Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1981 to 1990, 14 of 70 patients hospitalized at our institution for severe acute pancreatitis were selected to undergo percutaneous drainage of pancreatic abscess, under computed tomographic (CT) scan guidance. Pancreatic abscess was defined, on contrast-enhanced CT scan, as an infected fluid collection without pancreatic necrosis. There were nine men and five women, ranging in age from 28 to 46 years. The main cause of pancreatitis was alcohol abuse (eight patients). Other causes were gallstones (two patients), hyperlipidemia (two patients), postoperative (one patient) and one unknown. Ranson criteria were available in ten patients and ranged from three to six. Percutaneous drainage was performed as the primary treatment in 13 patients and for removal of a residual collection postoperatively in one patient. In two critically ill patients, percutaneous drainage was performed as a temporizing measure. In 12 patients with well-limited hypodense collections, percutaneous drainage was expected to result in the definitive cure of the abscess. Pigtail drains (No. 14F), were inserted using local anesthesia and CT scan guidance. Two patients had two drains and 12 patients had only one drain. Two patients were definitively cured by percutaneous drainage and all other patients were operated upon for removal of infected necrosis. In this study, the lack of accuracy of contrast-enhanced CT scan in the diagnosis of peripancreatic necrosis is highlighted and that percutaneous drainage has a better efficiency in the treatment of residual collections postoperatively than as a primary treatment of infected fluid collections is illustrated.
 ...
PMID:Failure of percutaneous drainage of pancreatic abscesses complicating severe acute pancreatitis. 173 73

Serum lipid (triglycerides and cholesterol) concentrations were studied in 49 patients with acute pancreatitis (AP). The aims of the study were to investigate the prevalence of hyperlipidemia (HL) in patients with AP according to etiology and to evaluate whether HL precedes or is a consequence of AP. Moreover, we analyzed the relationship between HL and the development of pancreatic necrosis. At admission, 23 patients (47%) had HL: 9 of 19 patients with alcoholic pancreatitis, 5 of 18 patients with biliary pancreatitis, and 9 of 12 patients with AP of miscellaneous etiologies (p less than 0.05). Severe HL (serum triglycerides greater than 20 mmol/L) was observed in five patients. Serum lipid levels in patients with AP and HL decreased markedly during the first 72 h of evolution, but remained slightly above the upper normal limit in most of them after 15 d. The prevalence of HL was similar in edematous and necrotizing pancreatitis. Necrotizing pancreatitis was significantly associated with the presence of hypertriglyceridemia in conjunction with hypercholesterolemia (p less than 0.05). The observations that a) hyperlipidemia is an early event in acute pancreatitis, (b) serum lipid values decrease during the acute phase of the disease, (c) hyperlipidemia has a different prevalence in different etiologies, and (d) high serum lipid levels are not always associated to pancreatic necrosis suggest that HL is a preexistent metabolic abnormality with respect to AP. On the other hand, HL may play a role in aggravating AP.
 ...
PMID:Hyperlipidemia in acute pancreatitis. Relationship with etiology, onset, and severity of the disease. 178 37

We report here a case of diabetic ketoacidosis associated with hyperlipidemia and acute pancreatitis following alcohol abuse. A 23-year-old man was admitted to the hospital because of right upper abdominal and back pain developing into a state of unconsciousness and shock. He had been drinking 720 ml of whisky daily for 4 years. Laboratory data on admission revealed metabolic acidosis (pH 7.01, PaO2 84.6 mmHg, PaCO2 41.1 mmHg, HCO3- 16.3 mmol/l, BE-16.4 mmol/l), a high blood glucose level (640 mg/dl), strongly positive urinary ketone bodies, hypercholesteremia (913 mg/dl) and hypertriglyceridemia (8500 mg/dl). Furthermore, the levels of pancreatic enzyme including serum amylase (770 U/l) and elastase I (2721 ng/dl) were elevated. After successful treatment of the diabetic ketoacidosis with insulin and fluid supplementation, serum cholesterol, triglyceride and pancreatic enzyme levels decreased concomitantly with stabilization of the blood glucose level. From these findings, it is suggested that hyperlipidemia might have caused the acute pancreatitis which developed into diabetic ketoacidosis in this patient.
 ...
PMID:[A case of non-insulin-dependent diabetes mellitus associated with diabetic ketoacidosis after the onset of hyperlipidemia and acute pancreatitis following alcohol abuse]. 193 46

