| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Lack of effect of lovastatin therapy on the parameters of whole-body cholesterol metabolism Goldberg, I. J., S. Holleran, et al. (1990), J Clin Invest 86(3): 801-8. Abstract: The effects of lovastatin therapy on the parameters of body cholesterol metabolism were explored in nine hypercholesterolemic patients. Long-term cholesterol turnover studies were performed before therapy, and were repeated after 15 mo of lovastatin therapy (40 mg/d) while continuing on therapy. The major question addressed was whether a reduction in plasma cholesterol level with lovastatin would be associated with a reduction in the whole-body production rate of cholesterol or with the sizes of exchangeable body cholesterol pools as determined by the three-pool model of cholesterol turnover. The mean plasma cholesterol level decreased 19.4% (from 294 to 237 mg/dl), and low-density lipoprotein cholesterol decreased 23.8% (from 210 to 159 mg/dl) with lovastatin therapy. Changes in high-density lipoprotein cholesterol level were not significant. The cholesterol production rate did not change significantly with therapy (1.09 +/- 0.10 mean +/- S.D. vs. 1.17 +/- 0.09 g/d). By comparison, colestipol and niacin treatment in three other subjects more than doubled the cholesterol production rate (1.14 +/- 0.28 vs. 2.42 +/- 0.34 g/d). Thus, hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibition by lovastatin at the therapeutic dose used here did not change the steady-state rate of whole-body cholesterol synthesis. Despite the changes in plasma cholesterol levels, no significant changes were seen in the values of M1, of M3 or of Mtot, the sizes of the pools of rapidly, of slowly, and of total body exchangeable cholesterol. Conclusion: lovastatin therapy to lower plasma cholesterol does not lead to corresponding reductions in body cholesterol pools or to a reduction in the rate of whole-body cholesterol synthesis. In the new steady state that exists during long-term lovastatin therapy, along with increased expression of the genes for HMG-CoA reductase and the LDL receptor, the body compensates for the effects of the drug so that cholesterol production rate and tissue pool sizes are not changed from pretreatment values. |
| Lack of effect of vitamin E on cholesteryl ester transfer and lipoprotein composition in cholesterol-fed rabbits Liu, X. Q., W. Buchanan, et al. (1997), Comp Biochem Physiol B Biochem Mol Biol 117(4): 553-9. Abstract: The concentration and activity of cholesteryl ester transfer protein (CETP) is increased in plasma in hypercholesterolemic humans and in experimental animals fed cholesterol. While the concentration of lipo-proteins appears to be the major determinant of CETP activity, we have found previously that dietary measures and pharmacologic agents that alter their lipid composition reduce the activity of CETP in plasma (CET). Since vitamin E is lipophilic and is incorporated into lipoproteins, we have examined the question of whether it too attenuates CET in cholesterol-fed New Zealand White rabbits prior to and 14 weeks after treatment with differing doses (5, 15, 30, 45 mg/kg) of vitamin E. Plasma triglycerides (TG), cholesterol (TC) and phospholipids (Lys, Sph, Lec, PI, PE) all increased significantly to a comparable degree in the rabbits fed cholesterol compared to those fed chow (p < 0.05; p < 0.01); the levels achieved were similar in the vitamin E-treated and untreated groups. As was observed with plasma lipids, cholesteryl ester transfer (CET) was accelerated to the same degree in each of the cholesterol-fed groups independent of whether they received vitamin E compared to chow-fed controls (p < 0.01) and the distribution of cholesterol in apo-B containing lipoproteins (VLDL, IDL, and LDL) was similar in the vitamin E-treated and untreated groups. These findings indicate that vitamin E has no discernible effect on CET when cholesterol levels are markedly elevated. |
