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)

Lipoprotein patterns and cholesteryl-ester transfer activity (CETA) were examined in a patient with familial hyperalphalipoproteinemia (FHALP). The proband was a 41-year-old Japanese male. He was found to have hypercholesterolemia, with a serum total cholesterol level of 382 mg/dl and a HDL-cholesterol level of 177 mg/dl. HDL showed a high cholesterol/Apo AI ratio. His father, all of his siblings and one of his children showed high HDL-cholesterol levels (91, 100, 70, 108, 75 and 98 mg/dl, respectively). These data suggest that all members of his family were heterozygotes. He had neither cutaneous or tendinous xanthomas nor any clinical signs of atherosclerosis. The proband appears to have only one-tenth of the normal level of CETA. However, the level of lipid-transfer protein I (LTP-I) activity was near normal. Thus, this patient is most likely to have an exaggerated level of LTP-I inhibitor(s). Effects of probucol on serum lipoprotein and apolipoprotein levels were studied in our patient. Treatment with 250 mg of probucol twice daily reduced total serum cholesterol, low density lipoprotein (LDL) and HDL-cholesterol levels by 33.32 and 33%, respectively. Apo AI, B and E levels decreased by 22, 16 and 35% respectively. HDL-cholesterol/Apo AI ratio decreased from 0.9 to 0.76. CETA showed no significant changes. However, cholesterol ester mass transfer increased from 10.8 to 14.9% after treatment with probucol. These results suggest that probucol appears to be a useful drug for FHALP.
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PMID:Decreased serum cholesteryl-ester transfer activity in a patient with familial hyperalphalipoproteinemia. 319 60

Acute myocardial infarction was precipitated by hyperventilation in a 65 year old man. His coronary arteriogram in the chronic phase showed almost normal coronary arteries. Injection of acetylcholine (50 micrograms) into the left coronary artery induced spasm of the circumflex artery with chest pain in association with ST-segment elevation in the inferior leads and ST-segment depression in the precordial leads. In this patient there may have been atherosclerosis of the coronary arteries with absent or dysfunctional endothelium, despite an almost normal angiographic appearance. In the absence of endothelium the response of the smooth muscle to acetylcholine is constriction.
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PMID:Possible role of coronary spasm in acute myocardial infarction precipitated by hyperventilation. 334 64

Hyperlipoproteinemia type V, with serum triglyceride concentrations of about 20 mmol/l, was detected in a pair of monozygotic, 40-year-old twin brothers. One of them had had recurrent attacks of pancreatitis, the other not. The endocrine and exocrine pancreatic functions were apparently normal, supporting that the pancreatitis was secondary to the hypertriglyceridemia. After successful lipid-lowering therapy the attacks of abdominal pain disappeared and remained absent during a 13-year follow-up period. The other twin died of ischemic heart disease nine years after the discovery of his lipid abnormality. The reduction of his lipid levels had been much less successful. His average "atherogenic index" (the ratio of cholesterol in low density to that in high density lipoproteins) was normal but increased to a very high value if cholesterol in very low density lipoproteins was also included together with the low density ones in the numerator. Lipoprotein particles modified in composition may have contributed to an increased uptake through a scavenger pathway and promoted atherosclerosis.
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PMID:Hypertriglyceridemia--acute pancreatitis--ischemic heart disease. A case study in a pair of monozygotic twins. 359 70

