Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum thyroid parameters show substantial inter-individual variability, in which genetic variation is a major factor. Findings in patients with subclinical hyper- and hypothyroidism illustrate that even minor alterations in serum thyroid function tests can have important consequences for a variety of thyroid hormone-related clinical endpoints, such as atherosclerosis, bone mineral density, obesity, and heart rate. In the last few years, several studies described polymorphisms in thyroid hormone pathway genes that alter serum thyroid function tests. In this review, we discuss the genetic variation in the TSH receptor and iodothyronine deiodinases. We discuss the possible consequences of these studies for the individual patient and also the new insights in thyroid hormone action that can be obtained from these data.
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PMID:Genetic variation in thyroid hormone pathway genes; polymorphisms in the TSH receptor and the iodothyronine deiodinases. 1706 80

The diagnosis of subclinical hypothyroidism and detection of its effects on cardiovascular system is important. Also, the patients with subclinical hypothyroidism even at the very early stage are at increased risk for developing atherosclerosis. We evaluated coronary microvascular circulation and endothelial dysfunction of epicardial coronary arteries by the measurement of coronary flow velocity reserve via a non invasive technique, transthoracic Doppler echocardiography in subclinical hypothyroidism. Coronary flow reserve in patients with subclinical hypothyroidism such as in overt hypothyroidism was lower than that of euthyroid subject. As a conclusion, endothelial and microvascular dysfunction, which are early harbingers of atherosclerosis, are shown in overt and subclinical hypothyroidism.
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PMID:Coronary flow reserve is also impaired in patients with subclinical hypothyroidism. 1709 81

The relationship of hypertensives and many pathological syndromes still remains unclear. A mathematical model in terms of the fluid mechanics and physicochemical analyses is established to correlate the plasma viscosity, the shear stress and the rate of shear in blood stream with the ligand-receptor dissociation constant. This model has arrived at the conclusive results that high viscosity, high rate of shear created in the blood streams, and the peripheral resistance may act as important preceding factors to induce a serial subsequent pathological clinical manifestations. High viscosity may interfere with the ligand-receptor combination, in contrast, high rate of shear may knock the ligand (s) off the existing ligand-receptor complex, while elevation of peripheral resistance may slow down the blood flow rate, resulting in a diminished dissociation of ligand-receptor complex. This model has successfully interpreted the possible cause of some post-hypertensive abnormal outcome manifestations involving obstructive and degenerative stenosis (such as renal artery stenosis), growth retardation, blood vessel detriment, coarctation of aorta, coronary thrombotics, atherosclerosis, hyperinsulinemia, diabetes, obesity, hypothyroidism, infertility, and at the worst, carcinoma, etc.
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PMID:Fluid mechanical and physicochemical modeling interprets hypertension to be capable of inducing secondary complications. 1714 24

Sub-clinical hypothyroidism is defined by elevated serum thyroid-stimulating hormone level in the face of normal free thyroid hormone values. The role of sub-clinical hypothyroidism as independent risk factor for atherosclerosis has been suggested by clinical studies which demonstrated a higher prevalence of peripheral arterial disease, aortic atherosclerosis and coronary artery disease, in patients affected by this pathological condition. This association have been confirmed by the assessment of subclinical atherosclerosis by means of B-mode ultrasonography. Using this method an higher intima-media thickness (IMT) of carotid artery, a close marker of early atherosclerosis changes, have been found in patients with subclinical hypothyroidism compared to control euthyroid subjects. Levothyroxine replacement therapy of sub-clinical hypothyroidism was able to improve both the carotid IMT and atherogenic lipid profile, suggesting that lipid infiltration of the endothelium may represent a mechanism underlying the atherosclerotic process in patients with this pathological condition. Morphologic and functional changes of the myocardial tissue has been also demonstrated in patients with sub-clinical hypothyroidism, using ultrasonic backscatter video densitometry. All these data provide evidence of cardiovascular remodelling in patients with sub-clinical hypothyroidism. Vascular remodelling in sub-clinical hypothyroidism patients could be also studied by means of backscatter analysis of carotid artery, a method which allows the assessment of vascular sclerosis. Our preliminary results using this method suggested that not only atherosclerosis by also sclerosis characterises vascular remodelling in sub-clinical hypothyroidism patients.
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PMID:[Cardiovascular remodelling in patients with sub-clinical hypothyroidism]. 1739 36

