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)

Nicotinic acid (niacin) is a water-soluble vitamin widely used for the treatment of lipid disorders. In pharmacologic doses (1 g or more/day), alone or in combination with other lipid-lowering drugs, nicotinic acid lowers very low-density (VLDL) and low-density lipoprotein (LDL) levels, while concurrently increasing high-density lipoprotein (HDL) levels. It may reduce long-term mortality in patients with known coronary artery disease and may slow or reverse the progression of atherosclerosis. A major consideration against using nicotinic acid is the occurrence of frequent, bothersome, adverse reactions such as cutaneous flushing, skin rash, and gastric upset. Careful dosing titration may, however, minimize these effects. The beneficial effects, taken together with the low cost of nicotinic acid therapy and the relative freedom from serious side effects, have made nicotinic acid the agent of choice for the treatment of many patients with hyperlipidemia.
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PMID:Nicotinic acid: a review of its clinical use in the treatment of lipid disorders. 267 60

Cholestyramine, colestipol, clofibrate, gemfibrozil, nicotinic acid (niacin), probucol, neomycin, and dextrothyroxine are the most commonly used drugs in the treatment of hyperlipoproteinaemic disorders. While adverse reaction data are available for all of them, definitive data regarding the frequency and severity of potential adverse effects from well-controlled trials using large numbers of patients (greater than 1000) are available only for cholestyramine, clofibrate, nicotinic acid and dextrothyroxine. In adult patients treated with cholestyramine, gastrointestinal complaints, especially constipation, abdominal pain and unpalatability are most frequently observed. Continued administration along with dietary manipulation (e.g. addition of dietary fibre) and/or stool softeners results in diminished complaints during long term therapy. Large doses of cholestyramine (greater than 32 g/day) may be associated with malabsorption of fat-soluble vitamins. Most significantly, osteomalacia and, on rare occasions, haemorrhagic diathesis are reported with cholestyramine impairment of vitamin D and vitamin K absorption, respectively. Paediatric patients have been reported to experience hyperchloraemic metabolic acidosis or gastrointestinal obstruction. Concurrent administration of acidic drugs may result in their reduced bioavailability. Serious adverse reactions to clofibrate will probably limit its role in the future. Of particular concern are ventricular arrhythmias, induction of cholelithiasis and cholecystitis, and the potential for promoting gastrointestinal malignancy which far outweigh the reported benefits in preventing new or recurrent myocardial infarction, cardiovascular death and overall death. Patients with renal disease are particularly prone to myositis, secondary to alterations in protein binding and impaired renal excretion of clofibrate. Drug interactions with coumarin anticoagulants and sulphonylurea compounds may produce bleeding episodes and hypoglycaemia, respectively. Nicotinic acid produces frequent adverse effects, but they are usually not serious, tend to decrease with time, and can be managed easily. Dermal and gastrointestinal reactions are most common. Truncal and facial flushing are reported in 90 to 100% of treated patients in large clinical trials. Significant elevations of liver enzymes, serum glucose, and serum uric acid are occasionally seen with nicotinic acid therapy. Liver enzyme elevations are more common in patients given large dosage increases over short periods of time, and in patients treated with sustained release formulations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adverse effects of hypolipidaemic drugs. 354 4

We reviewed clinical findings in 740 patients over age 65 who consulted the Otological Medical Group, Inc., during a one-year period for dizziness. A thorough neurotologic evaluation is indicated in every such case to determine the specific cause of dizziness. In 21 per cent of these patients, a specific cause of dizziness was found. In the remaining 79 per cent, the diagnosis of primary dysequilibrium of ageing (presbyastasis) was made. We classified dysequilibrium of ageing (presbyastasis) according to the character, time course, and precipitating factors of dizziness. Two clinical types were described: constant and episodic; episodic dizziness was subdivided into orthostatic, positional, and unclassified. The histological findings in the temporal bones of four cases with dysequilibrium of ageing were reviewed. Pathological changes other than those in the peripheral vestibular system seem to be responsible for dysequilibrium of ageing. In the present series, about three-fourths of the patients had a daily dose of nicotinic acid to produce flushing of the skin. In 16 per cent, the dizziness was minor, requiring no special treatment. In the remaining 9 per cent with incapacitating vertigo, a vasodilator regimen, antivertiginous drugs, and Cawthorne's vestibular exercises were prescribed.
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PMID:Dysequilibrium of ageing (presbyastasis). 376 Jun 85