It is estimated that over 60% of the variability in serum lipids is genetically determined, most of this variation being due to polygenic influences. Interaction between the latter and environmental factors is probably the commonest cause of hyperlipidaemia in the general population. Familial forms of hyperlipidaemia are usually more clearly defined, especially those which have a monogenic or dominant pattern of inheritance, but are less common. This type of disorder, exemplified by familial hypercholesterolaemia, is expressed independently of environmental influences. In contrast, in familial type III hyperlipoproteinaemia inheritance of the underlying gene defect is often insufficient to produce hyperlipidaemia unless additional environmental or genetic influences coexist. Rarely, hyperlipidaemia is recessively inherited, as in familial deficiency of lipoprotein lipase and of apolipoprotein CII. Primary hyperlipidaemias characterized by severe hypertriglyceridaemia predispose to acute pancreatitis whereas those disorders characterized by hypercholesterolaemia, apart from hyper alpha lipoproteinaemia, are associated with an increased risk of premature vascular disease.
 ...
PMID:Primary hyperlipidaemia. 210 Jun 94

Acute pancreatitis is a disease characterized by abdominal pain, low-grade fever, abdominal tenderness and rigidity, and moderate elevation of the white blood cell count. A widely used revised classification of pancreatitis is that proposed in 1984 at Marseille. It only distinguishes between acute and chronic pancreatitis. In 61 cases were 40 men and 21 women. The mean age in the total series was 52.5 years. The etiology of the acute condition was alcoholism in 32.8% and biliary tract disease in 23%. In 9.8% the acute pancreatitis is associated with alimentary tract diseases (adipositas, hyperlipidemia). The severity of acute pancreatitis is pathological anatomy determined by three stages. In pathogenesis the process of digestion is caused by activated pancreatic enzyme with acinar cell injury. The acinar cell is normally protected from the action of its own enzymes by elaborate intracellular compartmentation of enzymes. Acute pancreatitis is triggered by pancreatic phospholipase A leading to necrosis of lipolytically active fat cells with release of membrane-toxic fatty acids with following destruction of adjacent tissue. Fat necrosis initiates an acute inflammatory reaction with immigration of granulocytes and liberation of kinins, which activate pancreatic enzyme. Pancreatic enzymes are similar to lysosomal enzymes with regard to substrate specificity. Activation will be also triggered by lysosomal enzymes of necrotic acinar cells.
 ...
PMID:[Acute pancreatitis--etiology, pathological anatomy and pathogenesis]. 226 Mar 61

The majority (about 75%) of patients who suffer from acute pancreatitis do so as a consequence of gallstones or alcohol abuse. The other 25% of patients often present difficult diagnostic problems. Over several years the author has accumulated a series of patients with remedial causes of pancreatitis. They include a group of congenital conditions such as pancreas divisum, choledochal cysts and congenital abnormalities of the pancreatic ductal system. Patients who have had pancreatitis and who have an intact gallbladder often have stones that are difficult to identify. Repeated attacks of pancreatitis in the absence of any other apparent cause justifies cholecystectomy, which will often identify the cause so that recurrence can be prevented. A group of nonanatomic causes are also known. They include hyperlipidemia, drugs and toxins, certain systemic illnesses such as systemic lupus erythematosus, pregnancy, hypercalcemia, hereditary causes and occasionally cancer. In his lecture the author reviews the various etiologies of acute pancreatitis and describes an algorithm that can be used when the diagnosis is difficult.
 ...
PMID:Recurrent acute pancreatitis--rarely idiopathic: 1989 Du Pont lecture. 226 8

