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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histological, histochemical and electron-microscopical examinations have been performed on xanthoma of the skin and palmar creases in 5 patients with hyperlipoproteinemia type III, to follow the dynamics of xanthoma formation. The results were as follows: 1. There are no basic differences in histomorphology between xanthomas in type III-HLP and other types of HLP. Typical findings are: Rather dense distribution of relatively small foam cells within the dermis, only a few foam giant cells, great amounts of cholesterol intra- and extracellulary, and circumscribed necrobioses. 2. Xanthoma formation in type III-HLP is induced by pathological plasma lipoproteins. These seem to pass the endothelial barrier via pinocytosis or/and filtration. Between endothelial cells and their basal lamina plasma components sometimes could be observed. 3. The pathological lipoproteins induce a phagocytic reaction with foam cell formation in the dermal tissue. At first an augmentation of lymphocytoid or histiocytoid tissue macrophages could be detected in the dermis and especially in the perivascular region of venous blood vessels in the middermis. Perithelial cells as well as lymphocytoid and histiocytoid tissue macrophages engulve lipoproteins. Cytoplasmic enrichment of vacuoles with an electron opaque content (lipoproteins) are typical for type III-HLP; they lead to formation of typical foam cells. Within those cells lysosomal intracellular degradation of the engulved lipoproteins takes place; free cholesterol cristals, phospholipid-containing myelinic figures and residual bodies are endproducts of this process. They can lead to cellular necrosis with cellular remnants, lipoprotein vacuoles, free cholesterol and phospholipids lying free within the dermal tissue. 4. Factors are not well understood which control circumscribed xanthoma formation in type III-HLP. 5. These investigations show, that xanthomas are reactive new formations. The leading cellular substrate is the tissue macrophage, which is transformed into a foam cell by intake of lipoproteins. Foam cell formation, however, is not the result of a simple process of storage: after lipoprotein intake numerous, to a part lysosomal processes of chemical degradation and transformation, take place with an appearance of intracellular endproducts (free cholesterol, residual bodies, phospholipid-containing membranes). It is suggested that the dynamics of xanthoma formation might be importance in understanding of the process of atherosclerosis in those patients.
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PMID:[Sturcture and morphogenesis of xanthomas in hyperlipoproteinemia type III. A morphologic, histochemical and electron microscopy study]. 17 29

Lipid fluidity of the erythrocyte membrane and intact platelets was examined in 32 male patients affected by types IIA, IIB and IV primary hyperlipoproteinemia and 15 control subjects. Lipid fluidity was determined by fluorescence polarization using two probes: DPH and TMA-DPH which are localized in different lipid areas of the cell membrane. Classical haemorheological tests were also performed including plasma viscosity, whole blood viscosity and erythrocyte aggregation. As compared to a control group, plasma viscosity and whole blood viscosity at low shear rate was significantly increased in types IIB and IV, but not in type IIA patients. In contrast, the increase in erythrocyte aggregation was significant in all HLP types. Concerning lipid fluidity, the results recorded with red cells and platelets were not significantly different for type IIA HLP compared to the control group. In contrast, erythrocyte membranes from patients with types IIB and IV HLP had a significantly higher level of fluidity in lipid regions characterized by TMA-DPH. Using DPH as a fluorescent probe, identical results were only noted in type IIB patients. Regarding intact platelets of IIB and IV patients, an increase in lipid fluidity was noted for two fluorescent probes. These findings suggest that HLP associated erythrocyte and platelet fluidity alterations are not related to hypercholesterolemia but to the triglyceride level.
Atherosclerosis 1990 Aug
PMID:Rheological properties and membrane fluidity of red blood cells and platelets in primary hyperlipoproteinemia. 224 99

Platelets from patients with familial hypercholesterolemia (type IIa hyperlipoproteinemia), a condition associated with a high prevalence of atherosclerosis and its ischemic complications, are claimed to be hyperresponsive to aggregating stimuli. We investigated the platelet responsiveness to and the binding of PGD2, a potent endogenous inhibitor of platelet aggregation via stimulation of adenylate cyclase, in a group of 7 patients affected by IIa hyperlipoproteinemia (IIa HLP) and in a control group of 10 healthy subjects. Inhibition by PGD2 of ADP-induced platelet aggregation was significantly lower in IIa HLP patients than in controls. The number of binding sites for PGD2 of platelets from IIa HLP patients was significantly reduced in comparison with that from controls (93 +/- 19 and 232 +/- 23 receptors/platelet, respectively), whereas the affinity for PGD2 was comparable to that of controls (Kd = 68.8 +/- 19.8 nM in patients and 66.1 +/- 15.9 nM in controls). The reduced number of platelet PGD2 binding sites in IIa HLP patients may account for the impaired sensitivity to PGD2 shown in vitro by platelets and may contribute to the increased tendency to thrombotic manifestations observed in IIa HLP.
Atherosclerosis 1985 Feb
PMID:Decreased number of PGD2 binding sites on platelets from patients with type IIa hyperlipoproteinemia. 385 47

