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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most important side effects of oral contraceptives (OCs) and their incidence, together with advice and monitoring of the patient at risk, are pointed out. There is a mild increase in blood pressure in longterm contraceptive use caused by increased angiotensinogen production by the liver. It is significant only for women with a history of familial hypertension, diabetes mellitus, or pre-eclampsia. Smoking increases this risk. Urinary tract infections are 25-50% more frequent in pill users. Glucose tolerance is slightly decreased. Contraceptives' diabetogenic effect is higher in women with hereditary tendency for diabetes, latent diabetes, and/or obesity. They are contraindicated in latent diabetes. Findings are contradictory in their effects on cholesterol and triglyceride serum level, but the pill is contraindicated in lipid metabolism disorders. There is an increased incidence in cholecystitis and cholelithiasis in pill-users (70-80 additional cases/100,000 user years). Liver diseases, intrahepatic cholestasis, occur rarely and benign liver tumors have not conclusively been proved to be caused by the pill. A variety of laboratory findings have been related to contraceptive use and drug interactions occur with barbiturates, rifampicin, hydantoin, and phenylbutazone. Blood coagulation is increased, partially by increased production of various blood coagulation factors; but more importantly, by a decreased synthesis of antithrombin III, a natural protective mechanism against intravascular coagulation. This increases thrombosis risk. Risk doubles with simultaneous cigarette smoking. Various epidemiological studies indicate a 5-10 fold increase in thromboembolism and thrombophlebitis, deep vein thrombosis, and pulmonary embolism. There is a correlation between contraceptive use and cerebrovascular disorders and myocardial infarction. This risk increases with age and years of pill use. The pill is contraindicated with symptoms of thrombophlebitis and thromboembolism, sickle cell anemia, proposed surgery, and longterm immobilization. Overall risk factors are not too high. Recommendations for rational pill use related to age are given and further contraindications are mentioned.
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PMID:[Adverse effects of oral contraceptives]. 55 52

Familial dyslipidemic hypertension (FDH) is a syndrome recently described from sibships selected for early familial hypertension and found to have one or more of three fasting lipid abnormalities [high triglycerides, low high density lipoprotein (HDL) cholesterol, high low density lipoprotein (LDL) cholesterol]. In further analyses of these same 131 hypertensive subjects, apolipoprotein A-I and B, fasting plasma insulin (adjusted for body mass index), and detailed anthropometrics were different in two subgroups of FDH. Of 63 FDH patients, 19 met the criteria for familial combined hyperlipidemia (FCHL); 44 did not, but still had high triglyceride and/or low HDL cholesterol levels. When compared to 20 normolipidemic hypertensive patients, the 19 hypertensive patients with FCHL had 196% higher very low density lipoprotein cholesterol (p = 0.0001), 33% higher apolipoprotein B (p = 0.0002), smaller LDL particles (p = 0.007), and 73% higher fasting insulin (p = 0.003), but no significant differences in body mass index or skinfold thicknesses. The other 44 FDH patients without FCHL had 33% lower HDL (p = 0.0001), with only 8% lower apolipoprotein A-I levels (p = 0.20); significantly higher subscapular skinfolds (p = 0.02), weights (p = 0.002), body mass index (p = 0.006), knee widths (p = 0.0007), and wrist circumferences (p = 0.0009); smaller, denser LDL subfractions (p = 0.001); and increased apolipoprotein B levels (p = 0.01) compared to the normolipidemic hypertensive group. Increased fasting insulin levels were similar to the normolipidemic group and significantly lower than the FCHL group after adjustment for body mass index, suggesting a relationship between obesity and fasting insulin levels only in the non-FCHL group. We conclude that FDH consists of at least two subgroups: 1) FCHL with high apolipoprotein B, small LDL particles, and increased fasting plasma insulin levels, and 2) a less well-defined residual having upper central obesity with low HDL cholesterol and high triglyceride levels. Elevated insulin levels found in both groups, but possibly originating through different physiological mechanisms, may provide the pathophysiological connections between dyslipidemia, obesity, and hypertension.
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PMID:Apolipoprotein, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidemia. Study of Utah patients with familial dyslipidemic hypertension. 249 19

