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)

Lp(a) has been considered as an independent risk factor for atherosclerosis, mainly for coronary heart disease. Recent epidemiologic studies have demonstrated elevation of Lp(a) serum concentration in diabetes mellitus. Atherosclerosis is the most common cause of death in diabetic patients, but there is little information available concerning the importance of Lp(a) in these patients. We investigated the relationship between Lp(a) serum concentration and the presence of chronic diabetic complications. Lp(a) was determined in 14 IDDM patients and 62 NIDDM patients. Median Lp(a) serum concentration in diabetics was 21.8 mg/dl, which was significantly higher than in nondiabetic controls described before. Glucose, HbA1c, fructosamine, total cholesterol, triglycerides, HDL-cholesterol, apolipoprotein A1, B and E were not associated with raised Lp(a) values. With increasing Lp(a) levels, higher prevalences of retinopathy and of albuminuria were observed. We conclude that in diabetic patients, Lp(a) levels are elevated compared with non-diabetic subjects, and that higher Lp(a) levels are associated with higher prevalences of retinopathy and of albuminuria.
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PMID:[Lp(a) serum concentrations in diabetes mellitus]. 786 92

Small concentrations of albumin detected in the urine predict renal dysfunction and reflect vascular abnormalities such as atherosclerosis, retinopathy and, probably, neuropathy. Although microalbuminuria is not specific for diabetic complications, it has been most extensively studied in diabetics. The rate of urinary albumin excretion can also be used to determine therapeutic response to pharmacologic and lifestyle interventions such as diet, smoking cessation and physical activity. The pathophysiology of microalbuminuria and its clinical significance in diabetes is presented, along with a discussion of measurement issues and implications for clinical management. An algorithm for the evaluation of diabetic patients is included.
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PMID:Microalbuminuria and diabetes mellitus. 824 73

To determine whether young patients with IDDM already have atherosclerosis and what factors would relate to atherosclerosis, we examined the intimal-medial thickness (IMT) of the common carotid artery by ultrasonography. Subjects were 29 young patients with IDDM (aged 17-39 years, duration 4-31 years) without manifest macroangiopathy and 13 healthy controls of comparable age (22-29 years). The carotid artery IMT of young patients with IDDM were significantly higher than those of controls (0.60 +/- 0.09 vs. 0.46 +/- 0.02 mm, P < 0.0001). The levels of IMT significantly correlated to diastolic blood pressure (r = 0.45, P < 0.02), and were higher in those with proliferative retinopathy than those without retinopathy (0.66 +/- 0.09 vs. 0.55 +/- 0.08 mm, P < 0.02). The levels of IMT showed no significant correlation to the attained age, duration of IDDM, HbA1c, systolic blood pressure, and cholesterol level. These findings suggest the usefulness of this examination for the early detection of diabetic macroangiopathy, and point to a close relationship between microangiopathy and macroangiopathy in IDDM.
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PMID:Carotid atherosclerosis in young-aged IDDM associated with diabetic retinopathy and diastolic blood pressure. 826 16

We report a Canadian kindred with a novel mutation in the apolipoprotein (apo) A-I gene causing analphalipoproteinemia. The 34-yr-old proband, product of a consanguineous marriage, had bilateral retinopathy, bilateral cataracts, spinocerebellar ataxia, and tendon xanthomata. High density lipoprotein cholesterol (HDL-C) was < 0.1 mM and apoA-I was undetectable. Genomic DNA sequencing of the proband's apoA-I gene identified a nonsense mutation at codon [-2], which we designate as Q[-2]X. This mutation causes a loss of endonuclease digestion sites for both BbvI and Fnu4HI. Genotyping identified four additional homozygotes, four heterozygotes, and two unaffected subjects among the first-degree relatives. Q[-2]X homozygosity causes a selective failure to produce any portion of mature apoA-I, resulting in very low plasma level of HDL. Heterozygosity results in approximately half-normal apoA-I and HDL. Gradient gel electrophoresis and differential electroimmunodiffusion assay revealed that the HDL particles of the homozygotes had peak Stokes diameter of 7.9 nm and contained apoA-II without apoA-I (Lp-AII). Heterozygotes had an additional fraction of HDL3-like particles. Two of the proband's affected sisters had documented premature coronary heart disease. This kindred, the third reported apoA-I gene mutation causing isolated complete apoA-I deficiency, appears to be at significantly increased risk for atherosclerosis.
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PMID:Apolipoprotein A-I Q[-2]X causing isolated apolipoprotein A-I deficiency in a family with analphalipoproteinemia. 828 91

