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)

Two cases of severe acute pancreatitis associated with type V hyperlipoproteinemia are reported. A 39-year-old obese woman was hospitalized with continuous severe abdominal pain. The diagnosis was made on the day of admission to our hospital, and treatment using continuous regional arterial infusion of a protease inhibitor and an antibiotic was performed with good results. The other patient was a 35 year-old woman in the 35th week of pregnancy, and a diagnosis of gestational hyperlipidemic pancreatitis was made on the day of onset. She was treated supportively using intravenous hyperalimentation, protease inhibitors, and antibiotics. She recovered from the acute pancreatitis and delivered a healthy term infant. It is difficult to diagnose acute pancreatitis in patients with type V hyperlipoproteinemia, because even when serum amylase levels are high, the value is reduced by high serum triglycerides. Early diagnosis was achieved in both of the present cases, and early intensive therapy was performed, which may be of the utmost importance in saving the life of a patient.
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PMID:Severe acute pancreatitis associated with hyperlipidemia: report of two cases and review of the literature in Japan. 1057 88

An elderly woman with a history of cholecystectomy and a re-operation for postoperative peritonitis underwent extracorporeal shock wave lithotripsy (ESWL) for right and left renal pelvic calculi, 11 x 6 and 12 x 5 mm in size, to which 2400 and 1400 shots at 20 kV were given, respectively, on the same day. During the evening after the operation, the patient started to complain of upper abdominal pain. Laboratory examination on the next day revealed elevations in blood and urine amylase levels and a diagnosis of pancreatitis was made. Conservative treatment, including administration of protease inhibitor, did not improve her symptoms; abdominal distension became marked and she underwent laparotomy. Necrosection and indwelling of several drain tubes in abdomen were performed with an operative diagnosis of acute necrotic pancreatitis. With daily irrigation of drain tubes and treatment for methicillin-resistant Staphyloococcus aureus infection of the lungs and abdominal cavity, septicemia and duodenal fistula, the patient gradually recovered and was discharged on postoperative day 151. It was suggested that ESWL was responsible for the acute pancreatitis. Either an obstruction of the pancreatic duct by fragments of common duct stone, or mechanical injury of the pancreas due to adhesion between the pancreas and surrounding tissue caused by the lapalotomy, was considered as a possible cause of pancreatitis. To our knowledge, there has been no previous report of severe acute pancreatitis and the present case suggests that ESWL may cause severe pancreatic even in cases without stone shadow in the bile, common duct or pancreatic duct.
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PMID:Acute pancreatitis caused by extracorporeal shock wave lithotripsy for bilateral renal pelvic calculi. 1071 Feb 51

Despite potent antiretroviral activity, the HIV-1 protease inhibitors have recently been associated with abnormal serum lipoprotein concentrations. The purpose of this review is to describe serum lipid abnormalities related to protease inhibitor use. A MEDLINE search up to June 1, 1999, and abstracts from recent scientific meetings were primary data sources. Lipid disturbances in HIV-infected patients receiving protease inhibitors generally consist of elevated triglycerides and total cholesterol levels; HDL cholesterol is often reduced. The pathophysiological mechanism by which the protease inhibitors induce these lipid abnormalities has been hypothesized, but is unknown. Cases of pancreatitis and coronary heart disease have been described in hyperlipidemic patients receiving protease inhibitors. Treatment of protease inhibitor-related hyperlipidemia is unknown. Exchanging the offending protease inhibitor for nevirapine may be helpful in certain patients. Atorvastatin in combination with gemfibrozil has been used with limited success in a small number of individuals.
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PMID:Hyperlipidemia associated with HIV protease inhibitor use: pathophysiology, prevalence, risk factors and treatment. 1082 94

