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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A serie of 12 cases of hypopituitarism (Sheehan's syndrome, pituitary adenoma, idiopathic) associated with hyperlipidemia (type IIb in general), is reported. It is suggested that: 1--Growth hormone deficiency seems to have a protective effect against atherosclerosis in hyperlipidemia because there are no cardiovascular signs in 10 cases with a history of growth hormone deficiency lasting from 5 to 57 years and a manifesting hyperlipidemia (lasting a mean of 23 years), and there is stabilisation or improvement of ischemic signs in 2 other cases. 2--Lipid abnormalities are frequently seen in hypopituitarism even after thyroid replacement therapy. 3--The hyperlipidemia can be familial or can result from growth hormone deficiency alone.
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PMID:[Hypopituitarism and hyperlipidemia. Protective effect of growth hormone deficiency against atherosclerosis (author's transl)]. 54 77

Twelve cases of hypopituitarism (Sheehan's syndrome, pituitary adenoma, idiopathic) associated with hyperlipidemia (type IIb in general) are reported. It is suggested that: 1 - Growth hormone deficiency seems to have a protective effect against atherosclerosis in hyperlipidemia because there are no cardiovascular signs in 10 cases with a history of growth hormone deficiency lasting from 5 to 57 years and a patent hyperlipidemia (lasting a mean of 23 years), and there is stabilisation or improvement of ischemic signs in 2 other cases. 2 - Lipid abnormalities are frequently seen in hypopituitarism even after thyroid replacement therapy. 3 - The hyperlipidemia can be familial or can result from growth hormone deficiency alone.
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PMID:[Hypopituitarism and hyperlipidemia. Protective effect of growth hormone deficiency against atherosclerosis (author's transl)]. 54 16

It has been known for more than 30 years that growth hormone has a lipolytic properties and growth hormone excess (acromegaly) and growth hormone deficiency have been reported to be associated with abnormalities in serum lipoprotein concentrations. Due to the lipolytic effect of growth hormone, its administration in man has been reported to increase plasma nonesterified fatty acid (NEFA) concentrations. Ketone body production increases during acute growth hormone excess as a result of increased NEFA concentrations; similarly, the increase in serum triglycerides may be explained by an increase in substrate (NEFA) supply to the liver for VLDL production. The effect may be enhanced by a simultaneous decrease of serum lipoprotein lipase activity. The cholesterol-lowering effect of growth hormone administration has not been investigated in detail, specifically, the effect of growth hormone on LDL kinetics is unknown. Growth hormone-excess and growth hormone deficiency have been reported to be associated with increased risk for atherosclerosis; an association with serum lipoprotein changes is likely but evidence for a causal link is yet lacking.
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PMID:Growth hormone and lipids. 180 82

A non-invasive pulse-wave-velocity Doppler ultrasound technique for the assessment of aortic compliance is described. A computational approach for correcting for the effect of non-chronic changes in blood pressure is considered and applied to compliance measurements performed on an age-select cohort of 70 normotensive, normal healthy volunteers. In order to permit the wider availability of the pulse-wave-velocity Doppler ultrasound technique, the authors have developed a MkII system based on a standard 80486/33 MHz IBM compatible WINDOWS based personal computer; real-time spectral analysis being achieved using a relatively inexpensive but fast analogue to digital signal processing card. An overview of the new apparatus is provided and verification work to compare the repeatability of the MkI and MkII systems is described. Medical disorders such as atherosclerosis, diabetes mellitus, familial hypercholesterolaemia, growth hormone deficiency, and Ehlers-Danlos and Marfan's syndromes have all been shown to affect arterial wall compliance. We suggest that the in vivo clinical measurement of blood pressure corrected aortic distensibility using the MkII system may be a useful, reproducible, non-invasive tool for assessing such patients' susceptibility to atheromatous arterial disease as well as for monitoring their response to therapeutic interventions. Measurements in the aorta may be especially pertinent since the natural history of fatty streaks there tends to parallel that in the coronary vasculature thereby potentially affording a convenient surrogate estimate of coronary heart disease.
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PMID:Aortic compliance measured by non-invasive Doppler ultrasound: application of a personal computer based MkII system and its repeatability. 806 7

