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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of neopterin were determined in patients with different clinical stages of atherosclerosis. Non-hospitalized patients with atherosclerosis had serum and plasma neopterin levels within the normal range of the assay (6 +/- 2 nM). These values were not significantly different from those reported for healthy blood donors (5 +/- 2 nM). In contrast, about 50% (29 out of 61) of hospitalized patients undergoing conservative or surgical therapy had neopterin plasma levels, which exceeded the normal range (greater than 10 nM) up to 10-fold. The two groups differ on a significance level of P less than 0.01. For further evaluation hospitalized patients were subgrouped according to neopterin levels. In the subgroup with elevated neopterin levels patients with higher Frederickson types of atherosclerosis were overrepresented compared to patients with normal neopterin levels. Type 4 differed significantly from patients without pathological changes of lipoprotein (P less than 0.05). Only 3 patients suffered from minimal skin necrosis, two of them had elevated neopterin levels. Significantly more patients with peripheral artery occlusions had elevated neopterin levels than patients with occlusions of central arteries (P less than 0.05). All other criteria used for comparison (sex, age, smoking, antioxidant status, diabetes, hypertension, adipositas, hyperuricemia) did not vary significantly in both subgroups. These data indicate that neopterin plasma levels might be a valuable parameter in activity staging and therapeutic follow up of atherosclerotic patients. Additionally, an involvement of the nonspecific immune system in atherogenesis is suggested by the increased plasma neopterin concentrations.
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PMID:Elevated serum neopterin levels in atherosclerosis. 179 48

In forty patients with mild to moderate essential hypertension correlation between serum uric acid as well as renal excretion of urate and the transport of uric acid in nephron was evaluated. Quantity of the separate phases of uric acid transport in nephron was calculated based upon pharmacological tests with pyrazinamide and benzbromarone. The results obtained in twenty normotensive subjects were assumed to be a normal values. Positive correlation between serum uric acid and presecretory reabsorption of urate was found in hypertensive patients. However presecretory reabsorption of urate did not significantly differ between hypertensive patients with concomitant hyperuricemia and normotensive subjects. Tubular secretion of uric acid was significantly lower in hypertensive patients in comparison with normotensive subjects. Plasma uric acid correlated inversely++ with tubular secretion of urate in patients with essential hypertension. There was no difference in postsecretory reabsorption of uric acid between the groups. Plasma uric acid did not correlate with postsecretory reabsorption of urate in hypertensive patients. These findings suggest that decreased uric acid clearance in hypertension with concomitant hyperuricemia is connected with impaired tubular secretion of urate.
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PMID:[Uric acid and arterial hypertension. II. Evaluation of uric acid transport in the nephrons in primary arterial hypertension]. 180 1

In forty patients with essential hypertension correlation between serum uric acid and some clinical features of hypertensive disease i.e. severity and time of duration of arterial hypertension, the extent of vascular, retinal changes and left ventricular wall thickness was evaluated. Results showed that diastolic arterial pressure and the extent of retinal changes are significantly higher in hypertensive patients with concomitant hyperuricemia in comparison with normal uricemia patients with essential hypertension. Positive correlation was found between serum uric acid and diastolic as well as mean arterial pressure. Moreover, patients with essential hypertension and hyperuricemia demonstrated left ventricular hypertrophy in comparison with normal uricemia in hypertensive patients. Elevated serum uric acid in essential hypertension should be regarded as an early "harbinger" of disposition to the quick progress of vascular changes.
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PMID:[Uric acid and arterial hypertension. IV. Relation between serum uric acid level, the extent of vascular changes and heart enlargement in primary arterial hypertension]. 183 99

