Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The failure of patients to adhere adequately to prescribed medication and behavioral regimens is an important medical problem. Poor adherence is most common when the treatment regimen is preventive rather than curative, when patients are asymptomatic, and when the duration of treatment is long. For these reasons, adherence with dietary therapy for hypercholesterolemia is well recognized to be a significant clinical and research challenge. Medication adherence has been acknowledged to be a problem for those treatments with significant side effects, such as flushing and pruritus or the low palatability of bile acid sequestering agents. The availability of drugs that lack these effects has long been viewed as an important contribution to improving overall patient compliance. However, the literature on patient adherence with life-long treatment regimens that are simple and palatable (e.g., antihypertensives) suggests that while these improved treatments can enhance adherence, the overall rates of patient compliance still average only 50%. The fact that patients with heterozygous familial hypercholesterolemia are at high risk for early coronary artery disease and death if they fail to adhere to therapy is not sufficient to assure high rates of appropriate therapy over long periods of time, as demonstrated by the poor or erratic adherence commonly reported to treatments for other life-threatening diseases, such as advanced renal disease, hemophilia, and type I diabetes. The measurement of patient adherence to hypercholesterolemia therapy is often neglected in clinical practice and inadequate in hypercholesterolemia research.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Measuring adherence with therapy for chronic diseases: implications for the treatment of heterozygous familial hypercholesterolemia. 821 1

Nicardipine is a second generation dihydropyridine calcium antagonist which selectively inhibits vascular smooth muscle contraction. In elderly patients, the drug has demonstrated clinical efficacy in the management of hypertension, angina pectoris and ischaemia-related cerebrovascular disease. In particular, nicardipine effectively controls blood pressure in elderly hypertensive patients with or without coexistent disease. In noncomparative trials, a regimen containing nicardipine has been associated with an improvement of symptoms in hypertensive patients with concurrent coronary artery, cerebrovascular or peripheral vascular disease, while in essentially 'healthy' elderly hypertensive patients, nicardipine monotherapy has resulted in improved indices of mobility and cognitive function. As yet, however, there is no evidence that nicardipine (and/or other calcium channel antagonists) decreases cardiovascular morbidity and mortality in elderly patients, as has been demonstrated for more established antihypertensive therapies, namely diuretics and/or beta-blockers. The pharmacokinetic properties of nicardipine in elderly hypertensive patients appear to be similar to those in younger patients. The main adverse events associated with nicardipine in the elderly are related to the vasodilator properties of the drug and include pedal oedema, headache and flushing. However, the drug does not exacerbate spontaneous postural hypotension in the elderly, nor does it adversely affect the coronary artery disease risk profile, even in patients with type II diabetes mellitus. In summary, widespread clinical experience in the elderly indicates that nicardipine monotherapy or a regimen containing nicardipine is useful for the treatment of hypertension, particularly in patients with coexistent coronary artery, cerebrovascular or peripheral vascular disease. Nicardipine monotherapy has also demonstrated efficacy in angina pectoris and shown promise in the management of ischaemia-related cerebrovascular diseases, notably subarachnoid haemorrhage.
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PMID:Nicardipine. A review of its pharmacology and therapeutic efficacy in older patients. 847 49

Echocardiography and thallium-201 imaging with coronary vasodilators such as dipyridamole have been shown to be useful in detecting the presence and prognostic significance of coronary artery disease. Adenosine, a potent and direct coronary vasodilator, has a shorter physiologic half-life than dipyridamole, which exerts its effect by blocking the cellular uptake of adenosine. Because of the potential advantage of dipyridamole, we undertook this study to determine the correlation of adenosine echocardiography with thallium scintigraphy. Forty-two patients (18 men and 24 women; mean age 64) who were unable to undergo treadmill exercise and were known or suspected to have coronary artery disease were studied. A baseline echocardiogram was obtained in four standard views followed by adenosine infusion at a rate of 140 micrograms/kg/min for 6 minutes. Thallium-201 was administered 3 minutes into the infusion while a second echocardiogram was performed. Thallium-201 imaging was begun immediately after the infusion of adenosine and repeated 4 hours later. Sixteen patients underwent coronary angiography within 1 month of the adenosine echocardiogram and thallium-201 study. At the peak infused dose of adenosine there was a significant increase in heart rate (12 beats/min; p = 0.0001) and rate-pressure product (1.3 x 10(3) beats/min x mm Hg; p = 0.02) and statistically insignificant decreases in systolic and diastolic blood pressures. Sixty-two percent of patients experienced side effects during the adenosine infusion, with chest pain, shortness of breath, and flushing occurring most frequently. These side effects resolved within 1 to 2 minutes after the infusion was stopped. Ischemic electrocardiographic changes occurred in 19% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation of adenosine echocardiography and thallium scintigraphy. 849 1

