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)

Balb/c weanling mice were intraperitoneally inoculated with a myocarditic variant of coxsackievirus B3, with the aim of characterizing more thoroughly the features of virus-induced cell injury in pancreas and heart, as well as to compare ultrastructural alterations with histological and virological findings. During the first week post-infection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. At electron microscopy, acinar cells showed patent distortion, including marked loss of organelles and zymogen granules, together with gross dilatation of rough endoplasmic reticulum. Cardiac cells presented severe cytoskeletal changes, as myofibrillar collapse with a haphazard arrangement, concomitant with a decrease in myofibril number; besides, irregular pattern of nuclear chromatin and increased presence of swollen mitochondria were often observed. As the few initially detected lymphocytes tended to disappear in necrotic foci, there was an increase in fibroblast number concurrent with progressive scarring. Ultrastructural changes in both pancreas and heart correlated with local viral replication, suggesting that cell damage is attributable to direct viral action.
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PMID:Ultrastructural study of cell injury induced by coxsackievirus B3 in pancreatic and cardiac tissues. 820 11

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

In acute destructive pancreatitis due to rapidly developing endotoxicosis, marked circulatory disturbances, deep disturbance of homeostasis and functional insufficiency of vital organs, urgent surgery is necessary in order to remove necrotic parts of the pancreas as the main source of heavy toxemia resulting in shock and collapse.
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PMID:[Current aspects of acute destructive pancreatitis]. 958 94

Severe trauma, infection, burn, pancreatitis and major surgery often induce circulatory collapse leading to multiple organ failure and death. It is hypothesized that therapy for the attenuation of circulatory collapse may improve the prognosis in these diseases. Previous work has documented that pretreatment with a deleted form of hepatocyte growth factor (dHGF) in normal rats increases the circulating plasma volume that reflects its accelerating action of hepatic protein synthesis. Therefore, the effects of pretreatment with dHGF on hypovolemic shock models were studied in rats. Rats were intravenously administered dHGF (1 mg/kg, twice daily for 5-6 days) or vehicle, and subjected to a 25% total body surface area full-thickness burn or a trypsin-induced acute pancreatitis. In rats that were receiving vehicle, survival rates on day 7 after injury induction were 12% in the burn model and 5% in the pancreatitis model, respectively. In both models, hematocrit values were apparently increased and circulating plasma volumes were decreased compared to sham-operated rats at 6 h after injury induction. The pretreatment of animals with dHGF increased the survival rates on day 7 to 40% in the burn model and 29% in the pancreatitis model. dHGF-treatment in normal rats decreased the hematocrit values and increased the circulating plasma volumes, and these changes of hematocrit value and circulating plasma volume were also maintained after injury induction. These findings suggest that dHGF pretreatment prevents the mortality in the severe burn and acute pancreatitis, and that its effect may contribute to ameliorating the progressing of plasma-loss-induced hypovolemia.
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PMID:Pretreatment with a deleted form of hepatocyte growth factor (dHGF) prevents the mortality of plasma-loss-induced hypovolemic shock in rats. 1177 41

Respiratory complications are major factors contributing to death in acute pancreatitis. However, the mechanisms of these pulmonary complications are not completely elucidated. We studied the effects of pretreatment with purified crotapotin (a phospholipase A2 inhibitor), N-acetylcysteine (a reactive oxygen species inhibitor), and a combination of both on the pulmonary mechanical and morphometric changes secondary to severe acute necrohemorrhagic pancreatitis in Wistar rats. A total of 69 male Wistar rats were studied. Pancreatitis was induced by infusion of 0.5 mL of a 4% solution of sodium taurocholate into the biliopancreatic duct. Crotapotin, N-acetylcysteine, or a combination of both was given intraperitoneally 30 min before inducing pancreatitis. Data were compared with data from sham-operated animals with or without those pretreatments. The severity of pancreatic and pulmonary injuries was evaluated 4 h after inducing pancreatitis by morphometric and pulmonary mechanical studies. N-acetylcysteine prevented the development of alveolar edema, alveolar distention, and collapse. Crotapotin prevented alveolar distention and collapse, and pulmonary dynamic elastance increase. When used in combination, crotapotin and N-acetylcysteine prevented both pulmonary morphological and mechanical changes induced by acute pancreatitis, suggesting an increase in protective effect when these drugs are used together compared with individual effects. However, the severity of pancreatic necrosis and the increase in polymorphonuclear cells in alveolar septa induced by pancreatitis were not reduced by previous administration of crotapotin, N-acetylcysteine, or both. These results suggest that the protective effects of these drugs are probably due to an extra-pancreatic action in the circulation, or even directly in the lung.
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PMID:Acute lung injury in experimental pancreatitis in rats: pulmonary protective effects of crotapotin and N-acetylcysteine. 1241 21

