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)

Hyperglycemia may occur as a complication in patients with leukemia during induction therapy with L-asparaginase and steroids. The reported incidence is about 10%. The present report concerns three patients with acute lymphoblastic leukemia (ALL), complicated by hyperglycemia. Their ages were 10, 12, and 9 years, respectively. Past histories were normal, with no diabetes mellitus or other endocrine disorders in their families. Case 1 was an obese boy who developed pancreatitis and diabetic ketoacidosis (DKA) in his remission induction therapy which had included both L-asparaginase and steroids. Cases 2 and 3 both presented with polyuria and elevated postprandial blood sugar. For all patients, insulin was administered to control their blood sugars; the maximal daily dosage of insulin dispensed was 2.1 U/kg, 0.5 U/kg, and 0.7 U/kg, respectively. Increased plasma insulin and C-peptide levels suggestive of insulin resistance were observed in Case 3. The outcome of hyperglycemia in these three patients was good. The symptoms of this complication may vary from mild glucose intolerance to severe, or even fatal, DKA. Thus, periodic determinations of urine glucose and postprandial blood sugar are important for early recognition to prevent further life-threatening consequences.
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PMID:Hyperglycemia induced by chemotherapeutic agents used in acute lymphoblastic leukemia: report of three cases. 828 94

A randomized clinical trial of combination chemotherapy for adult acute lymphoblastic leukemia (ALL) with doxorubicin, vincristine and prednisolone with and without L-asparaginase (AdVP vs L-AdVP) was conducted, involving 58 institutions throughout Japan. After reaching complete remission (CR), patients were treated with the same regimen for more than 2 years. Among 166 evaluable cases of the 198 cases enrolled, CR rates were 63.1% (53/84) with AdVP and 64.6% (53/82) with L-AdVP (P = 0.837). Median survival times and 7-year survival rates were 12.7 months and 21.2% with AdVP, and 16.0 months and 22.3% with L-AdVP (P = 0.955 by generalized Wilcoxon test [GW], P = 0.952 by log-rank test [LR]). Median disease-free survival times and 7-year survival rates were 13.5 months and 23.8% with AdVP and 17.0 months and 30.6% with L-AdVP, showing some increments for L-AdVP but no statistical significance (P = 0.141 by GW, P = 0.300 by LR). Among the cases of extramurally confirmed FAB subtypes, CR rates were 75.9% (63/83) for the L1 subtype and 51.3% (39/76) for the L2 subtype (P = 0.001). As to adverse effects, pancreatitis was complicated more frequently in L-AdVP than in AdVP (P = 0.039). Other side effects such as hyperbilirubinemia, diabetes mellitus, diarrhea and hypofibrinogenemia were observed more frequently with L-AdVP, but with no statistical significance. Thus, addition of a single course of L-asparaginase in the induction phase of combination chemotherapy with doxorubicin, vincristine and prednisolone did not significantly enhance the effect of antileukemic treatment of adult ALL.
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PMID:Nation-wide randomized comparative study of doxorubicin, vincristine and prednisolone combination therapy with and without L-asparaginase for adult acute lymphoblastic leukemia. 830 8

A comprehensive literature search was performed to collect all available data on drug-induced pancreatitis. Strong evidence for an association with acute pancreatitis has been described for anticholinesterases, calcium 2',3'-dideoxyinosine, estrogen, L-asparaginase, salicylates, thiazide-diuretics, valproic acid, and vinca alkaloids. Weak evidence has been found for antituberculous agents, azathioprine, biguanides, cisplatinum, cyclosporine A, H2-blocking agents, loop diuretics, 6-mercaptopurine, metronidazole, pentamidine, steroids, sulfonamides, sulindac and tetracycline. Many cases were associated with underlying conditions known to induce acute pancreatitis themselves. It is concluded that for none of the drugs studied the available data are consistent enough to support a definite association with acute pancreatitis. Nevertheless, the data suggest that drugs may be a trigger or a cofactor in inducing pancreatitis.
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PMID:Drug-induced acute pancreatitis: further criticism. 833 61

L-asparaginase has been used clinically for treatment of a wide variety of pediatric neoplastic diseases (e.g. acute lymphocytic leukemia, malignant lymphoma, etc.) A 14-year-old female patient, is a victim of acute lymphocytic leukemia, Pre T type. She got acute pancreatitis after the L-asparaginase therapy. We reported her clinical course and our management. It is concluded that early diagnosis of pancreatitis is usually difficult, because the symptoms are vague, physical findings may be minimal, and laboratory studies are frequently inconclusive until the injury is severe. Therefore, physicians must be cautious to the patient's chief complaint before administering the next dose of L-asparaginase, because it may occur more earlier than the laboratory or image studies and thus could be used to predict pancreatitis.
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PMID:Acute pancreatitis in association with L-asparaginase therapy: report of one case. 838 60