In 521 pregnancies complicated by hypertensive disorders (PHD) and in 200 control cases, we studied the incidence of intrauterine growth retardation (IUGR), depression in the newborns, general morbidity of live newborns requiring admission and perinatal mortality. We also analyzed the relationship between these conditions and the type and severity of hypertension, gestational age, presence of symptoms of the classic EPH triad and of abnormal uric acid values, hemoconcentration, and low urinary estriol values. Perinatal mortality (especially antepartum) was significantly increased in severe pre-eclampsia, chronic hypertension and chronic hypertension with superimposed pregnancy-induced hypertension (PIH); in all the cases with PHD it was three times higher than that of the control group (59% versus 20% and five times higher than the global perinatal mortality of the 25,763 deliveries attended during the same period (12% General morbidity reached 44% in severe pre-eclampsia and 75% in antepartum eclampsia. But the preterminal deliveries were also more frequent in PHD, especially in severe pre-eclampsia-eclampsia. Nevertheless, the perinatal morbidity and mortality in general increased when proteinuria and edema plus proteinuria were associated with hypertension, and the incidence was significantly higher when proteinuria surpassed 100 mg/dl. Morbimortality also increased in the presence of hemoconcentration, hyperuricemia, and low estrioluria.
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PMID:Perinatal morbidity and mortality in pregnancy hypertensive disorders: prognostic value of the clinical and laboratory findings. 197 14

Hyperuricemia is present in 20-40% of pediatric and adult patients with essential hypertension. This metabolic abnormality may represent an additional risk factor for the development of cardiovascular disease. Therefore, we performed the following studies to determine 1) whether hyperuricemia is more prevalent in the spontaneously hypertensive rat (SHR) and 2) whether allopurinol treatment has a beneficial effect on the development of hypertension in this strain, based on its capacity to lower the serum uric acid concentration and to act as an antioxidant agent. SHR and control Wistar-Kyoto (WKY) rats were assigned to two groups, one given tap water to drink and the other provided water containing allopurinol (400 mg/l) to furnish an approximate daily dose equal to 100 mg/kg body wt. This treatment was maintained for 15 weeks. The serum uric acid levels were similar in untreated SHR and WKY rats (1.85 +/- 0.10 versus 1.66 +/- 0.14 mg/dl; p = 0.28). In the control WKY rat strain, allopurinol therapy did not adversely affect weight gain or hematocrit and did not cause an increase in mortality. It resulted in a moderate decrement in kidney function (creatinine clearance: allopurinol-treated group 0.32 +/- 0.09 versus control group 0.46 +/- 0.04 ml/min/100 g body wt, in conjunction with mild-to-moderate tubulointerstitial inflammation (allopurinol-treated group 0.9 +/- 0.4 versus control group 0).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Feb
PMID:Nephrotoxicity of allopurinol is enhanced in experimental hypertension. 199 52

Epidemiologic research indicates that glucose intolerance and hypertension are interrelated phenomena, each powerfully predisposing to atherosclerotic cardiovascular disease. Both diabetic and hypertensive patients have greater amounts of atherogenic risk factors, including dyslipidemia, hyperuricemia, elevated fibrinogen, and left ventricular hypertrophy. Diabetic persons have an increased prevalence of hypertension (50%), and glucose intolerance is more common in hypertension (15% to 18%). Both share a strong relationship to excess weight, but the excess of hypertension in diabetic persons occurs in both lean and obese subjects. Diabetes doubles the risk of hypertension associated with overweight. The risk of coronary disease, stroke, and peripheral arterial disease increases with increasing blood pressure to the same degree in diabetic persons as in nondiabetic persons, but at any level of blood pressure, diabetic persons have a doubled risk of these outcomes. Both diabetic and hypertensive patients are particularly prone to silent or unrecognized myocardial infarctions. Greater efforts at primary prevention of both hypertension and diabetes are clearly needed, including efforts at weight control, exercise, limitation of salt intake, and control of blood lipid levels. In either diabetic or hypertensive candidates for cardiovascular disease, optimization of the chances of avoiding sequelae requires a comprehensive multifactorial approach. Prevention requires more than normalization of either the blood sugar or blood pressure. Rational preventive measures must also include weight reduction, a fat-modified diet, cessation of smoking cigarettes, raising high-density lipoprotein, lowering low-density lipoprotein, and reduction of fibrinogen. Hypertension, obesity, insulin resistance, hyperinsulinemia, hypertriglyceridemia, and low high-density lipoprotein cholesterol tend to coexist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The epidemiology of impaired glucose tolerance and hypertension. 200 55

