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)

Heel pain is most commonly the result of mechanical abnormality in foot structure or function. Systemic disease, however, may also affect the heel, resulting in pain, deformity, or both of the rearfoot. This article discusses and reviews notable systemic conditions, exclusive of the seronegative spondyloarthropathies, which may produce subjective or objective heel findings. Specific conditions discussed are rheumatoid arthritis, crystal deposition arthropathies, osteoporosis, diffuse idiopathic skeletal hyperostosis, diabetes mellitus, hypertrophic osteoarthropathy, Paget's disease, hyperlipidemia, sarcoidosis, sickle cell anemia, and acromegaly and their effects on the heel.
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PMID:The heel in systemic disease. 218 35

Automated methods, with and without cyanide (+CN and -CN), for whole blood hemoglobin (Hb) determination were evaluated on the Technicon H*1TM System. Both automated Hb methods were linear over the range 0-250 g/L (0-25 g/dL) and correlated well with the International Committee for Standardization of Hematology (ICSH) reference method and with the Coulter S+II. Both methods quantitatively converted whole blood containing up to 100% carboxyhemoglobin in less than 24 seconds to their respective end products. With respect to abnormal samples (sickle cell anemia, multiple myeloma, and hyperlipemia), both H*1 methods gave Hb results that were equivalent to the (postfiltration) ICSH method. For samples with white blood cell (WBC) counts less than 36 X 10(9)/L, the +CN method was equivalent to the (postfiltration) ICSH method, whereas for WBC counts greater than 20 X 10(9)/L, the -CN method showed acceptable recovery of the mean but unacceptable imprecision. For WBC counts of 36-164 X 10(9)/L, the +CN method yielded acceptable Hb recovery with unacceptable imprecision. Hyperlipemia, resulting from addition of Intralipid directly to the blood samples, caused large errors in both H*1 methods.
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PMID:Evaluation of 24-second cyanide-containing and cyanide-free methods for whole blood hemoglobin on the Technicon H*1TM analyzer with normal and abnormal blood samples. 277 49

Methodologies for T and B lymphocyte quantitation, lymphocyte blast transformation (LBT) and carbohydrate (CHO) metabolism are important for assessing host lymphocyte response in the clinical laboratory. Modifications of methods for each of these techniques are presented. Results from studies of normal ambulatory adults, patients with diabetes mellitus, sickle cell disease and hyperlipidemia are reported. LBT of normal lymphocytes before and after ethanol exposure are examined. LBT during pregnancy is evaluated. T cell populations are abnormally high in black diabetics and decreased in patients with sickle cell anemia. B cell subpopulations are increased in patients with sickle cell anemia. LBT responses are decreased in maturity onset diabetes, during pregnancy and in patients with sickle cell disease. Ethanol in amounts attainable during human consumption results in significantly decreased LBT response. CHO metabolism (especially hexose monophosphate shunt [HMPS] and HMPS by pentose sugar recycling) is abnormal in diabetic lymphocytes. The low HMPS activity is partially reversible by treatment with prostaglandin synthetase inhibitors. Information related to lymphocytes in normal states remains to be collected by further clinical application of these techniques of quantitation and in vitro function.
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PMID:B and T lymphocytes: quantitation, function, and clinical applicability. 696 70