Hypothyroidism may result in accelerated atherosclerosis. Hyperhomocysteinaemia is an independent risk factor for premature atherosclerotic vascular disease. The aim of the present study was to assess plasma total homocysteine (tHcy), folate and cobalamin concentrations in hypothyroid patients before and after treatment. Thirty-one hypothyroid and thirty health young women were studied. The hypothyroid patients were investigated in the untreated state and again after restoration of euthyroidism. The levels of homocysteine, folate, cobalamin and thyroid stimulating hormone (TSH), free thyroxine (fT(4)), free triiodothyronine (fT(3)) and renal function were measured before and after treatment. In hypothyroidism tHcy was higher but not statistically significant than in control group. Serum level of folate was higher and serum cobalamin was lower in the hypothyroid state. Following L-thyroxine therapy tHcy significantly decreased as well as the concentration of cobalamin. Level of folate remained unchanged. Univariate analysis in hypothyroid group indicated that tHcy negative correlated with creatinine clearance, fT(3), fT(4), cobalamin and positive with TSH. In multivariate analysis tHcy correlated with creatinine clearance, cobalamin and fT(4). Thyroid status influences the plasma tHcy. Free triiodothyronine and next free thyroxine have the greatest negative influence. This would account for hyperhomocysteinemia in the hypothyroid state and premature atherogenesis.
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PMID:Homocysteine, folate and cobalamin levels in hypothyroid women before and after treatment. 1746 93

By affecting the metabolism of lipids, hypothyroidism accelerates the process of atherogenesis and increases cardiovascular risk. In manifest hypothyroidism the number of LDL receptors in the liver decreases and there is an increase in levels of overall cholesterol, LDL-cholesterol and apolipoprotein B in the blood. Levels of HDL particles remain normal or even rise slightly as a result of reduced activity of the Cholesterol ester transfer protein (CETP) and hepatic lipase. This leads to a reduction in the transport of cholesterol esters from HDL-(2) to VLDL and IDL. Subclinical hypothyroidism also has a negative effect on the lipid profile, but is more likely to lead to pro-atherogenic changes in the proportion of lipid particles than to a reduction in overall cholesterol. Subclinical hypothyroidism leads to the manifestation of certain risk factors of atherosclerosis. Although studies of overall mortality and cardiovascular morbidity have not been completely unanimous in their conclusions, increased cardiovascular risk can be considered likely in subclinical hypothyroidism. It remains an open question whether the treatment of subclinical hypothyroidism with levothyroxine. At present we have only indirect proof from studies that assessed the effect of levothyroxine treatment on risk factors of atherosclerosis. Starting treatment with lipid lowering agents (especially statins) for (sub)clinical hypothyroidism is extremely risky though due to the risk of the development or worsening of myopathy, which is a further cogent argument for the active screening and treatment of(sub)clinical hypothyroidism for all patients with dyslipidemia.
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PMID:[Thyroid diseases, dyslipidemia and cardiovascular risk]. 1757 70

Reactive oxygen species (ROS) are considered to be chemically reactive with and damaging to biomolecules including DNA, protein, and lipid, and excessive exposure to ROS induces oxidative stress and causes genetic mutations. However, the recently described family of Nox and Duox enzymes generates ROS in a variety of tissues as part of normal physiological functions, which include innate immunity, signal transduction, and biochemical reactions, e.g., to produce thyroid hormone. Nature's "choice" of ROS to carry out these biological functions seems odd indeed, given its predisposition to cause molecular damage. This review describes normal biological roles of Nox enzymes as well as pathological conditions that are associated with ROS production by Nox enzymes. By far the most common conditions associated with Nox-derived ROS are chronic diseases that tend to appear late in life, including atherosclerosis, hypertension, diabetic nephropathy, lung fibrosis, cancer, Alzheimer's disease, and others. In almost all cases, with the exception of a few rare inherited conditions (e.g., related to innate immunity, gravity perception, and hypothyroidism), diseases are associated with overproduction of ROS by Nox enzymes; this results in oxidative stress that damages tissues over time. I propose that these pathological roles of Nox enzymes can be understood in terms of antagonistic pleiotropy: genes that confer a reproductive advantage early in life can have harmful effects late in life. Such genes are retained during evolution despite their harmful effects, because the force of natural selection declines with advanced age. This review discusses some of the proposed physiologic roles of Nox enzymes, and emphasizes the role of Nox enzymes in disease and the likely beneficial effects of drugs that target Nox enzymes, particularly in chronic diseases associated with an aging population.
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PMID:Nox enzymes, ROS, and chronic disease: an example of antagonistic pleiotropy. 1760 48