Recent information about drugs implicated in causing pancreatitis is summarized. Although the frequency of drug-induced acute pancreatitis is generally low, the disease is associated with substantial morbidity and mortality, which makes timely identification of the offending agent important. Mechanisms suggested for drug-induced pancreatitis include pancreatic duct constriction; immunosuppression; cytotoxic, osmotic, pressure, or metabolic effects; arteriolar thrombosis; direct cellular toxicity; and hepatic involvement. Agents reported to have a definite association with pancreatitis are asparaginase, azathioprine, didanosine, estrogens, furosemide, mercaptopurine, pentamidine, sulfonamides, sulindac, tetracyclines, thiazides, and valproic acid. Agents reported to have a probable association with pancreatitis include cimetidine, clozapine, corticosteroids, endoscopic retrograde cholangiopancreatography contrast media, methyldopa, metronidazole, salicylates, and zalcitabine. Agents reported to have a questionable association with pancreatitis include acetaminophen, cyclosporine, cytarabine, erythromycin and roxithromycin, ketoprofen, metolazone, and octreotide. When ethanol abuse and biliary disease are ruled out as etiologies for pancreatitis, the possibility of drug-induced disease should be investigated.
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PMID:Drug-induced pancreatitis. 840 15

We reported a case of ALL complicated with acute pancreatitis caused by L-asparaginase (L-Asp). The patient was a 42-year-old man, who showed eosinophilia in peripheral blood and an increase of lymphoblast in bone marrow. He was diagnosed as ALL (L2) and treated by JALSG '87 protocol. Remission induction chemotherapy including L-Asp was administered by 5,000 IU i.v. for 10 days. The day after giving all dose of L-Asp, slight epigastralgia developed and then became severe. After two days, s-amylase was markedly elevated, and the patient was diagnosed as acute pancreatitis caused by L-Asp. He was treated conservatively, but hyperglycemia occurred. The epigastrial tumor was palpable and gradually grew in size. CT-scan and abdominal ultrasonography revealed pancreatic pseudocyst, so he was treated by percutaneous cyst drainage. The patient died of a relapse of ALL. The prophylaxis and early diagnosis of the pancreatitis and hyperglycemia caused by L-Asp are very difficult. We have to examine more cases and pay greater attention to the chemotherapy, including L-Asp.
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PMID:[A case of ALL complicated with acute pancreatitis and pancreatic pseudocyst caused by L-asparaginase ]. 842 80

Acute necrotic pancreatitis was diagnosed in two patients treated with asparaginase for, in the first case a highly malignant lymphoma and in the second an acute lymphoblastic leukemia. The diagnosis on clinical findings and amylase assay results was confirmed by LDH and/or C reactive protein values and abdominal CT scans. Both patients recovered after drainage of peripancreatic fluid collections, in the first patient by surgical followed by cutaneous drainage and in the second by cutaneous drainage of a pancreatic pseudocyst. In addition to the frequent pancreatic reaction observed during asparaginase treatment, signs of pancreatic necrosis requiring urgent treatment have to be identified. The necrotic nature of the pancreatitis was confirmed by clinical examination, assay to biologic markers and abdominal CT scans, eliminating other causes of the pancreatitis.
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PMID:[Acute necrotic pancreatitis secondary to asparaginase. Role of drug combinations--early diagnosis and treatment. Apropos of 2 cases]. 851 31

Few data exist about the incidence of drug-induced pancreatitis in the general population. 20 cases of drug-related pancreatitis were reported in Switzerland over a period of 12 years. The proportion of cases of pancreatitis caused by drugs is estimated to be around 2% in the general population, with much higher proportions in specific subpopulations, such as children and patients who are HIV positive. The literature about drug-induced pancreatitis consists mainly of anecdotal case reports. Clear evidence of a definite association with pancreatitis, by means of rechallenge tests, or consistent case reports, supported by animal experiments or data on the incidence of acute pancreatitis in drug trials exists for didanosine, valproic acid (sodium valproate), aminosalicylates, estrogen, calcium, anticholinesterases and sodium stibogluconate. An association with drug-induced pancreatitis is likely but not definitely proven for thiazide diuretics, pentamidine, ACE inhibitors, asparaginase, vinca alkaloids, some nonsteroidal anti-inflammatory drugs and clozapine. Pancreatitis is possibly caused by azathioprine, furosemide (frusemide), tetracycline, metronidazole, isoniazid, rifampicin (rifampin), sulphonamides, cyclosporin and some antineoplastic drugs. Many drugs have been reported to be associated with acute pancreatitis. However, lack of rechallenge evidence, consistent statistical data, or evidence from experimental studies on a possible mechanism prohibit definitive conclusions about most of them. The high incidence of concurrent illnesses known to induce acute pancreatitis, makes a trigger role or co-factor role for the drug seem most likely.
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PMID:Drug-induced pancreatitis. 882 18