The non-healing leg ulcer is examined by discussing three disease processes: peripheral vascular occlusive disease (PVOD), chronic venous insufficiency (CVI), and vasculitis. For PVOD, management decisions are based on risk factors and disease history. Comprehensive management includes the discontinuation of smoking, exercise conditioning and regulation of diabetes, hyperlipidemia, hypertension, and the appropriate application of anticoagulant/antiplatelet drugs. Methods of surgical management include bypass with autogenous or synthetic material in addition to reconstructive surgery with patch angioplasty or extra-anatomic bypass, amputation, percutaneous transluminal angioplasty/stents, thrombolytic infusion, atherectomy, intraluminal ultrasound, and angioscopy. The optimal healing environment for all ulcers prevents contamination, pain, and fluid loss. In CVI, higher venous pressure in the veins of the lower limb during exercise results in ambulatory venous hypertension and ulceration. Various theories are associated with the disease and ulceration process; the classic treatment of elevation, ambulation, and compression for venous disease remains unchallenged. Diagnosis is based on history, physical examination, invasive venography, and/or non-invasive studies. Two groups of vasculitic disorders that share varying degrees of vascular inflammation and necrosis are arteritis (lupus, erythematosus, periarteritis nodosa, dermatomyositis) and blood dyscrasias (sickle cell disease, thalassemia). Leg ulcers associated with vasculitis are due to inadequate tissue oxygenation at the local level, are typically chronic, slow to heal, and commonly recur.
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PMID:The non-healing leg ulcer: peripheral vascular disease, chronic venous insufficiency, and ischemic vasculitis. 939 80

Autonomic functions, such as increased sympathetic and parasympathetic activity and the brain's suprachiasmatic nucleus, higher nervous centres, depression, hostility and aggression appear to be important determinants of heart rate variability (HRV), which is, itself, an important risk factor of myocardial infarction, arrhythmias, sudden death, heart failure and atherosclerosis. The circadian rhythm of these complications with an increased occurrence in the second quarter of the day may be due to autonomic dysfunction as well as to the presence of excitatory brain and heart tissues. While increased sympathetic activity is associated with increased levels of cortisol, catecholamines, serotonin, renin, aldosterone, angiotensin and free radicals; increased parasympathetic activity may be associated with greater levels of acetylecholine, dopamine, nitric oxide, endorphins, coenzyme Q10, antioxidants and other protective factors. Recent studies indicate that hyperglycemia, diabetes, hyperlipidemia, ambient pollution, insulin resistance and mental stress can increase the risk of low HRV. These risk factors, which are known to favour cardiovascular disease, seem to act by decreasing HRV. There is evidence that regular fasting may modulate HRV and other risk factors of heart attack. While exercise is known to decrease HRV, exercise training may not have any adverse effect on HRV. In a recent study among 202 patients with acute myocardial infarction (AMI), the incidence of onset of chest pain was highest in the second quarter of the day (41.0%), mainly between 4.0-8.0 AM, followed by the fourth quarter, usually after large meals (28.2%). Emotion was the second most common trigger (43.5%). Cold weather was a predisposing factor in 29.2% and hot temperature (> 40 degrees celsius) was common in 24.7% of the patients. Dietary n-3 fatty acids and coenzyme Q10 have been found to prevent the increased circadian occurrence of cardiac events in our randomized controlled trials, possibly by increasing HRV. We have also found that n-3 fatty acids plus CoQ can decrease TNF-alpha and IL-6 in AMI which are pro-inflammatory agents. There is evidence that dietary n-3 fatty acids canenhance hippocampal acetylecholine levels, which may be protective. Similarly, the stimulation of the vagus nerve may inhibit TNF synthesis in the liver and acetylecholine, the principal vagal neurotransmitter, significantly attenuates the release of pro-inflammatory cytokines TNF-alpha, interleukin 1,6 and 18, but not the anti-inflammatory cytokine IL-10 in experiments. Therefore, any agent which can enhance brain acetylecholine levels, may be used as a therapeutic agent in protecting the suprachiasmatic nucleus, higher nervous centres, vagal activity and sympathetic nerve activity which are known to regulate the body clock and HRV and the risk of SCD and heart attack.
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PMID:Brain-heart connection and the risk of heart attack. 1265 78

