Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review, the cardiac lesions which develop in association with the various collagen-vascular diseases are described. In rheumatoid arthritis, the most frequent lesions are: fibrous obliterative pericarditis, with pericardial deposits of calcium, fibrin, cholesterol, and rheumatoid granulomas; granulomatous or nonspecific myocarditis; valvulitis, vasculitis, and amyloid deposits. In ankylosing spondylitis, the lesions involve mainly the valves (aortic and mitral valves) and the aorta. In systemic lupus erythematosus, the predominant cardiovascular lesions are: pericarditis, Libman-Sacks endocarditis, nonspecific myocarditis, vasculitis with fibrinoid necrosis, and acceleration of atherosclerosis. In scleroderma, the main cardiac lesion is fibrosis with only scanty inflammatory cells; pericarditis and nonbacterial thrombotic endocarditis also occur. In dermatomyositis/polymyositis, fibrous or fibrinous pericarditis can occur, as well as myocarditis with infiltrates of lymphocytes and plasma cells and with degeneration and necrosis of myocytes; valvulitis is uncommon except when the disease is related to mucinous adenocarcinoma. In polyarteritis nodosa, various stages of necrotizing vasculitis involve all layers of the arterial walls; foci of myocardial necrosis of various sizes can occur in association with these lesions; cardiac hypertrophy related to hypertension and pericarditis related to uremia, may also be found. In Wegener's granulomatosis, pericarditis, inflammatory infiltrates, necrotizing granulomas, and vasculitis have been observed in the heart.
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PMID:Cardiovascular lesions in collagen-vascular diseases. 391 76

A 30-year-old man presented at the diagnosis of an insulin dependent diabetes mellitus with pronounced and multiple complications, such as retino-, nephro-, dermo- and neuropathy. His diabetes had a malignant course and he died from uremia within one year after diagnosis. There were no signs of atherosclerosis at autopsy but in several organs there were pronounced diabetic small vessel lesions.
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PMID:Malignant diabetes mellitus--a case report. 400 39

A defect in cholesterol transport was detected in patients with uremia who were receiving long-term hemodialysis when the rate of cholesterol transfer (RCT) from high-density lipoprotein (HDL) to very low-density (VLDL) and low-density lipoproteins (LDL) was compared with that in controls. The RCT (mean +/- SD) in 29 men with uremia (1.85 +/- 1.29 mg/hr/100 ml) and 11 women with uremia (1.84 +/- 1.00 mg/hr/100 ml) was significantly lower (P less than 0.001) than values in 55 healthy men (4.50 +/- 2.61 mg/hr/100 ml) and 23 healthy women (3.72 +/- 1.92 mg/hr/100 ml), respectively. Six patients, but none of the controls, totally lacked the ability for cholesterol transfer. The decreased RCT of the patients could not be completely accounted for by their decreased HDL cholesterol levels, because patients matched with controls for HDL cholesterol within 1 mg/100 ml also had lower RCT (P less than 0.0025). Recombination and crossover of serum fractions of patients and controls separated by ultracentrifugation revealed that the defect in cholesterol transfer of the patients was in the d greater than 1.063 gm/ml fraction (containing HDL and other serum proteins), which not only contained less HDL cholesterol, but was also qualitatively inferior as donor for cholesterol transfer. In one of four patients studied, the d less than 1.063 gm/ml fraction (VLDL and LDL) also had deficient ability to accept cholesteryl esters in the transfer. These in vitro data indicate a defect in cholesterol transport in the patients who are undergoing hemodialysis. Whether this defect exists in vivo and creates the risk of accelerated atherosclerosis warrants further study.
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PMID:Defect in cholesterol transport in patients receiving maintenance hemodialysis. 400 22

A new dyslipoproteinemic state, characterized by two populations of very low density lipoprotein particles giving the electrophoretic appearance of two pre-beta bands, the double pre-beta lipoproteinemia, is described. Based upon the lipid and apoprotein composition, it can be inferred that the slow moving pre-beta component is probably made up of remnant very low density lipoprotein particles; the absence of apo B 48 in the very low density lipoprotein fraction in these subjects rules out the intestinal origin of this remnant. Clinical interest in the double pre-beta lipoproteinemia relates to its potential atherogenicity; in fact it seems to be causally associated with such pathological conditions as hypothyroidism, uremia and dialysis, which are frequently accompanied by clinical complications of atherosclerosis. Double pre-beta lipoproteinemia also shows familial aggregation. Six years follow-up in a large family kindred has demonstrated that the family members carrying the double pre-beta lipoproteinemia, develop an incidence of coronary and cerebrovascular events higher than that of family members without the double pre-beta lipoproteinemia.
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PMID:The double pre-beta very low density lipoprotein lipoproteinemia (DPBL): a new dyslipoproteinemic state. 408 82

Three labile diabetic patients had recurring episodes of altered sensorium. Each had severe cerebrovascular disease with superimposed metabolic derangements, including ketoacidosis, hyperglycemia without ketosis, mild uremia, and possibly cerebral edema. Two of the patients were examined postmortem. Severe leptomeningeal scarring, basal ganglial calcification and destruction of small intracerebral vessels without evidence of large vessel atherosclerosis were found unexpectedly in one patient, a rare occurrence in this country although recently reported from Europe. The other patient had large vessel atherosclerosis only. The clinical expression of the vascular disease was modified by concurrent abnormalities and reflected the sum total of the complexities which coexisted. The pathophysiology of the unconscious state necessarily depends on the inciting factors. Ketoacidotic coma is associated with depressed cerebral oxygen consumption. Spinal fluid pH is usually maintained during ketosis but is sometimes lowered inadvertently during bicarbonate therapy, with resultant coma. Other variables influencing the clinical expression, with or without ketosis, would include, among others, blood viscosity alterations, rapid decrements in blood sugar, and existing degrees of lactic acidosis. The increasing life-span of the juvenile diabetics, favorably influenced by improved management and recently by hemodialysis, may uncover vascular complications heretofore rarely seen and create additional diagnostic and therapeutic enigmas.
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PMID:Cerebral syndromes of diabetes mellitus. 579 97