Niacin is the oldest and most versatile agent in use for the treatment of dyslipidemia. It has beneficial effects on low-density lipoprotein cholesterol; high-density lipoprotein cholesterol; the apolipoproteins B and A-I constituting these fractions; triglyceride; and lipoprotein(a). Together, these benefits lead to a diminished incidence of coronary artery disease among niacin users. The chief constraints against niacin use have been flushing, gastrointestinal discomfort, and metabolic effects including hepatotoxicity. Time-release niacin has been developed in part to limit flushing, and now a nighttime formulation (Niaspan) has been developed that assists in containing this untoward effect. In a pivotal metabolic study, bed-time administration of 1.5 g time-release niacin was shown to have the same beneficial effects as 1.5 g plain niacin in 3 divided doses and to be well tolerated. Previous studies suggest that bedtime niacin administration diminishes lipolysis and release of free fatty acids to the liver; this, in turn, leads to an abolition of the usual diurnal increase in plasma triglyceride, which may result in diminished formation and secretion of triglyceride in the very-low-density lipoprotein fraction.
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PMID:Clinical profiles of plain versus sustained-release niacin (Niaspan) and the physiologic rationale for nighttime dosing. 991 59

Usual risk factors for coronary artery disease account for only 25-50% of increased atherosclerotic risk in diabetes mellitus. Other obvious risk factors are hyperglycemia and dyslipidemia. However, hyperglycemia is a very late stage in the sequence of events from insulin resistance to frank diabetes, whereas lipoprotein abnormalities are manifested during the largely asymptomatic diabetic prodrome and contribute substantially to the increased risk of macrovascular disease. The insulin-resistant diabetes course affects virtually all lipids and lipoproteins. Chylomicron and very-low-density lipoprotein (VLDL) remnants accumulate, and triglycerides enrich high-density lipoprotein (HDL) and low-density lipoprotein (LDL), leading to high levels of potentially atherogenic particles and low levels of HDL cholesterol. Hyperglycemia eventually impairs removal of triglyceride-rich lipoproteins, the accumulation of which accentuates hypertriglyceridemia. As triglycerides increase-still within the so-called normal range-abnormalities in HDL and LDL became more apparent. Thus, when triglycerides are >200 mg/dL, LDL particles are small and dense (when they are <90 mg/dL, the particles are of the large, buoyant variety). The atherogenicity of small, dense LDL particles is attributed to their increased susceptibility to oxidation, but in many patients they may be a marker for insulin resistance or the presence of atherogenic VLDL. Hypertriglyceridemia is associated with atherosclerosis because (1) it is a marker for insulin resistance and atherogenic metabolic abnormalities; and (2) the small size of triglyceride-enriched lipoproteins enables them to infiltrate the blood vessel wall where they are oxidized, bind to receptors on macrophages, and ingested, leading to the development of the atherosclerotic lesion. Various studies (primary prevention with gemfibrozil: Helsinki Heart Study; secondary prevention with simvastatin and pravastatin: Scandinavian Simvastatin Survival Study [4S] and Cholesterol and Recurrent Events [CARE], respectively) have demonstrated that lipid-lowering therapy in type 2 diabetes is effective in decreasing the number of cardiac events. Risk reduction was 22% to 50% (statins) and approximately 65% (fibrate) relative to placebo. It was also noted (in 4S and CARE) that the risk of major coronary events in untreated diabetic patients was 1.5-1.7-fold greater than in untreated nondiabetic patients. Although gemfibrozil (fibric acid derivative) is more effective in decreasing triglycerides and increasing HDL cholesterol in diabetic patients than the statins, it does not change and may even increase LDL-cholesterol levels (fenofibrate may be an exception, decreasing LDL cholesterol by 20-25% in some studies). However, gemfibrozil does increase LDL particle size. Nevertheless, the statins are the current lipid-lowering drugs of choice because the change in LDL-cholesterol-to-HDL-cholesterol ratio is better than with gemfibrozil. Moreover, the diabetic patient may be more likely to benefit from statin therapy than the nondiabetic patient. It should be noted that, in theory, nicotinic acid can correct or improve all lipid or lipoprotein abnormalities in patients with type 2 diabetes. Unfortunately, it is relatively contraindicated because it causes insulin resistance and may precipitate or aggravate hyperglycemia (in addition to its other well-known side effects such as flushing, gastric irritation, development of hepatotoxicity, and hyperuricemia). It is unknown at present whether newer formulations such as once-daily Niaspan may be better tolerated in diabetes. In any case, most patients with type 2 diabetes have risk factors for coronary artery disease and qualify for aggressive LDL cholesterol-lowering therapy. At the same time, it is presently unknown whether improved glycemic control decreases coronary artery disease risk in such patients.
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PMID:Diabetic dyslipidemia. 991 65

