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)

The fatty acid profiles of plasma phospholipids have been compared in 53 elderly subjects suffering from malnutrition (group U, 17 subjects) or from atherosclerosis (group A, 15 subjects). A control group was also included in the study (group C, 21 subjects). Main differences were observed in phosphatidylcholine (PC). In group U, the proportion of monounsaturated fatty acids increased in PC, which was reflected by an increase in unsaturated fatty acids without significant modification of essential fatty acids. In group A, no major modification has been observed statistically, although the proportion of saturated fatty acids tended to increase.
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PMID:Effects of malnutrition and atherosclerosis on the fatty acid composition of plasma phospholipids in the elderly. 928 66

Lysosomal acid lipase (LAL) deficiency leads to two phenotypically different diseases: cholesteryl ester storage disease (CESD) and Wolman's disease. Lysosomal acid lipase hydrolyzes cholesteryl esters and triglycerides. Deficiency of LAL results in intralysosomal storage of cholesteryl esters and triglycerides. CESD has a chronic and benign course and is characterized by hepatomegaly and mild hypercholesterolemia. It leads to fibrosis (cirrhosis) and early atherosclerosis. This report presents the clinical, biochemical and microscopic data of seven patients with CESD followed up over 10 years. The physical development of all the study children remained within the normal range; 7 patients had hepatomegaly and 6 also had splenomegaly. Three patients had normal cholesterol, triglycerides and transaminases values; the other four had slightly elevated levels for these parameters. The activity of LAL in all patients was reduced to below 30% of the lower normal value. Histologically, cholesteryl crystals and lipid storage vacuoles in Kupffer cells were present in all examined patients except one. Accumulation of cholesteryl esters was visible on thin-layer chromatography of lipid extracts obtained from liver biopsies.
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PMID:Clinical, biochemical and histological analysis of seven patients with cholesteryl ester storage disease. 944 50

Prostatic atrophy (PA) is one of the most frequent mimics of prostatic adenocarcinoma. It occurs almost exclusively in the peripheral zone of the gland and gained importance with the increasing use of needle biopsies for the detection of prostatic carcinoma The etiopathogenesis is unknown, and there is controversy related to the potential of PA as a precancerous lesion. The frequency increases with age. Compressions caused by hyperplastic nodules, inflammation, hormones, nutritional deficiency, or systemic or local ischemia, are all possible factors in the pathogenesis of PA. The peripheral zone of the prostate was step-sectioned and totally embedded from the bodies of 100 consecutively autopsied men more than 40 years of age. The fragments were microscopically studied for presence of PA, latent (histologic) carcinoma, high-grade prostatic intraepithelial neoplasia, local arteriosclerosis, and prostatitis. The prostates were macroscopically examined for the presence of nodular prostatic hyperplasia. The autopsy reports provided information concerning the presence of generalized atherosclerosis and benign or malignant nephrosclerosis. PA was seen in 85 of the 100 prostates examined and histologically was subtyped into simple, hyperplastic, and sclerotic atrophy. In 65 (76.47%) of 85 cases, the histologic subtypes were combined. In 33 (50.76%) of these 65 cases, the three subtypes were seen concomitantly, favoring the hypothesis that they represent a morphologic continuum of only one lesion. Fibrosis of the stroma may or may not be present in simple and hyperplastic atrophy. Hyperplastic atrophy associated with fibrosis of the stroma is the histologic subtype that most frequently mimics adenocarcinoma Sclerotic atrophy always presents fibrosis of the stroma. PA increases with age, and, in our study, ischemia caused by local intense arteriosclerosis seems to be a potential factor for its etiopathogenesis. Because there was no relation to latent (histologic) carcinoma or high-grade prostatic intraepithelial neoplasia, PA is probably not a premalignant lesion.
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PMID:Prostatic atrophy: an autopsy study of a histologic mimic of adenocarcinoma. 955 22