The ideal body weight (kg) of each individual can be calculated by the following formula: ideal body mass index x the height (m)2, since body mass index is expressed by the body weight in kilogram divided by the height squared in meters. We investigated an ideal body mass index with respect to morbidity in 4565 Japanese men and women aged 30-59 years. Ten medical problems served as indices of morbidity: lung disease, heart disease, upper gastrointestinal disease, hypertension, renal disease, liver disease, hyperlipidemia, hyperuricemia, diabetes mellitus and anemia. The value of body mass index associated with the lowest morbidity was 22.2 kg/m2 in men and 21.9 kg/m2 in women, according to the quadratic regression curves relating body mass index to morbidity. From these findings, we propose that the ideal body weight is 22 x height (m)2. Our recommendations apply to the age group studied, namely 30-59 years.
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PMID:Ideal body weight estimated from the body mass index with the lowest morbidity. 201 Feb 54

Type I glycogen storage disease (GSD-I) is due to the deficiency of glucose-6-phosphatase activity in the liver, kidney and intestine. Although kidney enlargement occurs in GSD-I, renal disease has not been considered a major problem until recently. In older patients (more than 20 years of age) whose GSD-I disease has been ineffectively treated, virtually all have disturbed renal function, manifested by persistent proteinuria; many also have hypertension, renal stones, altered creatinine clearance or a progressive renal insufficiency. Glomerular hyperfiltration is seen in the early stage of the renal dysfunction and can occur before proteinuria. In younger GSD-I patients, the hyperfiltration is usually the only renal abnormality found; and, in some patients, microalbuminuria develops before clinical proteinuria. The predominant underlying renal pathology is focal segmental glomerulosclerosis. Renal stones and/or nephrocalcinosis are also common findings. Amyloidosis and Fanconi-like syndrome can occur, but rarely. The risk factors for developing the glomerulosclerosis in GSD-I include hyperfiltration, hypertension, hyperlipidemia and hyperuricemia. Dietary therapy with cornstarch and/or nasogastric infusion of glucose, aimed at maintaining normoglycemia, corrects metabolic abnormalities and improves the proximal renal tubular function. Long-term trial will be needed to assess whether the dietary therapy may prevent the evolution or the progression of the renal disease.
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PMID:Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment. 202 44

The risk factors vascular disease, smoking, alcohol, a diet high in saturated fat and cholesterol, sedentary life style, obesity, glucose intolerance and diabetes, high salt intake, oral contraceptives, left ventricular disease, hyperlipidemia, hyperfibrinogenemia, and uricemia are discussed in terms of evidence for added risk to hypertensive patients. Most of these risk factors have been extensively studied as contributors to the vascular diseases of the heart, brain and peripheral circulation, but not specifically in hypertensive people. For example, there is definite evidence that women with high blood pressure are at risk for coronary heart disease, and that oral contraceptives may raise blood pressure, but there are not large studies examining the level of risk for vascular disease for hypertensive women who take the pill. Similarly, the vascular risks to women who smoke and use orals are known to be multiplied, but one can only assume that hypertensive women smokers who contemplate using the pill would be at even higher risk. An exception is exercise, which has been shown to be as effective as drug therapy in lowering blood pressure and other cardiac risk factors. Generally many of these risk factors interact in a logarithmic, rather than additive manner. Furthermore, these risk factors tend to occur together more frequently in the same patient with high blood pressure more than they do in the normotensive population. High blood pressure is itself an independent risk factor for vascular disease, in proportion to its height, for all ages and sexes, whether systolic or diastolic, labile or fixed, and the threat is further aggravated by surges in blood pressure throughout the person's daily activities. In pharmacologic management of hypertension, it is important to ensure that the drug chosen does not aggravate other risk factors, such as hyperglycemia, cardiac arrhythmias or mobilization of uric acid.
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PMID:Management of vascular risk factors in the hypertensive patient. 214 91

The prevalence of gout in the United States has been rising steadily for the past two decades. Hyperuricemia is considered a necessary but not sufficient precondition for gout. Known risk factors for gout include male sex, hypertension, renal insufficiency, obesity/weight gain, diuretic use, lead exposure, and family history. The association of gout and hyperuricemia with coronary artery disease is controversial. Current evidence from the Framingham Study suggests that gout is in fact an independent risk factor for CHD. These data suggest that patients with gout should be screened for modifiable risk factors for CHD, and that early intervention in such patients may be worthwhile. Finally, the effect of AHU as risk factor for CHD remains unclear but is probably a weak one.
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PMID:Gout and hyperuricemia. 221 57


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