Obstructive sleep apnea, a syndrome leading to recurrent intermittent hypoxia (IH), has been associated previously with hypercholesterolemia, independent of underlying obesity. We examined the effects of experimentally induced IH on serum lipid levels and pathways of lipid metabolism in the absence and presence of obesity. Lean C57BL/6J mice and leptin-deficient obese C57BL/6J-Lep(ob) mice were exposed to IH for five days to determine changes in serum lipid profile, liver lipid content, and expression of key hepatic genes of lipid metabolism. In lean mice, exposure to IH increased fasting serum levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, phospholipids (PLs), and triglycerides (TGs), as well as liver TG content. These changes were not observed in obese mice, which had hyperlipidemia and fatty liver at baseline. In lean mice, IH increased sterol regulatory element binding protein 1 (SREBP-1) levels in the liver, increased mRNA and protein levels of stearoyl-coenzyme A desaturase 1 (SCD-1), an important gene of TG and PL biosynthesis controlled by SREBP-1, and increased monounsaturated fatty acid content in serum, which indicated augmented SCD-1 activity. In addition, in lean mice, IH decreased protein levels of scavenger receptor B1, regulating uptake of cholesterol esters and HDL by the liver. We conclude that exposure to IH for five days increases serum cholesterol and PL levels, upregulates pathways of TG and PL biosynthesis, and inhibits pathways of cholesterol uptake in the liver in the lean state but does not exacerbate the pre-existing hyperlipidemia and metabolic disturbances in leptin-deficient obesity.
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PMID:Intermittent hypoxia induces hyperlipidemia in lean mice. 1612 34

Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (CIH) and associated with dysregulation of lipid metabolisms and atherosclerosis. Causal relationships between OSA and metabolic abnormalities have not been established because of confounding effects of underlying obesity. The goal of the study was to determine if CIH causes lipid peroxidation and dyslipidemia in the absence of obesity and whether the degrees of dyslipidemia and lipid peroxidation depend on the severity of hypoxia. Lean C57BL/6J mice were exposed to CIH for 4 wk with a fractional inspired O2 (FI(O2)) nadir of either 10% (moderate CIH) or 5% (severe CIH). Mice exposed to severe CIH exhibited significant increases in fasting serum levels of total cholesterol (129 +/- 2.9 vs. 113 +/- 2.8 mg/dl in control mice, P < 0.05) and low-density lipoprotein cholesterol (85.7 +/- 8.9 vs. 56.4 +/- 9.7 mg/dl, P < 0.05) in conjunction with a 1.5- to 2-fold increase in lipoprotein secretion, and upregulation of hepatic stearoyl coenzyme A desaturase 1 (SCD-1). Severe CIH also markedly increased lipid peroxidation in the liver (malondialdehyde levels of 94.4 +/- 5.4 vs. 57.4 +/- 5.2 nmol/mg in control mice, P < 0.001). In contrast, moderate CIH did not induce hyperlipidemia or change in hepatic SCD-1 levels but did cause lipid peroxidation in the liver at a reduced level relative to severe CIH. In conclusion, CIH leads to hypercholesterolemia and lipid peroxidation in the absence of obesity, and the degree of metabolic dysregulation is dependent on the severity of the hypoxic stimulus.
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PMID:Hyperlipidemia and lipid peroxidation are dependent on the severity of chronic intermittent hypoxia. 1715 41

Traditional risk factors associated with adult arterial ischemic stroke (AIS; ie, hypertension, hyperlipidemia, diabetes, smoking, and atherosclerosis) are relatively rare in children. Childhood AIS is instead associated with a variety of conditions including cerebral arteriopathies, congenital heart disease, infection, head and neck trauma, sickle cell anemia, and prothrombotic abnormalities. Although the pathophysiology and outcomes of adult AIS differ significantly from those in childhood AIS, therapeutic management remains similar, largely because of the paucity of evidence from devoted pediatric observational studies and clinical trials. The purpose of this article is to review the current guidelines and evidence in the treatment of childhood AIS, within the context of that which exists in adult AIS. Medical management of hypoxia, hyperglycemia, fever, blood pressure, and increased intracranial pressure has been insufficiently investigated in childhood stroke, resulting in a lack of guidance in these areas. Although acute antithrombotic management in childhood AIS has received relatively greater attention in published recommendations, it is based almost exclusively on consensus and expert opinion, and differs considerably among existing pediatric guidelines. Rehabilitation therapy in childhood AIS has great potential for meaningful improvements in long-term outcomes, especially given the plasticity of the young brain; however, little guidance for rehabilitative measures is provided by published recommendations. Ongoing and future multicenter cohort study efforts, and ultimately devoted pediatric clinical trials, will be essential to establish comprehensive evidence-based guidelines for the treatment of childhood AIS.
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PMID:Treatment of childhood arterial ischemic stroke. 1849 44

