Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1) In two patient with excessive hyperlipidemia diet in the post-partum days resulted in a rapid reduction of the high neutral fats in the serum which were 6,150 mg/dl and 6,290 mg/dl respectively. In one patient the hyperlipidemia was reduced by diet during the pregnancy. The course of the pregnancies and the puerperium were uneventful. Complications during delivery were not related to the hyperlipidemia. Coagulation defects were not tested.--2) Excessively high serum lipid values of the mother only had a minor influence on the serum lipid values of the mother only had a minor influence on the serum lipid values of the infants. The infants had slightly elevated values compared to controls. One infant was tested at age 7 months and showed definitely elevated lipids with higher values than neonatally. A familial hyperlipidemia was confirmed in this case.--3) The milk fat values (Total Cholesterol and Neutral fats) were not influenced by the hyperlipidemia. Breast feeding was therefore safe.--4) Both infants of the mothers with hyperlipidemia had neonatal hyperbilirubinaemia with values of maximal 16.2 mg% and 16.7 mg% which required phototherapy.
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PMID:[Excessive hyperlipidemia during pregnancy (author's transl)]. 740 9

Each hyperlipidemia patient requires individual management. Treatment choices are thus made for each patient on the basis of evaluation of their overall cardiovascular risk. This evaluation involves four types of characteristics: those which cannot be changed (age, gender), classical lipid and non-lipid risk factors, and finally cardiovascular status with two types of evaluation (clinical status and sub-clinical, atherosclerosis). Three examples are presented here, enabling more precise assessment of lipid risk: syndrome X which shows to what extent risk factors are often associated, combined familial hyperlipidemia which emphasises the importance of family history, and lipoprotein (a). The latter is a risk factor relatively inaccessible to treatment but which enables better evaluation of the risk of the patient and choice of a stricter treatment goal when it is very high.
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PMID:[New lipid factors of cardiovascular risk]. 782 48

Familial hyperlipidemia has received little attention as a possible cause of stroke in young patients. Some recent studies have demonstrated that lipoprotein (a) is a key factor for atherogenesis in familial hypercholesterolemia. Hypogonadism may also contribute to the elevation of serum lipids, but their influence as a risk factor for stroke is still less understood. A 34-year-old patient with heterozygous familial hypercholesterolemia presented with a left pure motor hemiparesis secondary to a right striatocapsular infarction. Arteriography showed atherosclerotic lesions in both internal carotid arteries. High levels of cholesterol, cLDL, apo B, and lipoprotein (a) were found. Clinical signs of hypogonadism were present and the karyotype led to the diagnosis of Klinefelter's syndrome (47,XXY). The early clinical course was excellent, and the levels of serum lipids were normalized with diet, lipid-lowering drugs and androgens. The importance of hyperlipidemia as a risk factor for stroke in the young, specially when it occurs in the context of familial hypercholesterolemia with elevated lipoprotein (a) levels, as well as the possible contribution of hypogonadism to the development of accelerated atherosclerosis in young patients, are discussed upon.
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PMID:[Striatocapsular infarct in a young patient with heterozygous familial hypercholesterolemia and Klinefelter's syndrome]. 828 24