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two etiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilisation, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin-resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons: i.e. non insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing: mainly neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism--whose non response to dexamethasone suppression test appears the simplest marker--may concern immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycemia, hyperlipidemia, atherosclerosis, disturbances in mood and mental performances through accelerated hippocampal ageing particularly. Treatment of magnesium deficiency requires simple oral physiological magnesium supplementation. Treatment of the different types of magnesium depletion leads to a more or less specific control of pathophysiological disturbances of the required magnesium substrate. Open and double blind studies on the effects of the treatments of magnesium deficiency and of magnesium depletions in geriatic populations are too scarce. Further study is necessary to assess the accurate place of magnesium deficit in the physiopathology of ageing.
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PMID:Magnesium status and ageing: an update. 959 47

Evidence continues to accumulate on the importance of neutrophils (PMNs) and phagocytes in the causation of tissue and endothelial injury that frequently accompanies the inflammatory response. Increased production of superoxide anions in combination with decreased endothelial antioxidant activity may contribute to the development of vascular disease including atherosclerosis, vasospasm, diabetic vascular complications, tissue damage in ischemia-reperfusion, and hypotension. Free radicals generated in the vascular wall may act directly on smooth muscle or interact with each other thus producing biologically active endogenous mediators. Derangement of macrophage function may occur in conditions characterized by protein malnutrition, thus leading to failure to develop a specific immunoresponse and to an increase in the production of oxygen intermediate radicals, which may cause tissue damage. A local inflammatory response followed by endothelial cell activation could also facilitate migration of immunocompetent cells into the parenchyma of grafted organs and stimulate dendritic cells in the graft. There is now convincing evidence that excessive and prolonged production of NO contributes to tissue damage in septicemia, ischemia/reperfusion injury, and other inflammatory conditions. There is also increasing evidence that the complement system plays an important role in tissue damage in association with phagocytes, e.g., in ischemia/reperfusion injury, carcinogenesis, and aging. It can therefore be surmised that phagocytic cells may act both as "friends" and as "foes" and that they are important mediators of tissue damage in a variety of conditions.
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PMID:Host tissue damage by phagocytes. 970 69

Serum lipoproteins including lipoprotein(a), Lp(a), are emerging as possible biological markers for cerebrovascular disease. Existing data on Lp(a) and serum lipids levels following acute ischemic stroke (AIS) are however equivocal. To determine whether serum Lp(a) and other lipid levels obtained within 24 h of acute ischemic stroke onset changed over the ensuing 4 weeks and whether these levels are related to an acute phase response, acquired nutritional deficiency, and neurovascular data, we conducted repeated measurement analyses among 19 subjects (mean age 65.0 +/- 12.1 years; 32% women) presenting with AIS (evaluated within 9.7 +/- 12.7 h). Eleven of the subjects had a moderate-to-severe stroke, defined by NIH stroke severity scale, and seven patients had a large cerebral infarction. Seven serial measurements of Lp(a), total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, and other lipoproteins, major acute phase reactants and albumin levels were collected for each subject over 4 weeks. The mean initial levels, (mg/dl), of total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, Lp(a), apolipoproteins A-I and B were: 225 +/- 57.6, 154 +/- 56.0, 40 +/- 10.4, 181 +/- 93.7, 52 +/- 28.6, 130 +/- 24.6, and 141 +/- 46.1, respectively. There were no significant changes in mean serum lipid, apolipoprotein or Lp(a) levels over the 4-week study period, analyzed by a random effects model to test for time trend. In addition, there were no significant changes in established acute phase or nutritional markers (C-reactive protein, alpha 1-glycoprotein, haptoglobin or serum albumin). Our findings suggest that serum lipid, apolipoprotein and Lp(a) levels remain stable following AIS, consistent with the absence of acute phase response or nutritional deficiency.
Atherosclerosis 1998 Aug
PMID:Lipid and lipoprotein levels remain stable in acute ischemic stroke: the Northern Manhattan Stroke Study. 971 47

Malnutrition and hypoalbuminemia, which are prevalent in patients with end-stage renal disease (ESRD), are strong predictors of increased mortality. However, cardiovascular disease predominates among direct causes of death, whereas malnutrition appears to be of minor importance in this respect. Reports in the literature demonstrate that cardiac failure may cause malnutrition and that infection/inflammation may predispose to atherosclerosis as well as to catabolism and hypoalbuminemia. Proinflammatory cytokines, generated in response to cardiac failure, infection, and other inflammatory stimuli, appear to play a pivotal role by causing muscle wasting, hypoalbuminemia, and anorexia as well as reduced cardiac contractility and atherosclerotic vascular disease. We hypothesize that this scenario also applies to ESRD patients, in whom congestion, hypertension, cardiac failure, and ischemic cardiovascular disease are common. Malnutrition rarely may be the direct cause of death, except in elderly dialysis patients, but may contribute to a poor prognosis by aggravating pre-existing heart failure and increasing the susceptibility to infections.
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PMID:Malnutrition, cardiac disease, and mortality: an integrated point of view. 982 Apr 57

