| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Lovastatin lowers serum cholesterol levels in non-insulin-dependent diabetes mellitus patients without altering their insulin sensitivity Hwu, C. M., K. C. Shih, et al. (1996), Zhonghua Yi Xue Za Zhi (Taipei) 57(3): 169-76. Abstract: BACKGROUND: Lovastatin, a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, has been widely used in the treatment of hypercholesterolemia. It is also applied to dyslipidemia in patients with diabetes mellitus. The influence of lovastatin on insulin sensitivity was evaluated in twelve Chinese non-insulin-dependent diabetes mellitus (NIDDM) patients with hypercholesterolemia. METHODS: This double-blind, randomized, placebo-controlled, and two-period cross-over experiment enrolled 12 patients. After a run-in period of two months, the patients were randomized into 2 groups to receive either lovastatin (20 mg once daily) or placebo treatment. Eight weeks later, two groups of patients exchanged their treatment for another 8 weeks. Blood samples were collected at the end of the run-in period and at 4-week intervals during the study to observe serum lipid profiles. A modified insulin suppression test was made to assess insulin sensitivity three times: at the end of run-in period, in week 8 and week 16, respectively. Wilcoxon signed rank test was used for analysis of statistical significance of the difference between lovastatin and placebo treatments. RESULTS: As compared with the placebo, lovastatin reduced serum total cholesterol (TC) levels significantly. Serum total triglyceride (TG) concentrations decreased slightly by lovastatin. The ratio of TC to high density lipoprotein-cholesterol (HDL-C) also decreased significantly in lovastatin period. No difference was found in serum apolipoprotein A1 levels. A significant reduction of serum apolipoprotein B concentrations was also noted in lovastatin period. No difference in glycemic indices and insulin sensitivity was observed in the base-line, placebo or lovastatin periods. CONCLUSIONS: The results demonstrated that lovastatin significantly lowered the serum TC levels without perturbation of insulin sensitivity in hypercholesterolemic NIDDM patients. |
| Lovastatin prevents the impairment of endothelium dependent relaxation and inhibits accumulation of cholesterol in the aorta in experimental atherosclerosis in rabbits Senaratne, M. P., A. B. Thomson, et al. (1991), Cardiovasc Res 25(7): 568-78. Abstract: STUDY OBJECTIVE--The aim was to determine the effect of the HMG CoA reductase inhibitor, lovastatin, on the loss of endothelium dependent relaxation and the accumulation of cholesterol in the aorta produced by feeding a diet enriched with cholesterol. DESIGN--The study was conducted in two stages. In stage 1, New Zealand white rabbits were randomised into four groups. Group 1 (n = 15) was fed standard rabbit diet for 6 weeks. Groups 2 (n = 15), 3 (n = 12), and 4 (n = 12) were fed standard rabbit diet supplemented with 2% cholesterol for 2 weeks followed by standard rabbit diet only for the next 4 weeks. In addition, lovastatin (4 mg.kg-1.d-1) was given for the entire 6 weeks in group 3 and for the first 2 weeks only in group 4. In stage 2 a second group of animals was fed a diet supplemented with 0.5% cholesterol for 2 weeks in order to match the serum cholesterol levels in groups 3 and 4 of stage 1. EXPERIMENTAL MATERIAL--Aortic tissue was removed for measurement of cholesterol content, endothelium dependent relaxation (to acetylcholine), contractile responses (to noradrenaline), relaxant responses (to sodium nitrite), and sudan staining. Serum was obtained for measurement of cholesterol and triglyceride concentrations. MEASUREMENTS AND MAIN RESULTS--In stage 1, at the end of 2 weeks, the serum cholesterol was significantly lower in groups 3 and 4 than in group 2. At 6 weeks, endothelium dependent relaxation to acetylcholine (-6.0 log mol.litre-1) was impaired in group 2 compared to the other groups: group 1 78.5(SEM 5.0); group 2 43.5(7.8)%; group 3 79.4(4.6)%; group 4 84.7(3.4)%. The relaxant response to sodium nitrite was not impaired in group 2. Further, the aortic tissue cholesterol concentration in group 2 was significantly greater than that in group 1, at 355(65) v 105(10) nmol.mg-1 protein. In groups 3 and 4, the aortic cholesterol concentrations were significantly lower than those in group 2, at 74(4) and 94(17) nmol.mg-1 protein respectively. In stage 2, the serum cholesterol values were matched to those in groups 3 and 4 of stage 1. In these animals, after a further 4 weeks the aortic cholesterol was significantly greater than in group 3. CONCLUSIONS--Lovastatin attenuates the accumulation of cholesterol and preserves endothelium dependent relaxation in this model of experimental atherosclerosis. It is likely that the latter is a secondary phenomenon. |
