| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Prevention and treatment of coronary heart disease. The importance of cholesterol synthesis enzyme inhibition Kostner, K. (2003), Pharm Unserer Zeit 32(6): 480-7. |
| Prevention of arteriosclerosis and consumption of olive oil. Is there more to it than its effect on cholesterol? Perez Jimenez, F. (1995), An Med Interna 12(3): 105-6. |
| Prevention of cholesterol cholelithiasis by dietary unsaturated fats in hormone-treated female hamsters Ayyad, N., B. I. Cohen, et al. (1996), Lipids 31(7): 721-7. Abstract: We examined the effect of diet on gallstone incidence and the composition of biliary phosphatidylcholines in methyltestosterone-treated female hamsters. These hamsters were fed a nutritionally adequate purified lithogenic diet containing 2% corn oil, 4% butterfat, 0.3% cholesterol, and 0.05% methyltestosterone, resulting in a cholesterol gallstone incidence of 86%. This incidence was lowered when mono- and polyunsaturated fats or fatty acids were added to the diet: 2.5% oleic acid resulted in total prevention of cholesterol cholelithiasis, 2.5% linoleic acid, and 4% safflower oil (78% linoleic acid content) reduced gallstone incidence to 26 and 8%, respectively. An additional 4% butterfat (29% oleic acid content) produced gallstones in 50% of the animals. At the end of the 6-wk feeding period, the bile of all hamsters was supersaturated with cholesterol. The major biliary phosphatidylcholine species in all groups were (sn-1-sn-2): 16:0-18:2, 16:0-18:1, 18:0-18:2, 16:0-20:4, and 18:2-18:2. The safflower oil- and linoleic acid-fed hamsters exhibited an enrichment of 16:0-18:2 (16-18%); added butterfat or oleic acid increased the proportion of 16:0-18:1 (9 and 25%, respectively). We conclude that the phosphatidylcholine molecular species in female hamster bile can be altered by dietary fats/fatty acids and that mono- and polyunsaturated fatty acids play a role in suppressing the induced cholelithiasis. |
| Prevention of cholesterol gallstone disease by FXR agonists in a mouse model Moschetta, A., A. L. Bookout, et al. (2004), Nat Med 10(12): 1352-8. Abstract: Cholesterol gallstone disease is characterized by several events, including cholesterol precipitation in bile, increased bile salt hydrophobicity and gallbladder inflammation. Here, we describe the same phenotype in mice lacking the bile acid receptor, FXR. Furthermore, in susceptible wild-type mice that recapitulate human cholesterol gallstone disease, treatment with a synthetic FXR agonist prevented sequelae of the disease. These effects were mediated by FXR-dependent increases in biliary bile salt and phospholipid concentrations, which restored cholesterol solubility and thereby prevented gallstone formation. Taken together, these results indicate that FXR is a promising therapeutic target for treating or preventing cholesterol gallstone disease. |
| Prevention of cholesteryl ester accumulation in P388D1 macrophage-like cells by increased cellular vitamin E depends on species of extracellular cholesterol. Conventional heterologous non-human cell cultures are poor models of human atherosclerotic foam cell formation Asmis, R., V. C. Llorente, et al. (1995), Eur J Biochem 233(1): 171-8. Abstract: Since the cellular role of the antioxidative vitamins in the formation of foam cells has not yet been studied in detail, we investigated the effect of alpha-tocopherol and ascorbic acid loading of P388D1 macrophage-like cells on their cholesterol and cholesteryl ester levels and their response to the exposure to different lipoproteins. alpha-Tocopherol loading, but not ascorbic acid loading, of P388D1 cells strongly reduced their cellular cholesteryl ester/cholesterol ratio (the crucial indicator of foam cell formation) when fetal calf serum was the only extracellular source of cholesterol. Balance studies suggest that this effect of alpha-tocopherol was mainly due to a reduced uptake of fetal-calf-serum-derived cholesterol. alpha-Tocopherol loading, however, did not reduce the cholesteryl ester/cholesterol ratio when human unmodified low-density lipoprotein (LDL) was added to culture medium containing fetal calf serum. Thus, the uptake of fetal-calf-serum-derived cholesterol was competitively reduced by human LDL, the uptake of which remained unaffected by alpha-tocopherol. Similarly, alpha-tocopherol loading did not prevent cholesteryl ester formation induced by human LDL either oxidized with Cu2+, ultraviolet light or HOCl, or modified by acetylation, aggregation or by malondialdehyde treatment. The present experimental conditions lacked any pro-oxidative