In order to study the relationships between serum lipoprotein lipid concentrations and the concentrations of apo E in serum and interstitial fluid, we have developed a specific, sensitive and rapid radioimmunoassay for this apolipoprotein. Studies of the interstitial fluid lipoproteins and of the gradient between the lipoprotein concentrations in interstitial fluid and serum may add to our understanding of the development of atherosclerosis and xanthomatosis. Serum, interstitial fluid, lipoproteins or standards were incubated with 125I-labelled apo E and rabbit antiserum against apo E for 90-120 min at room temperature. The immune complexes were harvested with the use of formalin-treated staphylococci. The displacement curves produced by standard and samples of serum, interstitial fluid and isolated lipoproteins were linear in logit-log plots and had identical slopes. Delipidation did not change the results and the recovery of added apo E to a serum sample was 96 +/- 5% (n = 5). Apo E was found in all major lipoprotein classes and the concentrations of apo E in serum and in interstitial fluid were 36 +/- 19 mg/l and 8 +/- 4 mg/l, respectively, in normals (n = 21) and 305 +/- 125 mg/ml and 20 +/- 9 mg/l, respectively, in patients with HLP type III (n = 11). Highly significant positive correlations were found in HLP type III between the interstitial fluid level of apo E and the corresponding concentrations of cholesterol and triglyceride. Interstitial fluid apo E concentrations were significantly correlated to apo E but not to the lipid levels in serum, indicating that only some subclasses of the serum lipoproteins are transported to the interstitial compartment.
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PMID:Serum and interstitial fluid apolipoprotein E levels in the healthy and in hyperlipoproteinemia type III as studied by radioimmunoassay. 404 71

The influence of the efficacy of triglyceride and cholesterol correction on cardiovascular complications and mortality was analysed in a follow-up study with 260 patients with primary HLP (triglycerides before entry greater than 2.9 mmol/l and/or cholesterol greater than 7.8 mmol/l). The follow-up time was 67.4 +/- 27 months. It was hypothesised that reduction of elevated levels of triglycerides and/or cholesterol influenced favourably the incidence of angina pectoris, MI, stroke and total mortality. For ethical reasons, it was not possible to carry out the investigations with a control group. Therefore, we performed an internal comparison of 3 categories of lipid correction achieved during the trial (effective, moderate, insufficient). A substantial improvement of the lipid disorder was obtained by individualizing the therapy. Triglycerides and cholesterol decreased on average by 50% and 20%, respectively. The incidence of MI was 10 times higher than in the general population. With respect to the type of HLP, hypertriglyceridemia revealed a significantly higher incidence of MI compared with hypercholesterolemia and mixed HLP. The therapy variant was only of importance with respect to gallstone diseases accumulating in the CPIB-treated subgroups. We found a majority of cases with newly manifested angina pectoris and stroke in the group with moderate correction of both triglycerides and cholesterol. Patients with effective triglyceride and cholesterol correction suffered less frequently from MI than those with insufficient correction. This was also the case with secondary prevention in cases with MI prior to entry. There was no significant difference in the distribution of lipid categories at entry between those with and without recurrent infarction. In the group without reinfarction, however, the percentage with insufficient control diminished significantly. Associated risk factors such as hypertension, diabetes, smoking and obesity were of minor or no significance. In subjects with effective triglyceride correction, the total mortality was 0.97/1000 treatment months vs. 3.63 in insufficiently treated patients. The figures for MI mortality were 0.36 and 1.91, respectively.
Atherosclerosis 1984 Oct
PMID:Reduced incidence of cardiovascular complications and mortality in hyperlipoproteinemia (HLP) with effective lipid correction. The Dresden HLP study. 649 44

The incidence of fasting HLP in 326 diabetics was 68.4 percent. The common types of HLP were type IV, IIb, IIa and III respectively. There was one case of type V. HDLC was decreased in all three groups of diabetics together with elevated ratio of TC to HDLC comparing with the controls of similar age and sex VLDL and TG were significantly elevated in NIDDM aged 60 and over comparing with IDDM but not significantly different from NIDDM aged below 60. The early detection and treatment of HLP along with optimum control of blood glucose are of utmost importance to prevent further complications caused by atherosclerosis.
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PMID:Lipid disorders in Thai diabetics. 668 May 38