| Lovastatin therapy for cholesterol ester storage disease in two sisters Tarantino, M. D., D. J. McNamara, et al. (1991), J Pediatr 118(1): 131-5. Abstract: We administered lovastatin to two sisters, aged 4 and 17 years, who had cholesterol ester storage disease, an autosomal recessive disorder manifested by hypercholesterolemia and hypertriglyceridemia. The drug, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was taken orally for 6 months. Serum lipid concentrations were determined monthly. Computed tomography of the liver was performed before and during therapy to evaluate liver fat content. The younger sister had liver biopsies before and after 6 months of lovastatin therapy to assess hepatic cholesterol stores. Both patients had marked decreases in serum levels of cholesterol, triglycerides, and low-density lipoprotein-cholesterol; high-density lipoprotein-cholesterol levels increased. Computed tomography during treatment demonstrated a significant increase in linear attenuation, suggesting a decreased liver fat content. Liver tissue obtained 6 months after lovastatin therapy was initiated had 13% less esterified cholesterol than the liver sample obtained before treatment. We conclude that lovastatin may be effective in treating children with cholesterol ester storage disease. |
| Lovastatin to prevent acute coronary events with average cholesterol levels MacFarlane, L. L. and P. J. Carek (1998), J Fam Pract 47(2): 91-2. |
| Low adherence of General Practitioners to National Cholesterol Education Program guidelines for the management of hyperlipidaemia Fornengo, P., G. Bruno, et al. (2000), Diabetes Nutr Metab 13(5): 263-8. Abstract: Aim of our study was to assess adherence to the National Cholesterol Education Program Adult-Treatment Panel II (NCEP-ATP II) in patients cared for by General Practitioners (GPs) in an Italian community. The design of the work was cross-sectional cohort study; the base was an unselected cohort of 1,168 patients cared for by GPs and screened at our lipid clinic in 1994-1995 in the Province of Turin (Italy). Blood samples were collected after 12-hr fast to measure plasma levels of total cholesterol, triglycerides, HDL-cholesterol, glucose and thyroid-stimulating hormone (TSH). LDL-cholesterol was calculated using Friedewald's formula. In patients with body mass index (BMI) >30 kg/m2, an oral glucose tolerance test was performed. Blood pressure was measured in all patients, and a baseline ECG or a stress test was performed in those with unknown cardiovascular disease (CVD), then they were classified following the NCEP-ATP II criteria. Primary hyperlipidaemia accounted for 86.9% of the cohort with most patients requiring pharmacological treatment; in 34.4% of the patients, LDL-cholesterol values were > or = 6.46 mmol/l (250 mg/dl) and in 23.7% with established CVD, LDL-cholesterol levels were > or = 5.68 mmol/l (220 mg/dl). In only 7.3% of patients the NCEP treatment goals were achieved, with 1.3% among those in secondary prevention. We observed great discrepancies between clinical practice and international recommendations for the management of hyperlipidaemia. |
| Low- and high-density lipoprotein cholesterol and ischemic cerebrovascular disease: the bezafibrate infarction prevention registry Koren-Morag, N., D. Tanne, et al. (2002), Arch Intern Med 162(9): 993-9. Abstract: BACKGROUND: Despite increasing evidence that beta-hydroxy-beta-methyglutaryl coenzyme A reductase inhibitors reduce the incidence of stroke in patients with coronary heart disease (CHD), the associations between blood lipid levels and cerebrovascular disease (CVD) are not clear. OBJECTIVE: To evaluate whether blood cholesterol level and its fractions are risk factors for stroke in a large group of patients with CHD. METHODS: We followed up 11 177 patients with documented CHD who were screened for but not included in the Bezafibrate Infarction Prevention study, a secondary prevention randomized clinical trial of lipid modification, and had no history of stroke for subsequent CVD. During a 6- to 8-year follow-up period, 941 patients were identified as having nonhemorrhagic CVD, of whom 487 had verified ischemic stroke or transient ischemic attack (TIA). RESULTS: Increases in age-adjusted rates of both nonhemorrhagic CVD and verified ischemic stroke or TIA were identified with increasing cholesterol and low-density lipoprotein cholesterol levels, decreasing high-density lipoprotein cholesterol levels, and decreasing percentage of total serum cholesterol contained in the HDL moiety. In logistic regression models, adjusting for clinical covariates, the following odds ratios (95% confidence intervals) were identified for lipid values in the upper vs lower tertile for the end point of nonhemorrhagic CVD: total cholesterol, 1.43 (1.20-1.70); low-density lipoprotein cholesterol, 1.52 (1.27-1.81), high-density lipoprotein cholesterol, 0.84 (0.70-1.00); and percentage of serum cholesterol contained in HDL, 0.69 (0.58-0.83). Similar trends appeared for the end point of verified ischemic stroke or TIA. CONCLUSION: These findings clearly support the role of total cholesterol and its fractions in prediction of ischemic CVD among patients with established CHD. |