An epidemiological study has been carried out on a group of 622 students (10 to 13 years old) from a secondary school in Naples. Aims of the present work were: the evaluation of the prevalence of hypertension in an adolescent population; the association with familial hypertension and obesity; the persistence of high blood pressure values at follow-up. Blood pressure data obtained in these subjects by the use of a standard evaluation scale based on body surface percentiles were compared with those obtained by two major current methods used for the definition of "normal" blood pressure values in pediatric age. The method based on body surface percentiles has shown the highest specificity. The prevalence of hypertension, as detected by this method, has been of 3,5% as compared to 12,9% and to 9,5% of the other two methods. In a follow-up at one year, while the percentage of hypertensive students remained unchanged in the group detected by the method of body surface percentiles, it decreased from 12,9% to 9,3% and from 9,5% to 7,8% in the other two groups. The high prevalence of obesity and familial hypertension observed in these young hypertensive subjects suggest the possibility of selecting, by body surface percentiles, well defined group of subjects at risk, characterized by borderline hypertension, high grade of familial aggregation, high prevalence of obesity and by the persistence of hypertension at the follow-up.
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PMID:[Juvenile arterial hypertension and body surface area. Initial results of a longitudinal epidemiologic study]. 653 82

Studies with school aged children of several communities of the United States have indicated that between one and two percent of them should be considered hypertensive. These findings contradict previous statements of a very rare incidence of hypertension in childhood. Some studies show that children of Black and Hispanic American ancestry, especially females, have a higher incidence of hypertension. The highest incidence of hypertensive children was related to a history of familial hypertension and obesity. In children less than three years of age and in infants, hypertension is less frequent. A disease of the urinary apparatus (nephropathy) or of the cardiovascular system (aorta coarctation) can often be identified as the primary cause of the hypertension. Less frequent is hypertension sustained by adrenal cortical dysfunction or a neoplasm of the adrenal medulla. Hypertensive crisis also frequently develops in children after thermal injury or renal transplant. In children, the use of antihypertensive drugs should be reserved for cases where the disease is very severe. Effective regulation of dietary and hygienic habits should be recommended, particularly for those cases of "mild" or "borderline" essential hypertension.
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PMID:Considerations of the renin-angiotensin aldosterone system in the pathogenesis of hypertension in infancy. 675 76

The epidemiologic links among essential hypertension, obesity, and noninsulin-dependent diabetes mellitus (NIDDM) are well recognized, and it has been proposed that these links may reflect an underlying common pathophysiologic link of resistance to the action of insulin (insulin resistance). In essential hypertension, data suggest the insulin resistance pertains predominantly to nonoxidative glucose disposal, especially in skeletal muscle and adipose tissue, which contrasts with a more generalized deficit in obesity and NIDDM. A number of animal studies of genetic hypertension have confirmed the presence of insulin resistance, whereas acquired models of animal hypertension have not. The clinical significance of insulin resistance on long-term morbidity in hypertension remains unclear; there is limited evidence that insulin resistance may be an independent risk factor for subsequent vascular events, but it is more likely that it clusters with other better defined risk factors for the vascular complications of hypertension. The potential clinical sequelae of insulin resistance and hyperinsulinemia and the effect of antihypertensive medication on insulin resistance in general are addressed.
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PMID:Insulin resistance and essential hypertension: mechanisms and clinical implications. 814 Nov 65

The association of arterial hypertension and diabetes mellitus is frequent: one third of patients attending a diabetic clinic. Excess hypertension frequency is marked in type II, non insulin-dependent diabetes, a condition often associated with other vascular risk factors such as obesity and lipid disorders. Insulin resistance is a common feature between type II diabetes, hypertension and other risk factors. In type I, insulin-dependent diabetes, hypertension is often linked to diabetic nephropathy. There is a genetic basis for diabetic nephropathy, which may share a common background with familial hypertension. Apart from possible genetic predispositions to hypertension diabetes association, chronic hyperglycaemia can lead to alteration in functional and structural properties of blood and vessels, which both contribute to elevated vascular resistance and blood pressure. From a therapeutic viewpoint, blood pressure values above 140/90 mmHg are not tolerable in diabetic subjects under 40 years of age. Due to their renal haemodynamic effects, angiotensin I converting enzyme inhibitors may be of special interest to protect kidney function in diabetic subjects.
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PMID:Hypertension and diabetes mellitus. 821 50