To further elucidate the incidence and potential mechanism of asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia (ALL), we serially obtained fasting lipid and lipoprotein studies on 38 of the 43 consecutively diagnosed children with ALL before, during, and after asparaginase therapy. We also evaluated a second population of 30 long-term survivors of childhood ALL; a fasting lipid and lipoprotein profile was obtained once at study entry. The mean peak triglyceride level during asparaginase of 465 mg/dL (standard deviation [SD] 492) was significantly higher (P = .003) than the level of 108 mg/dL (SD 46) before the initiation of asparaginase therapy. Sixty-seven percent of the newly diagnosed patients had fasting triglyceride levels greater than 200 mg/dL during asparaginase therapy; 15 patients (42%) had levels greater than 400 mg/ dL, 7 with levels greater than 1,000 mg/dL. The incidence of hypertriglyceridemia did not vary by type of asparaginase or risk status of ALL (defined by white blood cell count and age). None of the 7 patients with triglyceride levels greater than 1,000 mg/dL developed pancreatitis. In contrast, 4 of the 13 patients without triglyceride elevation developed pancreatitis; 3 of the 4 patients had fasting studies at the height of their abdominal pain. Nuclear magnetic resonance analysis of lipid subclasses showed a significant increase in the smaller, denser forms of very low density lipoprotein (VLDL) and negligible chylomicron fraction in a subset of patients with marked triglyceride elevation. Lipoprotein lipase activity was consistently above normative values for all levels of triglyceride and could not be explained by obesity or hyperglycemia. Apolipoprotein B(100) levels increased during asparaginase therapy, although the mechanism of this remains unclear. LDL reciprocally decreased with increased VLDL during asparaginase therapy. After asparaginase therapy, triglyceride levels (mean, 73 mg/dL [SD 33]) were significantly lower than levels obtained during asparaginase therapy. Triglyceride levels for survivors did not differ from the normal range or postasparaginase levels in the newly diagnosed patients. These data show a striking temporal association between asparaginase therapy and hypertriglyceridemia. Changes in cholesterol, in contrast, were not temporally related to asparaginase treatment. Cholesterol levels were elevated (>200 mg/dL) in 20% of the patients after asparaginase, which may be due to continued treatment with corticosteroids. The mean cholesterol level of long-term survivors of 177 mg/dL was significantly higher than the norm (P = .045). High-density lipoprotein (HDL) levels were significantly lower than normal at all time periods and for both populations; 25% of survivors had HDL levels less than 35 mg/dL. We conclude that modifications in asparaginase therapy are not necessary. In cases of triglyceride elevation greater than 2,000 mg/dL when the risk of pancreatitis is increased, close clinical monitoring is imperative. Larger studies are needed to determine the incidence of dyslipidemia in long-term survivors of ALL as well as the relationship between lipid abnormalities and other late effects of treatment, notably obesity and cardiomyopathies.
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PMID:Asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia. 905 8

Pancreatitis has been noted to be a potential complication in 2% to 16% of patients undergoing treatment with L-asparaginase for a variety of pediatric neoplasms, but rarely has surgical intervention been necessary. The authors present two fulminant cases of L-asparaginase-induced pancreatitis and review the current literature. The first patient is a 15-year-old boy who underwent induction chemotherapy with L-asparaginase for non-Hodgkin's lymphoma with bone marrow involvement. He presented with diffuse patchy necrosis of the pancreas as well as a large infected pancreatic pseudocyst. He subsequently required operative debridement of the pancreas and external drainage of the pseudocyst. He is currently doing well. The second patient is a 5-year-old boy who was treated with L-asparaginase for a diagnosis of acute lymphocytic leukemia. Within 3 weeks of initiation of therapy, fulminant pancreatitis developed, which progressed to multisystem organ failure. Computed tomography scan demonstrated extensive pancreatic necrosis involving 90% of the gland. He underwent surgical debridement of his necrotic pancreas and wide drainage of the lesser sac. Postoperatively he improved but subsequently multiple complications developed including erosion of his gastroduodenal artery with significant intraabdominal bleeding, which was controlled with angiographic embolization. Subsequently erosion of his endotracheal tube into the innominate vein developed, and he died. L-asparaginase-induced pancreatitis has been described after therapy for various pediatric neoplasms, and the reported cases have usually been self-limiting. However, our cases demonstrate potentially fatal sequelae of this complication and mandate early diagnosis with appropriate surgical intervention in this setting.
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PMID:Surgical pancreatic complications induced by L-asparaginase. 920 86


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