International journal of clinical practice. Supplement最新文献

It is becoming increasingly clear that hypertension and metabolic risk factors in women are inter-related and often share underlying causes. Menopause acts explicitly as a risk factor by reducing the direct beneficial effect of ovarian hormones upon cardiovascular functions and indirectly by negatively influencing other risk factors for coronary artery disease--i.e. hyperinsulinaemia, blood cholesterol, blood pressure, coagulation etc. Adverse changes in one factor may induce adverse changes in a variety of other risk factors and it is important to consider co-ordinated changes when evaluating these patients rather than attempt to isolate independent factors. Similarly with treatment, the prevalence of metabolic syndrome in postmenopausal hypertensive women has important implications and some antihypertensive drugs may worsen the already altered metabolic profile of these patients while others may be beneficial. Centrally-acting sympatholytic agents, e.g. moxonidine, are therefore important to consider in hypertensive postmenopausal women who experience other symptoms of metabolic syndrome.

Hypertension is more common in younger men than women but this trend is inverted at approximately 60 years of age--thereafter hypertension is more common in women. Menopause's contribution to this phenomenon is complex. Oestrogen deficiency after menopause precipitates a number of factors and these have established the 'menopausal metabolic syndrome' as a concept in postmenopausal women. However, studies have indicated that changes in the prevalence of hypertension, and overall cardiovascular risk profiles in postmenopausal women, might be due to ageing and not oestrogen deficiency. Undoubtedly, there is a strong multicolinearity between the two phenomena. Furthermore, hormone replacement therapy (HRT) may reduce age-induced blood pressure increases, thus decreasing cardiovascular risks. However, recent results have questioned HRT's role in cardiovascular disease (CVD) prevention in postmenopausal women and trials have unequivocally shown that CVD risk in postmenopausal women with hypertension can be effectively reduced by common antihypertensive drugs.

Women typically experience increased cardiovascular disease (CVD) following menopause. Major risk factors for CVD include hypertension and, after menopause, blood pressure increases in women. The mechanism(s) responsible for this increase are not determined. Changes in oestrogen/androgen ratios, possible activation of the renin-angiotensin system, and increases in endothelin and oxidative stress, are hallmarks in postmenopausal women. Obesity, type 2 diabetes and activation of the sympathetic nervous system may also play important roles. However, progress in clarifying the mechanisms responsible for postmenopausal hypertension has been hampered by lack of a suitable animal model. We have recently characterised the ageing female spontaneously hypertensive rat (SHR) as a model of postmenopausal hypertension, since this strain exhibits many of the humoral characteristics of postmenopausal women. This review discusses some of the mechanisms that could play a role in postmenopausal hypertension, as well as the characteristics of the ageing female SHR as a model.

This study compared the effects of two sympatholytic agents--one central (moxonidine) and one peripheral (atenolol)--on blood pressure and other metabolic syndrome factors in postmenopausal hypertensive women who were not taking hormone replacement therapy. Atenolol and moxonidine led to a statistically significant reduction in diastolic blood pressure of 9.5 mmHg and 5.5 mmHg, respectively. A clear rebound effect was observed in the atenolol patients whereas the moxonidine group exhibited a slightly further decrease in blood pressure. Moxonidine also caused a profound decrease in both mean plasma-glucose area under the curve (AUC) during oral glucose tolerance test (-0.96 mmol/L x H, NS) and mean plasma-insulin AUC (-6.15 mU/L x H). Therefore, moxonidine displayed a slightly less potent antihypertensive effect than atenolol in hypertensive postmenopausal women, but it demonstrated a better metabolic effect. To conclude, moxonidine could benefit hypertensive postmenopausal women who display other signs of metabolic syndrome.

Ibuprofen is prescribed for children for the treatment of acute pain and fever, and for juvenile idiopathic arthritis. The pharmacokinetic characteristics of ibuprofen in children are similar to those in adults and the relationship between dose and response is linear over the range 5-10 mg/kg. Clinical trials of ibuprofen have shown the effective dose range to be 7.5-10 mg/kg. The maximum reduction in temperature occurs 3-4 hours after administration. In comparative clinical trials, ibuprofen has been shown to be equally as effective as or more effective than paracetamol as an analgesic and antipyretic and to have a longer duration of action; it is also as effective as aspirin. The adverse effects of ibuprofen are similar to those of other non-steroidal anti-inflammatory drugs but clinical experience suggests that ibuprofen is better tolerated by children than adults and it is safer in overdose than paracetamol and aspirin.