| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Cholesterol. Myth vs reality in pediatric practice Berenson, G. S. (1993), Am J Dis Child 147(4): 371-3. |
| Cholesterol. The complex relation of an indispensable enemy. Interview by Robert Henry. Castelli, W. P. (1990), Union Med Can 119(3): 129-35. |
| Cholesterol: a rational approach Schofield, T. (1996), Practitioner 240(1563): 364-70. |
| Cholesterol: a renal risk factor in diabetic nephropathy? Mulec, H., S. A. Johnsen, et al. (1993), Am J Kidney Dis 22(1): 196-201. Abstract: In a prospective follow-up of 30 patients with type 1 diabetes and nephropathy, serum cholesterol, triglycerides, apolipoprotein Al and B, and lipoprotein(a) were determined to study their relationship to the rate of decline in glomerular filtration rate. The patients had proteinuria and advanced nephropathy with a mean +/- SD glomerular filtration rate of 39 mL/min/1.73 m2. The decline in glomerular filtration rate was determined during 2.5 +/- 0.5 years. High serum cholesterol, triglycerides, and apolipoprotein B were correlated to a more rapid deterioration in kidney function. The rate of decline in glomerular filtration rate was 1.0 +/- 2.5 mL/min/yr in the 10 patients with the lowest cholesterol level, compared with 4.5 +/- 3.2 mL/min/yr in the patients with the highest serum cholesterol (P = 0.015). The combined effect of the measured lipids, blood pressure, type of antihypertensive treatment, protein intake, proteinuria, and hemoglobin A1C on the rate of decline in glomerular filtration rate was assessed by multiple regression analysis. The measured factors together had a high explanatory power for the rate of decline in glomerular filtration rate. In this model, 73% of the variation in decline in glomerular filtration rate was explained by the measured variables (multiple r2 = 0.73). Low cholesterol and treatment with an angiotensin-converting enzyme inhibitor were the strongest predictors of a favorable renal prognosis. This suggests that hypercholesterolemia is an important risk factor for diabetic nephropathy. |
| Cholesterol: a two-edged sword in brain aging Joseph, J. A., R. Villalobos-Molinas, et al. (1997), Free Radic Biol Med 22(3): 455-62. Abstract: Previous research from several laboratories has indicated that cholesterol (CHO) accumulates in neuronal membranes and alters their structural and signal transduction (ST) properties during aging. The possible reasons for these increases in membrane CHO have not been specified. However, present findings suggest that such accumulation may actually serve to protect neuronal tissue from oxidative damage. Striatal slices (6, 24 month rats) were preincubated in 1 mM CHO (30 min) followed by incubation with H2O2 (10 microM, 30 min). The slices were then either superfused with 30 mM KCl in the presence or absence of 500 microM oxotremorine (Ox), and K(+)-evoked dopamine release (K(+)-ERDA) examined or assessed for carbachol-stimulated low K(m) GTPase activity. The results indicated that CHO incubation prior to H2O2 in either age group was effective in preventing H2O2 reductions in both non-Ox-enhanced K(+)-ERDA and Ox conditions, as well as sodium nitroprusside (SNP 150 microM)-induced decreases in K(+)-ERDA. In addition, H2O2-induced deficits in carbachol-stimulated low K(m) GTPase activity were reduced in the striatal tissue from the old animals pretreated with CHO. However, if the slices were incubated in H2O2 prior to CHO exposure, CHO enhanced the H2O2 effects in the tissue from the old animals. Thus, depending upon the order of exposure, CHO functioned to enhance or retard the effects of oxidative stress, in an age-dependent manner. |
| Cholesterol: a useful parameter for distinguishing between pleural exudates and transudates Valdes, L., A. Pose, et al. (1991), Chest 99(5): 1097-102. Abstract: Previously established criteria were used to classify 253 pleural effusions as transudates (65 cases), neoplastic exudates (67 cases), tuberculous exudates (65 cases), or miscellaneous exudate (56 cases). The parameters pleural LDH (PLDH), pleural LDH/serum LDH ratio (P/SLDH), and pleural protein/serum protein ratio (P/SPROT) were compared with pleural cholesterol (PCHOL) and the pleural cholesterol/serum cholesterol ratio (P/SCHOL) with regard to their usefulness for distinguishing between pleural exudates and transudates. The PCHOL