogenesis of pancreatitis after renal transplantation cannot be precisely assessed. Possible contributing factors are treatment with corticosteroids, azathioprin, and L-asparaginase, early hypercalcaemia after transplantation, surgery, infections of bacterial or viral origin, and unknown immunological processes.
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PMID:Pancreatitis after renal transplantation. 109 48

Seven hundred fifty-eight unselected children entered into the United Kingdom Medical Research Council acute lymphoblastic leukaemia UKALL VIII Study and Trial were studied for differences in early treatment-related toxicity according to the type of intramuscular L-asparaginase received. Two hundred seventy-five received a product obtained from Escherichia coli and 483 the enzyme from Erwinia chrysanthemi. The E. coli patients had a significantly higher incidence of neurotoxicity, pancreatitis, and life-threatening sepsis (4%, 2%, and 20%, respectively) when compared with the Erwinia group (2%, 0%, and 18%). Severe hypersensitivity was seen in one patient from both groups and the incidence of glucose intolerance was not significantly different. These findings indicate that E. coli asparaginase may be more toxic. With a minimum follow up of 4 1/2 years there is no evidence that either product has made a significantly different contribution to disease-free survival.
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PMID:Non-randomised study comparing toxicity of Escherichia coli and Erwinia asparaginase in children with leukaemia. 223 23

Ninety-two children with pancreatic disorders were treated over a 10-year period. Thirty-three had blunt trauma, while 69 had medical, metabolic, or neoplastic diseases. Children with trauma had either duct disruption (3), gland fracture (4), or pseudocysts formation (26). Operation was required in 30. Pseudocysts were treated with observation alone in three cases, ultrasound-guided percutaneous aspiration in three, surgical external drainage in two, distal pancreatectomy in four, cyst gastrostomy in ten, and cyst-Roux-en-Y jejunostomy in six. Other disorders included pancreatitis (44), neoplasms (10), nesidioblastosis (4), and pancreaticosplenic abscess (2). Treatment for neoplasms included surgical excision in nine and biopsy in one (adenocarcinoma). Patients with nesidioblastosis underwent 95% (near total) pancreatic resection (two after previous unsuccessful 80% resection). Pancreatitis was familial in two cases, necrotizing in two, idiopathic in 11, and secondary to medications in six cases (steroids, 2; L-asparaginase, 4), gallstones in 17, and choledochal cysts in 6. Pancreatitis resolved after observation and conservative therapy in ten idiopathic cases, 4/6 medication-related cases, and following correction of biliary tract disease (15/17) or choledochal cysts (6). Pancreatic resection or drainage was required in the remaining cases. Pancreatic disorders can be accurately detected with computed tomography (CT) scan in most cases (excluding insulinoma). Ultrasound (US) is useful in cases of biliary tract disease and pseudocyst formation. Traumatic pseudocysts can resolve spontaneously or with US-guided percutaneous drainage (in the presence of normal ducts). Children with neoplasms, abnormal pancreatic ducts, or recurrent pancreatitis require resection or appropriate drainage procedures. Overall survival was 95%.
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PMID:Pancreatic disorders in infancy and childhood: experience with 92 cases. 276 44

The clinical, laboratory, and ultrasonographic findings in children receiving L-asparaginase therapy were retrospectively reviewed and correlated to determine the diagnostic reliability and clinical usefulness of serial pancreatic sonograms in detecting L-asparaginase-induced pancreatitis. A total of 217 sonograms were obtained in 92 patients. Six of the 92 (6.5%) had L-asparaginase-induced pancreatitis. The diagnosis of pancreatitis was based solely on clinical symptoms in three patients, on clinical and laboratory findings in two, and on sonographic and laboratory findings in one. No confirmed cases of pancreatitis were detected solely by ultrasonography before clinical or laboratory evidence was obtained. Sonograms were useful only in confirming clinical and/or laboratory evidence of pancreatitis, but were of no value in making the early or preclinical diagnosis of drug-induced pancreatitis. We have discontinued the practice of obtaining routine serial pancreatic sonograms in children receiving L-asparaginase at our institution.
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PMID:Serial sonograms to detect pancreatitis in children receiving L-asparaginase. 330 44

