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)

We reviewed adverse event (AE) data in the National Cooperative Growth Study from start-up (1985) until January 1, 1999. Enrollment was 33,161. A total of 2,632 AE reports were received; 863 were serious events, with 156 deaths. The most common cause of death was recurrence of intracranial neoplasm. There were 20 reports of leukemia, and the standard morbidity ratio (SMR) was 0.73 (95% CI: 0.20-1.86) for the four cases without risk factors. There were 35 reports of extracranial nonleukemic malignancy, and the SMR was 0.44 (95% CI: 0.24-0.74) for the 14 cases without risk factors. The recurrence rate for all brain tumors present at baseline was 7.6%, and for craniopharyngiomas, 6.4%. There were 49 reports of intracranial hypertension (20 patients had papilledema), 68 reports of diabetes/hyperglycemia, 45 of slipped capital femoral epiphysis, 136 of scoliosis, and five of pancreatitis. There was no evidence of increased incidence of leukemia or extracranial nonleukemic malignancies among patients without prior risk factors. Intracranial hypertension does not necessarily occur early in growth hormone therapy. Other findings were consistent with past observations.
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PMID:Growth hormone safety update from the National Cooperative Growth Study. 1108 59

The metabolism of acute pancreatitis is characterized by hypermetabolism and catabolism. Evidence for glucose intolerance occurs in anywhere from 40 to 90% of cases and urine urea nitrogen may increase up to 40 g/day. The most important aspect when considering nutritional therapy is determining the severity of the pancreatitis. The APACHE-II-scoring-system and the time honored Ranson criteria are useful for differentiating severe from mild pancreatitis. Despite some limitations in sensitivity and specificity, studies have suggested that patients with 2 or less Ranson criteria and an APACHE-II-score of 9 or less have mild pancreatitis, while patients with 3 or more Ranson criteria and an APACHE-II-score of 10 or more have severe pancreatitis. Evidence of organ failure on clinical presentation and pancreatic necrosis on dynamic CT scan are also important factors in determining severity of pancreatitis and are probably the two major indicators of patient outcome. Only 3 prospective randomized controlled trials have compared enteral to parenteral nutrition for pancreatitis. All studies described successful use of enteral feeding without exacerbating the disease process although a mild stimulation of exocrine pancreatic secretion could not be prevented, even when the tube was placed below the ligament of Treitz. Kalfarentzos [11] and McClave [14] could show that hyperglycemia was worse in the parenteral feeding patients compared to the enteral feeding group and Windsor [24] concluded with respect to the results of his study, that enteral feeding modulates the inflammatory response in acute pancreatitis. Conclusions regarding the use of enteral or parenteral nutrition in acute pancreatitis are difficult to form, as there is a need of more prospective studies. As ileus may be a problem in patients with greater severity of pancreatitis, limiting the application of early enteral feeding, the route of nutritional support should be determined by the clinical course and the severity of the disease.
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PMID:[Enteral nutrition in acute pancreatitis]. 1122 88

This paper describes a 6-year-old Simmental bull with diabetes mellitus. The animal was referred to our clinic because of severe weight loss and chronic indigestion. Clinical examination revealed markedly disturbed general condition, impaired forestomach function and polyuria. There was aciduria, glucosuria and ketonuria. The most important biochemical findings were severe hyperglycemia, markedly increased activities of hepatic enzymes and severe metabolic acidosis. Plasma concentrations of insulin, insulin-like growth factor-I, thyroxine and 3,5,3'-triiodothyronine were lower than normal, whereas those of glucagon were higher than normal. Based on these findings, a diagnosis (secondary) diabetes mellitus was made. The bull was slaughtered and histological examination revealed mixed cell pancreatitis with severe degeneration of islet cells. Immunohistochemical examination of the pancreas showed that very few insulin-, glucagon-, somatostatin- and pancreatic polypeptide, insulin-like growth factor-I and adrenomedullin-producing islet cells were present.
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PMID:[Diabetes mellitus caused by pancreatitis in a bull]. 1123 31