| Lack of effects of post-initiation cholesterol on 3,2'-dimethyl-4-aminobiphenyl-induced prostate carcinogenesis Tagawa, Y., K. Ozaki, et al. (1992), Prostate 20(3): 179-85. Abstract: The effects of cholesterol on 3,2'-dimethyl-4-aminobiphenyl (DMAB)-induced rat prostate carcinogenesis were investigated in male F344 rats. Animals were given 10 subcutaneous (s.c.) injections of 50 mg/kg body weight of DMAB at 2-week intervals, each time 2 days after transfer from 1 week on 0.75 ppm of an ethinyl estradiol (EE)-supplemented diet to a basal diet. From week 20, the animals received treatment with cholesterol (2 or 1%, in the diet), saponin (1 or 0.2 mg/rat/week, s.c.), or clofibrate (0.3%, in the diet) for 40 weeks. Although serum cholesterol levels were significantly increased by administration of cholesterol itself, and were decreased by clofibrate, the incidences of atypical hyperplasias and carcinomas of the ventral prostate were very similar with all treatments. Thus, under the present conditions, high or low cholesteremia did not affect rat prostate lesion development. |
| Lack of efficacy of low-dose sitostanol therapy as an adjunct to a cholesterol-lowering diet in men with moderate hypercholesterolemia Denke, M. A. (1995), Am J Clin Nutr 61(2): 392-6. Abstract: Plant sterols have been shown to reduce dietary cholesterol absorption and hence, total and low-density-lipoprotein (LDL)-cholesterol concentrations in humans. In this study the cholesterol-lowering effects of dietary supplementation with the hydrogenated plant sterol sitostanol (3 g/d) were tested in 33 men with moderate hypercholesterolemia who were consuming an outpatient diet in which dietary cholesterol was restricted to < 200 mg/d. Sitostanol therapy did not significantly lower LDL cholesterol compared with the diet alone. Similarly, sitostanol therapy in conjunction with a cholesterol-lowering regimen of diet and 8 g cholestyramine did not significantly lower LDL-cholesterol concentrations. Hence, although previous reports have suggested that low-dose sitostanol therapy is an effective means of reducing LDL-cholesterol concentrations, its effectiveness may be attenuated when the diet is low in cholesterol. |
| Lack of influence of low blood cholesterol levels on pancreatic carcinogenesis after initiation with N-nitrosobis(2-oxopropyl)amine in Syrian golden hamsters Ogawa, T., T. Makino, et al. (1994), Carcinogenesis 15(8): 1663-6. Abstract: The effects of a cholesterol-free diet, a cholesterol-free diet supplemented with sesamin, and a diet supplemented with sesamin on pancreatic carcinogenesis of N-nitrosobis(2-oxopropyl)amine (BOP) were investigated in 140 female Syrian golden hamsters. BOP (70 and 20 mg/kg body wt) was injected s.c. twice at an interval of 2 weeks at the beginning of the experiment. Starting 3 weeks thereafter, the animals were maintained on basal diet, cholesterol-free diet, basal diet plus sesamin, or cholesterol-free diet plus sesamin for a further 15 weeks. All surviving hamsters were killed at week 18, and the pancreatic tissues examined histologically. The incidences of pancreatic neoplastic and preneoplastic lesions in each group did not show any statistically significant variation. The cholesterol-free diet significantly decreased the cholesterol contents of the serum, pancreas and liver, and sesamin supplement significantly decreased the cholesterol contents of the serum and liver. Both the cholesterol-free diet and sesamin decreased the serum lipoperoxide levels. The results thus indicated that low cholesterol per se and sesamin exert no significant influence on BOP-initiated pancreatic carcinogenesis in hamsters, at least within the 4 month period after carcinogen treatment. |
| Lack of relationship between left ventricular mass and serum cholesterol in hypertensives Lip, G. Y., E. Edmunds, et al. (1998), J Hypertens 16(11): 1703-4. |
| Lack of requirement for sterol carrier protein-2 in the intracellular trafficking of lysosomal cholesterol Johnson, W. J. and M. P. Reinhart (1994), J Lipid Res 35(4): 563-73. Abstract: Previous work has established that the absence of peroxisomes, as occurs in Zellweger syndrome, is accompanied by the absence of cellular sterol carrier protein-2 (SCP2). In the present study, Zellweger-syndrome fibroblasts and peroxisome-deficient CHO-ZR78 cells were used to study the role of SCP2 in the intracellular transport of low density lipoprotein (LDL)-derived lysosomal cholesterol. By immunoblotting, peroxisome-deficient cells were confirmed to contain either no detectable SCP2 or far less SCP2 than corresponding normal cells. To monitor the transport of lysosomal cholesterol to the plasma membrane, we measured efflux of