burden, since (a) ascorbic acid, either alone or combined with alpha-tocopherol, did not affect cellular cholesteryl ester levels, (b) foam cell formation was not a linear function of the degree of oxidative LDL modification, and (c) alpha-tocopherol lacked specific effects on oxidatively modified LDL. Thus, the reduction of cellular cholesteryl esters by alpha-tocopherol in the absence of human unmodified LDL was hardly due to common antioxidative properties of vitamin E. In conclusion, the present observation that a desirable alpha-tocopherol effect on the cholesteryl ester balance in mouse-tumor-derived P388D1 cells strongly depended on the species of extracellular cholesterol carrier, cautions against premature generalizations of conventional non-human cell culture data. |
| Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial Sever, P. S., B. Dahlof, et al. (2004), Drugs 64 Suppl 2: 43-60. Abstract: BACKGROUND: The lowering of cholesterol concentrations in individuals at high risk of cardiovascular disease improves outcome. No study, however, has assessed benefits of cholesterol lowering in the primary prevention of coronary heart disease (CHD) in hypertensive patients who are not conventionally deemed dyslipidaemic. METHODS: Of 19 342 hypertensive patients (aged 40-79 years with at least three other cardiovascular risk factors) randomised to one of two antihypertensive regimens in the Anglo-Scandinavian Cardiac Outcomes Trial, 10,305 with nonfasting total cholesterol concentrations 6.5 mmol/L or less were randomly assigned additional atorvastatin 10 mg or placebo. These patients formed the lipid-lowering arm of the study. We planned follow-up for an average of 5 years, the primary endpoint being non-fatal myocardial infarction and fatal CHD. Data were analysed by intention to treat. FINDINGS: Treatment was stopped after a median follow-up of 3.3 years. By that time, 100 primary events had occurred in the atorvastatin group compared with 154 events in the placebo group (hazard ratio 0.64 95% CI 0.50-0.83, p = 0.0005). This benefit emerged in the first year of follow-up. There was no significant heterogeneity among prespecified subgroups. Fatal and non-fatal stroke (89 atorvastatin vs 121 placebo, 0.73 0.56-0.96, p = 0.024), total cardiovascular events (389 vs 486, 0.79 0.69-0.90, p = 0.0005), and total coronary events (178 vs 247, 0.71 0.59-0.86, p = 0.0005) were also significantly lowered. There were 185 deaths in the atorvastatin group and 212 in the placebo group (0.87 0.71-1.06, p = 0.16). Atorvastatin lowered total serum cholesterol by about 1.3 mmol/L compared with placebo at 12 months, and by 1.1 mmol/L after 3 years of follow-up. INTERPRETATION: The reductions in major cardiovascular events with atorvastatin are large, given the short follow-up time. These findings may have implications for future lipid-lowering guidelines. |
| Prevention of coronary heart disease by raising high-density lipoprotein cholesterol? von Eckardstein, A. and G. Assmann (2000), Curr Opin Lipidol 11(6): 627-37. Abstract: Consistent with several potentially anti-atherogenic activities of high-density lipoproteins in vitro, low plasma levels of high-density lipoprotein cholesterol are associated with an increased risk of coronary heart disease. In addition to genes, lifestyle factors (e.g. smoking, being overweight and physical inactivity) strongly affect plasma high-density lipoprotein cholesterol levels. Moreover, a low level of high-density lipoprotein cholesterol interacts with other risk factors. Raising of high-density lipoprotein cholesterol by either adjustments of lifestyle or drug intervention as well as elimination of additional risk factors are thus thought to affect coronary risk. Here, we summarize the outcomes of observational and interventional studies as well as genetic and experimental research which have recently much advanced our understanding of the function and regulation of high-density lipoprotein metabolism. We conclude from the data that changes in the kinetics and functionality of high-density lipoprotein rather than changes in plasma high-density lipoprotein cholesterol levels per se will affect the anti-atherogenicity of therapeutic interference with high-density lipoprotein metabolism. |
