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

In 12 dogs with acute experimental pancreatitis (AEP) and 6 control animals the "free", "latent" and "total" activity of acid phosphatase, beta-glucuronidase and cathepsins in whole homogenates of the pancreas, in a lysosomal-enriched subfraction and the supernatant of pancreatic tissue was estimated. AEP was induced by injection of bile salts and thrombin solution into the pancreatic duct. In 6 dogs the protection with heparin (1.5 mg/kg/body weight) immediately after producing AEP was applied. In AEP without any protection the free activity of hydrolases in the whole homogenate (80--90%) and in the lysosomal enriched subfraction (75--90%) was higher than in the controls (60--70% and 55--75% respectively), suggesting an augmented lysosomal fragility during the course of AEP. Heparin depressed the free activity of hydrolases to 60--80% in whole homogenates, and 64--75% in the lysosomal enriched subfraction. The release of cathepsins during incubation of the lysosomal-enriched subfraction in acidic medium was lower in the group with heparin treatment. The data obtained suggest the stabilising effect of heparin on the lysosomes of the pancreas during acute experimental pancreatitis in dogs.
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PMID:The effect of heparin on lysosomes of the dog pancreas during acute experimental pancreatitis. 47 25

Two cases of thrombocytopenia due to a low molecular weight heparin (Fraxiparine) are reported. The first case was a 35-year-old alcoholic man with acute mild pancreatitis. After having been treated with Fraxiparine for 12 days to prevent venous thrombosis, routine laboratory studies revealed a thrombocytopenia (49 G.l-1). At the same time, a minor haemorrhage occurred in the nasogastric tube. Prothrombin time, partial thromboplastin time, fibrin degradation products and D-dimers remained normal. There were no soluble fibrin monomers. Fraxiparine was discontinued. The thrombocyte count continued to decrease (12 G.l-1) up to the thirteenth day, it raised 3 days later to 110 G.l-1, and returned to normal after 9 days more (395 G.l-1). The second patient was a 58-year-old man given prophylactic Fraxiparine between the 5th and 16th days after admission for a severe asthma attack. Here again, after 12 days of treatment, the thrombocyte count decreased to 74 G.l-1. There were no other abnormalities, neither clinically nor in laboratory findings. Heparin administration was discontinued and the thrombocytopenia had resolved 3 days later. In both patients, the diagnosis of thrombocytopenia elicited by low molecular weight heparin was confirmed by finding, in vitro, a platelet aggregating factor in the presence of Fraxiparine. The literature concerning this topic is reviewed and discussed.
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PMID:[Thrombocytopenia induced by low molecular weight heparin]. 133 4

Ten patients with the syndrome of non-ketotic hyperosmolar coma are described. The mean age of the patients was 62.3 +/- 17.12 years. One patient was 16 years old. In 9 cases the patients had type II diabetes, one had type I diabetes. In 7 cases the coma was the first sign of diabetes. The factor predisposing in most cases was infection. In the treatment-acting insulin and hypotonic solutions were given. In 2 cases clinical signs of the DIS syndrome were observed manifesting themselves with local changes, including mental disturbances. Heparin was given with good effect. Three patients (30%) died in hospital. The cause of death was serious disease associated with this coma: pancreatitis and myocarditis, purulent bronchopneumonia, myocardial infarction.
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PMID:[Hyperglycemic hyperosmolar nonketotic coma]. 240 21

The pulmonary complications are severe sequeles of acute pancreatitis. The pathogenesis of these complications is unsolved. The purpose of this work was to evaluate the status of lung lysosomes and phospholipase A activity in acute experimental pancreatitis (AEP) and the effect of heparin as a potentially protective agent. Taurocholate-induced AEP in rats lasting 24 and 48 hours was treated with heparin intraperitoneally (2 mg/kg every 8 hours). The total activity of cathepsins and B-glucuronidase in lysosomal enriched subfraction increased markedly during 48 hours of AEP in untreated animals, but the relative free activity was maximal after 24 hours. Free activity of cathepsins and acid phosphatase in supernatant was maximal after 24 hours. The phospholipase A activity was maximally elevated (more than twofold) after 48 hours. Heparin prevented the increase of activity of B-glucuronidase, depressed the relative free activity of all investigated lysosomal hydrolases and inhibited the phospholipase A activity in the lung homogenate. Our results indicate the significance of labilization of lung lysosomes and increment of phospholipase A activity in the lungs in the damage of this organ during AEP in the rats, and suggest the beneficial effect of heparin on these factors.
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PMID:The lung lysosomal hydrolases and phospholipase A in acute experimental pancreatitis with reference to heparin treatment. 243