lysosomal cholesterol to HDL3 or phospholipid vesicles. SCP2-deficient cells, in comparison to normal cells, demonstrated little or no impairment in this efflux, suggesting that SCP2 is not required for the efficient delivery of lysosomal cholesterol to the plasma membrane. To examine the role of SCP2 in the delivery of lysosomal cholesterol to acyl-CoA:cholesterol acyltransferase (ACAT) in the rough endoplasmic reticulum (RER), the lysosomal and whole-cell cholesterol pools were differentially labeled, and then the ACAT-mediated esterification of each pool was measured in response to an 8-h incubation with native LDL. For both cholesterol pools, esterification was stimulated by LDL, and the responses in normal and Zellweger cells were similar, demonstrating that SCP2 is required for neither the stimulation of ACAT that follows LDL uptake nor for the transport of lysosomal cholesterol to the RER. These findings suggest that some major aspects of lysosomal cholesterol trafficking in cells can occur by mechanisms not involving SCP2. |
| Lack of the intestinal Muc1 mucin impairs cholesterol uptake and absorption but not fatty acid uptake in Muc1-/- mice Wang, H. H., N. H. Afdhal, et al. (2004), Am J Physiol Gastrointest Liver Physiol 287(3): G547-54. Abstract: Before cholesterol and fatty acid molecules in the small intestinal lumen can interact with their possible transporters for uptake and absorption, they must pass through a diffusion barrier, which may modify the kinetics of nutrient assimilation. This barrier includes an unstirred water layer and a surface mucous coat, which is located at the intestinal lumen-membrane interface. In the present study, we investigated whether disruption of the mucin gene (Muc)1 may influence intestinal uptake and absorption of cholesterol and fatty acid in male Muc1(-/-) mice. The wild-type mice displayed relatively high levels of Muc1, Muc2, Muc3, and Muc4 mRNAs and relatively low levels of Muc5ac and Muc5b mRNAs in the small intestine. The absence of Muc1 mRNA and protein in the small intestines of Muc1(-/-) mice confirmed complete knockout of the Muc1 gene, but the mRNA expression for other mucin genes remained unchanged. Intestinal uptake and absorption of cholesterol but not palmitic acid were significantly reduced in Muc1(-/-) mice compared with the wild-type mice. However, knockout of the Muc1 gene did not impair either expression levels of the genes that encode intestinal sterol efflux transporters Abcg5 and Abcg8 and fatty acid transporter Fatp4 or small intestinal transit rates. We conclude that physiological levels of the epithelial mucin produced by the Muc1 gene are necessary for normal intestinal uptake and absorption of cholesterol in mice. Our study implies that because cholesterol absorption efficiency is reduced by approximately 50% in Muc1-deficient mice, there may be one or more additional pathways for cholesterol absorption. |
| Lack of toxic effects of F 12511, a novel potent inhibitor of acyl-coenzyme A: cholesterol O-acyltransferase, on human adrenocortical cells in culture Junquero, D., A. Pilon, et al. (2001), Biochem Pharmacol 61(4): 387-98. Abstract: Inhibition of acyl-coenzyme A: cholesterol O-acyltransferase (EC 2.3.1.26; ACAT) reduces intracellular cholesteryl esters that are substrates for steroidogenesis in adrenal cells. The adrenal side effects of ACAT inhibitors remain a key point for their development as antiatherosclerotic agents. The aim of this study was to characterize the effects of a novel and powerful ACAT inhibitor, F 12511 (S)-2',3',5'-trimethyl-4'-hydroxy-alpha-dodecylthio-phenylacetanilide, on the NCI-H295R cell line, which has functional properties comparable to those of normal human adrenal cells. F 12511 incubated with cultured cells for 4-72 hr strongly inhibited cholesteryl oleate formation. The concentrations required to produce 50% inhibition (IC50) values) ranged from 20 to 50 nM; in the presence of low-density lipoproteins (LDL), this effect was paralleled by a decrease in cholesteryl ester mass and an increase in intracellular free cholesterol. At concentrations 100-fold larger than the IC(50) value for up to 48 hr, F 12511 reduced neither the basal release of cortisol and aldosterone nor the production of cortisol stimulated by forskolin. F 12511 did not modify the mRNA levels of the steroidogenic