| Prevention of coronary heart disease by therapy of hyperlipidemia. Between cholesterol hysteria and therapeutic realism Deller, M. and K. Huth (1992), Fortschr Med 110(25): 463-6. Abstract: OBJECTIVES: The present paper is intended to provide an overview of the arguments for and against drug treatment of hyperlipidemia. MAJOR TOPICS: An argument in support of lipid-lowering prophylactic and therapeutic programs is the close relationship between lipid levels and coronary heart disease, which has been documented both epidemiologically and by interventional studies. Arguments against comprehensive treatment of hyperlipidemia have to do with the fact that although large interventional studies have shown a reduction in mortality from coronary heart disease, there has been no reduction in overall mortality. Of decisive importance for the decision to apply lipid-lowering treatment is the overall risk profile of the patient concerned. This includes not only pathological lipid levels, but also numerous other factors that must be taken into account when considering the indication. CONCLUSIONS: Whether to initiate lipid-lowering treatment or not should be determined on the basis of the individual patient's risk profile, with additional consideration being given to age and sex. |
| Prevention of coronary heart disease through cholesterol reduction Grundy, S. M. (1997), Am Fam Physician 55(6): 2250-8. Abstract: Growing evidence suggests that lowering serum cholesterol levels, particularly low-density lipoprotein levels, will reduce the risk for coronary heart disease. The benefit of cholesterol-lowering therapy has been documented by many clinical trials. Two secondary prevention trials, the Scandinavian Simvastatin Survival Study and the Cholesterol and Recurrent Events trial, demonstrated a striking reduction in recurrent coronary heart disease without an increase in noncardiovascular mortality; treatment with simvastatin reduced total mortality by 30 percent. A primary prevention trial, the West of Scotland Coronary Prevention Study, demonstrated similar results in high-risk patients without established coronary heart disease. More recent angiographic trials revealed that cholesterol-lowering therapy will reduce progression of atherosclerosis and, in some cases, will reverse existing lesions. Use of HMG-CoA reductase inhibitors also appears to be beneficial and safe. Evidence supports cholesterol-lowering therapy in high-risk patients, both with and without established atherosclerotic disease. |
| Prevention of myocardial infarction by reducing serum cholesterol levels. High-risk strategies should be limited Jacobsen, B. K. (1991), Tidsskr Nor Laegeforen 111(17): 2159-61. Abstract: Prevention of premature myocardial infarction is an important public health issue. Two different approaches may be used in order to prevent premature myocardial infarction, a high-risk strategy and a population strategy. The report discusses prevention of myocardial infarction in middle-aged Norwegian individuals by reducing total serum cholesterol and using the high risk and population strategies. A combination of these strategies is recommended, but with major emphasis on the population approach. Both trials and calculations indicate that the high-risk strategy should be limited to subjects with very high serum cholesterol (e.g. greater than or equal to 8 mmol/l in middle-aged men). |
| Prevention of raised low-density lipoprotein cholesterol in a patient with familial hypercholesterolaemia and lipoprotein lipase deficiency Zambon, A., A. Torres, et al. (1993), Lancet 341(8853): 1119-21. Abstract: Raised low-density lipoprotein (LDL) cholesterol is believed to predispose to development of atherosclerosis and coronary heart disease. Increased plasma LDL concentrations and premature coronary heart disease are present in familial hypercholesterolemia (FH), and the enzyme lipoprotein lipase (LPL) seems to have a key role in production of LDL. We describe a unique French Canadian individual who is both heterozygous for FH and homozygous for LPL deficiency (FH/LPL). In this patient, LDL cholesterol was strikingly low compared with both his FH (0.65 vs 5.84 mmol/L) and normolipidaemic (2.77 mmol/L) age-matched relatives despite the defect of LDL-receptor-mediated removal. No LDL peak was present in the cholesterol profile of the FH/LPL-deficient subject, as determined by density-gradient ultracentrifugation. Our results suggest that most LDL particles, in vivo, originate from triglyceride-rich lipoproteins, that LPL plays a vital part in this process, and that absence of LPL activity protects FH subjects against the increase in LDL cholesterol. |