Lactic acidosis (LA), a rare but life-threatening adverse effect associated with antiretroviral therapy, has been reported with an increasing frequency since the mid-1990s. From June 1994 to June 2002, a total of six patients, four males and two females with a median age of 43 years (range, 30 to 74 years), had been diagnosed with LA. The estimated incidence of LA was 5.1 per 1000 patient-years (PYs) on highly active antiretroviral therapy (HAART) (95% confidence interval [95% CI], 4.5-5.5 per 1000 PYs) and 4.4 per 1000 PY on nucleoside analogues (NAs) (95% CI, 3.9-4.7 per 1000 PYs). Their median body mass index at diagnosis of LA was 17.6 kg/m(2) (range 16.3 to 22.6 kg/m(2)). The median CD4+ lymphocyte count at the initial diagnosis of HIV infection and at the onset of LA was 38 cells/ micro L (range, 4 to 103 cells/ micro L) and 108 cells/ micro L (range, 79 to 224 cells/ micro L), respectively. The most common symptoms were nausea, vomiting, and dyspnoea. All of the patients had findings suggestive of NA-related mitochondrial toxicity, such as myositis, pancreatitis, fatty hepatitis, peripheral neuropathy or lipodystrophy. The prescribed NA related to LA were stavudine in six patients, lamivudine, five, and didanosine, one. Despite treatment, all patients died of persistent circulatory collapse following LA. The median duration from diagnosis to death was eight days (range, 4-17 days). Our report highlights that clinicians caring for patients with AIDS should be alerted to the potentially fatal LA associated with antiretroviral therapy when patients present with low body mass index, lipodystrophy, unexplained abdominal symptoms, dyspnoea, or elevated aminotransferases.
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PMID:Fatal lactic acidosis associated with highly active antiretroviral therapy in patients with advanced human immunodeficiency virus infection in Taiwan. 1507 19

Propofol (2, 6-diisopropylphenol) is a potent intravenous hypnotic agent which is widely used for the induction and maintenance of anesthesia and for sedation in the intensive care unit. Propofol is an oil at room temperature and insoluble in aqueous solution. Present formulations consists of 1% or 2% (w/v) propofol, 10% soybean oil, 2.25% glycerol, and 1.2% egg phosphatide. Disodium edetate (EDTA) or metabisulfite is added to retard bacterial and fungal growth. Propofol is a global central nervous system depressant. It directly activates GABA(A) receptors. In addition, propofol inhibits the NMDA receptor and modulates calcium influx through slow calcium ion channels. Propofol has a rapid onset of action with a dose-related hypnotic effect. Recovery is rapid even after prolonged use. Propofol decreases cerebral oxygen consumption, reduces intracranial pressure and has potent anti-convulsant properties. It is a potent antioxidant, has anti-inflammatory properties and is a bronchodilator. As a consequence of these properties propofol is being increasingly used in the management of traumatic head injury, status epilepticus, delirium tremens, status asthmaticus and in critically ill septic patients. Propofol has a remarkable safety profile. Dose dependent hypotension is the commonest complication; particularly in volume depleted patients. Hypertriglyceridemia and pancreatitis are uncommon complications. Allergic complications, which may include bronchospasm, have been reported with the formulation containing metabisulfite. In addition, this formulation has been demonstrated to result in the generation of oxygen free radicals. High dose propofol infusions have been associated with the "propofol syndrome"; this is a potentially fatal complication characterized by severe metabolic acidosis and circulatory collapse. This is a rare complication first reported in pediatric patients and believed to be due to decreased transmembrane electrical potential and alteration of electron transport across the inner mitochondrial membrane.
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PMID:Propofol: therapeutic indications and side-effects. 1557 60

