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)

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93

The effects of oral contraceptives (OCs) on drug therapy are related mainly to the inhibition of microsomal oxidation as well as the induction of enzymes involved in conjugation reactions. Since many drugs share these catabolic pathways, their pharmacodynamics will be affected by OCs. Notable interactions include an increased bioavailability of analgesics, tranquilizers, and tricyclic antidepressants. OCs increase the risk for hypertension, and pharmacokinetic interactions are to be expected when OCs are administered with antihypertensive drugs. Likewise, OCs affect lipid metabolism and thus modify the effects of atherogenic drugs; however, the different forms of hyperlipidemia show a heterogeneous response to OCs. Another particular concern is that the gestagen components of OCs may cause peripheral insulin resistance and may require dose adaption with antidiabetic treatments. Two common nonprescription drugs, theophylline and caffeine, show decreased clearance rates due to OCs. All share a common oxidation pathway involving cytochrome P-450 and P-448. However, cigarette smoking stimulates these enzymes, and the decreased clearance of theophylline and caffeine is usually not observed in smokers. The reports of effects of OCs and alcohol taken together are mixed, and no clinically relevant conclusions can be drawn. Most vitamin and mineral levels are influenced by OCs, but this is a concern only under conditions of deprived diet, when normal dietary adjustments are impossible. An important caveat of the many documented effects of OCs on the pharmacodynamics of other drugs is that, in most instances, these effects will be counterbalanced with kinetic changes and result in no clinical manifestation. Nevertheless, clinicians must be aware of possible adverse reactions, particularly in predisposed patients.
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PMID:Influence of oral contraceptives on drug therapy. 225 28

An enzyme immunoassay technique (EMIT) for microdeterminations of caffeine was compared with high performance liquid chromatography (HPLC) and evaluated in 113 neonates and young infants, and in 18 asthmatic and 15 epileptic children. The EMIT assay was found reliable in therapeutic drug monitoring. It offers advantages over HPLC in its rapidity and simplicity. It is not affected by hemolysis, hyperbilirubinemia, or lipemia. In the neonate, greater accuracy is obtained with blood samples containing no heparin.
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PMID:Caffeine enzyme immunoassay in neonatal and pediatric drug monitoring. 355 32

Fifty subjects with peripheral vascular disease were randomly assigned to either the American Heart Association Hyperlipidemia Diet C (AHA, N = 23) or a higher fiber, low fat diet based on the Pritikin maintenance diet (HFD, N = 27) and studied for a 12-month period. Diet counseling was provided, and the subjects were encouraged to exercise regularly, to decrease their consumption of salt, alcohol, and caffeine, and to restrict cigarettes as much as possible. Dietary intake data showed that energy distribution was approximately 49% and 64% carbohydrate, 20% and 22% protein, and 31% and 14% fat for the AHA and HFD groups, respectively. Cholesterol and dietary fiber intakes averaged 201 mg and 23 gm per day, respectively, for the AHA group and 108 mg and 43 gm per day, respectively, for the HFD group. Generally, both groups showed tendencies toward decreased serum triglycerides, cholesterol, and LDL cholesterol and increased HDL cholesterol. The HFD group achieved a significant decrease in serum cholesterol (at month 12) (p less than .01). The only significant between-group difference was in serum cholesterol at 4 months (p less than .01), with the lower value in the HFD group. There was a consistent negative correlation between dietary fiber and serum cholesterol levels (p less than .01). Average weight loss was 4.1 kg for the AHA group and 6 kg for the HFD group. We concluded that both dietary regimens, combined with exercise, can be of benefit to patients with peripheral vascular disease.
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PMID:Effects of two "lipid-lowering" diets on plasma lipid levels of patients with peripheral vascular disease. 632 25