| Prevention of the angiographic progression of coronary and vein-graft atherosclerosis by gemfibrozil after coronary bypass surgery in men with low levels of HDL cholesterol. Lopid Coronary Angiography Trial (LOCAT) Study Group Frick, M. H., M. Syvanne, et al. (1997), Circulation 96(7): 2137-43. Abstract: BACKGROUND: Studies have shown that treatment of hyperlipidemia, especially lowering of plasma LDL levels, retards the progression of coronary atherosclerosis and prevents clinical cardiovascular events. No such studies have focused on subjects with low levels of HDL cholesterol. METHODS AND RESULTS: We randomly assigned 395 post-coronary bypass men, who had an HDL cholesterol concentration < or = 1.1 mmol/L and LDL cholesterol < or = 4.5 mmol/L, to receive gemfibrozil 1200 mg/d or placebo. Coronary angiography was performed at baseline and after, on average, 32 months of therapy. Changes in coronary dimensions were assessed by computer-assisted analysis. Average on-trial serum triglyceride concentrations were 1.69+/-0.68 and 1.02+/-0.37, total cholesterol 5.48+/-0.68 and 4.83+/-0.63, LDL cholesterol 3.84+/-0.59 and 3.39+/-0.56, and HDL cholesterol 0.88+/-0.15 and 0.98+/-0.17 mmol/L in the placebo and gemfibrozil groups, respectively (mean+/-SD, each P<.001). The change in per-patient means of average diameters of native coronary segments was -0.04+/-0.11 mm in the placebo group and -0.01+/-0.10 mm in the gemfibrozil group (P=.009). The equivalent changes in minimum luminal diameters of stenoses were -0.09+/-0.18 and -0.04+/-0.15 mm, respectively (P=.002). A similar, albeit nonsignificant, trend toward treatment benefit was found in the predefined primary study end point, segments unaffected by grafts and those distal to graft insertions. In aortocoronary bypass grafts, 23 subjects (14%) assigned to placebo had new lesions in the follow-up angiogram, compared with 4 subjects (2%) assigned to gemfibrozil (P<.001). CONCLUSIONS: Gemfibrozil therapy retarded the progression of coronary atherosclerosis and the formation of bypass-graft lesions after coronary bypass surgery in men with low HDL cholesterol as their main lipid abnormality. |
| Prevention-oriented life styles and diffusion of cholesterol screening and awareness: Massachusetts behavioral risk factor survey, 1987-1991 Stein, A. D. and R. I. Lederman (1996), J Clin Epidemiol 49(3): 305-11. Abstract: Universal screening of the adult population for detection of elevated serum cholesterol has been recommended. We examined the relation of eight risk factors for morbidity and mortality (hypertension, overweight, inactivity, tobacco use, safety belt nonuse, binge alcohol consumption, driving after alcohol consumption, and chronic alcohol consumption) to adoption of cholesterol screening and to awareness of cholesterol level. Data were collected through the Massachusetts Behavioral Risk Factor Surveillance System between 1987 and 1991 (mean number of respondents interviewed annually, 1240). We compared trends in prevalence of cholesterol screening and awareness within risk groups defined on the basis of the presence or absence of each risk factor. Cholesterol screening prevalence increased from 46.8% in 1987 to 67.9% in 1991. Overweight and hypertensive respondents were more likely to have been screened than nonoverweight or normotensive respondents; for the other six risk factors, individuals at increased risk were less likely to have been screened. The difference in cholesterol screening prevalence between increased-risk and lower-risk respondents increased between 1987-1988 and 1990-1991 for four risk factors. Prevalence of awareness of cholesterol level increased from 7.8% in 1987 to 35.4% in 19991. Trends by risk status were comparable to those observed for cholesterol screening. Individuals already motivated toward a preventive life style appear to be those most likely to avail themselves of a new prevention possibility. |
| Preventive effect of simvastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on coronary atherosclerosis in cholesterol-fed rabbits Oogushi, K. (1991), Fukuoka Igaku Zasshi 82(2): 36-47. Abstract: A study was made on the effect of simvastatin (the generic name of MK-733), a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, on coronary atherosclerosis in cholesterol-fed rabbits with focus on the serum lipids and morphology. Twenty-seven Japanese white rabbits were divided according to dosage of simvastatin into four groups as follows, group P (placebo, 5 rabbits), group MK 1 (simvastatin 1mg/kg, 5 rabbits), group MK 3 (simvastatin 3mg/kg, 6 rabbits) and group MK 5 (simvastatin 5mg/kg, 5 rabbits). They were placed on a 0.5% cholesterol atherogenic diet for 16 weeks and measurements were made of the concentration of serum lipids weekly. After sacrifice, the degree of surface involvement (SI) of aorta stained with Sudan III and the degree of coronary stenosis (CS) of the left circumflex artery