Familial Combined Hyperlipidemia is the most frequent familial hyperlipidemia with a high risk a early manifestation of arteriosclerosis. Endothelial dysfunction is the first step in the development of arteriosclerosis. The aim of our investigation was to examine selected markers of endothelial dysfunction in hyperlipidemic members of families with familial combined hyperlipidemia and their normolipidemia first-line relatives and to compare them with healthy individuals. The study includes non-smoking members of the affected families (probands and first-line relatives), who have not suffered from clinical manifestations of arteriosclerosis and/or hypertension during the start of the study. The cohort was divided into hyperlipidemic individuals (N = 25) and normolipidemic individuals (N = 21). Both groups were compared with control groups of healthy individuals (two groups, N = 17 each), who were adjusted by age and sex. The following markers of endothelial dysfunction were examined: 1. ultrasound--flow mediated dilatation of brachial artery and 2. humoral--serum levels of von Willebrand factor, inhibitor of activator of plasminogen-1 and vasoadhesive molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). The members of families with familial combined hyperlipidemia displayed symptoms of endothelial dysfunction. In comparison with healthy controls the endothelial dysfunction was more expressed in hyperlipidemic individuals. They displayed a significantly lower flow-mediated dilatation of brachial artery (3.6 +/- 3.3% versus 6.6 +/- 2.8%, P < 0.01), higher levels of von Willebrand factor (152.8% +/- 79.1% versus 110.4% +/- 24.8%, P < 0.05), inhibitor of activator of plasminogen-1 (94.6 +/- 30.8 ng/ml versus 60.4 +/- 38.0 ng/ml, P < 0.01) and vasoadhesive molecules: vascular cell adhesion molecule-1 (927.0 +/- 167.7 ng/ml versus 814.7 +/- 171.1 ng/ml, P < 0.05), intercellular adhesion molecule-1 (601.7 +/- 89.5 ng/ml versus 544.8 +/- 59.8 ng/ml, P < 0.05). The normolipidemic individuals displayed only a significantly lower flow-mediated dilatation of brachial artery (5.6 +/- 2.6% versus 7.5 +/- 2.8%, P < 0.05) and higher levels of von Willebrand factor (136.8 +/- 40.32% versus 104.1 +/- 24.9%, P < 0.05). No significant difference was found in the levels of inhibitor of activator of plasminogen-1 and vasoadhesive molecules. The results indicated that members of families with familial combined hyperlipidemia represent a high-risk group from the standpoint of early manifestation of arteriosclerosis.
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PMID:[Endothelial dysfunction in a family with familial combined hyperlipidemia]. 1451 86

Hyperlipidemia is a frequent complication after renal transplantation. Cyclosporine therapy is an important cause of hyperlipidemia. It is still controversial whether C0 or C2 is the most effective way to monitor blood cyclosporine concentrations to guide dosages. We sought to evaluate the relationship of C0 or C2 to serum lipid levels in the early and late posttransplant periods among adolescent renal transplant recipients. The posttransplantation charts of 26 adolescent renal transplant recipients were evaluated retrospectively. Serum C0 and C2 levels and serum lipid (triglyceride and total cholesterol) levels were analyzed both in the early (first 6 months) and the late (thereafter) posttransplant periods. Hypertriglyceridemia and hypercholesterolemia were defined as levels above the 95th percentile adjusted for age and gender. To evaluate the influence of C0 and C2 levels on serum lipids, we excluded one patient with familial hyperlipidemia. In addition, serum lipid levels of the remaining 25 patients were excluded in acute rejection periods and when the serum creatinine levels were above 2.5 mg/dL, representing chronic allograft nephropathy. Concurrently recorded serum C0 and C2 levels were present for only 21 patients. Overall, we evaluated the records of 245 visits for these 21 patients. The incidence of hyperlipidemia decreased in the late posttransplant period, being significant for hypercholesterolemia. C2 had strong negative correlation with serum lipids; it was significant for total cholesterol in the early posttransplant period (r=-0.542, P=.005), but weaker in the late posttransplant and whole posttransplant periods. Thus correlation of C2 with serum lipids showed differences during posttransplant follow-up. C0, on the other hand, was positively correlated with total cholesterol levels in all periods, being significant for the whole posttransplant period (r=0.293, P=.000) and for the late posttransplant period (r=0.196, P=.025). Although not statistically significant, C0 levels were higher among hypertriglyceridemic or hypercholesterolemic episodes both in the early and the late posttransplant periods. When only the C0 levels of all 25 patients were analyzed (789 visits), C0 and serum cholesterol levels were positively correlated both in the early and the late posttransplant periods (P=.013, r=0.198 and P=.000, r=0.177, respectively). We concluded that C0 has a more predictable correlation with serum cholesterol levels after renal transplantation in adolescent patients.
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PMID:Correlation of C0 and C2 levels with lipid profiles in adolescent renal transplant recipients in the early and late posttransplant periods. 1679 83

Background. We report a case of familial hyperlipidemia in pregnancy that resulted in hemorrhagic pancreatitis. Case. A patient at 27-week gestation was admitted for recurrent pancreatitis secondary to severe hyperlipidemia. With conservative care, the patient improved but on the fourth day of admission she experienced a sudden onset of hypotension and was diagnosed with hemorrhagic pancreatitis. Conclusion. Pancreatitis caused by hyperlipidemia is an uncommon event during pregnancy. A familiarity with the severe complications associated with this potentially life-threatening condition is important.
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PMID:Severe Hyperlipidemia Induced Hemorrhagic Pancreatitis during Pregnancy. 1994 46

