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)

A double-blind, randomized study was undertaken to evaluate the efficacy and safety of fluvastatin as monotherapy and as combination therapy with niacin in the treatment of hypercholesterolemia refractory to diet. Seventy-four patients with plasma low-density lipoprotein cholesterol (LDL-C) levels > or = 160 mg/dL were treated with fluvastatin, 20 mg/d, or placebo for 6 weeks. Thereafter, immediate-release niacin, at a dosage titrated to a maximum of 3 g/d, was added to both regimens for another 9 weeks. All adverse events were monitored, with particular attention to the evaluation of liver and muscle enzymes. Initial analysis of the data shows that fluvastatin and its combination with niacin was well tolerated and was not associated with any serious adverse events. Small, transient, asymptomatic rises in aspartate aminotransferase (AST) occurred in 28.9% of fluvastatin-niacin treated patients compared to 8.3% in the niacin-placebo control arm (p < 0.05). These were considered clinically insignificant in that no transaminase elevations > 3 times the upper limit of normal occurred. No evidence of myopathy, creatine kinase levels exceeding 10 times the upper limit of normal, myositis, or rhabdomyolysis were demonstrated in this short-term trial. The majority of adverse events resulting in patient withdrawals were ascribed to niacin therapy and included cutaneous vasodilatation, flushing, itching, and rash. These preliminary results suggest that fluvastatin, both alone and combined with niacin, is an effective, safe, and well-tolerated treatment for hypercholesterolemia.
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PMID:Combination therapy with fluvastatin and niacin in hypercholesterolemia: a preliminary report on safety. 819 20

Telangiectasia macularis eruptiva perstans (TMEP) is a rare form of mastocytosis. It appears most frequently in adults and only occasionally will affect young children or infants. In this disease, multiple brownish-red confluent macules and telangiectasias develop, primarily on the trunk. Pruritus frequently occurs, and may be mild to severe. Most patients have only skin involvement; however, involvement may be systemic as well. Clinical signs and symptoms of systemic mastocytosis are varied and depend on which internal organs are affected. Classic symptoms--such as episodic flushing, gastrointestinal complaints, heart palpitations, and syncope--may be confused with those of other diseases, most notably the carcinoid syndrome. A simple workup can help to differentiate between these two conditions. The authors describe a 48-year old woman who was seen with cutaneous features of TMEP and with multiple symptoms suggesting systemic mastocytosis. They discuss the clinical features, diagnostic workup, and therapeutic options in the management of this relatively rare condition.
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PMID:Telangiectasia macularis eruptiva perstans. 820 Aug 29

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

We describe the clinicopathologic features of 10 patients with recurrent unexplained flushing. These patients were referred to the National Institutes of Health with a diagnosis of mastocytosis or idiopathic anaphylaxis. Both diagnoses were eliminated after evaluation. Patients reported attacks of flushing lasting 15 minutes to 2 days and associated with such symptoms as anxiety, chest tightness, paresthesia, slurred speech, weakness, and pruritus. Abdominal pain was a constant feature, often associated with cramping and an increase in stool frequency. Attacks witnessed by physicians consisted of an exaggerated blush response of the face and upper part of the chest, and were sometimes associated with tachycardia, mild hypertension, and tachypnea. Hives, angioedema, wheezing, and hypotension were not observed. Routine laboratory studies and 5-hydroxyindoleacetic acid, vanillylmandelic acid, and plasma histamine levels were normal. Plasma histamine levels did not elevate during attacks. When performed, results of bone marrow examinations, skin biopsies, and bone scans were normal. Psychiatric examinations frequently revealed somatization disorders. Patients had often been prescribed a wide variety of medications including antihistamines, nonsteroidal anti-inflammatory drugs, and steroids, with little or no benefit. Despite the benign nature of the clinical and laboratory findings, patients had undergone repeated, often invasive, examinations for several years. Whether such patients have a prominent flush response exaggerated through a somatization disorder or a relatively benign flushing disorder associated with putative mediator release remains to be determined. Recognition of this category of patients with unexplained flushing will avoid subjecting such patients to unwarranted repeated examinations, procedures, and inappropriate therapy.
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PMID:A clinicopathologic study of ten patients with recurrent unexplained flushing. 830 82