were measured using an image-processing system. Serum total cholesterol (TC) level and beta-lipoprotein level decreased dose-dependently in MK groups compared with group P. High density lipoprotein cholesterol level increased in groups MK 3 and MK 5 slightly. Triglyceride level decreased in groups MK 3 and MK 5. The progressions of SI and CS were suppressed in MK groups dose-dependently. Integrated TC, that is, sum of the serum TC values obtained at each week multiplied by 7 corresponded more closely to CS than SI. Intimal thickening constructed from large foam cells originated from macrophages and proliferating smooth muscle cells included lipid droplets in MK groups was almost similar in group P. But it was likely that lipid droplets in each smooth muscle cell in MK groups were less than in group P. In conclusion, the development of coronary atherosclerosis in cholesterol-fed rabbits was suppressed dose-dependently by simvastatin and it was suggested that this preventive effect was due to reducing the integrated TC and local action to vessel walls by simvastatin. (Fukuoka Acta Med.) |
| Preventive effects of eicosapentaenoic acid (EPA) on cholesterol gallstone formation in hamsters Mizuguchi, K., T. Yano, et al. (1997), Nippon Yakurigaku Zasshi 110 Suppl 1: 50P-55P. Abstract: Polyunsaturated fatty acids (PUFA) regulate various biological functions and are involved in a variety of diseases. Eicosapentaenoic acid (20:5, EPA), one of the omega-3 PUFA, has been reported a number of actions including suppression of platelet aggregability and decrease in serum lipids and is well known to be useful in preventing the atherosclerotic diseases. In this paper, we demonstrated that highly purified ethyl eicosapentaenoate (EPA-E) prevents cholesterol (CH) gallstone formation in hamster model. Repeated administration of EPA-E to animals fed a lithogenic diet for 6 weeks decreased the incidences of both CH crystal and CH gallstone formations in gallbladder bile. Contrary, bezafibrate, one of fibric acid derivative which were reported to increase CH saturation index (CSI) in bile, significantly increased the incidences of CH crystal and gallstone formations. EPA-E did not affect the CSI, but markedly increased biliary phospholipid concentration. In the same model, ethyl palmitate (16:0), ethyl oleate (18:1), ethyl linolate (18:2, omega-6) and ethyl arachidonate (20:4, omega-6) had no effects both on biliary lipids composition and CH gallstone formation. These result suggest the benefit of EPA-E in the prevention of CH gallstone. |
| Preventive effects of magnesium on raised serum lipid peroxide levels and aortic cholesterol deposition in mice fed an atherogenic diet Yamaguchi, Y., S. Kitagawa, et al. (1994), Magnes Res 7(1): 31-7. Abstract: We examined the effects of various levels of magnesium intake on serum lipid levels and aortic cholesterol deposition in mice fed for 14 weeks on an atherogenic diet containing 10 per cent linoleic acid. During that time, the mice were given MgCl2.6H2O in drinking water at magnesium doses of 10, 50, 100, or 200 mg/kg/d. A magnesium dose of 50 mg/kg/d is approximately equivalent to the amount consumed in the normal daily diet. Throughout the experimental period, levels of both serum total cholesterol and lipid peroxides decreased relative to increases in the dose of magnesium, while levels of serum phospholipid, triglyceride, and high density lipoprotein (HDL)-cholesterol were unaffected. Levels of aortic cholesterol, particularly cholesteryl ester, decreased as the dose of magnesium increased. These findings indicate that adequate magnesium intake prevents cholesterol deposition in the aortas of mice fed an atherogenic diet, and that this was due to the inhibitory effect of magnesium on lipid peroxidation and its hypocholesterolaemic effect, suggesting in turn, that the antioxidative action of this element plays an important role in creating a defence against the development of atherosclerosis. |
