Long-term effects of weight-reducing drugs in hypertensive patients

Siebenhofer, Andrea; Horvath, Karl; Jeitler, Klaus; Berghold, Andrea; Stich, Anne Kathrin; Matyas, Eva; Pignitter, Nicole; Siering, Ulrich

doi:10.1002/14651858.cd007654.pub2

Cited by 37 publications

(48 citation statements)

References 58 publications

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“…Available weight reduction drugs include orlistat, a fat-absorption (lipase) inhibitor and sibutramine, an appetite-suppressing drug with central action (norepinephrine and serotonin reuptake inhibition). 81 Orlistat reduced BP 83 with side effect being the reduction of fat-soluble vitamins absorption. Sibutramine was reported to induce tachycardia and probably increased BP 83 as a result of the interaction between peripheral and central nervous system effects, peripheral stimulatory effects and inhibitory clonidine-like actions on the central nervous system.…”

Section: Endothelial Dysfunction and Changes In Vascular Structurementioning

confidence: 99%

“…81 Orlistat reduced BP 83 with side effect being the reduction of fat-soluble vitamins absorption. Sibutramine was reported to induce tachycardia and probably increased BP 83 as a result of the interaction between peripheral and central nervous system effects, peripheral stimulatory effects and inhibitory clonidine-like actions on the central nervous system. 84 Rimonabant, a novel CB 1 -receptor inhibitor at the CNS and peripheral tissues, has been associated with increased rates of anxiety and depression disorders, and the European Medicines Agency has recently recommended the suspension of the marketing authorization for the treatment of obesity.…”

Section: Endothelial Dysfunction and Changes In Vascular Structurementioning

confidence: 99%

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Mechanisms of obesity-induced hypertension

et al. 2010

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The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi:10.1038/hr.2010.9Keywords: leptin; obesity; pressure natriuresis; rennin-angiotensin-aldosterone system; sympathetic nervous system INTRODUCTION Obesity is a common disorder that develops from the interaction between the genotype and the environment and involves social, behavioral, cultural, physiological, metabolic and genetic factors. A large number of studies have shown that obesity has an important negative impact on health in a population, leading to the recommendation for general practitioners to have an important function in the management of this condition and of its associated comorbidities such as hypertension, hyperlipidemia and hyperinsulinemia/insulin resistance. The relationship between obesity and hypertension is well established both in adults and children. 1,2 Obese individuals exhibit higher levels of office as well as ambulatory blood pressure (BP) from childhood to old age. Obese subjects display higher BP levels than non-obese individuals even in the normotensive range. The combination of obesity, hypertension and other cardiovascular risk factors significantly increases the probability of adverse cardiovascular outcomes, and raises considerations for aggressive treatment strategies. 3 The mechanisms through which obesity directly causes hypertension are still an area of research. Human and animal studies have elucidated the function of adipose tissue derivatives (adipokines and cytokines), neurohumoral pathways, metabolic functions and modulation of pressor/depressor mechanisms. Although obesity-related hypertension may be the result of a combinatio...

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Section: Endothelial Dysfunction and Changes In Vascular Structurementioning

confidence: 99%

Section: Endothelial Dysfunction and Changes In Vascular Structurementioning

confidence: 99%

Mechanisms of obesity-induced hypertension

et al. 2010

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“…Furthermore, in animal studies, methylphenidate increased locomotor activity (24,25) and thus might be a helpful compound to overcome physical hypoactivity, which is common in patients with hypothalamic obesity (10,19,26). Orlistat, a gastrointestinal lipase inhibitor, has limited efficacy and can be associated with intolerable side effects that can preclude its use (27,28). Several other drugs have recently been withdrawn from the market due to severe side effects, e.g.…”

Section: Introductionmentioning

confidence: 99%

GLP-1 analogues as a new treatment option for hypothalamic obesity in adults: report of nine cases

Zoicas

Droste

Mayr

et al. 2013

European Journal of Endocrinology

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Background: Patients with hypothalamic pathology often develop morbid obesity, causing severe metabolic alterations resulting in increased morbidity and mortality. Glucagon-like peptide-1 (GLP-1) analogues improve glycaemic control in type 2 diabetic patients and cause weight loss in obese patients by yet unknown mechanisms. Here we tested whether GLP-1 analogues were also effective in the treatment of obesity and associated metabolic alterations in patients with hypothalamic disease. Methods: Nine patients (eight with type 2 diabetes mellitus) with moderate to severe hypothalamic obesity were treated with GLP-1 analogues for up to 51 months. Body weight, homeostasis model assessment -insulin resistance (HOMA-IR), HbA1c and lipids were assessed. Results: Eight patients experienced substantial weight loss (K13.1G5.1 kg (range K9 to K22)). Insulin resistance (HOMA-IR K3.2G3.5 (range K9.1 to 0.8)) and HbA1c values (K1.3G1.4% (range K4.5 to 0.0)) improved under treatment (24.3G18.9 months (range 6 to 51)). Five patients reported increased satiation in response to the treatment. Two of the eight patients complained about nausea and vomiting and one of them abandoned therapy because of sustained gastrointestinal discomfort after 6 months. One patient suffered from intolerable nausea and vomiting and discontinued treatment within 2 weeks. Conclusion: GLP-1 analogues can cause substantial and sustained weight loss in obese patients with hypothalamic disease. This offers a new approach for medical treatment of moderate to severe hypothalamic obesity and associated metabolic alterations.

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“…Existen una serie de drogas relacionadas con HTA como anorexígenos, antiinflamatorios no esteroidales, antijaquecosos, antidepresivos y ACO 28,29 .…”

Section: Hta Secundariaunclassified