There are several allergic responses that may occur in susceptible individuals as a result of exposure to physical stimuli. Most of these conditions are mediated by vasoactive substances and usually result in symptoms of urticaria and/or angioedema. There are 2 such conditions that may occur as a direct result from exercise. The first of these is cholinergic urticaria. Patients with cholinergic urticaria experience punctate (2 to 4mm) hives which occur reproducibly with exercise or with passive warming, such as might occur in a steam bath or hot pool. Life-threatening hypotension or angioedema usually do not occur with cholinergic urticaria. This condition usually responds well to oral hydroxyzine. Exercise-induced anaphylaxis (EIA) is a form of physical allergy that has been recognised with increasing frequency in recent years. This syndrome typically presents with generalised pruritus, a flushing sensation, a feeling of warmth and the development of conventional (10 to 15mm) urticaria in association with vigorous physical exertion only. Symptoms tend to occur variably with exposure to exercise and do not typically occur with passive warming. During symptomatic attacks, cutaneous mast cells degranulate and serum histamine levels increase. Treatment is problematic. Cessation of exercise with onset of symptoms and self-administration of epinephrine (adrenaline) are recommended. Other physical allergies that may affect exercising individuals include cold urticaria, localised heat urticaria, symptomatic dermatographism (dermographism), delayed pressure urticaria (angioedema), solar urticaria and aquagenic urticaria. Management of these conditions may include patient education, selective avoidance, antihistamines and, in some cases, induction of tolerance.
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PMID:Physical allergies and exercise. Clinical implications for those engaged in sports activities. 834 71

We report a case of diffuse erythrodermic cutaneous mastocytosis with bone marrow infiltration. An 11-month-old female patient was referred to our hospital for intermittent flushing, fever, intense itching, erythematous rash and bullous lesions. Cutaneous biopsy demonstrated diffuse cutaneous mastocytosis. The bone marrow aspirate revealed mast cell infiltration. Ketotifen treatment was very effective.
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PMID:Diffuse erythrodermic cutaneous mastocytosis with bone marrow infiltration. 835 1

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin--lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although these agents have been proven safe in clinical trials, like any drug, they carry the risk for adverse effects. The bile-acid sequestrants may cause constipation, reflux oesophagitis, and dyspepsia, and may bind coadministered medications such as digitalis glycosides, beta blockers, warfarin, and exogenous thyroid hormone. Nicotinic acid use is commonly associated with flushing and pruritus and may also cause non-specific gastrointestinal complaints, hepatotoxicity (hepatic necrosis, hepatitis, or elevated liver enzymes), gout, myolysis, decreased glucose tolerance and increased fasting glucose levels, and ophthalmological complications including decreased visual acuity, toxic amblyopia, and cystic maculopathy. The HMG-CoA reductase inhibitors may produce liver enzyme elevations, creatine kinase elevations and rhabdomyolysis. The combination of a reductase inhibitor and a fibrate increases the risk for rhabdomyolysis. Possible adverse effects of the fibric-acid derivatives include abdominal discomfort, nausea, flatulence, increased lithogenicity of bile, liver enzyme elevations and creatine kinase elevations. Probucol may increase the QTc interval and may cause non-specific gastrointestinal complaints.
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PMID:Currently available hypolipidaemic drugs and future therapeutic developments. 859 27

Eosinophilia and some acute dialysis side-effects, such as itching, flushing and bronchospasm, are often associated with the presence of ethylene oxide (ETO) as dialyzer sterilizing agent. This study evaluated the effects of two different polysulfone (PS) hollow-fiber dialysers sterilized with ETO and steam in 31 chronic dialysis patients with eosinophilia. Clinical symptoms, metabolic and biochemical parameters, complement (C3a and C5a) activation and production were evaluated in each patient dialysed for two months at a time with Cuprophan dialyser, ETO-PS dialyser and steam-PS dialyser. The steam-sterilizer agent does not alter the purifying capacity of the PS membrane which maintains its superiority over Cuprophan in terms of biocompatibility. Using steam-PS, intradialytic eosinophil kinetics seems to improve. In some patients with high serum levels of ETO-specific IgE these levels tend to diminish. Generic intradialytic symptoms do not differ between the two sterilization methods, although some hypersensitivity symptoms during the first dialysis hour are considerably lower in some patients when steam-sterilized PS is used.
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PMID:Ethylene-oxide and steam-sterilised polysulfone membrane in dialysis patients with eosinophilia. 881 94

