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)

On July 24, 2006, the U.S. Food and Drug Administration granted approval to pegaspargase (Oncaspar; Enzon Pharmaceuticals, Inc., Bridgewater, NJ; hereafter, O) for the first-line treatment of patients with acute lymphoblastic leukemia (ALL) as a component of a multiagent chemotherapy regimen. O was previously approved in February 1994 for the treatment of patients with ALL who were hypersensitive to native forms of L-asparaginase. The trial supporting this new indication was an open label, randomized, multicenter clinical trial that enrolled 118 children (age, 1-9 years) with previously untreated, standard risk ALL. Patients received either native Escherichia coli asparaginase (Elspar; Merck, Whitehouse Station, NJ; hereafter, E) or O along with multiagent chemotherapy during remission induction and delayed intensification (DI) phases of treatment. O, at a dose of 2,500 IU/m(2), was administered i.m. on day 3 of the 4-week induction phase and on day 3 of each of two 8-week DI phases. E, at a dose of 6,000 IU/m(2), was administered i.m. three times weekly for nine doses during induction and for six doses during each DI phase. This study allowed direct comparison of O and E for asparagine depletion, asparaginase activity, and development of asparaginase antibodies. An unplanned comparison of event-free survival (EFS) was conducted to rule out a deleterious O efficacy effect. Following induction and DI treatment there was complete (</=1 microM) or moderate (1-10 microM) depletion of serum asparagine levels in the large majority of samples tested over the 4-week period in both O-treated and E-treated subjects. Similarly, depletion of cerebrospinal fluid asparagine levels during induction was similar between O-treated and E-treated subjects. The number of days asparaginase activity exceeded >0.03 IU/ml in O-treated subjects was greater than the number of days in E-treated subjects during both the induction and DI phases of treatment. There was no correlation, however, between asparaginase activity and serum asparagine levels, making the former determination less clinically relevant. Using the protocol-prespecified threshold for a positive result of >2.5 times the control, 7 of 56 (12%) O subjects tested at any time during the study demonstrated antiasparaginase antibodies and 16 of 57 (28%) E subjects tested at any time during the study had antiasparaginase antibodies. In both study arms EFS was in the range of 80% at 3 years. The most serious, sometimes fatal, O toxicities were anaphylaxis, other serious allergic reactions, thrombosis (including sagittal sinus thrombosis), pancreatitis, glucose intolerance, and coagulopathy. The most common adverse events were allergic reactions (including anaphylaxis), hyperglycemia, pancreatitis, central nervous system thrombosis, coagulopathy, hyperbilirubinemia, and elevated transaminases. Disclosure of potential conflicts of interest is found at the end of this article.
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PMID:FDA drug approval summary: pegaspargase (oncaspar) for the first-line treatment of children with acute lymphoblastic leukemia (ALL). 1776 59

The gastrointestinal tract is the preferred route for nutritional support in hospitalized patients. Patients with a functioning gastrointestinal tract, including those with pancreatitis or inflammatory bowel disease and those receiving chemotherapy, should be fed enterally. Parenteral nutrition (PN) should be limited to patients with gastrointestinal failure, including those with short gut syndrome, high-output fistula, prolonged ileus, or bowel obstruction. PN is associated with numerous complications, most notably increased risk of serious infection. Emerging data suggest that immunologic complications of PN may result from hyperglycemia and use of n-6 polyunsaturated fatty acids. Safety may be improved with a low-calorie formula and ensuring tight glycemic control with an insulin protocol. A lipid emulsion containing fish oil, olive oil, or both should replace soybean-containing emulsions. Supplemental glutamine, 0.2 g/kg/d to 0.5 g/kg/d, has been shown to reduce the risk of infection and to improve glycemic control.
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PMID:Maximizing efficacy from parenteral nutrition in critical care: appropriate patient populations, supplemental parenteral nutrition, glucose control, parenteral glutamine, and alternative fat sources. 1788 85

Arsenic trioxide (ATO) induces remission in 85% of adults with refractory acute promyelocytic leukemia (APL). We conducted a phase 1 trial of ATO in children (median age 13 y, range, 2-19) with refractory leukemia. ATO was administered intravenously over 2 hours, 5 d/wk for 20 doses/cycle. Patients with APL (n=13) received 0.15 mg/kg per day, and patients with other types of leukemia received 0.15 mg/kg per day (n=2) or 0.2 mg/kg per day (n=4). Nineteen of the 24 enrolled patients were fully evaluable for toxicity. At 0.15 mg/kg per day, 2 of 15 patients experienced dose-limiting corrected QT interval (QTc) prolongation, pneumonitis, or neuropathic pain. At 0.2 mg/kg per day, 2 of 4 patients had dose-limiting QTc prolongation or pancreatitis. Non-dose-limiting toxicities included elevated serum transaminases, nausea, vomiting, abdominal pain, constipation, electrolyte imbalance, hyperglycemia, dermatitis, and headache. At 0.15 mg/kg per day, the median (range) plasma arsenic maximum concentration (Cmax) was 0.28 microM (0.11-0.37 microM) and at 0.2 mg/kg per day, Cmax was 0.40 and 0.46 microM; area under the concentration times time curve (AUC0-24) was 2.50 microM-hr (1.28-3.85 microM-hr) and 4.37 microM-hr and 4.69 microM-hr, respectively. Morphologic complete response (CR) was achieved in 85% of patients with APL; no responses were observed in non-APL patients. ATO is well-tolerated in children at the recommended dose of 0.15 mg/kg per day. The response rate in children with relapsed APL is similar to the response rate in adults. This trial was registered as #NCT00020111 at www.ClinicalTrials.gov.
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PMID:Phase 1 trial and pharmacokinetic study of arsenic trioxide in children and adolescents with refractory or relapsed acute leukemia, including acute promyelocytic leukemia or lymphoma. 1795 55