The relationship between consumption of decaffeinated coffee and acute myocardial infarction was analyzed in a case-control study conducted in Italy between 1983 and 1992. Case patients were 433 women with acute myocardial infarction, aged 24 to 69 years (median age, 52 years), and control subjects included 869 women in hospital for a wide spectrum of acute conditions, other than cardiovascular, neoplastic, digestive, and hormone-related diseases or conditions associated with long-term modification of diet. Regular use of decaffeinated coffee was reported by 11% of the case patients and 7% of the control subjects. Compared with women who did not drink decaffeinated coffee, the relative risk (RR) was 1.3 (95% confidence interval (CI), 0.8 to 2.2) for one cup/d and 2.1 (95% CI, 1.1 to 3.9) for 2 or more cups (chi 2(1) for trend = 5.62, P = 0.02). The estimates were somewhat higher after allowance for education, marital status, body mass index, and smoking status (RR for > or = 2 cups of decaffeinated coffee per day, 2.5; 95% CI, 1.2 to 4.9), and somewhat lower after further allowance for diabetes, hypertension, and hyperlipidemia (RR, 1.7; 95% CI, 0.8 to 3.6). There was no association between duration of use of decaffeinated coffee and infarction risk. The relationship between decaffeinated coffee and infarction was consistent across strata of age, education, smoking, and history of hyperlipidemia. Thus, a relationship of marginal significance was observed in this study between decaffeinated coffee and myocardial infarction, of similar magnitude to that described for caffeinated coffee. This indicates that (i) caffeine is unlikely to be a relevant factor in any potential coffee-myocardial infarction relationship, and (ii) shifting from caffeinated to decaffeinated coffee is unjustified in order to reduce any possible coffee-related infarction risk.
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PMID:Decaffeinated coffee and acute myocardial infarction. A case-control study in Italian women. 792 7

Coffee is the most commonly used drug in the United States. The medical literature is conflicted regarding the harmful effects of coffee and caffeine. Because the articles that have appeared are so different, a formal meta-analysis is not the ideal way to summarize the data. However, this literature review suggests that coffee does not have an appreciable effect on hyperlipidemia, hypertension, ischemic heart disease, or cancer. The effects of decaffeinated coffee are much less well-defined, and there is little rationale for recommending that patients switch to decaffeinated coffee. A less appreciated problem with caffeine is that it may increase the risk of osteoporosis and hip fracture.
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PMID:Coffee: brew or bane? 801 Mar 38

Morbidity and mortality of cardiovascular diseases are related to life-style (in particular diet, exercise and smoking). Many epidemiological studies have demonstrated that nutrition significantly affects cholesterol (C) and lipoprotein levels i.e. LDL-c and HDL-c, whereby an increase in LDL-c and a decrease in HDL-c represent independent primary risk factors for atherogenesis. For many years studies have been performed to discover other risk factors, one of the most important being the influence of coffee consumption. Epidemiological analysis of a single dietary factor produces many methodological difficulties, which may explain the inconsistent study findings regarding the effects of coffee. Thus, these studies have to be performed with large numbers of participants over many years, during which time dietary and drinking habits have to be stabilized in order to detect possible associations. Coffee contains a number of biochemically active substances, one of the most important being caffeine, a xanthine derivative. Recent studies have concentrated on the methods of preparation of coffee, which vary from country to country. A lipid fraction of boiled coffee, which is widely consumed in Northern European countries has been shown to significantly raise C and LDL-c in a dose-dependent manner. Filtered coffee, however, does not contain this lipid elevating fraction. Thus, recommendations concerning the consumption of coffee have to take into account the particular method of preparation, the amount consumed and predisposing risk factors that could interact with coffee consumption such as hypertension, hyperlipidaemia, cardiac arrhythmia.
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PMID:Coffee, lipoproteins and cardiovascular disease. 843 98

Dexfenfluramine increases serotonergic activity by stimulating serotonin (5-hydroxytryptamine; 5-HT) release into brain synapses, inhibiting its reuptake into presynaptic neurons and by directly stimulating postsynaptic serotonin receptors. On the basis of the serotonin hypothesis of appetite control, these actions would be expected to reduce appetite and, consequently, bodyweight. Studies conducted in animals and in overweight patients with and without associated disorders have confirmed the weight-reducing efficacy and good tolerability of dexfenfluramine. In 3-month clinical studies in obese patients, weight reductions with dexfenfluramine 15mg twice daily combined with dietary support were significantly higher than those achieved with placebo and similar to those with ephedrine/caffeine 20/20mg 3 times daily, sibutramine 10mg once daily and fluoxetine 60 mg/day. Furthermore, dexfenfluramine recipients with non-insulin-dependent diabetes mellitus, hyperlipidaemia or hypertension consistently show improvements in glycaemic control, blood lipid profiles and blood pressure. 12-month trial results indicate that most weight loss occurs in the initial 6 months and appears to be maintained for a further 6 months. Weight regain after withdrawal of treatment in 12-month studies demonstrates that dexfenfluramine is effective in maintaining a stable bodyweight at a lower level than placebo and in limiting food intake over this time period. Commonly reported adverse events with dexfenfluramine include diarrhoea, tiredness, dry mouth and somnolence; these symptoms are generally mild and transient. Approximately 7 and 10% of dexfenfluramine recipients in short and long term studies withdrew because of adverse events. Dexfenfluramine was better tolerated than ephedrine/caffeine and fluoxetine in short term studies. Obesity is a chronic condition that is accompanied by a number of metabolic complications. It is a significant health problem in developed countries, and as a major risk factor for many chronic diseases, including diabetes and cardiovascular disease, the economic burden of this condition is considerable. As with other chronic conditions, there is a role for pharmacological intervention in patients with severe obesity. However, drugs should be considered as only one component of a weight-control programme, since additional lifestyle modification is required to maintain weight loss. The promising data on the long term efficacy and tolerability of dexfenfluramine as well as its favourable effects on risk factors associated with obesity requires confirmation in long term studies. In the meantime, dexfenfluramine should be considered a valuable adjunct to a reduced-calorie diet in the management of severe obesity, particularly in patients with associated disorders and those unsuccessful with conventional weight loss measures. Available data support the use of the drug for up to 1 year to maintain weight loss and thus dexfenfluramine should be considered for long term administration.
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PMID:Dexfenfluramine. An updated review of its therapeutic use in the management of obesity. 911 19

