1,720,981 research outputs found
Supplemented {alpha}-tocopherol apparently does not enter the plaque compartment
No full textIn Response:
Kontush and colleagues claim that vitamin E is not deficient in
advanced atherosclerotic plaques of our patient cohort.1 They suggest
that our conclusion should not be based on the comparison of
vitamin E/cholesterol ratios in plaque versus control plasma nor on
the use of 7hydroxy-cholesterol/vitamin E ratios
MRC/BHF Heart Protection Study
No full textSir—The HPS Collaborative Group1
conclude that recommendation of
supplementation with antioxidants is
not justified and that observational
studies that indicate a lower risk of
vascular disease in patients with a higher
intake of antioxidant vitamins could be
largely or wholly artifactual
Low-density lipoprotein oxidation
No full textFree radical mediated oxidation of low-density lipoproteins (LDL), which has been extensively studied in the last two decades, plays a central role in the development of the atherosclerotic plaque. Oxidation involves the lipid moiety of LDL in a chain reaction mechanism. In the initial phase, free radicals preferentially attack highly oxidizable polyunsaturated fatty acids. Subsequent recruitment of other molecules includes cholesterol and phospholipids. The process of oxidation is counteracted by antioxidants present in LDL. By-products formed during oxidation of LDL lipids, which may have biological activity, react with amino acid residues of the LDL protein backbone with the consequent modification of chemical and immunological properties responsible for cellular receptor shift. Oxidation-altered apolipoprotein B of oxidized LDL is, in fact, recognized by the macrophage scavenger receptor responsible for foam cell formation. The mechanism of LDL oxidation and the impact on atherogenesis are discussed
How to select patient candidates for antioxidant treatment?
No full textIn their excellent review, Steinberg and Witztum1 focused
their attention on the different reasons why treatment with
natural antioxidants has so far not convinced us that they may
prevent atherosclerotic progression and its cardiovascular complications.
The use of reliable biological markers of oxidative
stress, identification of a population suitable for antioxidant
treatment, and the choice of an adequate daily regimen of
antioxidants are important points that would help us plan future
trials with antioxidants. In accordance with the authors, we
believe that knowledge of the intrinsic mechanism leading to
LDL oxidation in vivo and the balance between oxidant stress
and natural antioxidant defense is likely a crucial element for
exploring the role of oxidative hypothesis in human pathology
Vitamin E supplementation.
No full textSir—In their report, Mona Boaz and
colleagues1 conclude that, in haemodialysis
patients who have increased
oxidative stress and are at high risk of
atherosclerotic complications, 800 IU
vitamin E daily reduces the risk of
vascular accidents, including myocardial
infarction.
The results are consistent with our
study, in which we show that vitamin
E interferes with one of the most
important mechanisms in the initiation
and progression of atherosclerosis—
cholesterol accumulation in the
vessel wall.2 We have shown that autologous
radiolabelled LDL injected
in patients, who underwent carotid
endarterectomy, localised in the
macrophages of atherosclerotic plaque
and that 900 mg vitamin E daily
almost completely prevented this
effect.
Vitamin E, atherosclerosis and thrombosis.
No full textVitamin E, a major lipid-soluble, chain-breaking antioxidant includes
several tocopherols having the biological activity of RRR-alphatocopherol.
Vitamin E circulates in the blood as free tocopherol bound
to beta-lipoproteins and is present in cell membrane where it exerts a
potent defence against lipid peroxidation (1). Blood concentration of
vitamin E in humans ranges from 25 to 30 M, depending on daily
intake and body’s ability to absorb fat (1). In the last decade the scientific
interest on biological activity of vitamin E increased because of a
growing body of evidence linking this vitamin with atherosclerosis and
its complications (2). Thus, the oxidative hypothesis of atherosclerosis
suggests that LDL accumulates within vessel wall, in particular in the
macrophages, as a consequence of its oxidative modification mediated
by resident cells (3, 4). A reduced defence against LDL oxidation could
favour this process and accelerate atherosclerotic progression. Accordingly,
patients with coronary heart disease have lower plasma concentration
of vitamin E than controls (2) and prospective studies demonstrated
that a daily assumption of vitamin E reduces cardiovascular
events (5). According to the oxidative hypothesis of atherosclerosis,
this effect has been attributed to the inhibition of LDL oxidation. Alternative
mechanism potentially implicated in the antiatherosclerotic
activity of vitamin E includes its interference with the activity of
platelet and monocyte, in which the intracellular redox status plays an
important functional role (6, 7). As platelets and monocytes are both
involved in the pathophysiologic process leading to atherosclerotic
lesion, the interference of vitamin E with the biological function of
these cells may represent another important tool to explore the antiatherosclerotic
activity of vitamin E. This review will focus on the open
issues related to the use of vitamin E in clinical studies and the potential
usefulness in investigating platelet function and clotting activation
in patients treated with vitamin E
Bullous pemphigoid: an unusual and insidious presentation of breast cancer.
No full textBlistering skin lesions can be associated with internal malignancies,
and paraneoplastic pemphigus is the typical blistering disease
presenting as a paraneoplastic syndrome [1]. In contrast, bullous
pemphigoid, an autoimmune blistering skin disease that rarely involves
mucous membranes, is not widely considered in paraneoplastic syndromes
[2–4]. No studies have reported bullous pemphigoid as paraneoplastic
presentation of breast cancer. We describe a 75-year-old
woman with an underlying metastatic breast cancer presenting with
bullous pemphigoid. The clinical history of the patient began 3 months
previously when she was admitted to another facility for the onset of
pruritus and widespread bullous skin lesions
Effect of Ramipril and Vitamin E on Atherosclerosis.
No full textTo the Editor:
In their study, Lonn et al1 report on the results of the SECURE
study, which evaluated the effect of ramipril and vitamin E on
atherosclerosis. The authors conclude that long-term treatment
with ramipril has a beneficial effect on atherosclerosis progression
whereas vitamin E has no effect
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