We investigated the effects of nafamostat mesilate, a synthetic protease inhibitor clinically used for patients with pancreatitis or disseminated intravascular coagulopathy, on NO synthesis and apoptosis in lipopolysaccharide (LPS)-treated human trophoblasts. Nafamostat mesilate or aminoguanidine, an inhibitor of NO synthase, suppressed NO synthesis and apoptosis in trophoblasts induced by LPS. Both agents also suppressed matrix metalloproteinase-2 activity induced by LPS. LPS also stimulated secretion of IL-6 and IL-8 in cultured trophoblasts, which was suppressed by nafamostat mesilate. Protease inhibitors including nafamostat mesilate may be therapeutic agents for chorioamnionitis and various diseases including septic shock, ischemia-reperfusion injury in brain and heart, graft rejection, and acute phase inflammatory diseases, in which overproduction of NO or peroxynitrite is involved in tissue injury.
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PMID:Nafamostat mesilate, a serine protease inhibitor, suppresses lipopolysaccharide-induced nitric oxide synthesis and apoptosis in cultured human trophoblasts. 1095 57

Long-term effects of nafamostat mesylate, a protease inhibitor, and imipenem, an antibiotic, on trypsintaurocholate-induced acute pancreatitis were studied in rats. Sham-operated rats infused with a buffer solution into the pancreatic duct served as controls. Nafamostat (1 mg/kg), imipenem (10 mg/kg), or imipenem + nafamostat in saline was injected subcutaneously 0.25, 3, 24, and 48 hours after the induction of pancreatitis. In untreated rats and control rats, saline was injected at the same intervals as in the treated rats. All rats in an untreated group died within 3.5 days (median survival, 1.25 day) after the induction of pancreatitis. The 2-week survival rate was significantly (p < 0.05) improved by a combination of nafamostat and imipenem (42%), but not by nafamostat (17%), or imipenem (8%) alone. Bacterial culture at 24 hours revealed infection of necrotic pancreatic tissues and ascites by intestinal bacteria in all untreated rats but not in control rats. Bacterial counts were significantly reduced by imipenem, but not by nafamostat. In conclusion, bacterial infection occurred within 24 hours after the induction of trypsintaurocholate pancreatitis in rats. Early treatment with nafamostat + imipenem, but not nafamostat or imipenem alone, improves long-term survival.
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PMID:Long-term effects of nafamostat and imipenem on experimental acute pancreatitis in rats. 1103 74

We describe the case of a young HIV-positive patient undergoing three-drug antiretroviral therapy that included a protease inhibitor for 9 months, who was admitted to the hospital with an acute myocardial infarction. A coronary angiogram revealed occlusion caused by a thrombus in the proximal third of the anterior descending artery. Complete recanalization was obtained after an angioplasty was performed. At the time of the infarction, only the triglyceride levels were found to be high. Metabolic alterations associated with the prolonged use of protease inhibitors have been described such as an increase in the triglyceride and cholesterol serum levels, diabetes, resistance to insulin, lipodystrophy, and pancreatitis. The consequences of chronic hyperlipidemia are well known in the medical literature, especially premature coronary artery disease. No family history of coronary artery disease was identified in this patient. Whether the genesis of this localized coronary thrombosis was due to a change in the metabolism of the vascular endothelium caused by the protease inhibitors, or by related dyslipidemia, is still to be determined. In this case, the data suggest a strong link between coronary insufficiency and prolonged use of the protease inhibitor.
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PMID:Acute Myocardial Infarction in a 34-Year-Old HIV-Positive Female Patient While Undergoing Active Antiretroviral Therapy Containing a Protease Inhibitor. 1108 68