values determined were 28.5 +/- 12.8 mg/dl for transudates, 88.1 +/- 30 mg/dl for neoplastic exudates, 96.5 +/- 28 mg/dl for tuberculous exudates, and 88 +/- 35.9 mg/dl for the miscellaneous group; the differences between the transudate group and the others are statistically significant (p less than 0.001). The sensitivity and specificity of P/SPROT for diagnosis of exudates were both 89 percent; the sensitivity of PLDH was 67 percent and its specificity was 95 percent; the sensitivity and specificity of P/SLDH were both 84.6 percent. Using Light's three criteria as a battery, the sensitivity was 94.6 percent and its specificity was 78.4 percent. All the transudates and 17 (9 percent) of the 188 exudates had PCHOL values below 55 mg/dl, so that with this threshold, PCHOL had a sensitivity of 91 percent and a specificity of 100 percent for diagnosis of exudates. With a threshold of 0.3, P/SCHOL had a sensitivity of 92.5 percent and a specificity of 87.6 percent. The number of misclassifications by PCHOL was less than with any other of the parameters, with statistically significant differences with respect to PLDH (p less than 0.001) and P/SLDH (p less than 0.01). We conclude that determination of PCHOL and P/SCHOL is of great value for distinguishing between pleural exudates and transudates, and should be included in routine laboratory analysis of pleural effusions. |
| Cholesterol: an important but relatively overemphasized risk factor for ischemic heart disease Hellstrom, H. R. (2001), Med Hypotheses 57(5): 593-601. Abstract: Educational messages directed at the public to prevent ischemic heart disease (IHD) are generally based on cholesterol-reduction. However, IHD has multiple risk factors, and a study was performed to help determine whether or not the allocation of educational messages among risk factors is appropriate: The severity of high cholesterol was compared with the severity of multiple other major risk factors for IHD, and the beneficial effects of cholesterol-reduction was compared with the benefits of multiple other major preventative factors for IHD. It was found that high cholesterol levels, and multiple other risk factors, generally give a risk of around 2.0 for developing IHD. Cholesterol-reduction by statins, and multiple other factors which prevent IHD, generally reduce the risk of IHD by about 30-40%. It was concluded that the allocation of educational messages to reduce the incidence of IHD should significantly increase discussions of non-cholesterol risk and preventative factors. |
| Cholesterol: blood level and control by Swiss physicians Nigg, C. and F. Gutzwiller (1995), Schweiz Med Wochenschr 125(8): 355-60. Abstract: The high coronary heart disease morbidity and mortality and the economic costs have led to intensive prevention efforts in Switzerland, where the management of multiple risk factors plays a prominent role. An important risk factor is hypercholesterolemia, one of the main causes in the development of human atherosclerosis. However, the eminence of this risk factor is not yet sufficiently established in the awareness of many physicians. Inappropriate public discussions of the problem have caused confusion among patients and physicians. Therefore, the purpose of the Cholesterin Informations Program of the Swiss Heart Foundation is to work out a far-reaching and objective information strategy for experts and the general population, based on scientific knowledge, as a contribution to promoting the health of the Swiss population. |
| Cholesterol: blood levels or total risk as a guide to preventive treatment? Mathes, P. (2004), Z Kardiol 93 Suppl 2: II16-20. Abstract: The results of a cholesterol lowering therapy with statins do belong to the best documented steps in medical treatment. The newer studies like HPS and LIPID have shown a therapeutic benefit across all serum-cholesterol levels, nearly obviating the need for a prior determination of the cholesterol values. Why not using the serum-cholesterol level as the only guide to therapy? Since there is no threshold indicating the need for treatment, there is the danger of an unlimited inflation of the indications for therapy, possibly leading to a collapse of the health care system. At the upper extreme, therapy would have to start at a very young age, and no one can predict the side effects of a statin therapy over many