We evaluated the use of adenosine, dobutamine and arbutamine with (99m)Tc-tetrofosmin myocardial perfusion imaging. Forty patients under investigation for suspected coronary artery disease were recruited. Each had a resting scan and two separate stress scans on different days, in a randomized cross-over study. Resultant images were blindly reported in 13 segments per scan as normal, reversible or fixed defects. A score was given (0-3) for segmental defect severity. Haemodynamic responses were as expected for each agent. Subjective side effect scores did not differ overall between agents. Adenosine caused a significantly higher incidence of abnormal taste (54%) than dobutamine and arbutamine (both 23%) and a lower incidence of palpitations (25% vs 69% and 54%, respectively), all P<0.05. Arbutamine caused significantly more chest pain than adenosine (77% vs 46%) though less flushing (35% vs 68%), both P<0.05. Comparison of the results obtained showed highly significant levels of segmental agreement for visual and semi-quantitative analysis between adenosine and arbutamine, kappa value and correlation coefficient of 0.78 and 0.86, respectively, dobutamine and adenosine 0.69 and 0.78, and arbutamine and dobutamine 0.75 and 0.78, all P<0.0001. Adenosine, arbutamine and dobutamine differ in their haemodynamic response and side effect profile but provide highly comparable results during (99m)Tc SPECT imaging.
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PMID:Assessment of adenosine, arbutamine and dobutamine as pharmacological stress agents during (99m)Tc-tetrofosmin SPECT imaging: a randomized study. 1171

For the reconstruction of complex skull defects with individual prefabricated CAD/CAM-implants titanium is well established as bone substitution material. The aim of our studies was to optimize a composite material from polyesters and calcium phosphate. Therefore two different operating procedures (hot pressing and gas-flushing) were combined. As a result the graded composition and porosity of the implants allow a spatial guided degradation progress and cell ingrowth. First biocompatibility tests in vitro with primary human osteoblasts showed a much better pH-characteristic and a better biocompatibility of the composites in comparison with the pure polymers. Degradation experiments in vitro confirmed the different expected degradation rates of the composite materials. As a next step in vivo experiments in ovine skulls are in progress.
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PMID:[A graded composite material for use in the area of the cranial and facial skull]. 1245 2