A donkey developed abdominal discomfort and distension together with cardiovascular collapse and gastric reflux 24 to 36 hours after ingesting a large amount of poultry feed. Rectal findings prompted a laparotomy that identified extensive gastric dilation, an empty, atonic small intestine, dry colonic content and an easily corrected caecal displacement. These findings were not consistent with the severity of the signs, which were attributed to endotoxaemia. The donkey was euthanased during recovery. Necropsy revealed acute necrotising pancreatitis with massive gastric dilation and right dorsal colon impaction. The clinicopathological features of acute equine pancreatitis associated with grain overload are discussed.
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PMID:Acute necrotising pancreatitis following grain overload in a donkey. 1588 85

Babesia (canis) rossi infection is common in dogs in South Africa, and frequently causes severe, life-threatening disease. Acidemia, persistent hyperlactatemia, hemoconcentration, elevated creatinine, cerebral babesiosis, pulmonary edema and pancreatitis are all associated with mortality rates above 30%, compared with overall mortality of 12% in admitted cases. Although half the admitted cases are severely anemic, hemoconcentration is associated with far higher mortality. Cerebral babesiosis is uncommon, but carries a poor prognosis. The pathological mechanism has been suggested to be endothelial cell damage and necrosis, followed by segmental microvascular necrosis with perivascular edema and hemorrhage. Renal involvement in babesiosis resembles the functional renal failure of sepsis. Hypotension is common, and other cardiovascular disturbances have been documented. Cerebellar ataxia, rhabdomyolysis and pancreatitis are recently identified complications. While the previous categorization into "severe" (life-threatening anemia) and "complicated" (complications not directly attributable to anemia) disease has proved useful, the distinction is artificial and probably unnecessary. An updated approach to classification is suggested, aimed at grouping animals by severity and prognosis, and using simple measures, such as clinical collapse and abnormal breathing, as much as possible. Although inflammatory mechanisms are undoubtedly important in the pathophysiology of babesiosis, there can be little doubt that tissue hypoxia plays a major role in the disease process.
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PMID:The South African form of severe and complicated canine babesiosis: clinical advances 1994-2004. 1650 90

The major keratins in the pancreas and liver are keratins 8 and 18 (K8/K18), but their function seemingly differs in that liver K8/K18 are essential cytoprotective proteins, whereas pancreatic K8/K18 are dispensable. This functional dichotomy raises the hypothesis that K8-null pancreata may undergo compensatory cytoprotective gene expression. We tested this hypothesis by comparing the gene expression profile in pancreata of wild-type and K8-null mice. Most prominent among the up-regulated genes in K8-null pancreas was mRNA for regenerating islet-derived (Reg)-II, which was confirmed by quantitative reverse transcription-polymerase chain reaction and by an anti-Reg-II peptide antibody we generated. Both K8-null and wild-type mice express Reg-II predominantly in acinar cells as determined by in situ hybridization and immunostaining. Analysis of Reg-II expression in various keratin-related transgenic mouse models showed that its induction also occurs in response to keratin cytoplasmic filament collapse, absence, or ablation of K18 Ser52 but not Ser33 phosphorylation via Ser-to-Ala mutation, which represent situations associated with predisposition to liver but not pancreatic injury. In wild-type mice, Reg-II is markedly up-regulated in two established pancreatitis models in response to injury and during the recovery phase. Thus, Reg-II is a likely mouse exocrine pancreas cytoprotective candidate protein whose expression is regulated by keratin filament organization and phosphorylation.
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PMID:Reg-II is an exocrine pancreas injury-response product that is up-regulated by keratin absence or mutation. 1789 82


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