The hypolipidemic activity of the tetraester of pantethine with 3-(3-pyridinemethoxycarbonyl)propionic acid (MG 28362) was assessed in various experimental conditions versus the corresponding activities of nicotinyl alcohol (NA), nicotinyl alcohol hemisuccinate (NAH), nicotinic acid (NAC), and pantethine tetranicotinate (PTN). In the normolipidemic rat, MG 28362 causes a more durable reduction of non-esterified fatty acids (NEFA) and serum triglycerides than the reference products. NEFA values return slowly to pretreatment levels without causing the rebound effect typical of most nicotinic acid derivatives. Likewise in the test of ethanol-induced hypertriglyceridemia, MG 28362 shows more pronounced and sustained activity compared to the reference products. It is also more effective on Triton hyperlipidemia and on diet-induced hypercholesterolemia; in the latter test, MG 28362 caused no triglyceride accumulation in the liver. Even at high dosage levels, MG 28362 did not cause the characteristic flushing of nicotinic acid congeners. Last, the new substance displays a fairly marked antiaggregating activity on blood platelets, some anti-hypoxic activity, and a generally low order of toxicity.
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PMID:Pharmacological study of a new hypolipidemic drug of prolonged activity, the tetraester of pantethine with 3-(3-pyridinemethoxycarbonyl)propionic acid. 384 36

Acipimox, an analogue of nicotinic acid, is a hypolipidemic drug with antilipolytic activity. Ten patients with type III and 10 with type IV hyperlipoproteinemia participated in a comparative open cross-over study of the effect of acipimox (750 mg/day) and clofibrate (2 g/day) on lipoproteins, apoliproproteins and postheparin lipase activities during 6 weeks. During acipimox treatment 2 type III patients complained of flushing, resulting in one drop-out. In the type III patients serum cholesterol decreased 30% (P less than 0.01) during treatment with acipimox and 24% (P less than 0.01) with clofibrate, and serum triglycerides 48% (P less than 0.01) and 34% (P less than 0.01), respectively. In the type IV patients serum cholesterol remained unchanged and serum triglycerides decreased 34% (P less than 0.05) and 35% (P less than 0.01), respectively. HDL cholesterol increased during treatment with both drugs in both groups between 6 and 15% (P less than 0.05) mainly due to a rise in HDL3 cholesterol (d greater than 1.100 g/ml). LDL cholesterol increased significantly during treatment with clofibrate, but not with acipimox. There were no or slight changes in the apoproteins A and B. Postheparin lipoprotein lipase increased during clofibrate treatment and hepatic lipase decreased during acipimox treatment. We concluded that acipimox in a dose of 750 mg/day has a similar hypolipidemic effect as 2 g clofibrate daily in type III and IV hyperlipoproteinemia.
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PMID:A comparative study of the effects of acipimox and clofibrate in type III and type IV hyperlipoproteinemia. 392 65

A randomised controlled clinical trial was conducted to investigate the ability of nicotinic acid to reduce intestinal secretion in patients with severe cholera. Of the 62 adults investigated, 29 received either 1 or 2 g of nicotinic acid given orally in divided doses and 33 served as controls. Patients who received the 2 g dose had less fluid loss than did their controls during the first (p less than 0.01) and second (p less than 0.05) 8 h post-treatment periods. During the third and fourth 8 h periods, the rates were lower in the treatment groups, but not significantly so. The drug-specific stool reduction was 31%-47% during the first 16 h. Patients receiving 1 g consistently had lower rates of purging than had their controls during each 8 h observation period, but the differences were not significant. The effect of the 2 g dose was significantly better than that with the 1 g dose. The peak inhibition occurred 8-16 h after start of therapy. The drug was well tolerated, the only side-effect being transient flushing of the body in 1 patient.
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PMID:Reduction of fluid-loss in cholera by nicotinic acid: a randomised controlled trial. 614 May 41