| Low and lowered cholesterol and total mortality Criqui, M. H. and B. A. Golomb (2004), J Am Coll Cardiol 44(5): 1009-10. |
| Low blood cholesterol and low platelet serotonin levels in violent suicide attempters Alvarez, J. C., D. Cremniter, et al. (1999), Biol Psychiatry 45(8): 1066-9. Abstract: AIM OF THE STUDY: This study investigated the possible connection between serum cholesterol levels and platelet serotonin (5-HT) content in violent suicide attempters and matched controls. METHODS: Blood samples for cholesterol and platelet 5-HT levels were obtained from 17 drug-free patients within 3 days after the suicide attempt. RESULTS: Serum cholesterol and platelet 5-HT levels in the suicide attempters were significantly lower than in the controls; however, we did not find any significant correlation between these two variables. Indeed, three clinical dimensions are present in this patient group: suicidality, violence, and impulsiveness. Because we did not find a difference in cholesterol and platelet 5-HT levels between impulsive and nonimpulsive patients, these two indexes may more reflect the dimension of suicidality and/or violence. CONCLUSIONS: Further investigation is necessary to study the dependence of these two peripheral abnormalities within the context of violent suicidal behavior. |
| Low blood cholesterol and non-atherosclerotic disease mortality: where do we stand? Smith, G. D. (1997), Eur Heart J 18(1): 6-9. |
| Low blood total cholesterol and mortality: causality, consequence and confounders Lewis, B. and M. J. Tikkanen (1994), Am J Cardiol 73(1): 80-5. |
| Low cholesterol and cancer Kritz, H., C. Zielinski, et al. (1996), J Clin Oncol 14(11): 3043-8. Abstract: PURPOSE: The relation between plasma cholesterol (CH) concentration and mortality is complex. The plasma CH concentration correlates positively with mortality from coronary heart disease, but some studies have shown a negative relation with death from cancer. If these two relations reflect causal mechanisms that are reversible by changing the plasma CH concentration, the benefits of lipid reduction for heart disease might be offset by an increased mortality from cancer. Different aspects between lipid metabolism and cancer, as well as new insights into this interesting field, are discussed. METHODS: The literature was searched using MedLine through 1966 and January 1996. RESULTS: There is no evidence from the data available at present that the association between low CH and a higher risk of cancer is causal. CONCLUSION: This issue should not affect the advice on health matters offered by doctors, especially to patients with other risk factors for cardiovascular disease. The possibility that hypercholesterolemia (HC) drugs can induce a reduction of tumor-cell growth makes them potentially useful as an adjuvant to chemotherapy and ultimately increases the probabilities in the prevention and treatment of cancer. |
| Low cholesterol and coronary heart disease Leigh, T. H. (1991), Bmj 303(6808): 993-4. |
| Low cholesterol and excess mortality: a real relationship? Oranje, W. A. and B. H. Wolffenbuttel (1993), Neth J Med 42(3-4): 89-91. |
| Low cholesterol and impaired cardiac function following heart transplantation Kaye, D. M., L. Johnston, et al. (1994), Clin Exp Pharmacol Physiol 21(8): 659-61. Abstract: 1. During follow-up of 59 cardiac transplant recipients over 2 or more years, a small group of subjects was observed who displayed an unpredictable, relatively marked, reduction in plasma cholesterol. 2. A significant proportion of these subjects were subsequently observed as having experienced a marked decline in left ventricular function at the time of routine radionuclide ventriculography. 3. While the mechanism for this fall in cholesterol is unclear, the observation of such an unexpected reduction in total cholesterol, late after heart transplantation should be considered significant and prompt further investigation including an assessment of allograft function. |