Antihypertensive treatment in the diabetic patient is a critical issue because hypertension has an impact on all of the vascular complications of diabetes, including nephropathy, retinopathy, atherosclerosis, and left ventricular hypertrophy. These complications are a consequence of altered endothelial-vascular smooth muscle interrelations that ultimately enhance vasoconstriction and alter the remodeling processes in the vascular wall. Several observations suggest that the renin-angiotensin system (RAS) may be an important contributor to these processes in diabetes mellitus. In both animal and human studies, angiotensin-converting enzyme (ACE) inhibitors have been demonstrated to slow the progression of glomerulosclerosis, prevent abnormal remodeling processes in the heart following injury, and slow the progression of atherosclerosis. In particular, ACE inhibitors appear to protect the kidney more than would be expected from simply the lowering of blood pressure and decreasing of intraglomerular pressure, possibly because angiotensin II has both hemodynamic and direct effects on the glomerulus. Paradoxically, however, the activity of the circulating RAS is low in diabetic patients. Part of these seemingly inconsistent observations may be due to (1) potential activity of tissue RASs, (2) increased sensitivity to angiotensin II in diabetes, or (3) an effect of ACE inhibition on other systems in addition to the RAS. Investigation of these mechanisms will be important in determining the therapeutic role of inhibition of the RAS in diabetes mellitus.
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PMID:Systemic hypertension and the renin-angiotensin system in diabetic vascular complications. 828 77

Advanced glycosylation end products (AGEs) are a potentially useful marker for monitoring glycemic control, predicting the risk of diabetes- and aging-associated clinical complications, and monitoring the treatment of patients with micro- and macrovascular diseases, including retinopathy, atherosclerosis, nephropathy, and neuropathy. AGEs or AGE-proteins are derived from nonenzymatically glycated proteins (Amadori products) after further cross-linking with other proteins and additional rearrangement. AGE-proteins can be assayed by either radioreceptor or immunoassays in blood and tissues. No commercial kit is available at this time.
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PMID:Advanced glycosylation end products: a new disease marker for diabetes and aging. 841 Apr 84

The hallmark of diabetes mellitus, whether type I or type II, is hyperglycemia. Clinical complications associated with diabetes are most likely the consequence of hyperglycemia via both altered metabolic pathways and nonenzymatic glycation of proteins. The nonenzymatic glycation of proteins is accelerated in diabetes due to elevated blood glucose concentration. The Amadori product of nonenzymatic glycation will further cross-link with other proteins to form advanced glycosylation end products (AGEs). The reaction of AGEs with long-lived proteins, such as collagen, and the uptake of AGEs by the receptors on macrophages, endothelial cells, and platelets are major reasons for the development of various clinical complications in diabetes. Several markers have been identified for the screening, diagnosis, and monitoring of the disease. Autoantibodies against beta cells are the best markers for mass screening and for early detection of type I diabetes. In addition to glycated hemoglobin, AGEs and blood glycated proteins of various half-lives could be used for monitoring glycemic control. Several abnormal metabolites have been identified as potential markers for monitoring the severity of various clinical complications. The most interesting findings in diabetic markers could be AGEs. The amount of AGEs found in the tissues could be related to the extent of micro- and macrovascular damage and might prove useful for monitoring the treatment of patients at early stages of either nephropathy, atherosclerosis, retinopathy, or neuropathy.
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PMID:Review of diabetes: identification of markers for early detection, glycemic control, and monitoring clinical complications. 841 Apr 89