Coxsackieviral infections have been linked etiologically to multiple diseases. The serotype CB4 is associated with acute pancreatitis and autoimmune type 1 diabetes. To delineate the mechanisms of host survival after an acute infection with CB4 (strain E2), we have investigated the role of nitric oxide (NO), generated by the inducible form of nitric oxide synthase (NOS2), in viral clearance and pancreatic beta-cell maintenance. Mice deficient in NOS2 (NOS2-/- mice) and their wild-type (wt) counterparts were injected with CB4, after which both groups developed severe pancreatitis, hepatitis, and hypoglycemia within 3 days. Within 4 to 7 days postinfection (p.i.), most of the NOS2-/- mice died and at a strikingly higher mortality rate than wt mice. Histological examination of pancreata from both infected NOS2-/- and infected wt mice revealed early and complete destruction of the pancreatic acinar tissue, but intact, insulin-stained islets. When examined up to 8 weeks p.i., neither surviving NOS2-/-mice nor surviving wt mice developed hyperglycemia. However, the clearance of infectious CB4 was different between the mice. The spleens of NOS2-/- survivors were cleared of infectious virus with kinetics similar to that of wt mice, but the livers, pancreata, kidneys, and hearts of the NOS2-/- groups cleared virus more slowly than those of the wt group. This delayed clearance was particularly prominent in the livers of infected NOS2-/- mice, which also showed prolonged histopathological features of viral hepatitis. Taken together, this outcome suggests that NOS2 (and NO) is not required for the prevention of pancreatic beta-cell depletion after CB4 infection. Instead the critical actions of NOS2 apparently occur early in the host immune response, allowing mice to survive and clear virus. Moreover, the data support the existence of an organ-specific dependency on NO for a rapid clearance of CB4.
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PMID:A critical role for inducible nitric oxide synthase in host survival following coxsackievirus B4 infection. 1127 93

It is well recognized that acetaminophen overdose can cause severe hepatic injury. However, extra-hepatic manifestations may also develop following inappropriate use or ingestion of large amounts of acetaminophen. We present a 44-y-o female who manifested coma, metabolic acidosis, shock, hypothermia, hyperglycemia, rhabdomyolysis, hepatotoxicity, and renal insufficiency after suicidal ingestion of an unknown amount of acetaminophen. Although her consciousness and hemodynamic status gradually improved after treatment with N-acetylcysteine and other supportive measures, she was found to have pancytopenia, pancreatitis and hepatorenal failure during the hospitalization and eventually died 18 d post-admission. Review of relevant literature reports and the clinical findings in our patient suggests that direct toxic effects mediated by acetaminophen or its metabolites were most likely responsible for most of the observed clinical features.
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PMID:Pancytopenia, hyperglycemia, shock, coma, rhabdomyolysis, and pancreatitis associated with acetaminophen poisoning. 1175 93

The purpose of this retrospective study was to evaluate the use of partial parenteral nutrition (PPN) in dogs and cats. The medical records of all dogs and cats receiving PPN between 1994 and 1999 were reviewed to determine signalment, reasons for use of PPN, duration of PPN administration, duration of hospitalization, complications, and mortality. Complications were classified as metabolic, mechanical, or septic. One hundred twenty-seven animals (80 dogs and 47 cats) were included in the study, accounting for 443 patient days of PPN. The most common underlying diseases were pancreatitis (n = 41), gastrointestinal disease (n = 33), and hepatic disease (n = 23). Median time of hospitalization before initiation of PPN was 2.8 days (range, 0.2-10.7 days). Median duration of PPN administration was 3.0 days (range, 0.3-8.8 days). Median duration of hospitalization was 7 days (range, 2-20 days). In the 127 animals receiving PPN, 72 complications occurred. These included metabolic (n = 43), mechanical (n = 25), and septic (n = 4) complications. The most common metabolic complication was hyperglycemia (n = 19), followed by lipemia (n = 17) and hyperbilirubinemia (n = 6). Most complications were mild and did not require discontinuation of PPN. Ninety-three (73.2%) of the 127 patients were discharged. All 4 animals with septic complications were discharged from the hospital. The presence, type, and number of complications did not impact the duration of hospitalization or outcome. However, animals that received supplemental enteral nutrition survived more often than those receiving PPN exclusively. Although PPN seems to be a relatively safe method of providing nutritional support, future studies are warranted to determine its efficacy.
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PMID:Retrospective evaluation of partial parenteral nutrition in dogs and cats. 1214 6

Diabetic ketoacidosis (DKA) and pancreatic pseudocysts are rare complications following treatment of hematological malignancies with L-asparaginase (L-asp). Persistent hyperglycemia with recurrent DKA presenting as a long-term complication of L-asp-induced pancreatitis is even rarer. A 21-year-old man with pre-B-type acute lymphoblastic leukemia (ALL) developed pancreatic pseudocysts, DKA and persistent hyperglycemia after L-asp therapy. The patient was treated with oral hypoglycemic agents (OHA) for sugar control thereafter. Ten months later, another episode of DKA developed during relapsed ALL without having obvious precipitating factors. Insulin was then instituted for control of his blood sugar until death. The leukemic process may play some role in glucose homeostasis and may be considered as a precipitating factor for DKA. The patient finally died of disease progression of ALL and sepsis 2 years after the initial diagnosis of ALL.
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PMID:Diabetic ketoacidosis and persistent hyperglycemia as long-term complications of L-asparaginase-induced pancreatitis. 1243 31