A cockatiel (Nymphicus hollandicus) examined because of weight loss, polydipsia, and polyuria was diagnosed with diabetes mellitus based on the presence of glucosuria and marked hyperglycemia. Medical attempts to manage the diabetes mellitus were unsuccessful, and the bird was euthanatized. Histopathologic examination of the pancreas revealed a chronic active pancreatitis with herpesviral inclusions in many of the pancreatic acinar and duct cells. Psittacid herpesvirus-1 (PsHV-1) DNA was amplified from the lesion by polymerase chain reaction. Sequencing of the amplicon showed it to be the genotype 1 variant, which is most commonly associated with Pacheco's disease, an acute rapidly fatal systemic infection. The findings in this case suggest that the PsHV-1 genotype may also cause a localized disease of the pancreas. Infection with this virus should be considered as a differential diagnosis in birds with pancreatitis with or without diabetes mellitus.
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PMID:Endocrine pancreatic insufficiency secondary to chronic herpesvirus pancreatitis in a cockatiel (Nymphicus hollandicus). 1806 36

Pancreatic infiltration with leukemic cells is a rare manifestation of acute lymphoblastic leukemia. There are only a few reported cases. We report the clinical and radiologic findings of a 4-year-old boy with mature B-cell acute lymphoblastic leukemia and pancreatic involvement. A computed tomography scan of his abdomen demonstrated diffuse hypodense lesions in the pancreas. Plasma amylase and lipase levels at that time were high, but no signs of hypoglycemia or hyperglycemia were observed. After 2 cycles of chemotherapy, the lesions in his pancreas, liver, and kidney disappeared, and his pancreatitis resolved as well. At 11 months' follow-up, after completion of therapy, the patient continues to be in remission.
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PMID:A case with mature B-cell acute lymphoblastic leukemia and pancreatic involvement at the time of diagnosis. 1817 91

Hyperglycemia, abdominal pain, and vomiting are the most common manifestations of diabetic ketoacidosis in pediatric patients. The absence of ketonemia in these patients should prompt a consideration of acute pancreatitis. We report a case of an 11-year-old girl with acute necrotizing pancreatitis, who was initially diagnosed as having new onset diabetes with nonketotic hyperglycemia.
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PMID:A child with abdominal pain and hyperglycemia: is it diabetic ketoacidosis? 1821 9

We present a case of a 16-year-old adolescent boy with autoimmune pancreatitis and a review of the related literature. The patient was sent from a peripheral medical center, presenting with jaundice, pruritus, weight loss, and hyperglycemia of 20 days' duration. At admission, the patient was icteric, choluric, and acholic. His abdomen was soft and nontender, and the patient felt no pain in his abdomen. He had skin lesions because of scratching. Laboratory findings showed a blood glucose level of 135 mg%; total serum bilirubin, 29.4 mg%; direct bilirubin, 23 mg%; and alkaline phosphatase, 1100 IU/L. Abdominal ultrasound showed an enlarged head of the pancreas that was 30 x 35 mm. The parenchyma was slightly heterogeneous. Abdominal computed tomography showed an enlarged head of the pancreas with a normal body and tail, thickened duodenal wall, and dilated intra- and extrahepatic biliary tract, and the distal choledochus was not visible. Magnetic resonance imaging showed dilated intra- and extrahepatic biliary tract. The choledochus was not visible, and the cystic duct ended abruptly. The pancreas head was enlarged and homogenous, and there were no changes with contrast. Wirsung's duct was not dilated. Laparotomy was performed with a presumed diagnosis of pancreatic head tumor. The pancreas was diffusely indurated and enlarged; biopsy and intraoperative cholangiography were performed. The biliary tract was dilated with no duodenal passage of contrast, and the Wirsung's duct was not observed. Cholecystectomy was performed, and a transcystic drain was positioned. The histopathology was compatible with autoimmune pancreatitis. Prednisone treatment was started with good response. Autoimmune pancreatitis is a very rare entity among children and adolescents. It should be suspected when characteristic clinical signs and radiographic images are associated with a higher level of IgG4. Autoimmune pancreatitis is confirmed by biopsy. Treatment with prednisone often alleviates all the symptoms, as what happened in this case.
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PMID:Autoimmune pancreatitis: an adolescent case and review of literature. 1863 99

