Hormone replacement therapy pdf

EPR spectral peak heights were taken as posterior vessel walls together with the distension a good correlation of spin-adduct concentration after waveform diameter change as a function of time confirmation of peak to peak line width conformity and The distension waveform enables measurement of double integration on selected samples.

Measurement values of venous free radicals by photo-plethysmography Finapres, Omehda, Brussels, are expressed in arbitrary units. Belgium from a finger cuff on the middle finger of the ipsilateral arm.

Blood flow was measured throughout the study using an 8 MHz continuous wave Doppler Biochemistry probe mounted at an angle of in a Perspex block and Various metabolic factors implicated in the patho- positioned over the brachial artery distal to the 7. Fasting venous blood probe. The Doppler signals were analysed by a was drawn following a h overnight fast to enable spectrum analyser SciMed Dopstation and stored on measurement of insulin-like growth factor IGF -I, lipid a metal audiotape using a high performance recorder profiles, glucose and plasma insulin.

Total cholesterol Nakamichi BE. Brachial artery blood flow was and triglyceride concentrations were measured enzy- calculated by multiplying the mean blood velocity matically using standard techniques 23, HDL corrected for Doppler angle by the internal brachial concentrations were measured after precipitation of artery diameter measured by wall tracking.

LDL was calculated using the Friedewald equa- in measuring baseline arterial diameter for our group is tion IGF-I was measured after prior acid-ethanol 1.

Reactive free radicals decay too quickly to be observed Plasma glucose was measured by a hexokinase based directly by EPR spectroscopy under normal laboratory technique. While such spin traps are too toxic to be All studies were performed in the morning, following injected into humans, they can be conveniently used a h overnight fast, in a temperature-controlled to trap free radicals in blood samples ex vivo.

This room 21 8C—23 8C. Fasting venous blood was drawn technique has recently been used and validated to to enable biochemical analyses and free radical estima- identify lipid-derived free radicals generated post- tion. Venepuncture was conducted after the patient exercise in humans 20 , and in the coronary sinus had been in a supine position for 15 min, to reduce any of patients undergoing elective cardioplegia 21 and possible confounding effects of exertion on free radical coronary angioplasty Measurement of lipid- release.

Furthermore, each subject was asked to refrain derived free radicals ex vivo in venous blood was from any excessive physical exertion in the h period performed in a fasting state at h in all subjects. Baseline measurements of arterial of the spin trap, a-phenyl N-tert-butyl nitrone PBN diameter and baseline blood flow were made following 0.

These samples were centrifuged 15 min of supine rest. Further measurements were at r. The GTN — an endothelium-independent vasodilator. PBN adduct was extracted twice from the supernatant A paediatric sphygmomanometer cuff was inflated with an equal volume of toluene, and concentrated at the wrist to suprasystolic pressure systolic pressure to virtual dryness under nitrogen gas. Blood flow was recorded yellow oil was redissolved in ml pure chloroform and from 15 s before until 90 s after cuff release, internal analysed by EPR spectroscopy.

Samples were sealed brachial artery diameter was measured for 10 s at 60, in Pasteur pipettes and measured on a Varian E EPR , , and s after cuff release.

All measure- spectrometer operating at 9. Typical spectro- ments were repeated 15 min later when values reached meter settings were 10 mW power, 1 Gauss modulation, original baseline levels. Measurements were repeated 0. All target hor- of the study and were repeated after a 3-month period mones were maintained within the normal reference of GH replacement. The peak GH responses to insulin- Statistics induced hypoglycaemia demonstrate that these subjects Descriptive data are expressed as means 6 standard were severely GH deficient prior to inclusion in the deviation S.

The hypopituitary and control groups study. Paired t-test was used to analyse changes within individuals as a result of GH therapy. Relationships Metabolic and free radical data between endothelial function, oxidative stress and Table 3 illustrates the metabolic and free radical data various metabolic parameters were analysed using in both control and GHD study groups before and univariate and multivariate analyses. Statistical signi- after GH replacement therapy.