A noninvasive Doppler ultrasound technique for the assessment of aortic compliance based on the in vivo measurement of pulse wave velocity along the thoraco-abdominal aortic pathway is described. An approach for correcting for the effect of blood pressure on aortic distensibility is considered. The derivation of an index of intrinsic distensibility, Cp, which is independent of blood pressure, is provided and applied to data collected from normal, healthy volunteers. Overviews are provided of studies utilising the technique to determine aortic compliance in medical disorders, which are known to predispose to premature cardiovascular disease, such as diabetes mellitus, familial hypercholesterolaemia and growth hormone deficiency. The significance of correlations between in vivo aortic compliance measurements and plasma concentrations of total cholesterol, low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol and insulin-like growth factor-I are discussed. It is proposed that the measurement of aortic compliance in normal, healthy individuals may potentially be a useful in vivo research tool for investigating the effects of biochemical factors on the biophysical properties of the aortic wall. Furthermore, we believe that the routine measurement of blood pressure-corrected aortic distensibility may prove a useful, noninvasive clinical tool for assessing patients' susceptibility to atherosclerosis, as well as for monitoring their response to therapeutic interventions.
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PMID:Aortic compliance measurements using Doppler ultrasound: in vivo biochemical correlates. 813 72

A non-invasive Doppler ultrasound technique is described for the assessment of aortic compliance based on the in vivo measurement of pulse wave velocity along the thoraco-abdominal aortic pathway. A structured protocol, which has been developed to improve the reproducibility of the technique, is validated. A method of correcting for the effect of non-chronic changes in blood pressure on arterial elasticity is considered and applied to compliance measurements performed on 66 normal, healthy volunteers. The results of a study to ascertain the overall reproducibility of the method are provided and problems associated with the technique are discussed. Medical disorders such as atherosclerosis, diabetes mellitus, familial hypercholesterolaemia and growth hormone deficiency have all been shown to affect arterial wall compliance. It is suggested that the in vivo measurement of pressure-corrected aortic distensibility may be a useful, non-invasive tool for assessing such patients' susceptibility to atheromatous arterial disease and for monitoring their response to therapy. Measurements in the aorta may be especially pertinent since the natural history of fatty streaks there tends to parallel that in coronary arteries thereby potentially affording a convenient surrogate estimate of coronary heart disease.
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PMID:Validation and reproducibility of pressure-corrected aortic distensibility measurements using pulse-wave-velocity Doppler ultrasound. 832 Sep 81

The syndrome of growth hormone deficiency (GHD) in adults is associated with premature atherosclerosis, increased cardiovascular mortality, abnormal lipoprotein patterns and abnormal body composition. We have previously shown that GH-deficient adults have increased concentrations of fibrinogen and plasminogen activator inhibitor (PAI-1) activity. The aim of the present investigation was to study coagulation and fibrinolysis in 17 patients with adult-onset GHD during two years of treatment with recombinant human GH (12 micrograms/kg body weight/day). The impact of the contemporary changes in metabolic variables and body composition on coagulation and fibrinolysis was studied. The patients received conventional thyroid, adrenal and gonadal hormone replacement therapy. PAI-1 activity, PAI-1 antigen and tissue plasminogen activator (t-PA) antigen levels decreased during the GH treatment period (p < 0.05). The decrease was more pronounced in patients with high pre-treatment levels of the different variables. alpha 2-antiplasmin decreased (p < 0.05), while plasminogen was unchanged during two years of GH treatment. Fibrinogen concentrations tended to decrease after two years of GH treatment (p = 0.06), while the coagulation factors VII and VIII were unchanged. von Willebrand factor demonstrated a transient decrease after 18 months of GH treatment. The coagulation inhibitor, protein C, decreased (p < 0.05), while antithrombin was unchanged. Fasting plasma insulin increased (p < 0.01), but blood glucose did not differ after two years of GH treatment. Serum high-density lipoprotein cholesterol, total cholesterol and triglycerides were unaltered. Body fat decreased during the initial GH treatment but was unaltered after two years, while lean body mass increased (p < 0.001) and the waist over hip circumference ratio tended to decrease (p = 0.06). In conclusion, PAI-1 activity, PAI-1 antigen and t-PA antigen decreased during long-term GH treatment. These changes may be a direct effect of GH itself or may be secondary to the favourable changes in body composition. It remains to be seen whether changes in these fibrinolytic variables during rhGH treatment reduces the cardiovascular risk in patients with GHD. The present results suggest that GH plays a role in the regulation of fibrinolysis.
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PMID:Long-term treatment with growth hormone decreases plasminogen activator inhibitor-1 and tissue plasminogen activator in growth hormone-deficient adults. 888 81

