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)

Seven patients with hyperlipoproteinemia (HLP) type II (four patients with type II A and three patients with type II B), who were experienced to be resistant to hypolipidemic drugs, were treated for 6 months with etofibrate, a double-ester of nicotinic acid and clofibrinic acid, at a dose of 0.3 g t.i.d. Mean serum cholesterol level decreased by up to 18% from a pre-treatment value of 7.7 +/- 1.4 mmol/l. The reduction of serum cholesterol was due both to a decrease in very low density (VLDL) and low density (LDL) lipoprotein cholesteral by 61 and 25%, respectively (after 6 months). Furthermore alpha-LP (HDL) cholesterol increased by 8%, (after 6 months). All seven patients had previously received clofibrate and had obtained a mean decrease in plasma cholesterol by 6%. There was a slight transient increase in S-ASAT and S-ALAT simultaneous with in increase in serum urate. However, these values returned after 3 months to pre-treatment level. No influence on glucose tolerance was recorded. There were no bothersome side effects except a transient discomfort in the form of flushing or acid indigestion which occurred after 1--2 months of treatment with etofibrate.
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PMID:Treatment of hyperlipoproteinemia type II with etofibrate. 52 96

We studied the effects of nifedipine on blood pressure and on clinical and analytical parameters in hypertensive patients. Seven male and eight female subjects (mean age of 46.27 +/- 5.38 years, range of 41-56 years) with essential arterial hypertension were given nifedipine (20 mg b.i.d.) for 3 months. Before and after treatment, history, blood pressure, and biochemical values were recorded [blood: Na, K, Ca, creatinine, uric acid, triglycerides, cholesterol, HDL cholesterol, antidiuretic hormone (ADH), and aldosterone; urine: Na, K, Ca, creatinine, ADH, aldosterone, and percentage fraction of Na, K, and Ca excreted]. After 3 months of treatment, we found (a) significant decreases in systolic (147 +/- 18 vs. 166 +/- 16 mm Hg, p less than 0.001) and diastolic blood pressure (90 +/- 8 vs. 107 +/- 8 mm Hg, p less than 0.0007), triglycerides (107 +/- 47 vs. 120 +/- 49 mg/dl, p less than 0.0007), and cholesterol (236 +/- 4 vs. 257 +/- 44 mg/dl, p less than 0.00075) in blood, and in K excretion (50 +/- 19 vs. 46 +/- 19 mEq/g of creatinine, p less than 0.0007) and excreted fraction of K (49 +/- 6% vs. 8 +/- 5%, p less than 0.0012) in urine; (b) significant increases in HDL cholesterol (65 +/- 13 vs. 58 +/- 13 mg/dl, p less than 0.001) in blood, and in Na (115 +/- 73 vs. 109 +/- 69 mEq/g of creatinine, p less than 0.0007) in urine; and (c) no significant change in the remaining biochemical parameters, or in heart rate. Secondary effects included flushing (34%), headache (20%), ankle swelling (17%), dizziness (13%), palpitations (4%), and pruritus (4%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic and antihypertensive effects of nifedipine in hypertensive patients. 137 8

The antihypertensive effect of nitrendipine was examined in 29 outpatients with a mild or moderate hypertension and type II diabetes or a dyslipidemic condition. The drug was administered for 90 days at a daily dose of 10 to 40 mg. Following a washout period, the blood pressure (measured by a Dinamap device) was 181/99 mm Hg supine and 172/104 mm Hg standing. Nitrendipine caused a reduction in both pressures and after 90 days their values were 148/74 and 143/80 mm Hg, respectively. Heart rate was not affected by the drug, which also caused no variation in blood pressure, total and HDL cholesterol, and triglycerides. In more than 20% of the cases, treatment was associated with headache and flushing, which did not necessitate discontinuation of treatment. Thus, nitrendipine is an effective antihypertensive agent and causes no untoward metabolic effects.
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PMID:Nitrendipine efficacy and safety in patients with mild and moderate essential hypertension. 172 54