A 29-year-old man with Cockayne's syndrome (CS), presenting reversible ischemic neurological deficit is reported. In his past history, hearing disturbance developed at 6 years old and visual disturbance at 12 years old. His parents have consanguinious marriage. He came to our hospital complaining of right-sided hemiparesis and speech disturbance. He was 115.8 cm tall and his weight 20 kg. The characteristic manifestation of CS, i. e., dwarfism, mental retardadation, cachectic feature, retinal atrophy, neural deafness and calcification of bilateral basal ganglia were all noticed. A CT scan on admission revealed marked brain atrophy as well as the intracranial calcifications, while no lesions compatible with his neurological findings were detected. Cerebral ischemic state was mostly suspected. Following up with conservative therapy by the use of fibrinolytic agent, his neurological deteriorations disappeared on the 4th hospital day. Cerebral angiograms showed stenotic lesions of both C1-C2 portion of the left internal carotid artery and the right middle cerebral artery, and the aneurysm in the right internal carotid artery. Such atherosclerotic vascular change as observed in the cerebral angiograms in this case have progressed rapidly for his age. In this case, diabetes mellitus and hyperlipoproteinemia such as increased total cholesterol, increased triglyceride, decreased HDL and increased apoprotein B and C II were complicated for the risk factor of the atherosclerosis. It's controversial that early progress of atherosclerosis is due to ideopathic original feature of CS or to the secondary change from these complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cockayne's syndrome presenting cerebral ischemic attack: case report]. 379 Mar 68

In a family in which both parents had the heterozygous form of familial hypercholesterolaemia four of the children had the homozygous form. The three oldest homozygous children, two of whom did not receive any treatment and in one of whom treatment did not lower the plasma cholesterol concentration, developed xanthomas in early childhood and died aged 3, 9, and 10 years. The fourth homozygous child was treated with diet and drugs from the age of 1 and at the age of 15 had no xanthomas, no clinical evidence of heart disease, and a virtually normal coronary angiogram. His plasma cholesterol concentration was reduced by about 30% but remained considerably raised. It is concluded that treatment, if started before atherosclerosis develops, can delay the onset of atheroma and coronary heart disease even though normal plasma cholesterol concentrations are not achieved.
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PMID:Treatment of homozygous familial hypercholesterolaemia: an informative sibship. 393 3

Lipoprotein patterns and cholesteryl ester transfer activity (CETA) were examined in 2 patients with familial hyperalphalipoproteinaemia (FHALP). The proband was a healthy 58-year-old Japanese male who had an HDL cholesterol of 7.83 mmol/l (301 mg/dl). His sister's HDL cholesterol was 4.52 mmol/l (174 mg/dl), which suggested that both were homozygous carriers of FHALP. In both subjects HDL showed a high cholesterol/apo A-I ratio and appeared to be a larger-sized particle than normal HDL on agarose gel chromatography. Two of the proband's children showed higher HDL cholesterol levels (1.74 mmol/l, 2.16 mmol/l) than normal, but another 2 children showed normal levels (1.48 mmol/l, 1.40 mmol/l). However, the ratios of HDL cholesterol to total cholesterol and to apo A-I in all children were higher than normal. These data suggest, but do not prove, that all his children were heterozygotes. Apo B levels in all of the family members studied were lower than normal (47-80 mg/dl). Deceased members of the same family had not died from cardiovascular disease. Cholesteryl-ester transfer activity was studied in both patients. When serum or lipoprotein deficient serum (d greater than 1.21) and [3H]cholesteryl ester labelled HDL3 were incubated in the presence of an LCAT inhibitor, there was no evidence of cholesteryl ester transfer from HDL to VLDL and/or LDL, unlike normal subjects. The deficiency of CETA in these patients with FHALP presumably accounted for the increase in particle size and cholesterol enrichment of HDL.
Atherosclerosis 1985 Dec
PMID:Deficiency of serum cholesteryl-ester transfer activity in patients with familial hyperalphalipoproteinaemia. 393 35