enzyme genes cytochrome P450 cholesterol side-chain cleavage (P450scc), cytochrome P450 17alpha-hydroxylase (P450c17), or cytochrome P450 21-hydroxylase (P450c21) or those of the LDL receptor and high-density lipoprotein scavenger receptor class B, type I (SR-BI) genes, either in the presence or absence of adenosine 3',5'-cyclic monophosphate stimulation for 24 hr. Exposure to F 12511 at up to 3 microM for 24 or 48 hr did not result in significant change in morphological and ultrastructural characteristics; the cytoplasm contained large numbers of mitochondria with intact crystae, and the same typical features of secretory activity were observed in NCI-H295R control cells. Exposure to 3 microM of F 12511 for 96 hr also did not affect cell viability. These data demonstrate that reduction of the substrate for steroidogenesis by the ACAT inhibitor F 12511 impairs neither steroid production nor transcription of genes involved in steroidogenesis and lipoprotein uptake in the pluripotent human adrenal cell line NCI-H295R. |
| Lack of tumorigenicity of cholesterol epoxides and estrone-3,4-quinone in the rat mammary gland el-Bayoumy, K., B. Y. Ji, et al. (1996), Cancer Res 56(9): 1970-3. Abstract: The purpose of this study is to test the long-standing hypothesis that endogenous agents found in human breast fluid and in plasma are potential initiators of breast cancer. Therefore, we evaluated the tumorigenicity in the mammary glands of female CD rats of cholestan-5 alpha,6 alpha-epoxy-3 beta-ol (cholesterol-alpha-epoxide), cholestan-5 beta,6 beta-epoxy-3 beta-ol (cholesterol-beta-epoxide), and 1,5(10)estradiene-3,14,17-trione (estrone-3,4-quinone). As a positive control, trans-3,4-dihydroxy-anti-1,2-epoxy-1,2,3,4-tetrahydrobenzocphenanthren e (BcPDE) was used. Rats were fed a high-fat AIN-76A diet (23.5% corn oil) to mimic the Western dietary composition. Because literature data suggest that the endogenous agents tested in this study are weak electrophiles, the total doses of cholesterol epoxides (12.3 mumol/rat) and of estrone-3,4-quinone (30 mumol/rat)were 10- and 25- fold higher, respectively, than that of BcPDE (1.2 mumol/rat). Each agent was dissolved in DMSO, and one-sixth of the total dose was injected under each of six nipples on the right side. The thoracic glands of the rat were treated at 30 days of age, and those located in the inguinal area were treated on the following day. The experiment was terminated at 44 weeks after treatment. Consistent with our previous study, BcPDE was a strong mammary carcinogen. However, there were no differences between rats treated with DMSO alone or those receiving DMSO containing cholesterol-alpha-epoxide, cholesterol-beta-epoxide, or estrone-3,4-quinone. The results of this study clearly indicate, for the first time, that metabolites derived from cholesterol and estrone lack tumorigenic activity in the rat mammary gland, at least under the conditions of the present protocol. |
| Lactoferrin inhibits cholesterol accumulation in macrophages mediated by acetylated or oxidized low-density lipoproteins Kajikawa, M., T. Ohta, et al. (1994), Biochim Biophys Acta 1213(1): 82-90. Abstract: When macrophages are incubated with acetylated or oxidized low-density lipoproteins (Ac- or OxLDL), cellular cholesteryl esters (CE) increase significantly. In the present study, we investigated the effect of whey protein on Ac- or OxLDL mediated accumulation of CE in macrophages and found that lactoferrin (Lf), a minor protein component of whey, inhibits the accumulation of CE dose-dependently. In the presence of bovine Lf (1 mg/ml), CE accumulation in macrophages incubated with AcLDL (100 micrograms of protein/ml) decreased by more than 80%. Human Lf was less potent than bovine Lf, and bovine transferrin had no effect. Binding of 125I-AcLDL to macrophages was also inhibited by Lf. Agarose gel electrophoresis revealed that Lf binds to Ac- or OxLDLs and neutralizes their negative charges. These results indicate that Lf inhibits the binding of modified LDLs to macrophages by direct interaction with modified LDLs, resulting in their loss of function as ligands of the scavenger receptor. Modification of the arginine residues of Lf with 1,2-cyclohexanedione abolished its ability to bind to AcLDL, suggesting that a region rich in basic amino acid residues near the N-terminus of Lf, which resembles the ligand-binding site of the scavenger receptor, may be responsible for this binding ability. As a result, the inhibitory effect of Lf on CE accumulation in macrophages was significantly weakened by this modification. Our results suggest the possibility that Lf in the blood stream may act as an anti-atherogenic agent in vivo. |