The generation of thromboxane B2 (TxB2) from its natural precursor, arachidonic acid, was studied in vitro in order to assess further the prostaglandin pathway in the platelets of patients with chronic renal failure. Some, but not all patients with conservatively treated uraemia synthesised significantly less TxB2 then controls and the same patients were also hypo-aggregable to arachidonic acid. The synthesis of TxB2 appeared normal in a group of patients on chronic ambulatory peritoneal dialysis (CAPD). In contrast, a group of patients on long-term maintenance haemodialysis produced significantly greater amounts of TxB2 and were hyper-aggregable to arachidonic acid, a finding which may be relevant to the high incidence of atherosclerosis and vascular disease in these patients.
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PMID:Synthesis of thromboxane B2 in uraemia and the effects of dialysis. 686 24

Atherosclerosis in 50 nondiabetic patients undergoing hemodialysis was assessed at the time of renal transplantation by intraoperative examination and histologic evaluation of the iliac vasculature. Patients were grouped accordingly: minimal (group 1), moderate (group 2) or severe (group 3) atherosclerosis. Sixty-two per cent of the patients had atherosclerosis, half of them with severe involvement. No sex differences were noted. There was a significant correlation between the patient's age and the degree of atherosclerosis (p less than 0.02). Thirty-five per cent of the patients under 30 years of age had atherosclerosis whereas similarly studied nonuremic control subjects had no atherosclerosis. Metabolic and lipid abnormalities, and duration of hemodialysis did not correlate with degree of atherosclerosis. Hypertension was present in 90 per cent of the patients in groups 2 and 3. When patients between the ages of 25 and 40 years were selected, atherosclerosis was present only in previously hypertensive patients (p less than 0.02). Atherosclerosis may not be accelerated by hemodialysis and may be prevented by more stringent control of hypertension in uremia.
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PMID:The role of hypertension in hemodialysis-associated atherosclerosis. 2665 40

The ways by which uremia may lead to atherosclerosis are still unknown. Furthermore, whether atherosclerosis is accelerated with prolonged hemodialysis is still under debate. The results of a longitudinal study carried out in 47 selected patients who were treated first with dietary regimen followed by dialysis and then transplantation indicate: 1) The longer the duration of uremia on low protein diet, the worse are the clinical and metabolic problems of atherosclerosis. 2) In subsequent regular dialysis treatment 2 distinct clinical and metabolic pictures may emerge, slowly progressive or comparatively accelerated, according to whether dialysis is initiated early or late. 3) In subsequent transplantation the avoidance of risk factors largely depends on the time at which regular dialysis begins. 4) Early direct transplantation without dialysis proves similar to transplantation in patients treated with early dialysis as far as prevention of accelerated atherosclerosis is concerned.
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PMID:Atherosclerosis in uremia: a longitudinal study. 699 73

Concentrations of peptidic compounds in blood plasma of uremics are increased. Evidence for participation of intestinal bacteria in the production of such peptides (presumably toxic) was obtained by isolation of a strongly basic peptide containing covalently bound spermidine from peritoneal dialysate of patients with chronic uremia. The same peptide was found in blood plasma of patients with end-stage chronic renal failure. The absence of glutamic acid in the spermidinepeptide molecule suggests that an enzyme different from the transglutaminase of mammalian cells must take part in the synthesis of spermidinepeptide. This conjugate forms a relatively stable complex with insulin, thus altering the action of the hormone on adipose cell metabolism. Also, interaction of spermidinepeptide with insulin and lipoproteins may contribute to hypertriglyceridemia and accelerated atherosclerosis in patients with chronic uremia.
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PMID:A uremic peptide containing polyamine: formation and possible role in uremic hypertriglyceridemia. 701 Mar 92

The development of experimental atherosclerosis was studied in subtotally nephrectomized rats which were subjected to preimmunization with horseradish peroxidase and subsequent feeding with atherogenic diet. Both in sham-operated pair-fed control animals and in uremic animals, the atherogenic diet caused hyperlipemia which was more pronounced in uremic than in control animals (control animals: triglycerides 1.11 +/- 0.04 mmol/l; cholesterol 5.82 +/- 0.21 mmol/l; uremia: triglycerides 1.33 +/- 0.06; cholesterol 10.9 +/- 0.31). An increase of cholesterol was seen both in the VLDL and in the LDL fractions. Despite more pronounced hyperlipemia, lipid concentration in the aortic wall was not increased nor were more marked histological abnormalities encountered in the aorta of uremic animals (cholesterol-fed control: cholesterol 95.4 +/- 4.4 micrograms/mg protein; phospholipids 2.42 +/- 0.9 micrograms/ml protein; cholesterol-fed uremia: cholesterol 96.8 +/- 4.9; phospholipids 2.52 +/- 0.8). The results suggest that despite hyperlipemia short-term experimental renal insufficiency does not promote atherogenesis.
Atherosclerosis
PMID:Atherogenesis in experimental uremia. 733 7


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