Nicotinic acid flushing after placebo and 975-mg oral doses of aspirin was assessed in 29 normal subjects over a range of nicotinic acid doses. Intensity of flushing was assessed by the change in malar thermal circulation index (delta MTCI). Aspirin pretreatment resulted in smaller delta MTCIs at the higher doses of nicotinic acid. At the lower doses the change in the index after pretreatments with both aspirin and placebo remained low, suggesting that very little flushing was provoked by these doses. These results are compatible with the proposed mediation by prostaglandins of the nicotinic acid-induced flush. According to the delta MCTI method, flushing is quantitatively characterized as a nonquantal, dose-response reaction of variable intensity.
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PMID:Aspirin blocks nicotinic acid-induced flushing. 706 Mar 28

The intensity of erythema does not show a linear correlation with convective and conductive heat transport. In erythema induced by various means such as dermographism, the application of nicotinic acid benzylester, UV-B-irradiation, or dithranol, the mediators follow the direction of blood and lymph defluxion. As a result heat reflection occurs not only from the erythemic region, but also from the surrounding unaffected skin area. Venous blood vessel texture is increased within areas of blood defluxion. Erythemous flushing after alcohol uptake is characterized by an increase in skin temperature. This increase in temperature occurs prior to the appearance of erythema compared to exogenous skin irritation which first shows erythema and later on an increased temperature. An even further increment can be measured in the flushed area. An increase in acral temperature (hands, feet, nose) is an indication of the systemic effect of the resorbed alcohol.
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PMID:[Development of erythema in thermographic images]. 731 14

Lipid abnormalities are seen frequently in renal transplant patients. Cardiovascular disease is an important cause of morbidity and mortality in these patients. We assessed the efficacy and safety of the lipid-lowering drugs, nicotinic acid (short acting) and lovastatin, the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Twelve renal transplant patients who had persistent hyperlipidemia despite 6 weeks of dietary treatment participated in this prospective, randomized, open-labeled crossover trial. At 16 weeks, when compared with control values, nicotinic acid (> or = 1.5 g twice a day) significantly reduced the total cholesterol (from 312 +/- 18 [+/- SEM] mg/dL to 229 +/- 19 mg/dL; P = 0.03) and the low-density lipoprotein cholesterol (from 218 +/- 15 mg/dL to 142 +/- 13 mg/dL; P = 0.03) and significantly increased the high-density lipoprotein cholesterol (from 44 +/- 3 mg/dL to 58 +/- 5 mg/dL; P = 0.03). The triglyceride level was reduced from 255 +/- 40 mg/dL to 150 +/- 23 mg/dL (P = 0.09). At 16 weeks, lovastatin therapy (40 mg/d) significantly reduced the total cholesterol (from 285 +/- 13 mg/dL to 233 +/- 10 mg/dL; P = 0.005) and the low-density lipoprotein cholesterol (from 201 +/- 11 mg/dL to 147 +/- 7 mg/dL; P = 0.001). There were no significant changes in the triglyceride and high-density lipoprotein cholesterol levels. Although flushing developed in 67% of patients treated with nicotinic acid, this was not a reason for any of the study dropouts. During this short-term study period no adverse biochemical effects were noted with either of the drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of nicotinic acid and lovastatin in renal transplant patients: a prospective, randomized, open-labeled crossover trial. 770 60

Nicotinic acid and derivatives are effective in numerous forms of hyperlipoproteinemia. Its primary mode of action is to inhibit lipolysis in adipose tissue and to prevent the utilization of free fatty acids for TG-rich lipoprotein synthesis in the liver. Consequently, it decreases the plasma lipoproteins which are considered to be atherogenic--VLDL, LDL and Lp(a), while it increases the antiatherogenic lipoprotein--HDL. A gradual administration of nicotinic acid or derivatives is useful to reduce the side effects such as flushing and itching. In the secondary prevention trials, nicotinic acid therapy with other hypolipidemic drugs asserted protective effects on the development/progression of cardiovascular disease.
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PMID:[Nicotinic acid and derivatives for therapy of hyperlipoproteinemia]. 785 25


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