Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is the case of a 15 year old adolescent girl who refers recurrent chronic abdominal pain for a period of three months. She was diagnosed as having a chronic pancreatic pseudocyst, seen as a complication of an episode of hemorrhage acute pancreatitis secondary to the administration of L-asparaginase for the treatment of acute lymphoblastic leukemia. The abdominal ultrasonography allowed for a pre-operatory diagnosis to be made. An internal drainage and a cystogastrostomy were the procedures of choice. A review of the literature is included on the physiopathology, clinical history, diagnostic procedures and therapeutic conduct to be followed.
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PMID:[Pancreatic pseudocyst. A case report and review of the literature]. 191 May 61

A polyethylene glycol conjugate of L-asparaginase (PEGLA) was administered to 21 patients with refractory non-Hodgkin's lymphoma. The dose given was 2,000 mu/m2 intramuscularly every 2 weeks. Eligibility required at least one prior trial of chemotherapy and ambulatory performance status. At entry, all patients had measurable lesions and documented disease progression. The median age of the patients was 61 years; 18 (86%) were ambulatory with minimal symptoms, 12 patients (57%) had 3 or more prior regimens, and 13 (62%) had stage IV disease. Histologic subtype was low grade in 11 patients (52%), intermediate in 7 (33%), high grade in 2 (10%) and unclassifiable in one (5%). There were two partial responses (11%) noted (95% confidence interval of response of 1-30%). Eleven patients (52%) were removed from study due to disease progression. Nine patients (43%), required removal for toxicity (7 for protracted nausea and vomiting and 2 for confusion). One patient died of sepsis while on study but this was not considered drug related. Almost one third of patients complained of fatigue or loss of appetite. Nausea and vomiting occurred in approximately half the patients and was moderate to severe in 9. Diarrhea and abdominal pain were also noted in one-third of those treated. Changes in the partial thromboplastin time and fibrinogen were noted in most patients but resulted in no bleeding complications. In this trial, PEGLA displayed modest activity in a heterogenous group of patients with progressive non-Hodgkin's lymphoma.
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PMID:A phase II trial of PEG-L-asparaginase in the treatment of non-Hodgkins lymphoma. 234 67

In early 1984, we treated 13 consecutive patients with acute lymphoblastic leukemia (ALL) using an induction regimen of rapidly rotated combinations of prednisone, vincristine, asparaginase, teniposide (VM-26), cytosine arabinoside, and high-dose methotrexate (MTX) followed by leucovorin rescue. The intent of this clinical trial, designated Total Therapy Study XI, is to test the hypothesis that greater initial leukemia cell kill will decrease opportunities for the development of drug-resistant mutants, with resultant improvement in the length of disease-free survival. Five patients experienced life-threatening gastrointestinal toxicity within three weeks of the start of treatment. One died. Three other patients had severe abdominal pain, abdominal distention, diarrhea, and weight loss, but not gastrointestinal bleeding. In the remaining five patients, toxicity was rapidly reversible, and each child was able to complete the planned course of chemotherapy. The study was then amended to switch high-dose MTX from the induction phase to the consolidation phase, allowing at least one week for mucosal recovery. Among the next 28 patients who were treated, none showed evidence of severe gastrointestinal toxicity. Patients now receive high-dose MTX alone as consolidation therapy and are tolerating it adequately. Drug timing should be examined critically when intensified multiple-agent regimens are being devised for initial treatment of ALL.
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PMID:Unexpectedly severe toxicity from intensive early treatment of childhood lymphoblastic leukemia. 391 44

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

From January 1994 until May 1997, 54 children with leukemia and non Hodgkin lymphoma were analyzed. The enzymatic function and ultrasound examination of pancreas were estimated. In 17 of 54 patients the clinical symptoms suggesting pancreatitis or toxic lesion of pancreas were observed. In 13 cases L-asparaginase was administered. The main symptom of the pancreas disease was severe abdominal pain with vomiting. The typical ultrasound view of pancreatitis was observed in 4 cases, pancreas oedema was seen in 6 patients. The most serious course of pancreatitis was diagnosed in 3 children. Diabetes mellitus coexisted in two cases, in the third case osteoporosis was seen. Because of the toxic pancreas lesion in one patient the administration of L-asparaginase and cortical hormones was discontinued, in the remaining 2 children the therapeutic scheme was modified. In all 17 cases this side effect was completely reversible, as well as in 3 children with the most serious clinical course of pancreas lesions.
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PMID:[Clinical manifestation of toxic pancreas lesion in children with hematopoietic malignancies]. 1073 49