Recently, a high plasma level of lipoprotein(a) [LP(a)] has been considered an independent risk factor for atherosclerosis and its sequelae, particularly myocardial infarction. Patients with non-insulin-dependent diabetes mellitus (NIDDM) have an increased mortality rate from cardiovascular and cerebrovascular disease. Therefore, plasma concentrations of Lp(a) were determined and the relationship between fasting plasma Lp(a) level and diabetic control was investigated in NIDDM patients without any diabetic complications. Fasting plasma Lp(a) levels were measured using enzyme-linked immunosorbent assay kits [Terumo Medical Corp, Elkton, MD, Lp(a)] in 61 NIDDM subjects (30 men aged 56 +/- 2.0 years, 31 women aged 53 +/- 2.1 years [mean +/- SEM]) who were without any diabetic macroangiopathy and microangiopathy such as retinopathy, nephropathy, and neuropathy and in 56 healthy age- and sex-matched controls. Plasma Lp(a) levels were significantly higher in the diabetic group than in the control group (23.5 +/- 2.5 v 11.7 +/- 1.4 mg/dL [mean +/- SEM], P < .001). There was no significant correlation between log-transformed plasma Lp(a) levels and other factors such as age, sex, body mass index (BMI), blood pressure, duration of diabetes, fasting plasma glucose (FPG) level, glycosylated hemoglobin (HbA1C) level, and plasma lipid levels except for low-density lipoprotein cholesterol (LDL-C) levels in diabetic patients. A significant positive correlation was noted in diabetic patients between the changes of log Lp(a) and HbA1C levels after a 3-month follow-up period (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alteration of lipoprotein(a) concentration with glycemic control in non-insulin-dependent diabetic subjects without diabetic complications. 841 45

Epidemiologic studies have identified lipoprotein(a) (Lp(a)) as an independent risk factor for atherosclerosis, mainly for coronary heart disease. Atherosclerosis is the most common cause of death in diabetic patients, but there is little information available concerning the importance of Lp(a) in these patients. We compared the presence or absence of late diabetic complications with Lp(a) serum concentrations in 224 patients (82 IDDM, 142 NIDDM). Lp(a) distribution was skewed as described for non-diabetic patients. Despite highly significant differences for total cholesterol, total triglycerides, HDL-cholesterol, VLDL-cholesterol and VLDL-triglycerides (P < 0.001) and for LDL-cholesterol (P < 0.01) Lp(a) concentrations were similar in NIDDM and IDDM (mean: 27 vs. 30, median: 12 vs. 21 mg/dl, P = 0.10). Diabetic polyneuropathy, autonomic neuropathy, nephropathy, peripheral occlusive disease, diabetic gangrene and coronary heart disease were not associated with raised Lp(a) values. Non-insulin-dependent patients with retinopathy exhibited higher Lp(a) concentrations in serum than those without this complication. This significant association was lost when duration of diabetes was taken into account by logistic regression. We conclude, that other risk factors surpass the significance of Lp(a) in diabetic patients.
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PMID:Lipoprotein(a) in diabetes mellitus. 845 77

Many neurological disorders have been described in combination with sensorineural hearing loss and pigmentary retinopathy. We present the clinicopathological case of such a combination, associated with premature atherosclerosis of large cerebral arteries. In the literature dealing with the combination of deafness and pigmentary retinopathy, none of the many described syndromes was associated with premature atherosclerosis. The mitochondrial myopathy, encephalopathy, lactic acidosis, early atherosclerosis and stroke-like episodes (MELAS) syndrome can include deafness and blindness. In this syndrome small cerebral arteries are affected. In our case we did not find electron microscopic evidence of mitochondrial myopathy. Also the syndrome with encephalopathy, deafness, blindness and ataxia in young women is attributed to microangiopathy with small brain infarcts and retinal infarcts. In contrast, in our case, large cerebral arteries are affected. In the reverse order, none of the conditions with early atherosclerosis has been reported in combination with sensorineural deafness and pigmentary retinopathy. There is some similarity of our case to cases of Usher syndrome, type II. In the Usher syndrome, plasma lipid disturbances have been described and neuroradiological evidence of decreased circulation in the posterior cerebral circulation has been published. We suggest that in cases of congenital or acquired oto-ophthalmo-neurological disease the cerebral circulation and the lipid metabolism should be analyzed.
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PMID:A congenital syndrome of mental deficiency, gait disturbance, sensorineural deafness and pigmentary retinopathy associated with premature atherosclerosis. 852 24


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