| Low cholesterol and noncardiovascular mortality Abbott, C., A. B. Meadows, et al. (2000), Mil Med 165(6): 466-9. Abstract: Recent clinical trial data have suggested that low cholesterol might cause increased mortality from noncardiovascular conditions. Several randomized trials have suggested an increase in noncoronary deaths at low levels of total cholesterol. When subcategories for causes of death were investigated, it was noted that hemorrhagic stroke risk was inversely related to total cholesterol, whereas nonhemorrhagic stroke risk was positively related to total cholesterol. Certain cancers were shown to be more common at low total cholesterol levels, namely lung, liver, lymphatic, and hematopoietic cancer. Another issue to consider is whether increased mortality rates are seen in individuals with "naturally" occurring low cholesterol or whether they are seen in individuals whose cholesterol has been deliberately lowered through dietary or drug intervention, or in both. If an association between low cholesterol and noncardiovascular mortality is present, there is continuing uncertainty regarding the mechanism by which it occurs. |
| Low cholesterol and pathological manifestations Gomirato, G. and G. Nigro (1994), Minerva Pediatr 46(6): 307-8. Abstract: The paper reviews the literature on the association between hypocholesterolemia and various pathologies. There are few studies on this topic and these are often fragmented and uncertain, in particular with regard to children. However, studies with a wide statistical basis have focused on the different stages of adulthood. There does not appear to be a genuine link between "low cholesterol" and disease in childhood, although the contrary would appear to be true. The authors invite pediatricians to examine this aspect further in view of the major repercussions that it may have on a wide range of factors. For this reason the authors consider it worthwhile presenting this innovative topic and field of research. |
| Low cholesterol and pathological manifestations: Smith-Lemli-Opitz syndrome Franceschini, P. and D. Franceschini (1994), Minerva Pediatr 46(12): 579-80. |
| Low cholesterol and risk of non-coronary mortality Simes, R. J. (1994), Aust N Z J Med 24(1): 113-9. Abstract: Based on a systematic review of over 20 cohort studies, a clear association exists, for both men and women, between particularly low cholesterol levels and the rate of non-coronary mortality. The excess in women appears mainly confined to non-cancer causes, particularly respiratory and digestive diseases, while there is also an excess of deaths from cancer seen in men with low cholesterol levels. Higher mortality rates from trauma, haemorrhagic stroke and cirrhosis have also been observed. Much of this association is known to be as a consequence of the disease with a fall in cholesterol levels seen after developing a variety of inflammatory diseases. However, the excess risk of non-coronary heart disease deaths is still apparent by excluding deaths within five years suggesting that effect-cause is not the only explanation. Confounding still remains the most likely explanation for the association with an underlying chronic disease or risk factor causing both the low cholesterol and the fatal event. However, there is still the possibility that some of the increased risk is due to the low cholesterol. This makes it important that appropriately controlled trials of both drug and dietary interventions demonstrate net clinical benefit among those with low levels of coronary risk before cholesterol-lowering strategies are adopted more widely in these groups. |
| Low cholesterol and violence Golomb, B. (1995), Arch Intern Med 155(22): 2485. |
| Low cholesterol and violence Mufti, R. M., R. Balon, et al. (1998), Psychiatr Serv 49(2): 221-4. Abstract: OBJECTIVE: The association between violent behavior and low serum total cholesterol levels was examined in a psychiatric inpatient population with diverse diagnoses. METHODS: The study used a case-control design to compare the cholesterol levels of patients in a long-term psychiatric hospital who had a history of seclusion or restraints (N = 20) and those who did not (N = 20). A low cholesterol level was defined as less than 180 mg/dL. RESULTS: A strong association was found between low cholesterol levels and violent behavior (odds ratio = 15.49), an association that was not due to age, race, sex, or diagnosis. The finding was consistent whether mean levels or dichotomized levels of cholesterol were examined. Physical health, cholesterol-lowering medication, current alcohol use, or unusual diets could not explain the results. However, the raw frequency of episodes of seclusion or restraint as an indicator of the frequency of violent behavior was not associated with cholesterol level. Dichotomizing cholesterol levels at 180 mg/dL yielded high sensitivity (90 percent) for predicting violent behavior but at the cost of low specificity (65 percent). CONCLUSIONS: The results support the hypothesis that an association exists between low cholesterol and violent behavior among psychiatric patients but argue against using cholesterol level as a screening tool for predicting violent behavior. |