Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Benefits of high-dose progestational contraception (pregnanes [chlormadinone acetate] or norpregnanes, promegestone, nomegestrol acetate) are its anti-estrogenic effect and its overall absence of metabolic effects. It lowers apoprotein A1 and increases antithrombin 3, but these changes produce no adverse effects. High-dose progestational contraception is ideal for women with certain contraindications to combined oral contraceptive use: high blood pressure, hyperlipemia, diabetes mellitus, benign breast disease, and premenstrual tension. It inhibits ovulation. Nomegestrol acetate also changes the cervical mucus, making it inhospitable to sperm. The primary side effect of high-dose progestational contraception is menstrual cycle disturbances. A study of 5 mg nomegestrol acetate among women aged 19-40 used for 20 days of each 28 day cycle revealed no pregnancies. A preliminary study shows that transdermal administration of nomegestrol acetate and estradiol 17 beta adequately treats hypoestrogeny. In conclusion, high-dose progestational contraception produces excellent metabolic results and reduces clinical manifestations of hyperestrogeny.
...
PMID:[High-dose progestational contraception: advantages]. 1231 10

For about three decades glomerular diseases have been the most intensively investigated research area in nephrology. The increasing proportion of patients with end-stage renal disease (ESRD) secondary to hypertension has now revived interest in hypertension. Prospective studies have firmly established that high blood pressure is associated with an increased risk of renal failure independent of other risk factors. Hypertension-related renal injury might be interpreted in a general context taking into account genes, intrauterine growth and environmental factors. Disturbed intrauterine growth (due to malnutrition or other factors) has a negative influence on the development of the cardiovascular system and favours the occurrence of hypertension, insulin resistance, hypercholesterolaemia and hyperuricaemia in adult life (Barker's hypothesis). Altered intrauterine growth has also been associated with a reduced number of nephrons at birth. Damage attributable to glomerular hyperperfusion in kidneys with a reduced number of nephrons is aggravated by vascular lesions in middle and small arterial vessels (secondary to hypertension, hyperlipidaemia and environmental risk factors such as smoking). The observation that subjects homozygous for the D allele of the ACE gene are predisposed to both cardiovascular complications and nephrosclerosis, suggests that genetic factors may interact with altered intrauterine growth in determining the risk of cardiovascular and renal diseases.
...
PMID:[Nephropathy associated with arterial hypertension: genes and Barker's hypothesis]. 1243 39

Osteonecrosis has been increasingly associated with HIV disease throughout the 1990s, and the incidence appears to be rising. The hip is most commonly involved and often bilaterally. Although anecodotal reports suggest an association between osteonecrosis and highly active antiretroviral therapy, controlled epidemiologic studies do not support a direct link. Many patients with osteonecrosis have established risk factors, some of which may be related to HIV disease or its therapy, including corticosteroid use and hyperlipidemia. Alcoholism, hypercoagulability, megesterol acetate use, immune reconstitution, and other factors may also contribute. Plain radiographs and magnetic resonance imaging are the cornerstones of diagnosis. Management is dependent on the stage of bone disease and ranges from observation to total joint arthroplasty. Clinicians may help to prevent HIV-associated osteonecrosis by encouraging patients to limit their exposure to the established risk factors for the disease.
...
PMID:Osteonecrosis in HIV disease: epidemiology, etiologies, and clinical management. 1247 64

The aim of the present work was to test the effects of large-dose supplementation of vitamin E (Vit E) and selenium (Se), either singly or in combination, on fish oil (FO)-induced tissue lipid peroxidation and hyperlipidemia. The supplementation of Se has been shown to lower blood cholesterol and increase tissue concentrations of the antioxidant glutathione (GSH); however, the effects of Se supplementation, either alone or in combination with supplemental Vit E, on FO-induced oxidative stress and hyperlipidemia have not been studied. Male Syrian hamsters received FO-based diets that contained 14.3 wt% fat and 0.46 wt% cholesterol supplemented with Vit E (129 IU D-alpha-tocopheryl acetate/kg diet) and/or Se (3.4 ppm as sodium selenate) or that contained basal requirements of both nutrients. The cardiac tissue of hamsters fed supplemental Se showed increased concentrations of lipid hydroperoxides (LPO) but decreased oxidized glutathione (GSSG) concentrations. The higher concentrations of LPO in the hearts of Se-supplemented hamsters were not lowered with concurrent Vit E supplementation. In the liver, Se supplementation was associated with higher Se-dependent glutathione peroxidase activity and an increase in the GSH/GSSG ratio, whereas a lower hepatic non-Se-dependent glutathione peroxidase activity was seen with Vit E supplementation. Supplemental intake of Se was associated with lower plasma concentrations of total cholesterol and low density lipoprotein cholesterol plus very low density lipoprotein cholesterol. In view of the pro-oxidative effects of Se supplementation on cardiac tissue, a cautionary approach needs to be taken regarding the plasma lipid-lowering properties of supplemental Se.
...
PMID:The effects of vitamin E and selenium intake on oxidative stress and plasma lipids in hamsters fed fish oil. 1261 64