Thyroxine T4 , tri-iodothyronine T3 , testos- terone, oestradiol and plasma glucose concentrations Patient characteristics were similar in both control and study groups irre- Table 1 illustrates the original diagnosis, duration of spective of GH therapy. However, fasting insulin levels GHD, the peak GH response to hypoglycaemia and other were significantly elevated in the hypopituitary subjects pituitary hormone deficiencies.

Table 2 illustrates the prior to GH replacement and remained significantly demographic features of both control and GHD subjects. All patients had multiple pituitary hormone deficien- As expected, the GHD patients had significantly lower cies, which were adequately replaced with hydrocorti- IGF-I levels which increased to within the age-related sone, thyroxine, sex steroids and desmopressin where normal range for all patients following GH replacement.

Values are means 6 S. Results are expressed as means 6 S. These assignments, which agree with previous ficantly following three months of GH replacement studies 21 , suggest that these radicals are derived but still remaining elevated compared with the control from decomposition of lipid hydroperoxides in the subjects Fig.

Results are means 6 S. Vascular data endothelium-dependent vasodilatation, occurring at 1 min post-cuff release, and thus a measure of endo- Table 4 illustrates the vascular data in the control and thelial function, was significantly impaired in the study groups both before and after GH replacement.

Results were calculated as actual values but are Furthermore, the impairment in flow-mediated dila- expressed as percentage change from resting baseline tation was maintained at both 2 and 3 min post-cuff values.

There were no differences in baseline blood release Fig. Following GH therapy, however, peak flow, hyperaemic blood flow or resting vessel calibre flow-mediated brachial artery dilatation improved between patients and controls both before and after GH significantly in the GHD patients, such that there was therapy.

Endothelium-independent GTN-mediated bra- no difference in comparison with controls at 1 min. Peak flow-mediated cantly improved to a level comparable with controls Figure 2 Relationship between time and flow-mediated brachial artery dilatation in GHD adults before and after GH replacement and matched control subjects.

Shaded bars, control subjects; solid bars, pre GH replacement; open bars, post GH replacement. Of the other measured parameters in the the response of either endothelial function or oxida- pre-treatment GHD patients, plasma LDL-cholesterol tive stress to GH replacement would require larger demonstrated the strongest correlation with FMD, numbers of study subjects.

Similarly, following GH therapy plasma a standard per body weight GH replacement regime at LDL remained as the strongest, although non signifi- an accepted efficacious dose Adult GHD results in a state of volume depletion. This factor is, however, unlikely to have any effect on our measurement of FMD either before or after GH Discussion therapy. The stimulus of hyperaemic blood flow, which We have demonstrated that peak FMD, a measure of causes endothelium-dependent vasodilatation, is a endothelial function, was significantly reduced in the local phenomenon governed by hand hyperaemia.

In GHD adults compared with matched healthy controls, our study, the stimulus of hyperaemic blood flow whereas dilatation in response to GTN was normal.

The percentage increase from resting flow was similar in stimulus of increased blood flow causes a sheer stress control and GHD groups both before and after GH on the endothelium resulting in the release of NO, therapy.

GTN, by contrast, donates NO directly to profiles at base line between controls and the GHD vascular smooth muscle, thus causing vasodilatation subjects, and no changes were noted following GH by an endothelium-independent mechanism. The therapy. Furthermore, FMD was not significant, probably because of the relatively small also reduced at 2 and 3 min post-wrist-cuff release, number of subjects studied.

However, this observation further indicating endothelial dysfunction rather than is consistent with many other studies in which plasma delayed vascular smooth muscle responsiveness to LDL-cholesterol has a strong predictive value for NO. Since there were no quan- endothelium-independent dilatation is well described titative differences in lipids in comparison with controls in the presence of both overt vascular disease and or following GH replacement, the endothelial dys- many identified vascular risk factors 13, Indeed, then GTN causes vasodilatation irrespective of endo- GHD is associated with an excess of small dense LDL- thelial integrity, as this is an endothelium-independent cholesterol particles 7 which are particularly athero- mechanism.