| Prickly pear (Opuntia sp.) pectin alters hepatic cholesterol metabolism without affecting cholesterol absorption in guinea pigs fed a hypercholesterolemic diet Fernandez, M. L., E. C. Lin, et al. (1994), J Nutr 124(6): 817-24. Abstract: Prickly pear pectin intake decreases plasma LDL concentrations by increasing hepatic apolipoprotein B/E receptor expression in guinea pigs fed a hypercholesterolemic diet. To investigate whether prickly pear pectin has an effect on cholesterol absorption and on enzymes responsible for hepatic cholesterol homeostasis, guinea pigs were fed one of three semipurified diets, each containing 15 g lard/100 g diet: 1) the lard-basal diet with no added cholesterol or prickly pear pectin (LB diet); 2) the LB diet with 0.25 g added cholesterol/100 g diet (LC diet); or 3) the LC diet containing 2.5 g prickly pear pectin/100 g diet, added at the expense of cellulose (LC-P diet). Animals fed the LB diet had the lowest plasma LDL and hepatic cholesterol concentrations, followed by animals fed the LC-P diet (P < 0.001). Hepatic 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase activity was highest in the group fed the LB diet, with similar values for animals in the other two groups. A positive correlation existed between plasma LDL cholesterol concentration and hepatic acyl CoA:cholesterol acyltransferase activity (r = 0.87, P < 0.001). Cholesterol absorption was not different among the three dietary groups. These results indicate that the decreased plasma and hepatic cholesterol concentrations of animals fed prickly pear pectin are not explained by differences in cholesterol absorption but rather are due to mechanisms that alter hepatic cholesterol homeostasis, resulting in lower plasma LDL concentrations. |
| Primary care clinician compliance with cholesterol treatment guidelines Schectman, J. M., E. G. Elinsky, et al. (1991), J Gen Intern Med 6(2): 121-5. Abstract: OBJECTIVE: To determine the rate and predictors of clinician compliance with treatment guidelines for high cholesterol in a primary care practice and establish quality assurance thresholds for monitoring patient management. DESIGN: Retrospective chart audit one year after high (greater than 240 mg/dL) cholesterol level. PATIENTS: 257 (243 after exclusions) consecutive patients with serum cholesterol levels greater than 240 mg/dL. SETTING: Primary care practice of group-model university-based HMO. INTERVENTIONS: None. MEASUREMENTS and MAIN RESULTS: In the one-year interval following the index elevated cholesterol level, 67% of 243 patients had received documented dietary counseling, 53% had had a follow-up cholesterol test, and 8% were started on drug treatment. Only two patients (1.8%) without a history of hypercholesterolemia prior to the index level were started on drug treatment, compared with 18 patients (15%) with such a history. The odds (and 95% confidence intervals) of patient dietary counseling increased twofold (1.35 to 2.95) for each 25-mg/dL increment in serum cholesterol, and by 1.45 times (1.12 to 1.87) for each additional coronary risk factor. Patients who had high cholesterol levels obtained as isolated determinations had 2.46 times (1.32 to 4.64) higher odds of being followed by counseling than did those whose levels had been obtained as part of a chemistry panel. CONCLUSIONS: Compliance with National Cholesterol Education Panel guidelines for dietary counseling, but not drug therapy, was higher in this setting than in other published compliance studies. Quality assurance monitoring of compliance with dietary counseling and obtaining lipid measurements using a threshold approach are suggested. A similar approach to drug therapy of hypercholesterolemia appears premature. |
| Primary care physicians and children's blood cholesterol Kimm, S. Y., G. H. Payne, et al. (1992), Prev Med 21(2): 191-202. Abstract: BACKGROUND. In a national survey sponsored by the National Heart, Lung, and Blood Institute, 62% of primary care physicians of children (under age 18 years) believed that high levels of low-density lipoprotein cholesterol in childhood had a great effect on subsequent heart disease risk. RESULTS. About 75% believed high blood pressure, smoking, and diabetes had similar effects. Although routine cholesterol screening in children under age 10 was infrequent, 72% of physicians screened high risk children. The age at which screening was done varied markedly; more pediatricians screened children younger than 5 years. The majority of physicians who saw children with high blood cholesterol instituted nondrug therapy, with pediatricians being most apt to do so. Low saturated fat diets were prescribed by 26% of these physicians and 9% of physicians prescribed increased polyunsaturated diets. Twelve percent of physicians treating hypercholesterolemic children used lipid-lowering drugs. Among those using drugs, 9% based drug use on total blood cholesterol measurements only. Factors that affected physician treatment of childhood hypercholesterolemia included physician specialty type, organization of practice (group or solo), and the age distribution of the pediatric patient population. |
| Primary cholesterol hepatolithiasis: a disease with a different pathogenesis Soloway, R. D. (1993), Hepatology 17(4): 737-8. |