The hyperosmolar hyperglycemic nonketotic state (HHNS) is an acute metabolic complication occurring characteristically in elderly type-2 diabetic patients. It may account for 10 up to 47% of cases of severe hyperglycemia with or without ketoacidosis. Many factors associated with advanced age may explain the predilection of both elderly subjects in general and older diabetics in particular to develop hyperosmolar coma, including reduced glomerular filtration rate and elevated renal threshold for glucose (which fail to correct hyperglycemia by osmotic diuresis), lack of thirst appropriate to the state of hydratation and some iatrogenic factors. In HHNS the age of the patients is the best known prognostic indicator. The increased mortality rate in the elderly diabetics depends on the severity of precipitating acute diseases (gastrointestinal hemorrhage, cardiovascular accident, pneumonia, pancreatitis, etc.), but the frequent compromises of the hemodynamic state and renal function of aged subjects substantially contributes. However, the role of erroneous management is not negligible and difficulties may be encountered in conciliating correction of metabolic disorder with treatment of precipitating illness. Insulin, water and electrolytes are the most important therapeutical tools for the treatment of hyperglycemic emergencies. In HHNS, the aggressive fluid replacement with isotonic or hypotonic NaCl solutions have first priority. Such a type of strategy is difficult to perform in patients suffering from cerebral stroke (which needs of anti-edema therapy) or congestive heart failure (necessitating to avoid fluid excess). According to the literary data, in our experience these two precipitating factors are frequent causes of death. We outline the validity of prefixed protocols of management; on the other hand, we think that the pathophysiological understanding of HHNS in the single patient is essential to decide the proper corrections and to permit a successful outcome. The primary way aiming at diminishing mortality by HHNS is its prevention; it is fundamental to warrant an appropriate fluid intake and to utilize with caution some drugs (thiazides, steroids, phenytoin, etc.) in aged diabetics, especially when nephropathic or unable, or living in nursing homes.
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PMID:Diabetic non ketotic hyperosmolar state: a special care in aged patients. 1865 40

A 3-year-old male nanday conure (Nandayus nenday) was presented with acute lethargy, polyuria, and polydipsia. Marked persistent hyperglycemia, glycosuria, and ketonuria were also noted. The serum insulin concentration (< 3 microU/ml) was lower than reference ranges described for other psittacine birds. Initial treatment included insulin, antibiotics, and supportive care. Insulin therapy was adjusted based on results of serial blood glucose curves. Histopathologic examination of pancreatic biopsy samples revealed normal exocrine pancreatic tissue with rare lymphoplasmocytic infiltrates and absence of pancreatic islets, suggesting atrophy of endocrine pancreatic tissue. Resolution of clinical signs and a normalized blood glucose curve were obtained after administration of long-acting insulin (0.3 IU/kg IM AM and 0.25 IU/kg IM PM). One month after initial presentation, the conure was admitted for severe dyspnea and lethargy and died despite supportive care. Histopathologic examination of the pancreas revealed nearly total depletion of the endocrine pancreas with moderate lymphoplasmocytic pancreatitis. Immunohistochemical evaluation of the remaining pancreatic islets was negative for the presence of insulin and positive for glucagon. Results of polymerase chain reaction tests for Chlamydophila psittaci performed on tissues from the liver, spleen, and lung were negative. Transmission electron microscopy did not demonstrate viruses. Clinical and pathological findings observed in this case are consistent with insulin-dependant type 1 diabetes.
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PMID:Diabetes mellitus in a nanday conure (Nandayus nenday). 1901 99

Glucocorticoids are used as anti-inflammatory agents and are associated with many side effects including hyperglycemia, hypertension, pancreatitis, peptic ulcer, and so on. Hyperglycemia is a common side effect, but ketoacidosis is observed rarely. We present a girl who developed diabetic ketoacidosis after the administration of methylprednisolone during the treatment of acute rheumatic fever. She did not have diabetes and was not obese. She developed ketoacidosis after glucocorticoid therapy. Glucocorticoid-induced insulin resistance, lipolysis, and ketogenesis were likely to have precipitated ketoacidosis. During the treatment of ketoacidosis, the insulin need of the patient was gradually decreased by reducing glucocorticoid dose. In addition to the gradual reduction in glucocorticoid dose, salicylate therapy could be considered the treatment for insulin resistance. In this patient, screening for blood gases and urine was diagnostic in the diagnosis of ketoacidosis. The risk of ketoacidosis as well as hyperglycemia should be considered in the course of glucocorticoid therapy.
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PMID:Glucocorticoid-induced diabetic ketoacidosis in acute rheumatic fever. 1908 51


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