The efficacy and tolerance of 750 mg of Acipimox was tested in 38 pts with primary dyslipidemias: 20 type IIa, 12 type IIb, and 6 type IV. All pts had been poor responders to a 2 month diet according to the recommendations of the National Cholesterol Education Program. Clinical examination, eye fundus, and the following laboratory tests: total cholesterol (TC), HDL, triglycerides (TG), total bilirubin, alkaline phosphatase, oxalacetic and pyruvic transaminases, uric acid, plasmatic creatinine, albumin, postprandial glucose test, hematocrit, white blood and platelet count were performed 60 days before drug initiation, 60 and 180 days after treatment had been started. No side effects were observed (myositis, visual gastrointestinal). 50% of the pts had slight to moderate flushing which appeared the first 3 days and lasted 14 +/- 7 days after treatment had been started. Plasmatic creatinine increased from 0.89 to 1.86 mg/dl in pt with one kidney, returning to normal levels 30 days after Acipimox interruption. After 180 days of therapy in the IIa group TC was -27% (p < 0.001), HDL + 15% (p < 0.001); in the IIb group: TC-23% (p < 0.001), HDL +9% (NS), TG -48% (p < 0.001); and in the IV group: TC-10% (p < 0.05), HDL +20% (p < 0.001), TG-53% (p < 0.001). Acipimox is well tolerated and is useful as a lipid-lowering drug in type IIa, IIb and IV dyslipidemias. Further studies are necessary to clear effects of the drug on renal metabolism and on long term survival of coronary pts.
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PMID:[Acipimox in primary hyperlipidemias: safety and efficacy evaluated in six months]. 184 8

Twenty-five hypercholesterolaemic patients from three centres in the UK were investigated in an open study of the efficacy and side effects of niceritrol. Five patients dropped out of the study at an early stage and had insufficient data for analysis. There were 13 males and 7 females (mean age 49.2 years, range 18-69). Fourteen patients had heterozygous familial hypercholesterolaemia, and six polygenic hypercholesterolaemia. Niceritrol was started at a dose of 750 mg/day and this was increased at weekly intervals over 4 weeks to the maximum tolerated dosage up to 3 g/day. This was then maintained for a further 8 weeks. There were statistically significant decreases in total plasma cholesterol, total triglyceride, LDL cholesterol and VLDL triglyceride; HDL cholesterol remained unchanged after 12 weeks of treatment (Wilcoxon matched pairs, signed ranks test). The 14 patients with familial hypercholesterolaemia showed a 13.9% fall in total cholesterol and a 19.8% fall in LDL cholesterol. All patients reported flushing and some had gastrointestinal symptoms but 19 would have been prepared to continue with the therapy at doses up to 3 g/day. Thus niceritrol has been found to be beneficial in the treatment of both familial and polygenic hypercholesterolaemia.
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PMID:Clinical and laboratory responses to niceritrol in the treatment of hypercholesterolaemia. 307 43

Pentaerythritol tetranicotinate (Perycit), at an oral dosage of 750 mg daily, was given to 12 patients with idiopathic hyperlipidemia and to 12 patients with hyperlipidemia superimposed with diabetes mellitus (DM). With 2 months off-drug period as the baseline, each patient then received 3 months of placebo and 3 months of Perycit. The sequence of treatment was randomized and balanced in frequency. Blood glycosylated hemoglobin (Hb A1) and fasting plasma glucose (FPG) were used as indices of diabetic control. Serum triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), and TC/HDL-C ratio were measured and calculated in order to compare the antilipemic effectiveness of Perycit with that of placebo. The non-parametric Wilcoxon test was used for the statistical analysis. The results showed that in the idiopathic group, Perycit significantly lowered the serum level of TG and the ratio of TC/HDL-C, and elevated the serum level of HDL-C. In the diabetic group, although there was a similar improvement in diabetic control in both periods of placebo and Perycit treatments, there was no change in the serum levels of TG and HDL-C. There was a slight increase of the serum levels of TC in the periods of Perycit treatment, whereas a small increase of HDL-C resulted in a mild decrease of the TC/HDL-C ratio. There was mild and transient facial flushing during the Perycit treatment in 6 out of 12 diabetic patients. Otherwise, there was no side effects in either group. Pooling the two groups' data together, Perycit increased the serum levels of HDL-C and decreased the TC/HDL-C ratio. It is concluded that Perycit has antilipemic effects in patients with idiopathic hyperlipidemia, and may be helpful in reducing the atherogenic risks in these patients. In patients with hyperlipidemia superimposed with DM, although the serum lipids composition was not significantly changed after Perycit, the atherogenic risks might also be reduced as demonstrated by the decrease of the TC/HDL-C ratio.
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PMID:The antilipemic effectiveness of pentaerythritol tetranicotinate on hyperlipidemic patients with or without diabetes mellitus--a double-blind, randomized and two-period change-over experiment. 391 69