Reports of metabolic disorders, such as diabetes mellitus and hyperlipidemia, occurring during treatment with protease inhibitor (PI) regimens are prompting patients and providers to try to better understand the links between these disorders and antiretroviral treatments. The Food and Drug Administration (FDA) first reported PI-associated diabetes in June 1997. Diabetes mellitus can be managed by controlling diet and exercise, or by supplementing treatment with oral hypoglycemic drugs. Hypertriglyceridemia has also been associated with PI therapies, and is apparent even in patients experiencing good results from antiretroviral therapy. Treatment for hypertriglyceridemia encompasses monitoring diet and exercise, limiting alcohol, watching hypertension, and quitting smoking. Patients at higher risk for pancreatitis can consider using lipid-lowering drugs and fibric acid derivatives. Alterations in fat distribution have also been linked to PI use, particularly in the back of the neck and upper back, and abdominal area. Researchers have seen evidence of anomalous fat distribution in some patients prior to PI treatment. Management has not consistently been remedied by diet and exercise. Sustaining overall health, reducing blood lipids, and controlling risk factors for cardiovascular disease need to be implemented. Unless the abnormalities are severe and potentially harmful to the patient, it is not commonly recommended to change the PI treatment.
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PMID:Metabolic complications of antiretroviral therapies. 1136 97

Lipodystrophy is defined as the defective metabolism of fat, and it is characterized by distinct physical changes, such as an increased waist size or an accumulation of fatty tissue at the base of the neck. Lipodystrophy may be linked with protease inhibitor use and is sometimes called crixi-belly or buffalo hump. High triglyceride levels are associated with lipodystrophy and can lead to increased chances of heart disease, hardening of the arteries, and pancreatitis. Women at risk for lipodystrophy should consider using a different form of birth control if they are taking oral contraceptives. Contact information is provided.
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PMID:Update on lipodystrophy. 1136

The Food and Drug Administration (FDA) approved once-daily dosing of a new 200mg formulation of Bristol-Myers Squibb's nucleoside analog, ddI. The new tablet will be available in December 1999. Two tablets of ddI must always be taken together to minimize gastric acid degradation. The FDA will require the drug company to warn patients of the increased risk of developing pancreatitis, sometimes observed in persons on ddI therapy. The FDA also approved a 1,250mg twice-daily dosing of nelfinavir, a protease inhibitor manufactured by Agouron Pharmaceuticals.
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PMID:New dosing of ddI (Videx) and Nelfinavir (Viracept) approved. 1136 46

Many drugs besides lipid-lowering drugs affect serum lipid levels in either a potentially harmful or beneficial way, and may therefore increase or decrease the risk of cardiovascular disease. Diuretics, beta-blocking agents, progestogens, combined oral contraceptives containing 'second generation' progestogens, danazol, immunosuppressive agents, protease inhibitors and enzyme-inducing anticonvulsants adversely affect the lipid profile. They increase total cholesterol, low density lipoprotein cholesterol and triglycerides by up to 40, 50 and 300%, respectively, and decrease high density lipoprotein cholesterol by a maximum of 50%. Conversely, alpha-blocking agents, estrogens, hormone replacement therapy, combined oral contraceptives containing 'third generation' progestogens, selective estrogen receptor modulators, growth hormone and valproic acid show mostly beneficial effects on the lipd profile. Some drugs, for example, isotretinoin, acitretin and antipsychotics, mainly elevate triglyceride levels. Adverse or beneficial effects on serum cholesterol levels do not always translate into a higher or lower, respectively, incidence of cardiovascular disease. because these drugs may influence cardiovascular risk through multiple pathways. In some cases, excessive cholesterol levels occur, for example, with protease inhibitor therapy, and several cases of pancreatitis attributable to drug-induced hypertriglyceridaemia have been reported. Some general guidelines on the management of drug-induced dyslipidaemia can be given. Replacement of the dyslipidaemia-inducing drug by an equivalent alternative therapy is preferred. However, such alternatives are often difficult to find. If there is no equivalent alternative and treatment with the dyslipidaemia-inducing drug must be initiated, monitoring of serum lipid levels is important. If drug use is expected to be long term, the existing guidelines for the management of dyslipidaemia in the general population can be applied to drug-induced dyslipidaemia. In cases of extreme hyperlipidaemia, medication use should be reassessed.
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PMID:Drug-Induced lipid changes: a review of the unintended effects of some commonly used drugs on serum lipid levels. 1173 56


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