Hypertension affects 26% of adults and is in constant progress related to increased incidence of obesity and diabetes. One-third of hypertensive patients may be successfully treated with one antihypertensive agent, one-third may require two agents and in the remaining patients will need three agents for effective blood pressure (BP) control. The development of new classes of antihypertensive agents with different mechanisms of action therefore remains an important goal. Brain renin-angiotensin system (RAS) hyperactivity has been implicated in hypertension development and maintenance in several types of experimental and genetic hypertension animal models. Among the main bioactive peptides of the brain RAS, angiotensin (Ang) II and Ang III have similar affinities for type 1 (AT1) and type 2 (AT2) Ang II receptors. Following intracerebroventricular (i.c.v.) injection, Ang II and Ang III similarly increase arginine-vasopressin (AVP) release and BP. Blocking the brain RAS may be advantageous as it simultaneously (1) decreases sympathetic tone and consequently vascular resistance, (2) decreases AVP release, reducing blood volume and vascular resistance and (3) blocks angiotensin-induced baroreflex inhibition, decreasing both vascular resistance and cardiac output. However, as Ang II is converted to Ang III in vivo, the exact nature of the active peptide is not precisely determined. We summarize here the main findings identifying AngIII as one of the major effector peptides of the brain RAS in the control of AVP release and BP. Brain AngIII exerts a tonic stimulatory effect on BP in hypertensive rats, identifying brain aminopeptidase A (APA), the enzyme generating brain Ang III, as a potentially candidate target for hypertension treatment. This has led to the development of potent orally active APA inhibitors, such as RB150--the prototype of a new class of centrally acting antihypertensive agents.
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PMID:The role of the brain renin-angiotensin system in hypertension: implications for new treatment. 2176 94

Hypertension affects one-third of the adult population and is a growing problem due to the increasing incidence of obesity and diabetes. Brain RAS (renin-angiotensin system) hyperactivity has been implicated in the development and maintenance of hypertension in several types of experimental and genetic hypertension animal models. We have identified in the brain RAS that APA (aminopeptidase A) and APN (aminopeptidase N), two membrane-bound zinc metalloproteases, are involved in the metabolism of AngII (angiotensin II) and AngIII (angiotensin III) respectively. The present review summarizes the main findings suggesting that AngIII plays a predominant role in the brain RAS in the control of BP (blood pressure). We first explored the organization of the APA active site by site-directed mutagenesis and molecular modelling. The development and the use in vivo of specific and selective APA and APN inhibitors EC33 and PC18 respectively, has allowed the demonstration that brain AngIII generated by APA is one of the main effector peptides of the brain RAS, exerting a tonic stimulatory control over BP in conscious hypertensive rats. This identified brain APA as a potential therapeutic target for the treatment of hypertension, which has led to the development of potent orally active APA inhibitors, such as RB150. RB150 administered orally in hypertensive DOCA (deoxycorticosteroneacetate)-salt rats or SHRs (spontaneously hypertensive rats) crosses the intestinal, hepatic and blood-brain barriers, enters the brain, generates two active molecules of EC33 which inhibit brain APA activity, block the formation of brain AngIII and normalize BP for several hours. The decrease in BP involves two different mechanisms: a decrease in vasopressin release into the bloodstream, which in turn increases diuresis resulting in a blood volume reduction that participates in the decrease in BP and/or a decrease in sympathetic tone, decreasing vascular resistance. RB150 constitutes the prototype of a new class of centrally acting antihypertensive agents and is currently being evaluated in a Phase Ib clinical trial.
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PMID:A new strategy for treating hypertension by blocking the activity of the brain renin-angiotensin system with aminopeptidase A inhibitors. 2469 96

Chromogranin A (CgA)-the index member of the chromogranin/secretogranin secretory protein family-is ubiquitously distributed in endocrine, neuroendocrine, and immune cells. Elevated levels of CgA-related polypeptides, consisting of full-length molecules and fragments, are detected in the blood of patients suffering from neuroendocrine tumors, heart failure, renal failure, hypertension, rheumatoid arthritis, and inflammatory bowel disease. Full-length CgA and various CgA-derived peptides, including vasostatin-1, pancreastatin, catestatin, and serpinin, are expressed at different relative levels in normal and pathological conditions and exert diverse, and sometime opposite, biological functions. For example, CgA is overexpressed in genetic hypertension, whereas catestatin is diminished. In rodents, the administration of catestatin decreases hypertension, cardiac contractility, obesity, atherosclerosis, and inflammation, and it improves insulin sensitivity. By contrast, pancreastatin is elevated in diabetic patients, and the administration of this peptide to obese mice decreases insulin sensitivity and increases inflammation. CgA and the N-terminal fragment of vasostatin-1 can enhance the endothelial barrier function, exert antiangiogenic effects, and inhibit tumor growth in animal models, whereas CgA fragments lacking the CgA C-terminal region promote angiogenesis and tumor growth. Overall, the CgA system, consisting of full-length CgA and its fragments, is emerging as an important and complex player in cardiovascular, immunometabolic, and cancer regulation.
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PMID:Chromogranin A and its fragments in cardiovascular, immunometabolic, and cancer regulation. 3158 72