Chronic hyperglycemia and hypercholesterolemia have been shown to alter ionic currents in vascular smooth muscle. We tested the hypothesis that the combined effect of hyperglycemia and hyperlipidemia (diabetic dyslipidemia) would increase the Ca2+-sensitive K+ (KCa) current as a compensatory response to an increase in intracellular Ca2+ concentration. We also hypothesized that exercise training would prevent this elevation in KCa current. Miniature Yucatan swine were randomly assigned to five groups: control, standard pig chow (C, n = 6); hyperlipidemic, high-fat pig chow (H, n = 5); diabetic, standard pig chow (D, n = 7); diabetic, high-fat pig chow ("diabetic dyslipidemic," DD, n = 12); and exercise-trained DD (DDX, n = 9). High-fat chow consisted of standard minipig chow supplemented with cholesterol (2%) and coconut oil. Increased coronary vasoconstriction assessed in vivo and in vitro in DD was prevented by exercise. Patch-clamp experiments performed on right coronary artery smooth muscle cells resulted in greater K+ current densities in the H, D, and DD groups vs. the DDX group between -10 and 40 mV. In fura 2-loaded cells, current activated by caffeine-induced Ca2+ release was greater in H, D, and DD compared with C and DDX (P < 0.05), whereas intracellular Ca2+ concentration was not different across groups. Finally, there were no differences in the KCa or Kv channel protein content between groups. These data indicate that hyperglycemia, hyperlipidemia, and diabetic dyslipidemia lead to elevated whole cell K+ current and increased functional coupling of KCa and Ca2+ release. Endurance exercise prevented increased coupling of Ca2+ release to KCa channel activation in diabetic dyslipidemia.
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PMID:Altered functional coupling of coronary K+ channels in diabetic dyslipidemic pigs is prevented by exercise. 1277 9

In animals deprived of food for a long period, a drop in the fat mass below 5% of the total body mass results in an increase in blood glucocorticoids and uric acid levels, followed by foraging activity. Since the glucocorticoids increase the uric acid excretion, an increase in the level of uric acid in the bladder urine could be the signal for this feeding behaviour and subsequent fat storage. Accumulation of fat is associated with hyperglycaemia, hyperinsulinaemia, hyperlipidaemia, and hypercholesterolaemia as seen in the metabolic syndrome or hibernation. It is hypothesized that uric acid or its structurally related compound, 1-methyl uric acid (one of the metabolites of the methyl xanthines namely caffeine, theophylline, and theobromine present in coffee, tea, cocoa, and some drugs), can act on the urinary bladder mucosa and increases the blood glucose, insulin, triglyceride, and cholesterol levels. In rats, perfusion of the urinary bladder with saturated aqueous solution of uric acid or 1-methyl uric acid results in a significant increase in the serum levels of glucose, insulin, true triglyceride, and total cholesterol in comparison with perfusion of the bladder with distilled water at 20, 40, and 80 min. The uric acid or the 1-methyl uric acid acts on the urinary bladder mucosa and increases the serum glucose, insulin, true triglyceride, and total cholesterol levels.
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PMID:Uric acid or 1-methyl uric acid in the urinary bladder increases serum glucose, insulin, true triglyceride, and total cholesterol levels in Wistar rats. 1524 98


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