In patients who have undergone a heart transplant, the major cause of death is coronary artery disease (CAD). The etiology of cardiac-allograft vasculopathy is thought to be multifactorial, but due in large part to immune mechanisms that cause elevations in serum cholesterol levels. The dextran sulfate cellulose low-density lipoprotein (LDL) adsorption (DSA) apheresis procedure has been shown to reduce lipoprotein levels and markers of blood rheology to improve coronary perfusion to the transplanted heart. We report the first described case of the stabilization and reversal of progressive transplant CAD with DSA. We followed a 50-year-old male orthotopic heart transplant recipient with familial hyperlipidemia refractory to lipid lowering therapy with bi-weekly LDL-apheresis (DSA system) for 12 months. Quarterly pre- and post-apheresis blood investigations were obtained, as well as annual adenosine thallium (AT) studies. Creatinine kinase (CPK), creatinine, LDL, fibrinogen, and lipoprotein (a) were reduced by 70%, 26%, 23%, 47%, and 47%, respectively. AT before the initiation of apheresis revealed a small to medium sized, partially reversible perfusion defect in the anterolateral and inferoapical walls, with an ejection fraction (EF) of 49%, elevated left ventricular volume (171 mL), and an elevated pulmonary-to-myocardial (PMR) count ratio of 0.67 (normal <0.52). After 12 months of LDL apheresis with DSA, a repeat AT demonstrated no fixed or reversible perfusion abnormality, an EF of 51%, and the PMR had normalized (0.46). This is the first reported case demonstrating that in a heart transplant survivor with hyperlipidemia and progression of coronary artery disease, LDL apheresis with DSA therapy can lead to regression and is an effective treatment of post-transplant coronary disease.
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PMID:The first case report of the treatment of transplant coronary artery disease with dextran sulfate adsorption lipid apheresis. 2043 45

Familial hyperlipidemia is a group of genetic disorders with a predisposition to atherosclerosis. Hyperlipidemia causes increased atherosclerotic events through increased endothelial damage. In this report we aimed to measure the plasma fibrinogen and von Willebrand factor antigen (VWf:Ag) levels in pediatric patients with familial hyperlipidemias and to investigate the effects of serum lipid levels and antihyperlipidemic agents on these parameters. Of the 41 patients analyzed, vWf:Ag level was significantly lower in antihyperlipidemic receivers (132 +/- 51%, 102 +/- 19%; p = 0.010). This finding may indicate that early initiation of antihyperlipidemics in patients with familial hyperlipidemias may decrease the risk of future atherosclerotic events through not only decreasing the serum lipid levels, but also decreasing plasma vWf:Ag levels.
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PMID:Antihyperlipidemic agents cause a decrease in von Willebrand factor levels in pediatric patients with familial hyperlipidemia. 2107 19

Tenderness over the sternum is a clue for possible sternal fracture. Sternal fractures usually occur at the body or manubrium. Lateral chest radiography could detect a sternum fracture, but the diagnosis is usually made by chest tomography. Traumatic sternum fracture considered as a marker of seriously life-threatening, high-energy injury. In hyperlipidemia, oxidized lipids accumulate in vascular tissues and trigger atherosclerosis. Such lipids also deposit in bone tissues where they may promote osteoporosis. In the literature, there is no previously reported traumatic sternal fracture due to hyperlipidemia-induced osteoporosis. Here, we report a case of a combined mixed type familial hyperlipidemia-induced osteoporosis in which the patient having seat belt on had an unexpected sternum fracture in a low-energy motor vehicle accident.
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PMID:Dyslipidemia and sternum fracture. 2347 7

Recent epidemiologic studies and meta-analysis with triglyceride levels are revealing that hypertriglyceridemia is associated with coronary heart diseases independent of other coronary risk factors, although the direct effect of serum triglycerides to atherosclerotic lesion is still uncertain. Multiple genetic and environmental factors from familial hyperlipidemia to food and alcohol intake are implicated in elevating triglycerides. Especially, a number of investigators demonstrated a relationship between atherosclerotic diseases and postprandial hyperlipidemia, which may lead to nonfasting TG elevation. The purpose of this article is to review several clinical studies relating serum fasting and nonfasting triglyceride levels and coronary heart disease, and to discuss whether hypertriglyceridemia initiates atherosclerosis or plays a role as a biomarker for metabolic abnormalities.
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PMID:[Clinical science relating atherosclerotic diseases and hypertriglyceridemia]. 2420 12


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