AMPK (AMP-activated protein kinase) has been suggested to be a central player regulating FA (fatty acid) metabolism through its ability to regulate ACC (acetyl-CoA carboxylase) activity. Nevertheless, its involvement in insulin resistance- and TD2 (Type 2 diabetes)-associated dyslipidaemia remains enigmatic. In the present study, we employed the Psammomys obesus gerbil, a well-established model of insulin resistance and TD2, in order to appreciate the contribution of the AMPK/ACC pathway to the abnormal hepatic lipid synthesis and increased lipid accumulation in the liver. Our investigation provided evidence that the development of insulin resistance/diabetic state in P. obesus is accompanied by (i) body weight gain and hyperlipidaemia; (ii) elevations of hepatic ACC-Ser79 phosphorylation and ACC protein levels; (iii) a rise in the gene expression of cytosolic ACC1 concomitant with invariable mitochondrial ACC2; (iv) an increase in hepatic AMPKalpha-Thr172 phosphorylation and protein expression without any modification in the calculated ratio of phospho-AMPKalpha to total AMPKalpha; (v) a stimulation in ACC activity despite increased AMPKalpha phosphorylation and protein expression; and (vi) a trend of increase in mRNA levels of key lipogenic enzymes [SCD-1 (stearoyl-CoA desaturase-1), mGPAT (mitochondrial isoform of glycerol-3-phosphate acyltransferase) and FAS (FA synthase)] and transcription factors [SREBP-1 (sterol-regulatory-element-binding protein-1) and ChREBP (carbohydrate responsive element-binding protein)]. Altogether, our findings suggest that up-regulation of the AMPK pathway seems to be a natural response in order to reduce lipid metabolism abnormalities, thus supporting the role of AMPK as a promising target for the treatment of TD2-associated dyslipidaemia.
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PMID:Increased hepatic lipogenesis in insulin resistance and Type 2 diabetes is associated with AMPK signalling pathway up-regulation in Psammomys obesus. 1884 11

This report compares the relative rates and risk factors associated with stroke in adults versus children with sickle cell disease (SCD) in the United States over the last decade. We identified incident strokes in patients with SCD using ICD-9 codes for acute stroke and SCD and the California Patient Discharge Databases. We estimated SCD prevalence by using the incidence of SCD at birth with adjustment for early mortality from SCD. We identified 255 acute strokes (70 primary hemorrhagic and 185 ischemic) among 69,586 hospitalizations for SCD-related complications from 1998 to 2007. The rate of stroke in children [<18 years old (310/100,000 person-years)] was similar to young adults [18-34 years old (360/100,000 person-years)], but much higher in middle-aged [35-64 years old (1,160/100,000 person-years)] and elderly adults [> or =65 years old (4,700/100,000 person-years)]. Stroke was associated with hypertension in children and hypertension, diabetes mellitus, hyperlipidemia, atrial fibrillation, and renal disease in adults. Most acute strokes (75%) and in-hospital deaths from stroke (91%) occurred in adults. Our results suggest that the rate of stroke in SCD peaks in older adults and is three-fold higher than rates previously reported in African-Americans of similar age (35-64 years) without SCD. Stroke in SCD is associated with several known adult risk factors for ischemic and hemorrhagic stroke. Studies for the primary and secondary prevention of stroke in adults with SCD are urgently needed.
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PMID:The excess burden of stroke in hospitalized adults with sickle cell disease. 1962 72


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