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

To minimize the cutaneous flushing symptoms associated with niacin use, a time-release capsule form of niacin has been formulated. Thus study compares the effects of time-release niacin with those of unmodified niacin on lipoprotein lipids, including HDL2 and HDL3, apoproteins A-I and A-II, clinical chemistries, symptomatic side effects, and adherence to the medication regimen. Seventy-one primarily hypercholesterolemic subjects were randomized to either unmodified niacin or time-release niacin ad took medication for a six-month period. The two groups were closely matched on anthropomorphic and lipid variables. Adherence to the therapeutic regimen at a dose of 1.5 g/d in the first month of treatment was similar in the two groups. Thereafter, at a dose of 3.0 g/d, adherence was in excess of 90% among subjects taking unmodified niacin but only 64% among those taking time-release niacin, chiefly because of aggravated gastrointestinal symptoms; cutaneous flushing side effects, however, were slightly less common with time-release niacin. At these levels of adherence, LDL cholesterol (C) was reduced 21% by unmodified niacin and 13% by the time release form. Plasma total triglyceride was reduced more with unmodified niacin (27%) than with time-release niacin (8% maximum), and HDL-C and HDL2-C were increased significantly with unmodified niacin (26% and 36%) and were not significantly changed by time-release niacin. Increased to a similar degree on both regimens were HDL3-C (approximately 35%) and apoA-I (approximately 12%). ApoA-II was not affected by either drug regimen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contrasting effects of unmodified and time-release forms of niacin on lipoproteins in hyperlipidemic subjects: clues to mechanism of action of niacin. 392 90

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.
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PMID:The effects on lipids, blood viscosity and platelet aggregation of combined use of niceritrol (Perycit) and a low dose of acetylsalicylic acid. 400 83

Bezalip (bezafibrate), at an oral dosage of 200 mg three times a day, has been used on 12 patients with idiopathic hyperlipidemia, and on 12 patients with hyperlipidemia superimposed with diabetes mellitus. Each patient received bezafibrate for 3 months and placebo for 3 months. Blood glycosylated hemoglobin (HbA1) and fasting plasma glucose (FPG) were used as indices of diabetic control. Serum triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C), and TC/HDL-C ratio were measured and calculated in order to compare the antilipemic effects of bezafibrate with that of placebo. Non-parametric Wilcoxon test was used for statistical analysis. In both the idiopathic group and diabetic group, bezafibrate significantly lowered the serum levels of TG and TC/HDL-C, as well as elevated the level of HDL-C. The serum TC levels were not significantly altered in either of the groups. These effects could not be ascribed to an improved diabetic control, since the percent changes of HbA1 were not different between the bezafibrate periods and the placebo periods. There were no significant facial flushing, nor other side effects during the treatment with bezafibrate. It is concluded that bezafibrate has antilipemic effects, and may be helpful in reducing the atherogenic risks.
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PMID:A therapeutic trial of bezafibrate on patients with hyperlipidemia with or without diabetes mellitus. 657 90


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