decades. Improving the target for therapy can only be achieved via determination of the total risk of cardiovascular disease. Several algorithms like PROCAM (www.chd-taskforce.de), the risk chart of the European Society of Cardiology or the Framingham risk-scores will come to similar results. In this manner, one can differentiate further, and persons with a low risk of cardiovascular disease like women and young adults do not have to be treated unnecessarily. However, it must not be overlooked that the sensitivity of these risk-scores is rather low. The majority of myocardial infarctions occur in the average risk population, because of sheer numbers. Independent indicators of cardiovascular risk, such as the CRP, the intima-media thickness of the carotid artery and in particular the determination of the coronary calcium score via EBT or ultrafast scan can lead to more clarity. To improve the estimation of the individual risk, we will need a combination of risk-factors and -indicators. |
| Cholesterol: consensus and controversies, what is the trend in 1993? Fossati, P. (1993), Ann Endocrinol (Paris) 54(6): 389-97. Abstract: Anatomopathological, biological and epidemiological studies suggest that raised cholesterol concentrations are associated with heightened risk for coronary heart disease. Preventive measures have been recommended by consensus conferences (prudent diet and cholesterol lowering drugs) for a "desirable" level of plasma total cholesterol, i.e.: 1.80 g/l before thirty years and 2 g after thirty years. The debates about the advantage of plasma cholesterol lowering have boosted many controversies after the completion of randomized primary and secondary prevention trials analyses. It was showed an increase in total mortality and a no reduction in fatal coronary events. A series of papers have tried to discourage physicians from identifying subjects with high risk. One has to continue to detect subjects with familial hypercholesterolemia and to treat them following the recommendations of consensus conferences. In the other cases, one has to attach value to HDL-cholesterol and plasma triglyceride levels, especially in patients with hyperinsulinemia, insulin resistance, hypertension and visceral obesity. As lipid oxidation products toxicity, protective diets, as the traditional mediterranean diet containing antioxidant components are important too. Relationships between lipoprotein status and hypercoagulability remains to be investigated to identify predictive factors better than cholesterol for atherothrombosis diseases in subjects at risk. |
| Cholesterol: free radical peroxidation and transfer into phospholipid membranes Barclay, L. R., R. C. Cameron, et al. (1990), Biochim Biophys Acta 1047(3): 255-63. Abstract: Cholesterol, when sequestered in saturated liposomes of dimyristoylphosphatidylcholine (DMPC) or dipalmitoylphosphatidylcholine (DPPC), undergoes peroxidation thermally initiated either by a lipid-soluble or a water-soluble azo initiator and in both cases the reaction is inhibited effectively by the water-soluble antioxidant, 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylate (Trolox). Quantitative kinetic methods of autoxidation show that the oxidizability, kp/(2kt)1/2 (where kp and 2kt are the rate constants of radical chain propagation and termination, respectively) of cholesterol in DMPC or DPPC multilamellar liposomes, where kp/(2kt)1/2 is 3.0.10(-3) to 4.3.10(-3) M-1/2 s-1/2 at 37-45 degrees C, is similar to that measured in homogeneous solution in chlorobenzene, where kp/(2kt)1/2 is 3.32.10(-3). However, its oxidizability in smaller unilamellar vesicles of DMPC or DPPC increases by at least 3-times that measured in multilamellar systems. Autoxidation/antioxidant methods show that cholesterol partitions directly from the solid state into DMPC or DPPC liposomes by shaking and this is confirmed by 31P and 2H quadrupole NMR spectra of deuterated cholesterol when membrane bound. Analytical studies indicate that up to 21 mol% cholesterol will partition into the membranes by shaking. |
