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Lipids risk factors

Lamarche, B. (2008). Review of the effect of dairy products on non-lipid risk factors for cardiovascular disease. J. Am. Coll. Nutr. 27, 741S-746S. [Pg.37]

Wang GQ, DiPietro M, Roeder K et al. Cladistic analysis of human apolipoprotein a4 polymorphisms in relation to quantitative plasma lipid risk factors of coronary heart disease. Ann Hum Genet. 2003, 67 107-124. [Pg.168]

Jenkins, D.J. et al., Soluble fiber intake at a dose approved by the US Food and Drug Administration for a claim of health benefits serum lipid risk factors for cardiovascular disease assessed in a randomized controlled crossover trial, Am. J. Clin. Nutr., 75, 834, 2002. [Pg.140]

The management of liyperlipidacmia is an important aspect of coronary heart disease (CHD) risk factor correction. Modifying liyperlipidacmia together with the other non-lipid risk factors has been repeatedly shown to reduce the risk of developing CHD and to delay or even reverse the progression of established CHD. Risk factors for CHD (Table 1) fall into two groups those which can be corrected (such as smoking, hypertension, hyperlipidaemia and obesity) and those which cannot be inlluenced (such as age. sex and family history). [Pg.40]

Castelli WP, Lipids, risk factors and ischaemic heart disease. Atherosclerosis, Jul 1996 124 Suppl Sl-9. [Pg.19]

R 608 T. Handa, Lipid Risk Factor and Colloid Interface Science , Maku, 2004,29,202... [Pg.71]

Cholesterol is biosynthesized in the liver trans ported throughout the body to be used in a va riety of ways and returned to the liver where it serves as the biosynthetic precursor to other steroids But cholesterol is a lipid and isn t soluble in water How can it move through the blood if it doesn t dis solve in if The answer is that it doesn t dissolve but IS instead carried through the blood and tissues as part of a lipoprotein (lipid + protein = lipoprotein) The proteins that carry cholesterol from the liver are called low density lipoproteins or LDLs those that return it to the liver are the high-density lipoproteins or HDLs If too much cholesterol is being transported by LDL or too little by HDL the extra cholesterol builds up on the walls of the arteries caus mg atherosclerosis A thorough physical examination nowadays measures not only total cholesterol con centration but also the distribution between LDL and HDL cholesterol An elevated level of LDL cholesterol IS a risk factor for heart disease LDL cholesterol is bad cholesterol HDLs on the other hand remove excess cholesterol and are protective HDL cholesterol IS good cholesterol... [Pg.1096]

Increased risk factors for suffering retinoid side effects are adipositas, alcohol abuse, diabetes, nicotine abuse, familiar lipid metabolism alterations and other concommittant therapies (see below). [Pg.1077]

Cardiovascular disease (CVD) is characterized by the involvement of the heart and allied vascular system. High cholesterol, associated lipid abnormahties and high blood pressure are recognized as the major risk factors of CVD. There have been several animal experiments and clinical studies using rice bran and rice bran oil, which have demonstrated a hypocholesterolemic effect (Raghuram et al., 1989 Rukmini and Raghuram, 1991 Sugano and Tsuji, 1997). The mechanisms involved are briefly summarized. [Pg.366]

Fatty acids play an important role as a risk factor for cardiovascular diseases, that is by forming plaques within the arteria. Low density lipoproteins (LDL) are seen as the most important risk factor. In the clinical chemistry laboratory, both LDLs and HDLs (high density lipids, considered as an anti-atherogenic factor) are determined. [Pg.209]

Laboratory Tests The following tests may indicate additional cardiovascular risk factors or poor control of diabetes. Elevated fasting lipid panel Elevated fasting blood glucose Hemoglobin A1c greater than 7.0%... [Pg.14]

Hyperlipidemia has not clearly been established as a risk factor for stroke, although it is a modifiable risk factor for coronary heart disease. Recent studies show that statin use may reduce the incidence of a first stroke in high-risk patients (e.g., hypertension, coronary heart disease, or diabetes) including patients with normal lipid levels. A recent meta-analysis showed a 25% risk reduction for fatal and non-fatal strokes with statin use.4 Patients with a history of MI, elevated lipid levels, diabetes, and... [Pg.169]

The development of CHD is a lifelong process. Except in rare cases of severely elevated serum cholesterol levels, years of poor dietary habits, sedentary lifestyle, and life-habit risk factors (e.g., smoking and obesity) contribute to the development of atherosclerosis.3 Unfortunately, many individuals at risk for CHD do not receive lipid-lowering therapy or are not optimally treated. This chapter will help identify individuals at risk, assess treatment goals based on the level of CHD risk, and implement optimal treatment strategies and monitoring plans. [Pg.176]

Amphotericin B-induced ARF occurs in as many as 40% to 65% of patients treated with the conventional desoxycholate formulation.30 Nephrotoxicity is due to renal arterial vasoconstriction and distal renal tubule cell damage. Risk factors include high doses, treatment for at least 7 days, preexisting kidney dysfunction, and concomitant use of other nephrotoxic drugs.31 Three lipid-based formulations of amphotericin B have been developed in an attempt to decrease the incidence of ARF amphotericin B lipid complex, amphotericin colloidal dispersion, and liposomal amphotericin B. The range of... [Pg.369]

Response to antifungal therapy in invasive candidiasis is often more rapid than for endemic fungal infections. Resolution of fever and sterilization of blood cultures are indications of response to antifungal therapy. Toxicity associated with antifungal therapy is similar in these patients as described earlier with the caveat that some toxicities maybe more pronounced in crit-ically-ill patients with invasive candidiasis. Nephrotoxicity and electrolyte disturbances, with amphotericin B in particular, are problematic and may not be avoidable even with lipid amphotericin B formulations. Fluconazole and echinocandins are generally safer options, and are generally well tolerated. Decisions to use one class of agents over the other is principally driven by concerns of non-albicans species, patient tolerability, or history of prior fluconazole exposure (risk factor for non-albicans species.). [Pg.1223]

APOE Apolipoprotein E 19ql3 Risk factor Unknown (AP clearance Lipid metabolism )... [Pg.656]

A complete history and physical examination should assess (1) presence or absence of cardiovascular risk factors or definite cardiovascular disease in the individual (2) family history of premature cardiovascular disease or lipid disorders (3) presence or absence of secondary causes of hyperlipidemia, including concurrent medications and (4) presence or absence of xanthomas, abdominal pain, or history of pancreatitis, renal or liver disease, peripheral vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient ischemic attack). [Pg.113]

Women with controlled dyslipidemias can use low-dose CHCs, with periodic monitoring of fasting lipid profiles. Women with uncontrolled dysiipidemia (LDL greater than 160 mg/dL, HDL less than 35 mg/dL, triglycerides greater than 250 mg/dL) and additional risk factors (e.g., coronary artery disease, diabetes, hypertension, smoking, or a positive family history) should use an alternative method of contraception. [Pg.346]

Because of the similarity, it is difficult to conclude whether the lipid changes induced by SERMs offer any advantage over the profile determined by HT. Triglyceride levels have been proposed as an independent risk factor for CVD in postmenopausal women (Miller 1998). Further, there are some indications that increases in triglycerides may favor the reduction in the size of LDL particles. Smaller LDL particles are more susceptible to oxidation and have been associated with a higher risk potential (Austin et al. 1988), but whether this observation confers any clinical prejudice to hypertriglyceridemia has not been proven at present. [Pg.225]


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See also in sourсe #XX -- [ Pg.370 ]




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