The effect of growth hormone replacement therapy in near physiological doses on lipoprotein composition and serum lipoprotein(a) concentrations was investigated in growth hormone-deficient subjects. A randomised, double-blind, placebo-controlled trial of recombinant growth hormone was undertaken for 6 months followed by an open extension for a further 6 months (0.125 IU/kg per week for the first 4 weeks of each 6 month period and thereafter 0.25 IU/kg per week). A total of 18 patients with isolated growth hormone deficiency or hypopituitarism were studied. Lipid concentrations were estimated in lipoprotein fractions and protein concentrations were measured in low density lipoprotein (LDL). Glucose and glycated haemoglobin in blood and insulin, cholesterol, triglyceride, apolipoproteins A-I and B and lipoprotein(a) concentrations were measured in serum. In the placebo-controlled phase fasting blood glucose concentrations increased with growth hormone treatment from 5.0 +/- 0.2 to 5.8 +/- 0.2 mmol/l (P = 0.02) (mean +/- S.E.M.), although no significant changes were seen in lipids or lipoproteins. In the group receiving active treatment total serum cholesterol decreased from 6.0 +/- 0.4 to 5.2 +/- 0.3 mmol/l (P = 0.002) after 6 months, due to reduced LDL cholesterol concentrations. Low density lipoprotein protein concentrations fell (0.8 +/- 0.1 versus 0.7 +/- 0.1 g/l) (P = 0.005), and LDL phospholipid levels decreased from 0.9 +/- 0.1 to 0.7 +/- 0.1 mmol/l (P = 0.007). Serum cholesterol and LDL composition reverted to pre-treatment values by 12 months. Fasting blood glucose remained above pre-treatment values (P = 0.036) and fasting insulin was significantly increased (P = 0.044). There was no effect of growth hormone therapy on serum triglyceride, apolipoprotein or lipoprotein(a) concentrations. In conclusion, growth hormone therapy with near physiological doses has no long term effects on serum lipoprotein(a) concentrations or lipoprotein composition.
Atherosclerosis 1997 Aug
PMID:The effect of growth hormone replacement therapy for up to 12 months on lipoprotein composition and lipoprotein(a) in growth hormone-deficient adults. 925 15

Using stable isotope techniques to establish turnover rates for very low density lipoprotein (VLDL), a group of eight adult patients with growth hormone deficiency (GHD) exhibited an increased VLDL apoprotein B (apo B) secretion and decreased VLDL apoB metabolic clearance rate compared to controls. Such increased secretion is seen in some dyslipidemic states, including GHD, which are associated with atherosclerosis. The study of VLDL metabolism may provide a clue to the lipid metabolism disorder associated with GHD.
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PMID:The use of stable isotopes to unravel the hyperlipidemia of adult growth hormone deficiency. 943 55

Growth hormone-deficient hypopituitary patients on conventional replacement therapy have increased mortality and morbidity from atherosclerotic cardiovascular disease. Oxidation of low-density lipoprotein (LDL) is a key event in the development and progression of atherosclerosis. Antibodies against oxidatively modified LDL may reflect in vivo oxidation processes. The aim of this study is to determine the effect of growth hormone deficiency on oxidised-LDL antibody titres in panhypopituitary patients taking conventional replacement therapy. Twenty-one GH deficient, adult panhypopituitary patients and 17 age, sex and body mass index-matched healthy controls were studied. After an overnight fast, anthropometric parameters were measured and body composition was determined by a bioelectrical impedance analyser. Venous blood samples were obtained for the measurements of biochemical parameters. Antibodies to oxidised-LDL were analysed by an ELISA system in the patients' and controls' serum. No significant difference was observed between the oxidised-LDL antibody titres in hypopituitary patients and controls (395.4+/- 183.2 mU/ml and 393.2 +/- 186.2 mU/ml respectively, p = NS). A significant positive correlation was observed between oxidised-LDL antibody titres and total cholesterol concentrations in the patients (r = 0.449, p < 0.05). No significant correlation was observed between oxidised-LDL antibody titres and anthropometric/biochemical variables in the controls. It is concluded that relatively increased LDL oxidation may not contribute to the progression of atherosclerosis in hypopituitary patients.
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PMID:Antibodies against oxidised low-density lipoprotein in hypopituitary patients with growth hormone deficiency. 1178 63


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