| Lacunar infarctions due to cholesterol emboli Laloux, P. and J. M. Brucher (1991), Stroke 22(11): 1440-4. Abstract: BACKGROUND AND PURPOSE: Hypertension is commonly considered the major cause of lacunar infarctions. However, in some cases, it has been suggested that lacunes could be caused by cerebral emboli from cardiac or carotid sources. Cholesterol cerebral emboli have been rarely reported as a cause of lacunes. CASE DESCRIPTION: We describe a 79-year-old patient with a progressive multi-infarct dementia who developed transient motor aphasia and paresis of the right arm. Computed tomography showed lacunar infarcts in the right caudate nucleus, left thalamus, and left putamen, as well as an old right frontal infarction. Neuropathological examination demonstrated no prominent vascular hyalinosis, but did show multiple cholesterol emboli occluding small arteries around lacunar infarcts and leptomeningeal arteries near cortical infarcts. The cholesterol material presumably originated in the extended atheromatous changes along the aortic arch. CONCLUSIONS: Our report confirms that lacunes can be caused by cholesterol emboli in some patients. Small cerebral emboli should not be overlooked as a cause of lacunes. |
| Lamellar bodies coexist with vesicles and micelles in human gallbladder bile. Ursodeoxycholic acid prevents cholesterol crystal nucleation by increasing biliary lamellae Ginanni Corradini, S., G. Arancia, et al. (1995), J Hepatol 22(6): 642-57. Abstract: The aggregative forms of lipids in human gallbladder bile and their relation to cholesterol crystallization are controversial. Using combined chemical, gel-chromatographic, optical/electron microscopic and quasielastic light-scattering methods, we investigated this issue in native gallbladder bile obtained from nine untreated cholesterol gallstone patients and eight cholesterol gallstone patients treated for 1 week with 600 mg/day of ursodeoxycholic acid. Bile obtained at cholecystectomy was ultracentrifuged for 2 h at 150,000 g to obtain isotropic samples. The conventional cholesterol crystal observation time was 3.1 +/- 4.1 (SD) days in controls and 19.0 +/- 1.9 days in the ursodeoxycholic acid-treated group (p < 0.001). Bile was analyzed by high-resolution gel-chromatography using 7 mM sodium taurocholate in the elution buffer. Biliary lipids eluted in four chromatographic zones: zone #I, corresponding to the column void volume, contained only minimal amounts of lipids; zone #II (apparent m.w. 100-220 kDa) comprised 29.1 +/- 12.4% of biliary cholesterol in the untreated group and 8.3 +/- 4.3% in the ursodeoxycholic acid-group (p < 0.001). At negative staining electron microscopy, this region was composed of roundish vesicles ranging from 7 to 20 nm in diameter. Zone #III (apparent m.w. 50-100 kDa) carried 59.1 +/- 2.1% of cholesterol in untreated patients and 81.2 +/- 9.5% in ursodeoxycholic acid-rich biles, respectively (p < 0.001). At negative staining electron microscopy, this region was composed of lamellar stacks of variable length, usually with 5 nm interspaces and up to 30 nm in width. In ursodeoxycholic acid-rich biles, lamellae often appeared in the form of concentric fingerprint-like images. Quasielastic light-scattering measurements in this region were compatible with the size estimates obtained at electron microscopy. Zone #IV (apparent m.w. 6-50 kDa) carried 11.8 +/- 9.4% and 11.6 +/- 9.0% of cholesterol, respectively (not significant). Since this region comprised a considerable fraction of endogenous bile salts and had no distinct morphological structures, it was interpreted as mixed micelles. The cholesterol crystal observation time showed a significant inverse correlation (r = -0.85, p < 0.001) with percent cholesterol carried by vesicles (zone #II) and a direct correlation (r = 0.86, p < 0.001) with percent cholesterol carried by lamellar bodies (zone #III). Vesicles and lamellae identical to those observed in isolated gel-chromatographic fractions were observed also on direct electron microscopic examination of unfractionated isotropic native biles. Similar findings were observed also in matched model biles.(ABSTRACT TRUNCATED AT 400 WORDS) |