Rats on a stock diet with added cholesterol, cholic acid, and thiouracil developed increased concentrations of cholesterol, total lipide, and beta lipoprotein in the serum, and an increased content of cholesterol in the liver and carcass, despite the fact that the diet produced a cessation of endogenous cholesterol synthesis. Rats with high serum lipide concentrations developed intimal lesions similar to those of human atherosclerosis. The induction of hypertension by desoxycorticosterone and salt accelerated the development of hypercholesterolemia, hyperlipemia, increase in tissue cholesterol content, and atherosclerotic changes in the intima. Hypertension induced by renal artery constriction also intensified the hypercholesterolemia and hyperlipemia. On the other hand, rats receiving desoxycorticosterone acetate without salt or salt without desoxycorticosterone acetate did not show any intensification of hypercholesterolemia or hyperlipemia. The extent of the atherosclerotic lesions was correlated with the concentration of cholesterol in the serum. There was also a positive correlation between blood pressure and the degree of hypercholesterolemia. It remained uncertain whether the increase in atherosclerosis in the hypertensive animals was dependent on the increased lipide content of serum and tissues or on a local effect of the elevated blood pressure.
...
PMID:Blood pressure, cholesterol content of serum and tissues and atherogenesis in the rat. 1351 19

With the increased attention being given to cardiovascular risk factor reduction, the opportunity exists to substantially decrease the largest cause of mortality in diabetic patients. The concept that type 2 diabetes and CVD are linked via a common etiologic pathway (metabolic syndrome) has substantial ramifications for the care of individual patients. Many of the metabolic abnormalities that contribute to both glycemic disorders and CVD are interrelated. For example, hyperinsulinemia and insulin resistance coupled with abdominal obesity further worsens HTN and hyperlipidemia. Likewise, the procoagulant state and endothelial dysfunction increase with worsening glycemic control. Specific interventions include tobacco cessation, a food management and physical activity plan, choice of antidiabetic agent (such as metformin), and use of ACE inhibitors for hypertension and microalbuminuria (Table 5). Programs to enhance cardiovascular risk factor reduction as part of the comprehensive evaluation and management of diabetic patients have been described [95,99]. One community-based program provided free screening to diabetic patients with randomization to either annotated result reports provided to the patient and their physician or results provided by a project nurse (either face-to-face or over the phone). Greater improvements in mean glycohemoglobin, cholesterol, and blood pressure were noted with verbal presentation of results [99]. Recent data from the Centers for Disease Control and Prevention Diabetes Cost-effectiveness Group support the idea that interventions to decrease CVD in diabetics are economically beneficial. Intensive management of hypertension, glycemic control, and hyperlipidemia each improved health outcomes. Hypertension control reduced costs. Although intensive treatment of glucose and hyperlipidemia increased costs, the increase was comparable to that of other frequently used health care interventions [100]. Further directions include further exploration of the implications and management of metabolic syndrome as it relates to CVD prevention. Interventions such as exercise, which can impact on all outcomes, require special attention. Efforts by physicians, health systems, and society are necessary to increase physical activity for individuals of all ages. It makes clinical sense that the recommendations for prevention of CVD in diabetics described in this article may also benefit patients with prediabetes (fasting glucose 110-125 mg/dl), but this remains to be definitively shown.
...
PMID:Preventing cardiovascular disease in diabetes and glucose intolerance: evidence and implications for care. 1469 2

Systemic embolism is a frequent cause of stroke. At the beginning of the last decade by introduction of transesophageal echocardiography and other imaging techniques atheromatosis of the aortic arch has been recognized as an important source of embolism. Formerly in the pre-TEE era, this entity was included into cryptogenic strokes. Aortic atheromas are found in about one quarter of patients presenting with embolic events. The severity of atherosclerosis graded by TEE correlates with the risk for future embolism, especially if mobile lesions or superimposed thrombi are present. Independent of plaque extension, patients with unstable plaques characterized by echo-lucency, inhomogenity, lacking of calcifications, ulceration, mobile parts and concomitant spontaneous echo contrast within the aorta have a higher risk for embolic events. However, the diagnosis of aortic atheromatosis is mostly established if an embolic event has already occurred. Therefore, it is important to identify patients at risk, especially before they undergo interventions with manipulation at the aorta like coronary bypass surgery. Risk factors are age above 70, diabetes mellitus, hyperlipidemia, arterial hypertension, aortic calcifications on standard chest X-ray, elevated serum levels of C-reactive protein, other inflammatory markers, and an activated coagulation. Randomized studies for treatment of patients with severe aortic atheromatosis are not yet existing. Warfarin has been shown to prevent stroke in patients with mobile atheromas and superimposed thrombi, but there are case reports about aggravation of cholesterol embolism under warfarin treatment. It is concluded from other atherosclerotic manifestations that plaque stabilizing treatment with statins and ACE inhibitors is also beneficial.
...
PMID:Atheromatous disease of the thoracic aorta and systemic embolism. Clinical picture and therapeutic challenge. 1474 Feb 36

