Obesity and hypertension

Mikhail, Nasser; Golub, Michael S.; Tuck, Michael L.

doi:10.1016/s0033-0620(99)70008-3

Cited by 118 publications

(77 citation statements)

References 129 publications

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“…These results are interesting because of the strong association between RAS and the mechanisms of obesity. Obesity leads to hypertension and increases the cardiovascular risk (Mikhail et al, 1999). RAS has been implicated in obesity by several authors (Giacchetti et al, 2002), which is supported by recent investigations that show high plasma concentrations of angiotensinogen (ANG) (Umemura et al, 1997) and a rise in the expression of the ANG gene in obese humans (Van Harmelen et al, 2000).…”

Section: Discussionmentioning

confidence: 88%

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

et al. 2007

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Metabolic Syndrome (MS) is recognized as a cluster of cardiovascular risk factors. All components of MS have a genetic base. Genes of the renin angiotensin system are potential candidate genes for MS. We investigated whether angiotensin converting enzyme (ACE) gene polymorphism increases susceptibility to MS as an entity in a Mexican population. In a cross-sectional study, 514 individuals were studied including 245 patients with MS and 269 subjects without MS criteria. ACE gene polymorphism was detected using PCR. MS was defined according to The National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) criteria, except that the raised fasting plasma glucose ≥ 100 mg/dl criterion for identification of intolerance fasting glucose was modified in accordance with the suggestion of the American Diabetes Association. Patients with MS were significantly different from subjects without MS in relation to mean body mass index (BMI), waist circumference (WC), systolic blood pressure, diastolic blood pressure, glucose, total cholesterol (C), triglycerides, HDL-C, and LDL-C (P ＜ 0.0001). The differences in the mean BMI, WC, glucose, total cholesterol, triglycerides, LDL-C, and HDL-C were maintained in patients with the MS and DD genotypes (P ＜ 0.01). The DD genotype was strongly associated with MS (adjusted OR = 5.48, 95% CI 3.20-9.38, P ＜ 0.0001). We concluded that the DD genotype increases susceptibility to MS in a Mexican population. These results indicate that pharmacological and non-pharmacological treatment and a reduction in body fat will have important therapeutic implications in this disease.

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Section: Discussionmentioning

confidence: 88%

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

et al. 2007

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“…Hypertension is the most common obesity-related disease. 21 A case report of new-onset hypertension and peripheral oedema during treatment with orlistat has been published, however, there is disagreement over the cause of further episodes of oedema in this patient after treatment with orlistat was stopped. [22][23][24] One report of oedema and three reports of swelling of the ankles were assessed as causally related to orlistat in our study.…”

Section: Discussionmentioning

confidence: 88%

Safety profile of orlistat: results of a prescription-event monitoring study

2006

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Introduction: Orlistat, the first of a new class of drugs for the treatment of obesity, was launched in the UK in December 1998. The prescribing information recommends that treatment with orlistat should be discontinued after 12 weeks if the patient has not achieved a specified loss of weight. Objective: To monitor the safety of orlistat prescribed in the primary care setting in England using prescription-event monitoring (PEM). Methods: A postmarketing surveillance study using the observational cohort technique of PEM. Patients were identified from dispensed prescriptions issued by primary care physicians for orlistat between December 1998 and November 1999. The outcome data were event reports obtained by sending questionnaires (green forms) to the prescribing doctor at least 6 months after the first prescription for an individual patient. Incidence densities, expressed as number of first reports of an event/1000 patient-months of exposure, were calculated. Significant differences between incidence densities (IDs) for events reported in the 1st month (ID 1 ) and months 2 and 3 (ID 2-3 ) of exposure were regarded as potential signals. Reasons for stopping orlistat were analysed. Follow-up information was requested for selected events and used to assess the causal association with orlistat. Results: Green forms containing clinically useful information on 16 021 patients (median age 45 years (interquartile range 35-54); 80.1% females) were received. The events reported most frequently during the 1st month of treatment were 'not effective' (639; 4.0% of cohort), diarrhoea (371; 2.3%) and weight loss (230; 1.4%). Twelve clinical adverse events were identified for which ID 1 was significantly greater than ID 2-3 . These included non-specific events (e.g. intolerance, malaise/ lassitude, unspecified side effects), weight loss and vaginitis/vulvitis. The remaining events were gastrointestinal in nature and included diarrhoea, pain abdomen, flatulence, nausea/vomiting, rectal discharge, faecal incontinence and 'gastrointestinal unspecified' events. A similar pattern of predominately gastrointestinal events was seen for reasons for stopping and suspected adverse drug reactions. Review of selected events for causality revealed 45 events which were assessed as possibly or probably related to orlistat. Conclusions: This study shows that orlistat is fairly well tolerated. The safety profile of orlistat was similar to the prescribing information and experience reported in the literature.

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“…[63][64][65] CCB are considered metabolically neutral, as it does not affect insulin sensitivity or the levels of serum insulin, glucose and lipid. 8,63,65 CCB can reduce LVH more effectively than diuretics and BRB. 49 Nondihydropyridine CCB (diltiazem, verapamil) can also lower the heart rate, may reduce the rate of reinfarction and increase the patient survival after an AMI.…”

Section: Diureticsmentioning

confidence: 96%

“…3,6 There is cumulating evidence suggesting that obesity per se, is the cause of HTN in obese subjects. 3,[7][8][9] Obesity-associated HTN has a complex, multifactorial mechanism, including activation of the sympathetic nervous system (SNS) and the reninangiotensin systems (RAS), insulin resistance, excess renal sodium reabsorption, leptin-resistance and natriuretic peptides (NPs) downregulation. [7][8][9] Pressure natriuresis normally seen with increased blood pressure (BP) is blunted in obesity.…”

Section: Introductionmentioning

confidence: 99%

“…3,[7][8][9] Obesity-associated HTN has a complex, multifactorial mechanism, including activation of the sympathetic nervous system (SNS) and the reninangiotensin systems (RAS), insulin resistance, excess renal sodium reabsorption, leptin-resistance and natriuretic peptides (NPs) downregulation. [7][8][9] Pressure natriuresis normally seen with increased blood pressure (BP) is blunted in obesity. 9,10 Obesity-HTN causes haemodynamic and structural adaptations in the renal and cardiovascular systems.…”

Section: Introductionmentioning

confidence: 99%

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