They exhibit an increased propensity to At baseline, the GHD patients had significantly higher undergo oxidation, stimulate free radical release 32 levels of free radicals as measured by EPR spectroscopy and promote the uptake of lipids by macrophages to in comparison with control subjects.

From analysing form foam cells, culminating in increased toxicity coupling constants, the EPR spectra obtained appear to endothelial cells In addition, small dense LDL- to represent both lipid alkoxyl and carbon-centred cholesterol particles can directly induce free radical radicals. Detection of secondarily formed lipid free production Thus, improvement in endothelial radicals strongly supports the presence of peroxidative function and reduction in oxidative stress following GH damage in these patients.

This suggests that there is a therapy may, in part, be due to qualitative alterations milieu of increased oxidative stress in these patients in lipoprotein particles, possibly through improvements leading to a proatherogenic diathesis. This may contribute directly to the normal in the GHD adults. Oxidative stress also pathogenesis of ED, since free radicals can reduce bio- improved significantly with GH treatment but remained available NO 36 , are themselves directly toxic to endo- elevated compared with control subjects.

No gender thelial cells 37 , and facilitate the generation of toxic differences in either FMD or oxidative stress were oxidised LDL-cholesterol particles Thus, low completely reverse some of the mechanisms involved IGF-I levels in adult GHD may impair endothelial NO in atherogenesis and, although preliminary, provide a synthesis and so contribute to the pathogenesis of ED.

This mechanism could also contribute to the restoration of endothelial function following GH therapy. Premature mortality due to cardiovas- GHD patients and increase significantly following 3 cular disease in hypopituitarism.

The Lancet — The effects of hypopituitarism on life expectancy. Journal of Clinical Endocrinol- mediated endothelial NO synthesis may also play a role ogy and Metabolism 81 — NO has antioxidant properties.

Thus, GH-stimulated Body composition in growth hormone deficient adults. Growth hormone treatment in growth hormone deficient adults. Effects on exercise replacement.

Growth hormone deficient adults are insulin resistant. Metabolism GHD subjects indicates a state of insulin resistance 44 — The effect of GH replacement on serum oxidative stress and endothelial dysfunction seen in lipids, lipoproteins, apolipoproteins and cholesterol precursors the GHD patients. Insulin resistance is associated with in adult GHD patients. Clinical Endocrinology 41 — Insulin resistance may DG. Fasting and post-prandial lipid abnormalities in hypopituitary also contribute directly to the excess generation of free women receiving conventional hormone replacement therapy.

Following GH replacement there GH deficiency in adulthood and the effect of GH as evidenced by similar fasting insulin levels, and this replacement. Journal of Clinical Endocrinology and Metabolism may partially explain why oxidative stress still remained 83 — Nitric oxide NO in the cardiovascular system: role GH therapy significantly improves effort tolerance, in atherosclerosis and hypercholesterolaemia. Blood Pressure 5 — Oxidised lipoproteins and nitric oxide.

Current Opinion in subjects 4. Both regular exercise and physical training Lipidology 7 — Endothelium in control. British Heart Journal NO synthesis and release, together with significantly 65 — The observed bene- Non-invasive detection of endothelial dysfunction in children ficial effect of GH therapy on endothelial function may and adults at risk of atherosclerosis.

The Lancet thus be a consequence of the effect of GH on exercise — An introduction to oxygen free that exercise capacity is, at least partially, dependent on radicals. Heart and Lung 25 — Lipid peroxides and human diseases. Chemistry Physiology vascular function and NO release 46 , it is possible that Lipids 45 — Role of nitric oxide in cardiovascular disease.

Clinical contribute, in part, to its effect on endothelial function. Chemistry 44 — Is oxidative stress causally linked to unstable enhanced oxidative stress in adult hypopituitary angina pectoris? Cardiovascular Research 36 — This study would have benefitted from et al.

Oxidative stress during myocardial ischaemia and heart both a placebo control group and larger numbers of failure. Endothelial control of arterial distensibility on both endothelial function and free radical status is impaired in chronic heart failure.

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