This study compared the relative efficacy of a once-daily niacin extended-release (ER)/lovastatin fixed-dose combination with standard doses of atorvastatin or simvastatin, with a special emphasis on relative starting doses. Subjects (n = 315) with elevated low-density lipoprotein (LDL) cholesterol and decreased high-density lipoprotein (HDL) cholesterol blood levels (defined as LDL cholesterol blood levels > or =160 mg/dl without coronary artery disease, or > or =130 mg/dl if coronary artery disease was present, and HDL cholesterol <45 mg/dl in men and <50 mg/dl in women) were randomized to atorvastatin, simvastatin, or niacin ER/lovastatin for 16 weeks. The primary efficacy variables were the mean percent change in LDL cholesterol and HDL cholesterol levels from baseline. After 8 weeks, the starting dose niacin ER/lovastatin 1,000/40 mg and the 10-mg starting dose atorvastatin both lowered mean LDL cholesterol by 38%. After 12 weeks, niacin ER/lovastatin 1,000/40 mg lowered LDL cholesterol by 42% versus 34% with the 20-mg starting dose of simvastatin (p <0.001). Niacin ER/lovastatin increased HDL cholesterol significantly more than atorvastatin or simvastatin at all compared doses (p <0.001). Niacin ER/lovastatin also provided significant improvements in triglycerides, lipoprotein(a), apolipoprotein A-1, apolipoprotein B, and HDL subfractions. A total of 6% of study subjects receiving niacin ER/lovastatin withdrew because of flushing. No significant differences were seen among study groups in discontinuance due to elevated liver enzymes. No drug-induced myopathy was observed. Niacin ER/lovastatin was comparable to atorvastatin 10 mg and more effective than simvastatin 20 mg in reducing LDL cholesterol, was more effective in increasing HDL cholesterol than either atorvastatin or simvastatin, and provided greater global improvements in non-HDL cholesterol, triglycerides, and lipoprotein(a).
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PMID:Comparison of once-daily, niacin extended-release/lovastatin with standard doses of atorvastatin and simvastatin (the ADvicor Versus Other Cholesterol-Modulating Agents Trial Evaluation [ADVOCATE]). 1263 95

The efficacy and safety profiles of various forms of niacin for treating dyslipidemia are described. Niacin is well recognized for treating dyslipidemia in adults and has been shown to be effective in reducing coronary events. It has a broad range of effects on serum lipids and lipoproteins, including lowering total cholesterol, low-density-lipoprotein (LDL) cholesterol, and triglycerides. Niacin is the most effective lipid-modifying drug for raising high-density-lipoprotein (HDL) cholesterol levels and has been shown to lower Lp(a) lipoprotein. Niacin reduces triglycerides and very-low-density-lipoprotein and LDL cholesterol synthesis, primarily by decreasing fatty acid mobilization from adipose tissue. Niacin appears to raise HDL cholesterol by reducing hepatic apolipoprotein A-l clearance and enhancing reverse cholesterol transport. Niacin is metabolized through a conjugation or nicotinamide pathway. Standard immediate-release niacin is metabolized primarily through the conjugation pathway, which results in a high frequency of flushing. Long-acting niacin is metabolized through the nicotinamide pathway, which results in less flushing but increases the risk of hepatotoxicity. Extended-release niacin has a more balanced metabolism and causes fewer of both types of adverse effects. Improved serum lipid levels during niacin therapy have been associated with clinical and angiographic evidence of reduced coronary artery disease, especially when combined with statins. Niacin is particularly useful for managing high triglyceride and low HDL cholesterol levels as well as the lipid abnormalities associated with metabolic syndrome, including those commonly encountered in patients with diabetes. Several niacin products are available with significant differences in their safety and efficacy profiles. Health care providers must consider the differences between agents when recommending niacin for dyslipidemia treatment.
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PMID:Niacin for dyslipidemia: considerations in product selection. 1278 70

This was a double-blind, placebo-controlled, flexible-dose study of the efficacy and safety of sildenafil in men with erectile dysfunction (ED) and clinically stable coronary artery disease (CAD). Patients were randomized to receive sildenafil or placebo for 12 weeks. Primary outcomes were questions 3 and 4 of the International Index of Erectile Function (IIEF). Secondary outcomes included the other IIEF questions and functional domains, the Life Satisfaction Checklist, the Erectile Dysfunction Inventory of Treatment Satisfaction, 2 global efficacy assessment questions, and intercourse success rate. By week 12, sildenafil-treated patients (n = 70) showed significant improvements on questions 3 and 4 compared with placebo-treated patients (n = 72; p <0.01). Larger percentages of sildenafil-treated patients reported improved erections (64%) and improved intercourse (65%) compared with placebo-treated patients (21% and 19%, respectively). Sildenafil-treated patients were highly satisfied with treatment and their sexual life compared with placebo-treated patients. Forty-seven percent of sildenafil- and 32% of placebo-treated patients experienced adverse events, including transient headache, hypertension, flushing, and dyspepsia. There were no serious drug-related cardiovascular effects. Thus, sildenafil is an effective and well-tolerated treatment for ED in men with CAD. Sildenafil was not associated with additional safety risks in this patient population.
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PMID:Efficacy and safety of sildenafil citrate in men with erectile dysfunction and stable coronary artery disease. 1471 38


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