The treatment of anemia in hemodialysis patients is frequently hindered by the presence of suboptimal iron stores. Intravenous iron dextran is in common use to maintain iron stores in this population, but there are little published data regarding the incidence and type of adverse events. The purpose of this study was to evaluate the safety of this medication. Charts from four hemodialysis centers of all 573 patients treated with intravenous iron dextran (INFeD; Schein Pharmaceutical, Inc, Florham Park, NJ) between July 1, 1993, and June 30, 1995, were studied. Twenty-seven patients (4.7%) had adverse reactions that were related to iron dextran. Four patients (0.7%) had reactions classified as serious (one cardiac arrest; three others required hospitalization). Ten patients (1.7%) had reactions classified as anaphylactoid. No patients died or developed permanent disability as a result of reactions. The most common adverse reactions included itching (1.5% of patients) and dyspnea or wheezing (1.5%); others included chest pain (1.0%), nausea (0.5%), hypotension (0.5%), swelling (0.5%), dyspepsia (0.5%), diarrhea (0.5%), skin flushing (0.3%), headache (0.3%), cardiac arrest (0.2%), and myalgias (0.2%). Five of all the reactions occurred during a test dose; four of these were anaphylactoid. Several factors were studied as possible predictors of adverse reactions. A positive history of drug allergy (odds ratio, 2.4; P = 0.03) and history of multiple drug allergy (odds ratio, 5.5; P = 0.0004) were significant predictors of reactions. In summary, we found serious adverse reactions to be uncommon in hemodialysis patients treated with intravenous iron dextran. Future prospective studies will help confirm this finding.
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PMID:The safety of intravenous iron dextran in hemodialysis patients. 1067 41

There is increasing evidence that neuropeptides may be involved in the pathogenesis of atopic dermatitis (AD). This study examines whether neuropeptide distribution in the skin of patients with AD differs from normal controls. The distribution and density of several neuropeptides were examined in lesional and non-lesional skin of AD patients (n = 5) and in normal controls (n = 4) using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Staining with the general neuronal marker protein gene product 9 x 5 showed a subepidermal network of nerves with fibres penetrating the epidermis, and nerves around blood vessels, sweat glands and hair follicles. Image analysis of nerves around sweat glands showed a significantly higher nerve density in non-lesional compared with both normal controls and lesional skin (P < 0.05); lesional compared with control skin showed no significant difference. In the epidermis the density of nerves was not significantly greater in non-lesional compared with lesional skin and controls. Calcitonin gene-related peptide immunoreactivity was similar in all subjects except in three of the AD patients, where more nerves appeared to penetrate the epidermis. Substance P immunoreactivity in the papillary dermis was seen in all AD patients but no controls. Vasoactive intestinal polypeptide and neuropeptide Y staining were similar in all groups. Acetylcholinesterase-positive nerves were found around sweat glands in all subjects, the staining being greatest in non-lesional and least in lesional skin. Occasional nerves were seen in the papillary dermis in lesional skin of two out of the four patients. We have demonstrated quantitative differences in nerve growth in clinically normal skin of AD patients, and altered cutaneous neuropeptide expression in these patients which may contribute to the pathogenesis of AD. The cause of atopic dermatitis (AD) has not been fully established but it is believed that there is a complex interaction between genetic susceptibility, precipitating environmental factors and disordered immune responsiveness. There is increasing evidence that neuropeptides may be involved in the pathogenesis of AD. Exacerbations of the disease can be provoked by stress, scratching and sweating which may be the result of neurogenic inflammation. One of the first features of an exacerbation is flushing of the affected skin and pruritus. Several neuropeptides that have been identified in human skin are potent inducers of vasodilation and may induce pruritus. Substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) all cause vasodilation when injected intradermally, and SP and CGRP have been shown to be mediators of the weal and flare reaction. Spantide, a competitive antagonist of SP, has been shown to inhibit immediate and delayed-type hypersensitivity reactions. Part of these responses may be due to release of histamine and indeed elevated concentrations of histamine have been found in vivo in the skin and plasma of patients with AD. In this study the distribution and density of several neuropeptides were examined in lesional and nonlesional skin of AD patients and in normal controls using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Because many afferent fibres do not express CGRP or SP, the general neuronal marker protein gene product (PGP 9 x 5) was used to assess the overall nerve supply to the skin.
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PMID:Neuropeptides in the skin of patients with atopic dermatitis. 885 37


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