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

Elastin preparations from intimal layers and the media of normal and atherosclerotic human aortae were analyzed for protein and lipid content. In atherosclerotic aortae, elastin from plaques was compared with elastin from adjacent normal appearing areas of the same aorta. Arterial elastin purified by alkaline extraction appeared to be a protein-lipid complex containing free and ester cholesterol, phospholipids, and triglycerides. The lipid component of normal arterial elastin was small (1-2%). With increasing severity of atherosclerosis, there was a progressive accumulation of lipid in intimal elastin from plaques, reaching a mean lipid content of 37% in severe plaques. The increase in the lipid content of plaque elastic preparations was mainly due to large increases in cholesterol, over 80% of which was cholesteryl ester. This deposition of cholesterol in plaque elastin accounted for 20-34% of the total cholesterol content of the plaque. The increased lipid deposition in plaque elastin was associated with alterations in the amino acid composition of plaque elastin. In elastin from plaque intima, the following polar amino acids were increased significantly: aspartic acid, threonine, serine, glutamic acid, lysine, histidine, and arginine; whereas, cross-linking amino acids: desmosine, isodesmosine, and lysinonorleucine were decreased significantly. The amino acid and lipid composition of elastin from normal appearing aortic areas was comparable to that of normal arterial elastin except for intimal elastin directly adjacent to and medial elastin directly below the most severe plaques.The data indicate that the focal lipid deposition in early atherosclerotic plaques is due to a large extent to lipid accumulations in altered elastin protein of localized intimal areas. Continued lipid deposition in altered elastin appears to contribute substantially to the progressive lipid accumulation in the plaque. The study suggests that elastin of intimal elastic membranes may play an important role in the pathogenesis and progression of atherosclerosis.
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PMID:The protein and lipid composition of arterial elastin and its relationship to lipid accumulation in the atherosclerotic plaque. 509 73

We report here a peculiar case with premature corneal opacity and extremely high levels of HDL cholesterol in serum. The patient is a 54-year-old man who was first noticed to have marked corneal opacities at age 19. His serum HDL cholesterol level was elevated to the level of 135-160 mg/dl, while total serum cholesterol and triglyceride concentrations were 254 mg/dl and 56 mg/dl, respectively. Serum apoprotein A-I and E levels analyzed by single radial immunodiffusion method were elevated in the case. Serum lipoprotein fractions isolated by preparative ultracentrifugation revealed that increased levels of HDL cholesterol were accounted for solely by the HDL2 fraction. HDL2 of the patient contained relatively higher amounts of apoprotein E than normal control HDL2. Elution profiles of lipoproteins in high performance liquid chromatography revealed that HDL2 particles from the patient were larger in size than those from normal controls. These characteristics of HDL are in part similar to those of HDLC which appears in experimental animals after cholesterol feeding. Such abnormalities in HDL2 fractions associated with premature corneal opacity have not been reported so far and appear to constitute a new disease entity.
Atherosclerosis 1984 Nov
PMID:Marked hyper-HDL2-cholesterolemia associated with premature corneal opacity. A case report. 651 75

A lot of over 60 atherosclerotics with clinical manifestations of senile depressive illness was studied comparatively with a lot of subjects of the same age with essential arterial hypertension (EAH). As concerns the behaviour of the catecholamine content in CSF and blood, the total catecholamines are approxiately equal in the two lots, but with a clear difference of the catecholamine fractions. The CSF catecholamines behaviour in old atherosclerotics is characterized by the presence of increased values of noradrenaline (NA) and of adrenaline (A), with increased statistical significance, but without modifications of the adrenaline percentage (A %) from the total catecholamines, comparatively to the values found in normal subjects. The serotonin (5-HT) content of the CSF in men with atherosclerotic senile depressive illness was lower even than in subjects with coronary atherosclerosis. In atherosclerosis protides modifications precede the histologic changes. In CSF, GLU, ALA, TYR increase in old subjects. In blood, GLU, ALA, TYR, HIS, LEU, SER increase in the same subjects. ARG decreases with age. THR is higher in men than in women. In the urine of all the men as well as of all the women of more than 60 years, GLN and ALA have increased values. LYS increases with age. GLN and ARG are higher in men than in women.
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PMID:Pattern of the cerebrospinal fluid (CSF) and blood biogenic amines and of the CSF, blood and urine amino acids as pathogenetic ground of the senile depressive illness. 677 91


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