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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The main purpose of this study was to investigate the influence of early total parenteral nutrition on acute sodium-taurocholate-induced pancreatitis in rats. Total parenteral nutrition did not change the survival rate, serum amylase, calcium or liver transaminase level on the degree of pancreatic damage, but reduced serum acid phosphatase and lactate dehydrogenase levels. Hyperglycemia occurred during the use of total parenteral nutrition. Total parenteral nutrition is not harmful in the course of acute experimental pancreatitis, and could be used with few side effects.
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PMID:The influence of early total parenteral nutrition on experimental pancreatitis in rats. 768 45

The treatment of the acute lymphoblastic leukemia in childhood includes frequent administration of L-asparaginase by intravenous route. L-asparaginase is an enzyme produced by E. coli and Erwinia chrysanthemi strains. Adverse reactions produced by L-asparaginase are numerous, and pancreatitis is being the most severe. Children with the acute lymphoblastic leukemia were followed up for 2 years. Hyperglycaemia and glycosuria were noted in 10% of them resulting in L-asparaginase cessation or replacement by less toxic agents. The acute pancreatitis was produced in 8% of the patients, and was treated typically.
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PMID:[Acute pancreatitis in children with acute lymphoblastic leukemia treated with L-asparaginase]. 780 58

This study analyzed the prevalence, aggravating factors (including duration of diabetes, glycemic control, body mass index, hypertension, serum total cholesterol, changes of ST on ECG and diabetic therapies) and characteristics of diabetic retinopathy in 75 patients with pancreatic diabetes resulting from calcifying pancreatitis. The patients were divided into three Groups: Group I (27 patients in whom diabetes was detected earlier than pancreatic stones), Group II (36 patients in whom diabetes and pancreatic stones were simultaneously detected) and Group III (12 patients in whom pancreatic stones were detected earlier than diabetes). The prevalence of retinopathy was dependent on the duration of diabetes as well as poor glycemic control. It was significantly (p < 0.01) higher among the patient with the duration of diabetes that was more than 5 years than that of the patients whose duration was less than 5 years. The prevalence of retinopathy in Group I (63%) was significantly (p < 0.05) higher than that in Group II (30.6%) and Group III (12.5%). Proliferative retinopathy was not found in any patients with a duration of diabetes less than 5 years, while it was found in 5 patients with a duration of more than 5 years (5 cases out of 31 patients). Diabetic retinopathy was correlated with the duration of diabetes and glycemic control, and was not linked to frequency of hypoglycemia and family history of diabetes. From the results above, we concluded that diabetic retinopathy in patients with pancreatic diabetes due to calcifying pancreatitis might be taken as evidence that such complications are primarily due to chronic hyperglycemia and the duration of diabetes mellitus rather than to genetic factors and other factors (body mass index, hypertension, serum total cholesterol and diabetic therapies).
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PMID:Diabetic retinopathy in Japanese patients with long-standing pancreatic diabetes due to calcifying pancreatitis. 786 4

We show Escherichia coli derived L-asparaginase complications observed in 14 of 136 acute lymphoblastic leukemia patients during remission induction therapy according to St. Jude Children's Hospital Total XI Protocol. We observed hyperglycemia in six patients; two of them had accompanying ketoacidosis. One of the cases with ketoacidosis had peritonitis and pancreatitis. Central nervous system symptoms such as convulsions and depression with personality changes (in one case) were observed in four of these six hyperglycemic patients. Intracranial bleeding and ischemic infarction were shown in cranial computed tomographies in two cases. Hypersensitivity reactions were observed in seven patients. Patients were randomly assigned into two groups and treated with conventional dose steroids or high dose methylprednisolone. Although the frequency of hypersensitivity reactions were lower in the high dose methylprednisolone group, one patient in this group had an anaphylactic reaction. These findings once again high-light L-asparaginase complications which are not dose dependent and can be life threatening.
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PMID:Hyperglycemia, ketoacidosis and other complications of L-asparaginase in children with acute lymphoblastic leukemia. 799 65