We present a case of fatal mesenteric vein thrombosis (MVT) associated with L-asparaginase (L-asp) therapy and temporally related to cryoprecipitate infusion, in an adult with acute lymphoblastic leukaemia (ALL). Cryoprecipitate was given on two consecutive days to raise a low fibrinogen level of 0.7 g/L, in the presence of severe thrombocytopenia and mucocutaneous bleeding. The thrombotic event presented as sudden abdominal pain a day after the second cryoprecipitate infusion, which raised the fibrinogen to 1.5 g/L. Concurrent levels of antithrombin III (AT III), protein C (PC) and protein S (PS) were very low. The patient died after laparotomy and wide resection of gangrenous bowel. We believe this is the first reported case in the English literature of a patient who developed mesenteric venous thrombosis during L-asp therapy, and once more we advise caution in using conventional blood products, especially cryoprecipitate, and recommend restricting the use of cryoprecipitate and fresh frozen plasma (FFP) to the treatment of serious hemorrhagic manifestations, until new effective and safe therapies are available.
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PMID:Cryoprecipitate-induced mesenteric venous thrombosis during L-asparaginase therapy for acute lymphoblastic leukaemia. 1142 67

L-asparaginase, an effective antileukemia and antilymphoma agent, is toxic to many organ systems. We report a case of ureteral obstruction caused by L-asparaginase via the inflammatory complication of acute pancreatitis. The patient was an 11-year-old boy with acute lymphoblastic leukemia. Six days after completing a 4-week induction therapy containing 9 doses of L-asparaginase, severe left abdominal pain developed. Abdominal computed tomography showed phlegmon formation anterior to the pancreatic head and in the left posterior pararenal space. The strands of inflammatory soft tissues encased the upper third of the left ureter, causing left hydroureter and left hydronephrosis. The ureteral obstruction resolved after insertion of a double-J catheter that remained in place for 66 days. This case suggests that L-asparaginase may play a role in the pathogenesis of ureteral obstruction in children receiving chemotherapy.
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PMID:Ureteral obstruction caused by L-asparaginase-induced pancreatitis in a child with acute lymphoblastic leukemia. 1521 6

A major complication of L-asparaginase used in the treatment of paediatric malignancies in children is pancreatitis (2%-16%). However, only seven paediatric cases of pancreatic pseudocyst caused by the utilization of the agent have been reported in literature. We present the case of a 5-year old girl who had abdominal pain and epigastric dullness after the third course of BMF-95 protocol with a diagnosis of ALL. A pancreatic pseudocyst of 10 x 10 cm size was found by abdominal tomography. The cyst was treated by percutaneous external drainage, total parenteral nutrition (TPN), administration of octreotide and antibiotherapy for one month. Percutaneous external drainage has proven to be an effective, noninvasive method in this special case with a systemic disorder and the high risk of mortality should a surgical intervention have been performed.
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PMID:Pancreas pseudocyst associated with L-asparaginase treatment: a case report. 1643 84

A dog with lymphosarcoma was evaluated for vomiting, lethargy, and abdominal pain 48 h after treatment with L-asparaginase. Based on drug administration, clinical signs, bloodwork, and elevated canine pancreatic lipase immunoreactivity, L-asparaginase-associated pancreatitis was diagnosed. This is an acknowledged toxicity; however, its pathophysiology and incidence rate in veterinary patients are unknown and sparsely documented.
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PMID:Asparaginase-associated pancreatitis in a dog. 2237 3

Acute pancreatitis and diabetic ketoacidosis are unusual adverse events following chemotherapy based on L-asparaginase and prednisone as support treatment for acute lymphoblastic leukemia. We present the case of a 16-year-old Hispanic male patient, in remission induction therapy for acute lymphoblastic leukemia on treatment with mitoxantrone, vincristine, prednisone, and L-asparaginase. He was hospitalized complaining of abdominal pain, nausea, and vomiting. Hyperglycemia, acidosis, ketonuria, low bicarbonate levels, hyperamylasemia, and hyperlipasemia were documented, and the diagnosis of diabetic ketoacidosis was made. Because of uncertainty of the additional diagnosis of acute pancreatitis as the cause of abdominal pain, a contrast-enhanced computed tomography was performed resulting in a Balthazar C pancreatitis classification.
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PMID:Acute Pancreatitis and Diabetic Ketoacidosis following L-Asparaginase/Prednisone Therapy in Acute Lymphoblastic Leukemia. 2471 37


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