Neonatal diabetes mellitus (NDM) is defined as hyperglycemia occurring in the first few weeks of life. It can be either transient (TNDM) or permanent (PNDM). A 25 days old newborn was brought to the hospital with restlessness, respiratory depression and cyanosis. He was born at term with a birth weight of 2,000 g. There was no consanguinity between his parents. His physical examination findings were as follows: Weight and height were under 3th percentile, he was hypoactive and dehydrated. Serum glucose level was 800 mg/dl; C-peptide was 0.41 ng/ml. Upon investigation for dyslipidemia in association with his neonatal diabetes, hyperchylomicronemia was found both in the patient and his father. Pancreatitis, anemia and cholestasis were also observed. Insulin treatment was started for his diabetes together with a special diet for dyslipidemia. At the end of 28 months of follow-up, dyslipidemia has resolved but the need for insulin therapy was still existing. However, TNDM was considered in differential diagnosis because he was small for gestational age (SGA) at birth and his symptoms had started at the 25th day of the neonatal period. Delayed recovery from insulin dependency brought out the possibility of PNDM. Furthermore, neonatal diabetes combined with hypechylomicronemia is a rare clinical picture. Reported cases of NDM with different clinical evaluation will help to better understanding of this disorder.
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PMID:Neonatal diabetes with hyperchylomicronemia. 1255 65

Acute biliary pancreatitis (ABP) is a serious complication of biliary stones disease and is associated with significant morbidity and mortality. The role of ERCP in the management of ABP has been the focus of discussion in recent years. In this report, we evaluated a protocol of emergency Endoscopic retrograde Cholangiopancreatography (ERCP) (within 24 hours) and early ERCP (within 72 hours). From July 1997 to July 2000, were observed 45 patients (19 man and 26 women) with acute biliary pancreatitis. Mean age of patients was 63.4 years (range 21-87 years). Diagnosis of ABP was based on anamnesis and clinical assessment and was confirmed by specific laboratory data (hyperamylasemia, hyperlipasemia, total and fractionated bilirubinemia, gamma-GT, transaminase, alkaline phosphatase, hypocalcemia, hyperglycemia, leukocytosis). Ultrasound scanning within 24 h of admission was performed in 45 patients (100%) and it revealed gallbladder stones and muddy bile in 39 patients (87%). Computed tomography (CT) performed in all patients, showed a severe acute pancreatitis in the second or subsequent week following admission. The severity of acute pancreatitis was established by Glasgow's criteria and by clinical details of patients. ERCP and Endoscopic Sphinterotomy (ES) was performed in all 45 patients with acute biliary pancreatitis. Twenty-six patients (57%) were classified as having a severe attack (> 4) 19 as having a mild attack by Glasgow's criteria. ERCP associated with ES was performed within 24 hours in 22 patients (49%), 11 (50%) showed a severe attack and 11 (50%) showed a mild attack. A total of 2 complications (4%) occurred and the mortality was of 2 patients (4%). In 23 patients (51%) ERCP and ES was performed within 72 hours after conservative therapy, 8 (35%) showed a mild attack and 15 (65%) showed a severe attack. A total of 5 complications (9%) occurred and the mortality was of 3 patients (6%). Our study showed that ERCP with endoscopic sphincterotomy can be performed safely by skilled endoscopist, without adverse consequences soon after the onset of acute biliary pancreatitis even within the first 24 hours and it showed that is better than ERCP within 72 hours after conservative therapy.
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PMID:ERCP and acute pancreatitis. 1260 52

A 38-year-old man developed severe diabetic ketoacidosis complicated with rhabdomyolysis and acute renal failure after presenting hyperglycemic symptoms for 4 days. Initial investigation showed significant hyperglycemia (blood glucose level 1,593 mg/dl) with a relatively low level of HbA1c (7.0%) and a high pancreatic enzyme concentration without any signs of pancreatitis. Diabetes-related antibodies were absent except for the anti-glutamic acid decarboxylase antibody, which disappeared later on. Pancreatic biopsy examination showed the lack of insulin-secreting cells, without insulitis. These findings were almost consistent with non-autoimmune fulminant type 1B diabetes. The patient remained dependent on dialysis for 1 month, then his renal function recovered. In patients with this type of diabetes, the onset of overt diabetes, frequently accompanied with severe diabetic ketoacidosis, is rapid, hence, early detection, quick diagnosis and immediate treatment of this novel type of diabetes are important in the rescue of these patients.
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PMID:A case of acute renal failure due to rhabdomyolysis, associated with non-autoimmune fulminant type 1B diabetes mellitus. 1270 72


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