Malnutrition, inflammation and atherosclerotic cardiovascular disease occur at high prevalence, and often concomitantly, in conjunction with chronic renal failure. Several features of malnutrition (e.g., increased oxidative stress, increased plasma levels of fibrinogen, Lp(a), and inflammation) may all, alone or in concert, increase the risk of cardiovascular disease. Recent findings suggest malnutrition and hypoalbuminaemia in chronic renal failure to be largely the consequence of such factors as heart failure, chronic infection and inflammation, that simultaneously trigger the development of atherosclerotic cardiovascular disease. Central to this scenario is the involvement of proinflammatory cytokines which may cause muscle wasting, hypoalbuminaemia, anorexia, and accelerated atherosclerosis. It is unlikely that the high mortality due to atherosclerotic disease among patients with chronic renal failure can be substantially reduced unless new treatment strategies are developed which address the complex relationships that exist between malnutrition, inflammation and cardiovascular disease.
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PMID:[Strong connection between malnutrition, inflammation and arteriosclerosis. Improved treatment of renal failure if underlying factors are attacked]. 1057 60

Many factors, both intrinsic and extrinsic, may contribute to wound recalcitrance. For example, arterial circulation may be impaired by atherosclerosis, vasospastic disorders, microemboli, thromboangiitis obliterans, vasculitis, sickle cell anemia, and antiphospholipid syndrome, all of which may impair healing. Inflammatory disorders that may lead to recalcitrance include pyoderma gangrenosum and necrobiosis lipoidica. Chronic venous insufficiency, infection, diabetes mellitus, systemic malignancy, malnutrition, and exposure to pressure and shear prolong the healing process. Wounds secondary to primary skin carcinoma will not heal. Calciphylaxis, a life-threatening metabolic disorder, leads to multiple ulcerations that are especially difficult to heal. Knowledge of common factors that lead to wound recalcitrance is essential to the wound care clinician, as accurate diagnosis results in appropriate treatment. To arrive at the diagnosis, the wound care clinician must perform a thorough history and physical examination and order relevant investigative studies. Treatment is based on correction of the identified underlying condition. By utilizing a systematic approach in the management of each patient with a chronic wound, the wound care clinician increases the probability of achieving wound closure.
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PMID:Considerations for the global assessment and treatment of patients with recalcitrant wounds. 1073 37

Cardiovascular complications caused by an accelerated atherosclerotic disease represent the largest single cause of mortality in chronic renal failure patients. The rapidly developing atherosclerosis of the uremic syndrome appears to be caused by a synergism of different mechanisms, such as malnutrition, oxidative stress and genetic factors. Recent studies provide evidence that chronic inflammation plays an important role in the pathogenesis of cardiovascular diseases. Elevated serum levels of plasma C-reactive protein (CRP) are associated with an increased risk of experiencing myocardial infarction and sudden cardiac death in apparently healthy subjects. Several recently published papers have confirmed this strong association between CRP and the extent and severity of the atherosclerotic processes. In patients affected by predialytic renal failure, increased levels of CRP and interleukin (IL)-6 were recorded in 25% of our population; CRP and IL-6 were inversely related with renal function. These data suggest the activation - even in the predialytic phase of renal failure - of mechanisms known to contribute to the enhanced cardiovascular morbidity and mortality of the uremic syndrome. In recent years we have investigated the hypothesis that the chronic inflammatory state of the uremic patient could at least in part be due to the dialytic technique. We provide evidence suggesting that the increase of CRP in stable dialytic patients may be due to the stimulation of monocyte/macrophage by backfiltration of dialysate contaminants.
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PMID:C-reactive protein as a marker of chronic inflammation in uremic patients. 1085 21


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