Local microcirculatory dysfunction within the pancreatic gland might be an important factor in the conversion of oedematous to necrotizing pancreatitis. Therapeutic agents, improving the pancreatic blood flow, might be valuable in acute pancreatitis treatment. An influence of nitric oxide, heparin and procaine treatment on microcirculatory values in acute pancreatitis (AP) in rats was investigated. Acute pancreatitis was induced by i.p. injection of cerulein in four doses of 15 microg kg-1 each at 1-h intervals. The rats with pancreatitis were divided into five groups, 12 animals each. One group remained without treatment, four groups were treated i.p. either with NO synthase inhibitor L-NNA (2x25 mg kg-1 or heparin 2x2.5 mg kg-1 or L-arginine 2x100 mg kg-1 or procaine 2x25 mg kg-1. Five control groups, ten animals each, received saline, L-NNA, heparin, L-arginine or procaine only. Five hours after the first ceruleine injection microcirculatory values within the pancreas were measured by means of laser Doppler flowmetry. Acute pancreatitis caused a significant drop of microcirculatory value to 37% of the basal value. The L-NNA administration resulted in a further insignificant reduction of the pancreatic blood flow to 34%. An improvement of microcirculation was observed in rats with pancreatitis receiving heparin (76%) and L-arginine (72%). Procaine had no effect on microcirculatory disturbances within the pancreas in rats with pancreatitis. Cn-induced acute pancreatitis (AP) causes microcirculatory deterioration within the pancreas. Heparin and nitric oxide donor, L-arginine, might be considered as therapeutic agents, improving the diminished pancreatic tissue perfusion observed in acute pancreatitis. Procaine does not improve the pancreatic blood flow in acute pancreatitis.
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PMID:Microcirculatory disturbances of the pancreas in cerulein-induced acute pancreatitis in rats with reference to L-arginine, heparin, and procaine treatment. 934 40

Hypertriglyceridaemia is thought to be the aetiology in 3% of patients with acute pancreatitis, often associated with poorly controlled diabetes mellitus or chronic alcohol abuse. However, in patients with non-biliary pancreatitis, chylomicronaemia is an underrated cause of acute pancreatitis. The activity of lipoprotein lipase (LPL) is crucial in removing triglycerides from the plasma; LPL gene mutations combined with secondary alterations in plasma lipoproteins, such as occur in pregnancy, diabetes mellitus, and alcohol abuse can cause severe hypertriglyceridaemia and pancreatitis. Heparin and insulin stimulate LPL activity. During a 12 months' period we consecutively screened all patients with the diagnosis of acute non-biliary pancreatitis for hypertriglyceridaemia, to evaluate the prevalence of hypertriglyceridaemia-induced pancreatitis and to assess the outcome under standardised treatment with intravenous heparin and insulin. Hypertriglyceridaemia-induced pancreatitis was diagnosed in 5 out of 46 patients (11%) with acute pancreatitis. In 2 patients hypertriglyceridaemia was associated with diabetes mellitus, in one patient with pregnancy and in another with chronic alcohol abuse. Four patients had to be referred to the intensive care unit. Plasma concentrations of triglycerides were (median +/- range) 43 mmol/l (14.7 to 80.4); pancreas amylase was 574 U/l (155 to 1606), and lipase was 1003 U/l (330 to 3010). All patients had oedematous pancreatitis demonstrated by CT scan. Treatment with i.v. heparin and i.v. insulin decreased trigylceride levels to less than 10 mmol/l within 2.8 days (1 to 6), the amylase and lipase levels returned to normal after 3 and 4 days respectively, and the abdominal pain was resolved. Hypertriglyceridaemia is a common and under-diagnosed etiology of acute non-biliary pancreatitis. Intravenous heparin and insulin is safe and effective in the treatment of hypertriglyceridaemia-induced pancreatitis. Low fat diet, supplements of (n-3) fatty acids ("fish oil") and fibrates are recommended for long-term maintenance therapy.
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PMID:[Heparin and insulin in the treatment of acute hypertriglyceridemia-induced pancreatitis]. 1049 50

