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

We assessed the analytical performance of the co-immobilized hexokinase (EC 2.7.1.1) and glucose-6-phosphate dehydrogenase (EC 1.1.1.49) method for D-glucose analysis on the Technicon SMAC. The enzyme-containing coils were usable for one month, or 12 000 tests. Bilirubin, hemoglobin, lipemia, creatinine, uric acid, citric acid, and ascorbic acid did not interfere. Results with this method were compared to those by the National Glucose Reference Method. The upper limits of the total error estimate (a combination of random and systematic errors) were 76, 74, and 125 mg/liter at concentrations of 500, 1200, and 3000 mg/liter, respectively. The error estimates were less than allowable errors based on medical usefulness; thus the method was judged to perform acceptably with respect to the Reference Method. We also present performance data for the routine SMAC glucose oxidase (EC 1.1.3.4)/Peroxidase (EC 1.11.1.7) 3-methyl-2-benzothianolinone hydrazone-N,N-dimethylaniline method, the direct hexokinase method with the Du Pont aca, and the glucose oxidase oxygen-rate method with the Beckman Glucose Analyzer.
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PMID:Evaluation of the co-immobilized hexokinase/glucose-6-phosphate dehydrogenase method for glucose, as adapted to the Technicon SMAC. 65 1

We evaluated the performance of the Du Pont aca ammonia procedure with regard to (a) linearity, (b) precision, (c) interferences, and (d) effect of anticoagulants. Linearity extends to 2,000 mumol/L. The SD of the method was essentially constant (2 to 3 mumol/L) and independent of the NH3 concentration. Hemoglobin, bilirubin, and lipemia do not interfere. Either EDTA or heparin is suitable as anticoagulant. Recovery of NH3 added to plasma samples averaged 102% (range: 97--107%). We established normal values by measuring NH3 in 188 plasma samples from apparently healthy individuals. The 95% confidence range is from 10 to 35 mumol/L. The aca ammonia method compares very well with that of Kingsley and Tager but correlates less strongly with that of Reinhold and Chung. We describe a protein-based solution with stable NH3 concentration that is suitable as a control material.
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PMID:Performance of the Du Pont aca ammonia method. 76 61

The procedure used with the Du Pont aca for alpha-amylase (1,4,-alpha-D-glucan glucanohydrolase, EC 3.2.1.1) was evaluated in our laboratory and compared with the Roche Diagnostics "Amylochrome" and Perkin-Elmer Coleman 91 amylase assays. The within-run coefficients of variation (CV) for samples of fresh normal sera were: aca 5.8% and 4.3% on two different lots of reagent, Amylochrome 7.4%, and Coleman 91 3.3%. In sera with abnormally high amylase activity, the respective CV's were: aca, 1.2% and 0.8%; Amylochrome, 2.0%; and Coleman 91, 2.8%. Day-to-day precision studies on fresh and lyophilized normal and abnormal sera gave CV's in the following ranges: aca, 1.8% to 6.7%; Amylochrome, 3.0% to 5.2%; and Coleman 91, 4.5% to 5.9%. Results by the aca procedure were linearly related to activity to about 10-fold the upper limit of normal amylase activity. For serum, correlations were: r = 0.977 for aca vs. Coleman 91 and r = 0.974 for aca vs. Amylochrome. For urine they were: r = 0.978 for aca vs. Coleman 91 and r = 0.975 for aca vs. Amylochrome. Mean recovery from 53 supplemented samples was 98%. Icterus, hemolysis, and lipemia did not interfere with method correlation of aca vs. Coleman 91 or Amylochrome.
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PMID:Evaluation of the Du Pont aca alpha-amylase procedure. 83 42

A distict alcoholic withdrawal syndrome in chronic alcoholics cannot only be induced upon withdrawal of alcohol or dose reduction but also occurs upon continuous and long lasting consumption of larger quantities of alcohol. In the latter case we deal with an alcoholic predelirium which is characterized by simultaneous occurence of neurologic, vegetative and gastrointestinal disturbances as well as mental symptoms like anxiety, increased irritability and disturbance of sleep. In parallel to this alcoholic withdrawal syndrome from internal medical view a characteristic symptomatology can be observed in patients with chronic alcohol abuse. In most cases younger patients are concerned who, concomitantly with predelirant symptoms frequently display a labile hyperlipidemia and additional obesity, fatty liver, hyperlipidemia and often also hyperuricemia. Based on ten typical cases the combination of symptoms as described above is introduced. This combination can according to Feuerlein be defined as "alcohol-syndrome". The difficulties of diagnosis are shown because in many cases not the alcohol abuse but primarily vegetative and other functional disturbances dominate the clinical appearance. Additionally the pathogenetic connection between the described symptoms and alcohol abuse are discussed.
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PMID:[The "alcohol-syndrome" from internal medical view (author's transl)]. 86 89