Patients with the acquired immunodeficiency syndrome (AIDS) can develop pancreatic disease from causes unrelated to AIDS as well as AIDS-specific lesions. AIDS-specific causes include opportunistic infection, AIDS-associated neoplasia, and medications used to treat complications of AIDS. Reported pancreatic opportunistic pathogens include Mycobacterium tuberculosis, Mycobacterium avium intracellulare, Cryptococcus neoformans, Candida, Aspergillus, Toxoplasma gondii, Pneumocystis carinii, cytomegalovirus, herpes simplex, cryptosporidium, and microsporidium. Although cytomegaloviral pancreatic infection can occur without clinically evident pancreatic disease, cytomegalovirus can cause pancreatitis. Other opportunistic infections that can cause pancreatitis include Toxoplasma gondii, Cryptococcus neoformans, and Candida. Mycobacterial infection can produce a pancreatic abscess. Hepatobiliary or pancreatic duct infection by cytomegalovirus, cryptosporidium, and microsporidium causes irregular ductular narrowing and dilatation. This cholangiographic abnormality resembles the pattern found in idiopathic sclerosing cholangitis. Reported AIDS-associated pancreatic neoplasms include Kaposi's sarcoma and lymphoma. Pancreatic involvement is usually part of widely disseminated tumor and rarely produces clinical symptoms. Pentamidine, trimethoprim-sulfamethoxazole, and 2', 3'dideoxyinosine are medications commonly used in AIDS patients which can cause pancreatitis. Pentamidine also causes hypoglycemia or hyperglycemia.
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PMID:Pancreatic disease in AIDS--a review. 822 89

Eighteen patients with acute hemorrhagic necrotizing pancreatitis who survived from operation were followed up for 12 to 43 months. Late complications including pancreatic external fistula, pseudocyst, hyperglycemia, etc were reviewed. The pancreatic juice was collected through endoscopic cannulation. The volume and HCO3- concentration of the pancreatic juice and three kinds of pancreatic enzymes were measured. The results demonstrated that inspite of anatomic abnormality or functional impairment of the pancreas, the pancreatic insufficiency rarely manifested to be marked because of the compensative ability of the viable exocrine pancreas.
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PMID:Long-term results of surgical treatment for acute hemorrhagic necrotizing pancreatitis. 824 20

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

We report an autopsy case of acute-onset insulin-dependent diabetes mellitus, type I, that occurred in an adult. The patient died 3 days after the clinical onset of diabetes. Hyperglycemia, ketonuria, and hyperamylasemia were observed at admission. The pathologic examination of the pancreas showed a markedly decreased number of islets, and residual islets were small and shrunken. Diffuse inflammatory cell infiltrates, which were found in islets and also in acini, were mainly T lymphocytes. Shrunken islets were composed of insulin cells, glucagon cells, somatostatin cells, and pancreatic polypeptide cells. A decreased number of zymogen granules in acini were prominent [corrected]. This case suggested that pan-pancreatitis, destroying whole islets and acini, can initiate insulin-dependent diabetes mellitus.
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PMID:Vanished islets with pancreatitis in acute-onset insulin-dependent diabetes mellitus in an adult. 828 38

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

Triciribine is a purine analogue which inhibits DNA and protein synthesis. We performed two studies to define its activity against metastatic breast cancer. The first study was a phase II study in 14 patients with metastatic breast cancer who had received two or fewer chemotherapy treatments. The treatment schedule was tricirbine 20 mg/m2 per day by 24-h infusion (CI) daily for 5 days every 6 weeks as recommended by a previous open phase I trial. When neither response nor toxicity was seen in the phase II trial, we assumed the starting dose was too low for this group of patients with good performance status and repeated the phase I trial in patients with metastatic breast cancer with good performance status. The starting dose was 35 mg/m2 per day using the same 5-day CI schedule, and starting doses were increased in subsequent cohorts of three patients in increments of 5 mg/m2 until toxicity occurred. In the initial (phase II) study, one patient had stable disease for 18 weeks (three courses), the remainder progressed. There were no significant toxic effects. In the subsequent phase I study, ten patients were treated until the study was closed. The maximum dose was 40 mg/m2. Two patients died, one each at the 35 and 40 mg/m2 levels, respectively, 3 months and 6 weeks after their last course, one without intervening disease progression. Both had severe hypertriglyceridemia (18- and 21-fold elevation) and severe fatigue. At postmortem examination, one had congestive cardiomyopathy, and the other had severe pancreatitis and hypothyroidism. One patient had severe exacerbation of psoriasis which made her bedridden for more than 30 days. Four patients had hyperglycemia. Plasma pharmacology studies showed erratic drug levels, presumably related to enterohepatic circulation. Postmortem pharmacology studies showed residual drug present as long as 12 weeks after the last dose. We conclude that triciribine is ineffective at all doses tested and at doses of > or = 35 mg/m2 has unacceptable toxic effects.
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PMID:Phase I-II study: triciribine (tricyclic nucleoside phosphate) for metastatic breast cancer. 852 86


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