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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

L-asparaginase (L-Asp)-associated pancreatitis (AAP) occurs occasionally; however, this side-effect has predominantly been observed among pediatric patients. Usually, it is not life-threatening and generally responds to intensive medical therapy. The present study presents a rare case of lethal AAP in an adult. The patient was recently diagnosed with extranodal natural killer/T-cell lymphoma (ENKTL), nasal type, and the chronic hepatitis B virus (HBV) infection and was receiving L-Asp as part of a chemotherapy regimen. Severe acute pancreatitis occurred and the patient succumbed 72 h after completion of chemotherapy. The HBV infection and lipid disorders may have been potential risk factors for the development of severe acute pancreatitis in the patient.
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PMID:L-asparaginase-induced severe acute pancreatitis in an adult with extranodal natural killer/T-cell lymphoma, nasal type: A case report and review of the literature. 2494 14

A 15-year-old boy was admitted to our hospital with a recent increase in the size of a preexisting pancreatic pseudocyst. At 11 years of age, he was diagnosed with acute lymphoid leukemia (ALL) and received chemotherapy with L-asparaginase (L-Asp); he developed the pancreatic pseudocyst following L-Asp-induced acute pancreatitis. The pancreatic pseudocyst had increased to 120mm in diameter. He developed epigastralgia and portal hypertension. Endoscopic ultrasound (EUS)-guided cystogastrostomy with the placement of a 7-cm 7-Fr plastic stent and a 5-Fr NB pigtail catheter led to the near-complete resolution of the pseudocyst. There were no signs of recurrence within the first year after intervention. EUS-guided drainage, increasingly used for pseudocysts, should be considered as an effective treatment approach for pediatric pancreatic pseudocysts.
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PMID:Endoscopic ultrasound-guided cystogastrostomy for successful drainage of pancreatic pseudocyst: a pediatric case report. 2674 56

L-Asparaginase has significantly improved outcome for children with acute lymphoblastic leukemia and has become an essential component of multiagent chemotherapy. However, there are many adverse events due to L-asparaginase, including acute pancreatitis. The pathology of L-asparaginase-associated pancreatitis (AAP) remains unclear. We compared patients who developed AAP (n=29) and random matched controls (n=36) who had been enrolled in the Japan Association of Childhood Leukemia Study of the ALL-02 protocol. AAP and control patients were matched for age, sex, treatment, and protocol risk. We examined correlations between AAP development and clinical symptoms, laboratory data, and concomitant medication. Abdominal pain and nausea were common presenting symptoms for AAP. There was an increased risk of AAP in patients using gastric acid-suppressing agents and antithrombin (AT) supplementation. Mean fibrinogen and AT levels before the onset of AAP were lower in AAP patients than in controls. Decreased AT and fibrinogen levels resulting from the strong suppression of protein synthesis by L-asparaginase were predictive signs for AAP. Our epidemiological approach should prove clinically useful for the diagnosis the AAP as early as possible.
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PMID:Acid-suppressing Drugs and a Low 1 Level of Antithrombin as Risk Factors for L-Asparaginase-associated Pancreatitis: A Case-control Study in the Japan Association of Childhood Leukemia Study (JACLS). 2969 79

The chylomicronemia syndrome is characterized by severe hypertriglyceridemia and fasting chylomicronemia and predisposes affected individuals to acute pancreatitis. When due to very rare monogenic mutations in the genes encoding the enzyme, lipoprotein lipase, or its regulators, APOC2, APOA5, GPIHBP1, and LMF1, it is referred to as the familial chylomicronemia syndrome. Much more frequently, the chylomicronemia syndrome results from a cluster of minor genetic variants causing polygenic hypertriglyceridemia, which is exacerbated by conditions or medications which increase triglyceride levels beyond the saturation point of triglyceride removal systems. This situation is termed the multifactorial chylomicronemia syndrome. These aggravating factors include common conditions such as uncontrolled diabetes, overweight and obesity, alcohol excess, chronic kidney disease and pregnancy and several medications, including diuretics, non-selective beta blockers, estrogenic compounds, corticosteroids, protease inhibitors, immunosuppressives, antipsychotics, antidepressants, retinoids, L-asparaginase, and propofol. A third uncommon cause of the chylomicronemia syndrome is familial forms of partial lipodystrophy. Development of pancreatitis is the most feared complication of the chylomicronemia syndrome, but the risk of cardiovascular disease as well as non-alcoholic steatohepatitis is also increased. Treatment consists of dietary fat restriction and weight reduction combined with the use of triglyceride lowering medications such as fibrates, omega 3 fatty acids and niacin. Effective management of aggravating factors such as improving diabetes control, discontinuing alcohol and replacing or reducing the dose of medications that raise triglyceride levels is essential. Importantly, many if not most cases of the chylomicronemia syndrome can be prevented by effective identification of polygenic hypertriglyceridemia in people with conditions that increase its likelihood or before starting medications that may increase triglyceride levels. Several new pharmacotherapeutic agents are being tested that are likely to considerably improve treatment of hypertriglyceridemia in people at risk.
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PMID:A Comprehensive Update on the Chylomicronemia Syndrome. 3319 6


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