In most patients presenting with acute pancreatitis, the cause can be established on the basis of initial history, physical examination, laboratory studies, and abdominal sonography. Patients with unexplained pancreatitis at that point are often considered to have idiopathic disease. However, a cause and, often, effective treatment to prevent recurrent pancreatitis are possible in many of these patients if an aggressive diagnostic approach is taken to discover undiagnosed hyperlipidemia, occult gallstones, abnormalities of the bile and pancreatic ducts, sphincter of Oddi dysfunction, pancreatic cancer and other tumors, and cystic fibrosis (in children and young adults).
 ...
PMID:Idiopathic acute pancreatitis. 226 20

The use of total parenteral nutrition (TPN) in the treatment of 73 patients with acute severe pancreatitis was prospectively studied during a two year period. Patients were divided into three groups on the basis of calorie substrate used. Glucose and twice weekly lipid infusion (glucose based) were used in 60 per cent; 27 per cent required daily lipid infusion (lipid based), and 13 per cent received no lipid because of pre-existing hyperlipemia or thrombocytopenia (no lipid). Nutritional indices (albumin, transferrin and total lymphocyte count) were initially abnormal in more than 80 per cent of patients, and 50 per cent had three or more of Ranson's criteria. After TPN, 81 per cent had improved nutritional indices, and none had hypertriglyceridemia or aggravation of pancreatitis develop. Patients who received lipid based or no lipid had higher insulin requirements (p less than 0.01) than those receiving mainly glucose. Mortality was increased tenfold (2.5 versus 21.4 per cent, p less than 0.01) in patients who did not achieve positive nitrogen balance. We conclude that TPN, either lipid or glucose based, is a safe and effective therapy to reverse the malnutrition of acute pancreatitis and that failure to achieve positive nitrogen balance is associated with increased mortality.
 ...
PMID:Total parenteral nutrition and alternate energy substrates in treatment of severe acute pancreatitis. 249 6

Acute pancreatitis often results in a hyperdynamic, consumptive state. Hallmarks of this condition are decreased peripheral resistance with increased cardiac output. Hemodynamic and cardiovascular changes are accompanied by metabolic alterations. Increased protein catabolism, increased ureagenesis, glucose intolerance, increased lipolysis, and reduced servoregulation are metabolic changes commonly seen in this syndrome. To preserve organ structure and function, biochemical processes must be metabolically supported. Substrate needs change as stress level increases. The per cent of total calories provided as protein must increase. Branched-chain-enriched amino acid solutions have been shown to improve nitrogen utilization in hypermetabolic patients and may therefore be beneficial for the patient with acute pancreatitis. Glucose utilization decreases and free fatty oxidation increases. A mixed fuel system that provides fat, protein, and glucose is suggested for these patients. IV fat has been shown to be a safe energy substrate for patients with pancreatitis in the absence of hyperlipidemia. Failure to use fat as an energy substrate in conjunction with TPN may result in hepatic steatosis and excess carbon dioxide production. The decision of whether to use the parenteral or enteral route to nutritionally support the patient with pancreatitis remains controversial. TPN may allow maintenance of pancreatic rest. The role of enteral feedings is less clear. However, it has been shown that the further down the alimentary tract the feeding is infused, the less pancreatic stimulation occurs. Therefore, it seems wise to support the patient with TPN during severe acute pancreatitis. Jejunal enteral feedings should be initiated as a transitional feeding when the acute inflammatory episode begins to subside.
 ...
PMID:Nutritional support in acute pancreatitis. 250 54

A 29 year old woman with type V hyperlipidemia developed acute pancreatitis associated with severe hyper triglyceridemia when she coursed the 28th week of pregnancy. Plasma exchange was performed 3 times and plasma lipids became normal, while the acute pancreatitis subsided. Intravenous and then enteric nutrition followed and a successful cesarean section was performed 30 days after the initial episode.
 ...
PMID:[Plasmapheresis in acute pancreatitis secondary to familial hyperlipidemia in a pregnant woman]. 251 5


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>