Changes in the rate of the plasma cholesterol ester production mediated by lecithin: cholesterol acyltransferase (LCAT, E.C. 2.3.1.43) were examined in 15 patients suffering from types II and IV HLP who had been treated for 14 weeks with etiroxate. Whereas the plasma cholesterol concentration decreased significantly only in the initial phase of the therapy, the rate of cholesterol esterification increased gradually and attained at the end of the study a value exceeding by 50% the initial level. The final fractional turnover rate nearly equalled that characteristic for the control group of healthy subjects, in spite of the fact that the concentration of plasma cholesterol in the diseased subjects was higher by 50-100%. Triglyceride concentration decreased only transitorily in the course of the therapy with etiroxate. It is concluded that etiroxate is likely to normalize the rate of cholesterol turnover in the endogenous pool.
Atherosclerosis 1982 Apr
PMID:Rate of LCAT-mediated cholesterol esterification and serum lipids during etiroxate therapy in hyperlipoproteinemia. 707 4

The effect of guar (15.6 g/day), a dietary fibre, and simultaneous administration of bezafibrate (600 mg/day) during dietetic treatment on the plasma lipoproteins and apolipoproteins was investigated in 12 patients with familial hypercholesterolemia (corresponding to the HLP type IIa pattern). Either bezafibrate alone or bezafibrate in combination with guar was administered in a cross-over study for 3 months. Guar led to an additional lowering of the total cholesterol in the plasma by 7% (P less than or equal to 0.05) associated with a fall of the low density lipoprotein cholesterol (LDL-cholesterol (LDL-cholesterol) by 13% (P less than or equal to 0.01) without any changes in the very low density lipoprotein (VLDL) and high density lipoprotein (HDL) cholesterols. In parallel with the decrease in LDL-cholesterol, the apoprotein B also was diminished by 20% (P less than or equal to 0.05). The plasma triglyceride level and the triglyceride distribution within the individual lipoprotein fractions were not altered in any consistent manner by the addition of guar. Neither the fasting plasma glucose level nor the body weight were affected. The side-effects due to guar treatment consisted of slight nausea, meteorism and constipation, but this did not in any of the cases lead to early termination of the study. These results demonstrate that guar exerts its cholesterol-lowering effect in addition to that of bezafibrate.
Atherosclerosis 1982 Dec
PMID:Treatment of familial hypercholesterolemia with a combination of bezafibrate and guar. 715

Serial liver biopsies were carried out in 67 patients with HLP and/or fatty liver before, during short- and long-term therapy with CPIB and after termination of therapy. Results (1) Decrease of liver glycogen from 4.17% to 2.69% (wet weight, P less than 0.02). (2) Insignificant changes of liver triglyceride content. (3) Significant decrease of manganese, while the concentrations of zinc and copper in the liver biopsy specimens remained unchanged. (4) No signs of liver intoxication or cancerogeneous effects of light-microscopic pictures. (5) Significant increases in numbers of mitochondria and cristae as well as a hypertrophy of endoplasmic reticulum with longer lasting therapy. (6) Striking focal proliferation of cristae mitochondriales in 3 cases on longterm treatment. (7) Regression of the mitochondrial alterations after termination of the CPIB therapy. Our findings suggest that an increased number of mitochondria and of their inner membranes in the liver cells induced by CPIB could play an important role in the hypolipidemic action of the drug.
Atherosclerosis 1980 Jun
PMID:Effects of p-chlorophenoxyisobutyric acid (CPIB) on the human liver. 740 47

Probucol was administered for 4 months in 20 adult males with Type IIb HLP in a total daily dose of 1.0 g per day. All patients had achieved a stable weight and diet response prior to entering the study. Plasma lipid and lipoprotein determinations were done at monthly intervals. Probucol produced mean reductions to TPC of -38.8 mg/dl (P < 0.0001), in LDL of -26.7 mg/dl (P < 0.001) and HDL of -8.1 mg/dl (P < 0.0001) for the entire treatment period. The mean LDL/HDL ratio increased from 5.43 to 6.08 (P < 0.02). There was no significant change in TG levels. During the study a progressive decrease in mean HDL levels from 38.9 to 29.2 mg/dl was noted. A progressive increase in the LDL/HDL ratio from 5.43 to 6.35 was also observed. These findings suggest that probucol should be used cautiously in patients with Type IIb HLP, because an inverse relationship between HDL levels and IHD incidence has been demonstrated in epidemiologic studies.
Atherosclerosis 1980 Nov
PMID:Effect of probucol on plasma lipids and lipoproteins in type IIb hyperlipoproteinemia. 745 92


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