1. Hypothyroidism is accompanied by hyperlipidaemia and oxidative stress and is associated with several complications, such as atherosclerosis. Paraoxonase activity has been reported to decrease in several situations associated with atherosclerosis and oxidative stress. In the present study, the effects of different doses of taurine on serum paraoxonase and arylesterase activities, as well as on the serum lipid profile, were investigated in hypothyroid rats. 2. Forty male Sprague-Dawley rats were randomly divided into five groups as follows: Group 1, rats received normal rat chow and tap water; Group 2, rats received standard rat chow + 0.05% propylthiouracil (PTU) in the drinking water; and Groups 3-5, taurine-supplemented PTU groups (standard rat chow + 0.5, 2 or 3% taurine in the drinking water, respectively, in addition to PTU). Paraoxon or phenylacetate were used as substrates to measure paraoxonase and arylesterase activity, respectively. Plasma and tissue malondialdehyde (MDA) levels, indicators of lipid peroxidation, were determined using the thiobarbituric-acid reactive substances method. Serum triglyceride, total cholesterol and high-density lipoprotein-cholesterol (following precipitation with dextran sulphate-magnesium chloride) were determined using enzymatic methods. 3. Serum paraoxonase and arylesterase activities were increased and plasma and tissue MDA levels and serum triglyceride levels were reduced in a dose-dependent manner in taurine-treated hypothyroid rats. Taurine concentrations were positively correlated with enzyme activities and negatively correlated with MDA and triglyceride levels. 4. Further studies are needed to investigate the role of taurine supplementation in hypothyroidism in human subjects.
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PMID:High-dose taurine supplementation increases serum paraoxonase and arylesterase activities in experimental hypothyroidism. 1764 25

Retroperitoneal fibrosis (RF) is a clinical entity characterized by the progressive proliferation of connective tissue that rarely forms a mass involving the periaortic area of the abdomen, which may be idiopathic as well as a result of an inflammatory process after aneurysmal dilatation of the aorta. This fibrotic tissue may cover both aorta and iliac arteries, reach the retroperitoneum and surrounding ureters, and cause serious obstructions and renal insufficiency in three-quarters of patients. Most of the patients are known to have atherosclerosis and local inflammation against the antigens of the plaques. A systemic autoimmune disease presenting with retroperitoneal fibrosis seems to be pronounced more frequently nowadays because of the elevated acute-phase reactant levels, positive autoantibodies, and concurrent autoimmune diseases affecting other organs in majority of the diagnosed patients. Ultrasonography, computed tomography, magnetic resonance imaging, positron emission tomography, and retroperitoneal biopsy are useful in diagnosing and assessing the full extent of the disease. Surgical interventions such as ureterolysis and aneurysm repair are frequently performed, but medical therapy including steroids and immunosuppressants is often needed because of the inflammatory and chronic-relapsing nature of the disease. In this paper, we described two cases diagnosed with RF secondary to hemilaminectomy and hypothyroidism, and we summarized the literature related to RF.
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PMID:Retroperitoneal fibrosis secondary to different etiologies (hemilaminectomy and hypothyroidism): reports of two cases. 1765 30

The present study was designed to investigate the relationship between the serum levels of oxidant-antioxidant system (malondialdehyde (MDA) level, Paraoxonase (PON1) activity, nitric oxide (NO) level and superoxide dismutase (SOD) activity) and thyroid hormone status in hypothyroidism pre and posttreatment. The study group comprised 33 patients with primary hypothyroidism. 18 of these patients were reevaluated after euthyroid state i.e. at least 6 months of thyroxine replacement. The patients were compared with 26 normal healthy controls. Serum MDA level, PON1 activity, NO level and SOD activity were measured according to an enzymatic spectrophotometric method. MDA levels were found higher in patients with hypothyroidism before the treatment than the controls. MDA levels were also found to be decreased after the treatment in patients with hypothyroidism. However MDA were found still higher than the controls after the treatment. PON1 activity was found to be lower in patients pretreatment when compared to posttreatment hypothyroidism and controls. Posttreatment of hypothyroidism mean PON1 activity significantly increased compared to pretreatment level but it was still significantly lower than control level. NO level was higher in pretreatment hypothyroidism when compared to controls. SOD activity was not found different in patients before treatment when compared to controls. SOD activity was significantly higher in after treatment when compared to both pretreatment and control levels. In conclusion, increased ROS levels in hypothyroidism may result in a pro-oxidation environment, which in turn could result in decreased antioxidant PON1 activity, increased MDA and NO levels. As a result, lipid peroxidation may have a role in the pathogenesis of the atherosclerosis in hypothyroidism.
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PMID:Oxidative stress and enzymatic antioxidant status in patients with hypothyroidism before and after treatment. 1785 36


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