| Lanosterol 14 alpha-demethylase (cytochrome P-45014DM): modulation of its enzyme activity by cholesterol feeding Sonoda, Y., C. Amano, et al. (1995), Biol Pharm Bull 18(7): 1009-11. Abstract: Regulation of the activity of lanosterol 14 alpha-demethylase (cytochrome P-45014DM) by dietary cholesterol was studied in rats. In male rats fed a 3% cholesterol diet for 1 and 4 weeks, the activity of 24,25-dihydrolanosterol 14 alpha-demethylase was decreased in the liver. The cytochrome P-45014DM protein content detected by immunoblotting was also decreased by cholesterol feeding. These results demonstrate that dietary cholesterol acts as a repressive factor for lanosterol 14 alpha-demethylase. Further, the activity was enhanced by preincubation with phosphatase of the enzyme solution from both the control and cholesterol fed rats at the same rate. This result suggests that regulation of the activity involves phosphorylation of this enzyme. |
| Lanosterol 14alpha-demethylase (CYP51)--a cholesterol biosynthetic enzyme involved in production of meiosis activating sterols in oocytes and testis--a minireview Rozman, D. (2000), Pflugers Arch 439(3 Suppl): R56-7. Abstract: CYP51 is an evolutionarily conserved, housekeeping gene of the cytochrome P450 superfamily which is involved in cholesterol biosynthesis in animals. The two intermediates of cholesterol biosynthetis pathway, sterol FF-MAS, produced by CYP51 and the following sterol T-MAS, accumulate in follicular fluid and in testis. CYP51 is expressed in all tissues in mammals with the highest level in the testis. In rat, expression peaks in postmeiotic male germ cells of the testis. Promoters of the human and rat CYP51 genes contain SRE and CRE elements which indicate two main regulatory routes--the sterol-dependent regulation and the cAMP-dependent regulation. While feedback regulation by sterols is characteristic for all genes involved in cholesterol biosynthesis and homeostasis, the cAMP-dependent regulation is unique, indicating that CYP51 may play tissue-specific roles distinct from cholesterol biosynthesis. |
| Large and cholesteryl ester-rich high-density lipoproteins in cholesteryl ester transfer protein (CETP) deficiency can not protect macrophages from cholesterol accumulation induced by acetylated low-density lipoproteins Ishigami, M., S. Yamashita, et al. (1994), J Biochem (Tokyo) 116(2): 257-62. Abstract: High-density lipoprotein (HDL) has been speculated to have an anti-atherogenic function. Many in vitro studies have demonstrated that HDL has the ability to remove cholesteryl ester (CE) from lipid-laden macrophages. However, the effect of alteration in chemical composition and particle diameter on the in vivo function of HDL is unknown. In the study described here, we have isolated the HDL from patients homozygous for cholesteryl ester transfer protein (CETP) deficiency and examined its function in vitro, in order to clarify the anti-atherogenic property of HDL in CETP-deficient subjects. Apolipoprotein (apo) E-free HDL2 from the patients, separated by heparin-Sepharose column chromatography, was rich in CE, poor in triglycerides (TG), and enlarged in size on 4-30% nondenaturing polyacrylamide gradient gel electrophoresis. In contrast, HDL3 from the patients was normal in size and in its chemical composition. First, we examined the effect of HDL on CE accumulation in macrophages. After mouse peritoneal macrophages had been incubated with both acetylated low-density lipoproteins (Ac-LDL) and HDL, cellular CE content was determined by an enzymatic, fluorometric method. Ac-LDL alone induced a 9-fold accumulation of CE. The addition of apo E-free HDL2 and HDL3 from controls and patients' HDL3 prevented CE accumulation in macrophages, while patients' HDL2 had no preventive effect. We next investigated the in vitro ability of HDL to remove cellular CE from lipid-laden macrophages after incubation with Ac-LDL. After loading of macrophages with cholesterol by Ac-LDL, HDL was added to the culture medium and the cellular CE content was measured.