In the management of children with acute lymphoblastic leukemia, L-asparaginase has become established as an effective drug in the usual multi-agent therapy; and the significance of pancreatitis as a complication of this drug is well recognized. Less well appreciated, however, is the progression of such pancreatitis in some patients to pseudocyst formation and the possible necessity for surgical management. Two adolescent girls who developed pancreatic pseudocysts while being treated with L-asparaginase are described in this report. Both were being treated for acute lymphoblastic leukemia for periods of 18 and 4 months, respectively, prior to the onset of pancreatitis. Both were in remission of their leukemic disease when typical clinical and laboratory manifestations of acute pancreatitis developed. In one girl, a pancreatic pseudocyst became apparent 2 weeks following the diagnosis of acute pancreatitis and in the other girl, this complication developed over a period of 8 weeks. The usual nonsurgical management of pancreatitis over protracted periods of time was ineffective in the treatment of the pseudocysts. Surgical drainage (internal in one and external in the other) was successful in both in eradicating the pseudocyst, and in neither did further evidence of pancreatic disease subsequently occur. In both resumption of chemotherapy, omitting L-asparaginase, was well tolerated. One has been in remission of leukemia and in good health for a 3-year period of follow-up observation, while the other subsequently had a relapse of leukemia and died 18 months following the onset of pancreatitis.
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PMID:Pancreatic pseudocyst complicating treatment of acute lymphoblastic leukemia. 390 Mar 29

93 publications concerning drug-induced pancreatitis are reviewed. A confirmed causal relationship between drug and acute pancreatitis so far exists only for 8 compounds: azathioprine, chlorothiazide, furosemide, sulfonamides, tetracycline, estrogens, valproic acid and L-asparaginase. There is less convincing, but still suggestive, evidence for a causal relationship with 5 other drugs, namely: corticosteroids, chlorthalidone, ethacrynic acid, phenformin and iatrogenic hypercalcemia. Due to inadequate or contradictory evidence, the link between a number of additional drugs and acute pancreatitis is considered possible, conditional or doubtful. Finally, the scant literature concerning the pathogenesis and histological lesions of drug-induced pancreatitis is briefly reviewed.
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PMID:[Acute drug-induced pancreatitis]. 392 79

This paper reports the association of acute pancreatitis coincident with cytosine arabinoside (Ara-c) therapy in a single patient on at least two occasions. The patient had previously received L-asparaginase, but the last dose had been given 4 months prior to the onset of pancreatitis. A literature review provided two more cases of pancreatitis associated with Ara-c therapy in patients previously treated with L-asparaginase. In view of th extreme rarity of pancreatitis in patients receiving Ara-c, the possibility arises that prior treatment with L-asparaginase may predispose the pancreas to this complication.
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PMID:Acute pancreatitis in association with cytosine arabinoside therapy. 694 26

Adverse reactions to L-asparaginase in children undergoing induction therapy for acute lymphocytic leukemia have previously been described and have been noted to include hypersensitivity reactions, pancreatitis, hepatic dysfunction, nephrotoxicity, and central nervous system dysfunction. Recently, however, newly described abnormalities in hematological and hemostatic function have resulted in intracranial hemorrhage and thrombosis of the extremities, immune hemolytic anemia and abnormal collagen stimulated platelet aggregation. The coagulopathy appears to be a result of a combination of events related to decreased synthesis of fibrinogen, antithrombin III and plasminogen. Implications for future modifications of L-asparaginase therapy are further discussed.
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PMID:Adverse reactions of L-asparaginase. 695 44

The polyethylene glycol (PEG) adduct of Escherichia coli L-asparaginase was administered intravenously to 4 patients with chemotherapy refractory cancers. The PEG-enzyme in plasma exhibited a half-life of 16-25 days. Doses of 250IU/m2 or greater reduced plasma asparagine to undetectable levels for as long as enzyme was detectable in plasma. All doses of enzyme administered (250-1000 IU/m2) caused similar increases in plasma aspartate, i.e. no dose-response relationship. Pleural fluid and ascites contained detectable enzyme but at a value 10-15% of simultaneously drawn plasma levels. Toxicity in this small group of patients was minimal; nausea and transient fever predominated. There were no clinical signs of PEG-asparaginase-induced pancreatitis, renal dysfunction, hypocalcemia and hyperglycemia. No patient developed evidence of a PEG-asparaginase allergic reaction; no patient formed antibodies to asparaginase or PEG-asparaginase. Two patients with large cell lymphoma showed a partial response to treatment.
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PMID:Pharmacology of Escherichia coli-L-asparaginase polyethylene glycol adduct. 704 23


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