We evaluated a revised serum calcium method (o-cresolphthalein complexone) used with the Du Pont aca. Our results correlated well with those obtained by atomic absorption spectrometry. Within-run and day-to-day coefficients of variation were 0.5 and 1.5%, respectively. Color produced and calcium concentration are linearly related and the relation is not affected by hemolysis, lipemia, or icterus.
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PMID:Evaluation of the revised serum calcium procedure used with the Du Pont automatic clinical analyzer. 113 36

Malnutrition is common among alcoholics because alcohol displaces protein-, vitamin-, and mineral-containing foods in the diet, and chronic alcohol consumption results in maldigestion and malabsorption of essential nutrients. In addition, alcohol exerts direct toxic effects on both the liver and gut, resulting in structural alterations in the intestine and the development of fatty liver, alcoholic hepatitis, and cirrhosis. Liver injury is preceded by an adaptive phase characterized by accelerated metabolism of drugs (including ethanol), and hyperlipemia, secondary to hypertrophy and hyperactivity of the smooth endoplasmic reticulum. Side effects include enhanced hepatotoxicity of CCI4 and possibly energy wastage. Alcoholics should not be led to beleive that correction or prevention of nutritional deficiency will prevent liver damage in the face of continued alcohol abuse.
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PMID:Alcohol and malnutrition in the pathogenesis of liver disease.. 117 54

A total of 164 patients with alcoholism-induced osteonecrosis were seen over a 22-year period, from 1962 to 1984. Twenty-three percent of patients were female and 30.5% were black. The average duration of alcohol abuse was 9.5 years, ranging from 8 to 20 years. The presence of femoral head necrosis was diagnosed in patients aged 21-67 years; 28% of patients were under 40 years of age and 76% were under 50 years. Bilateral hip necrosis was present in 44.5% of patients and, within three years of the diagnosis of FHN, the presence of multifocal necrosis became evident in 23 cases at sites away from the hip (shoulders and knees). Hyperlipidemia was found in 38.4% of cases, involving both cholesterol and triglycerides. Serum amylase was elevated in 33 patients; liver dysfunction was present in 50; hepatomegaly was found in 32; and biopsy-confirmed cirrhosis was present in 22 cases. Hyperuricemia was found in 22 patients, some of whom had received steroids. Disabling hip pain was the first manifestation of disability related to alcohol abuse in 158 patients, most of whom required total hip joint replacement. This study supports the hypothesis that alcoholism-induced bone necrosis is caused by fat embolism linked to co-existent hyperlipidemia. The treatment of hyperlipidemia by dietary means or lipotropic medication and the cessation of alcohol abuse is advised. Multi-center studies employing such treatment should provide evidence of its effect on the evolution of necrosis as well as the incidence of bilateral hip femoral head necrosis and multifocal lesions.
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PMID:Alcoholism-induced bone necrosis. 151 11

Hepatobiliary characteristics of untreated obese patients and those of patients reducing weight through very-low-calorie diets (VLCDs) are reviewed. In untreated obesity, hepatobiliary abnormalities are prevalent. Fatty change is common and may be related to insulin resistance. Moreover, portal inflammation and fibrosis are prevalent findings, also in the absence of alcohol abuse. The liver plays a key role in the hyperinsulinism and hyperlipidemia, and hepatic drug metabolism is influenced by enhanced glucuronidation and sulphatation. Predisposition to gallstone formation can be ascribed to increased biliary cholesterol secretion in concert with changed nucleating factors and altered gallbladder motility. Weight loss by VLCD reduces fatty change but may induce slight portal inflammation and fibrosis. Insulin resistance and pharmacokinetic abnormalities regress. During VLCD the risk of gallstone formation is markedly increased. The deleterious effects described of a rapid weight loss should draw some attention to the liver and biliary tract during VLCD treatment.
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PMID:Liver and gallbladder disease before and after very-low-calorie diets. 161 89

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.
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PMID:Failure of percutaneous drainage of pancreatic abscesses complicating severe acute pancreatitis. 173 73

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.
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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


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