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Large artery stiffness is not related to plasma cholesterol in older subjects with hypertension Dart, A. M., C. D. Gatzka, et al. (2004), Arterioscler Thromb Vasc Biol 24(5): 962-8. Abstract: OBJECTIVE: Previous studies have demonstrated a prognostic role of large artery stiffness in hypertensive subjects and increased stiffness in subjects with coronary artery disease. Although plasma cholesterol is an established risk factor for cardiovascular disease, its relationship with large artery properties in a hypertensive population is unclear. METHODS AND RESULTS: Plasma cholesterol and large artery properties were measured at baseline in a subset of participants of a randomized controlled trial (ANBP2) evaluating hypertension treatment in older (65 to 84 years) subjects. Noninvasive measures of large artery behavior were central augmentation index (AI), systemic arterial compliance (SAC), and transverse expansion of the aortic arch (aortic distensibility). Arterial waveforms acceptable for analysis were obtained in approximately 80% of cases yielding valid measurements of AI in 868, SAC in 846, and aortic distensibility in 680 subjects. Mean total and high-density lipoprotein (HDL) concentrations were 5.5+/-1.0 and 1.4+/-0.5 mmol L(-1). Total and HDL cholesterol and AI were greater in females than males, whereas SAC and aortic distensibility were greater in males. In multiple regression analyses there were no significant associations between stiffness parameters and total or HDL cholesterol. Significant independent associations in such analyses were found for mean arterial blood pressure, gender, age, height, and heart rate, in keeping with previous findings. CONCLUSIONS: In the largest cohort of elderly hypertensive subjects studied to date, plasma cholesterol per se was not associated with large artery stiffness. Such independence from cholesterol increases the potential for artery stiffness measurements to additionally contribute to cardiovascular risk assessment in this population. |
| Large cholesterol granuloma arising from the frontal sinus--case report Ochiai, H., Y. Yamakawa, et al. (2001), Neurol Med Chir (Tokyo) 41(5): 283-7. Abstract: A 59-year-old male presented with a large cholesterol granuloma arising from the frontal sinus manifesting as a large, fluctuated, soft mass in his brow, compressing left eye. Skull radiography showed dilation of the frontal sinus. Computed tomography and magnetic resonance imaging revealed a cystic mass extending into the left orbit and anterior cranial fossa. Gross inspection at the frontal craniotomy showed mucinous, dark green fluid intermingled with shining material. The histological diagnosis was cholesterol granuloma with epithelial lining. Large cholesterol granuloma with facial deformity is always associated with bone and cosmetic problems. Wide opening of the frontal sinus followed by cyst wall removal and plastic repair of the skull is necessary. |
| Large cholesterol granuloma of the petrous apex treated via subcochlear drainage Jaramillo, M. and P. C. Windle-Taylor (2001), J Laryngol Otol 115(12): 1005-9. Abstract: This is a case report of a patient with bilateral cholesterol granuloma of the petrous apex, who presented with unilateral symptoms. Initially suspected as having a dermoid cyst, he underwent posterior fossa exploration, drainage and biopsy. Symptoms recurred one year later and subcochlear drainage of the petrous apex cyst was successfully performed. Follow-up for over 18 months shows no clinical nor imaging signs of recurrence. A MEDLINE literature search was carried out and relevant paper publications reviewed. Case presentation including initial, pre- and post-operative imaging is presented. This is followed by discussion of current concepts on the presentation and management of large cholesterol cysts of the petrous apex. |
| Large cholesterol polyp of the gallbladder mimicking gallbladder carcinoma Kaido, T., M. Kano, et al. (2004), Abdom Imaging 29(1): 100-1. Abstract: Gallbladder tumors larger than 10 mm in diameter have a high incidence of malignancy. We report an extremely rare case of a large cholesterol polyp of the gallbladder mimicking gallbladder carcinoma. Ultrasonography and computed tomography showed a larger papillary mass in the fundus of the gallbladder with a maximum diameter of about 30 mm, the largest gallbladder polyp ever reported to our knowledge. |