In the last decade the number of patients with congestive heart failure has increased noticeably and today heart failure is one of the major problems in civilized countries. While in earlier decades arterial hypertension was the main reason for developing heart failure, today coronary artery disease has become the focus of attention. However, arterial hypertension, diabetes and hyperlipidemia are also main risk factors for developing coronary artery disease. In addition to non-pharmacological management with reduced fluid intake and periodical exercise training particularly in stable heart failure, in the last decade some special drug compounds have demonstrated a significant reduction in mortality in great double blind randomized trials. ACE-inhibitors and betablockers are essential components in treating congestive heart failure. Angiotensin-II-receptorblockers are indicated if ACE inhibitors and/or beta-blockers are not tolerated. The combined use of all three compounds was shown to result in a further reduction of mortality in the recently presented CHARM study. In progressive heart failure the use of diuretics is necessary and effective especially when fluid overload exists. Not treating heart failure is followed by high mortality, as we know, and so adequate and uncompromising treatment of hypertension is the most important approach to prevent the further development of heart failure.
...
PMID:[Therapeutical strategies in hypertensive patients presenting heart failure symptoms]. 1500 83

The effect of hyperlipemia associated with diabetes on the contractility of resistance arteries to prostaglandin F2alpha (PGF2alpha) was investigated employing 4 weeks simultaneously hyperlipemic-diabetic (HD), hyperlipemic (H), diabetic (D) and normal hamsters (controls, C). The isometric force produced by explanted arteries in the presence of 10(-8) to 10(-5) M PGF2alpha was recorded by the myograph technique. The results showed that compared with controls, the contractile response to 10(-5) M PGF2alpha was approx. 2 fold increased in HD group, and approx. 1.75 and 1.62-fold enhanced in H and D groups, respectively. Activation of protein kinase C with 10(-6) M phorbol 12-myristate 13-acetate increased the contractility to PGF2alpha in all groups and particularly in HD hamsters (approx. 10.16-fold). Inhibition of cyclooxygenase by indomethacin increased approx. 1.81-fold the arterial contractility to PGF2alpha in C group, whereas in H, D and HD hamsters had no effect. Blockage of Ca(2+)-activated K(+)-channels with 10(-3) M tetraethylammonium augmented the contraction to PGF2alpha approx. 6.43-fold in C group, and at significantly lower levels in H, D and HD groups, i.e. approx. 3.84, 3.72 and 3.33-fold, respectively. The results validate two conclusions: (i) simultaneous insult of hyperlipemia-hyperglycemia is associated with the highest contractility of the resistance arteries to PGF2alpha; the highest circulating glucose and cholesterol levels, and the enhancement in the protein kinase C pathway underlay the augmented contractility; (ii) no matter the pathology induced (hyperlipemia, diabetes or both simultaneously) a common dysfunctional response to PGF2alpha was installed; this consists in a reduced effect of cyclooxygenase inhibition, and a altered activity of Ca(2+) dependent K(+) channels.
...
PMID:The contractile response of the mesenteric resistance arteries to prostaglandin F2alpha; effects of simultaneous hyperlipemia-diabetes. 1501 13

The purpose of this research project was to investigate potential matrix effects of anticoagulant and lipemia on the response of olanzapine, desmethyl olanzapine, olanzapine-D(3) and desmethyl olanzapine-D(8) in an LC/MS/MS assay. Blank human serum and sodium heparin, sodium citrate, and K(3)EDTA plasma with various degrees of lipemia were fortified with olanzapine, desmethyl olanzapine, olanzapine-D(3) and desmethyl olanzapine-D(8). Six replicates of each sample were extracted using Waters Oasis MCX cartridges and analyzed using electrospray LC/MS/MS. The analytes were separated on a Phenomenex LUNA phenyl hexyl, 2 mm x 50 mm, 5 microm, analytical column and a gradient rising from 2 to 85% mobile phase B. Mobile phase A consisted of acetonitrile-ammonium acetate (20 mM) (52:48 v/v) and mobile phase B was formic acid-acetonitrile (0.1:100 v/v). Ion suppression was investigated through post column infusion experiments. The degree of lipemia of each sample, indicated by turbidity, was ranked into categories from least to greatest and used for statistical analyses. The results from analysis of variance testing indicated that lipemia, anticoagulant and their interaction significantly influenced mass spectral matrix effects and extraction matrix effects. Differential behavior between the analytes and labeled internal standards contributed to variability. The most significant source of variability however, was ion suppression due to co-eluting matrix components.
...
PMID:A study of matrix effects on an LC/MS/MS assay for olanzapine and desmethyl olanzapine. 1533 61


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---