Heparin and insulin stimulate lipoprotein lipase and are known to decrease serum triglyceride levels. However, their efficacy in hypertriglyceridemia-induced acute pancreatitis is not well documented. We report a 51-year-old man in whom treatment with heparin and insulin was accompanied by reduction in serum triglyceride levels and resolution of pancreatitis.
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PMID:Hypertriglyceridemia-induced acute pancreatitis--treatment with heparin and insulin. 1283 85

We report the case of a 28-year-old secundipari with a history of severe hypertriglycideremia-induced pancreatitis 3 years ago who was admitted in the 37th week of gestation with abdominal pain. A blood sample had a milky aspect and plasma concentrations were as follows: triglycerides 8,5g/l, cholesterol 1000 mg/dl, amylase 574 IU/l, lipase 1310 IU/l. Acute pancreatitis was diagnosed, a caesarean was performed under spinal anaesthesia. The diagnosis was confirmed by CT-scan. Treatment with 15,000 IU heparin per day and intravenous nutrition decreased triglycerides level to less than 1g/l within 48 h. She was discharged 28 days later. Heparin could be a low-cost alternative to plasmapheresis in hypertriglycideremia-induced pancreatitis.
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PMID:[A case of hypertriglycideremia-induced pancreatitis in pregnancy: value of heparin]. 1534 58

We report the case of a 31-year-old pregnant patient in the 33rd week of gestation, with no history of dyslipidaemia, admitted for sub-acute epigastric pain. The milky aspect of blood samples was remarkable. Blood analysis showed a moderate increase in pancreatic enzymes but a major hyperlipaemia: triglyceridaemia 113 g/l and total cholesterolaemia 25 g/l. We suspected a hypertriglyceridemia-induced pancreatitis in pregnancy. The diagnosis was confirmed by CT-scan. Abdominal echography showed no abnormalities in biliary duct. After few hours, a caesarean was performed for acute fetal distress. The patient was admitted to the intensive care unit where a decrease of hypertriglyceridemia was already observed. Only one plasmapheresis was performed. Heparin was introduced. Rapid clinical improvement allowed discharge from intensive care at day 3. This case report illustrates lipid decrease with undertaken treatments. We discuss the management of hypertriglyceridemia-induced pancreatitis in pregnancy.
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PMID:[Hypertriglyceridemia-induced pancreatitis in pregnancy. A case report]. 1759 Mar 6

Of the cases of acute pancreatitis, 1-7% are caused by severe hypertriglyceridemia and can be treated with plasma exchange (PE). We report on a large series of patients with acute hyperlipidemic pancreatitis (HLP) treated with PE. In the 1992-2008 period, 50 patients (45 +/- 8 years old, 92% male) with acute HLP were treated with PE, during which 1-2 plasma volumes were exchanged. Heparin was used as anticoagulant in 85% of the procedures, and citrate in the rest. Cholesterol and triglycerides were measured before and after PE. In the 2003-2008 cohort of 40 patients, we retrospectively recorded an Acute Physiology and Chronic Health Evaluation II (APACHE II) score at the first PE session, hospital mortality, and length of hospital stay. A total of 79 PE treatments were done, 1-5 per patient. The volume exchanged was 4890 +/- 1300 mL over a duration of 3.5 +/- 2 h. During the first PE, the triglycerides were lowered from 58.9 +/- 40.8 to 10.8 +/- 10.8 mmol/L, and the total cholesterol was lowered from 20.0 +/- 7.6 to 5.7 +/- 4.3 mmol/L. In 10% of the procedures the plasmafilter was replaced, and in 3% the filter was clotted. Hypotension occurred in 3% of PE and there was one case of gastrointestinal bleeding after PE with heparin anticoagulation. In the 2003-2008 cohort, the median APACHE II score was 5 (range 0-15), the median overall hospital stay was 18 days (range 3-142 days) and the hospital mortality was 15%. To conclude, in acute hyperlipidemic pancreatitis, one to two plasma exchanges effectively reduce the serum triglyceride level. There is a low rate of procedure-related complications. A mortality rate of 15% is considerable.
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PMID:Treatment of hyperlipidemic acute pancreatitis with plasma exchange: a single-center experience. 1969 66


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