| Cholesterol: from heart attacks to Alzheimer's disease Raffai, R. L. and K. H. Weisgraber (2003), J Lipid Res 44(8): 1423-30. Abstract: The accumulation and aggregation of the amyloid-beta peptide (Abeta) in the brain are important contributing factors to Alzheimer's disease (AD). Consequently, blocking the generation of Abeta is a potentially important treatment strategy. Recent work on the metabolism of Abeta has identified several cellular proteins and proteases that collectively promote or prevent the generation of Abeta. In addition, accumulating in vitro and in vivo evidence suggests a role for cholesterol in modulating the cellular processing of Abeta with the potential to affect AD. |
| Cholesterol: how low is low enough? Rosengren, A. (1998), Bmj 317(7156): 425-6. |
| Cholesterol: how low is low enough? Doctors have been slow in getting evidence on lowering cholesterol into practice Wierzbicki, A. S. and T. M. Reynolds (1999), Bmj 318(7182): 539. |
| Cholesterol: how low is low enough? Effect of a given concentration depends on several factors Walker, A. R. (1999), Bmj 318(7182): 538-9. |
| Cholesterol: myth or reality? Thompson, W. G. (1990), South Med J 83(4): 435-40. |
| Cholesterol: myth vs reality? Newman, T. B. (1994), Arch Pediatr Adolesc Med 148(3): 330-1. |
| Cholesterol: point-of-care testing Taylor, J. R. and L. M. Lopez (2004), Ann Pharmacother 38(7-8): 1252-7. Abstract: OBJECTIVE: To review the literature regarding point-of-care (POC) cholesterol monitors and describe their role in pharmacy practice. DATA SOURCES: Primary articles were identified by a MEDLINE search (1966-May 2003); references cited in these articles provided additional resources. STUDY SELECTION AND DATA EXTRACTION: All of the articles identified from this search were reviewed, and all information deemed relevant was included. DATA SYNTHESIS: Hyperlipidemia is a well-established risk factor for coronary artery disease, which is the leading cause of death in the US. The use of POC cholesterol monitors may help to improve the identification and management of this disease. Pharmacists may use many of these devices in their practice and are also in an ideal position to provide patient education on selection and use of these monitors and interpretation of the results. CONCLUSIONS: The availability of POC cholesterol monitors has increased in recent years. Based on currently available data, these monitors are best suited for screening purposes and to assist in the management of hyperlipidemia. There is not enough evidence to support the notion that POC cholesterol monitors can replace laboratory or office monitoring. Their application in the diagnosis of hyperlipidemia is also currently limited. |
| Cholesterol: precursor to many lipid disorders Jones, P. H. (2001), Am J Manag Care 7(9 Suppl): S289-98. Abstract: Despite advances in treatment and prevention, coronary heart disease (CHD) remains the leading cause of death in the United States. A major risk factor for CHD is elevated low-density lipoprotein cholesterol (LDL-C). Randomized clinical trials have proven that lowering LDL-C to near target levels significantly reduces CHD risk. More aggressive LDL-C reductions would have an even greater impact on reducing CHD risk if these goal levels were applied to all patients at risk, as identified by a CHD risk prediction scoring system. In 1993 the second Adult Treatment Panel (ATP II) of the National Cholesterol Education Program issued guidelines that defined CHD risk on the basis of whether a patient qualified for primary or secondary prevention. The ATP III guidelines, issued May 2001, introduce the concept of CHD-equivalent risk in patients without known CHD, thereby expanding considerably the number of people eligible for lipid-lowering therapy. Unfortunately, many patients who are eligible for therapy are not receiving it, and among those on lipid-lowering therapy, less than half have achieved their treatment goals. As mentioned, findings from several large-scale primary- and secondary-prevention trials with statins and other lipid-lowering agents have shown that lowering LDL-C reduces the risk for fatal and nonfatal coronary events and results in fewer hospitalizations and revascularization procedures. In fact, a review of the 5 major statin trials reveals that the higher the patient's baseline CHD risk, the more striking the benefits of therapy are. Clearly, the need to lower LDL-C levels is crucial. Meeting this need involves targeting patients who are at risk, implementing appropriate treatment, and ensuring compliance with therapy. |
| Cholesterol: stuck in traffic Mukherjee, S. and F. R. Maxfield (1999), Nat Cell Biol 1(2): E37-8. |