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

The study was undertaken to determine the causes of the more frequent pre-term deliveries, fetal and neonatal deaths associated with maternal urinary-tract infections during pregnancy. The combined perinatal mortality rate for eight common placental and fetal disorders was 42 per thousand births in the infected vs. 21 per thousand in the noninfected, owing to a greater mortality from noninfectious placental and fetal disorders in the gestations with the urinary-tract infections (P less than 0.001). All the mortality excess took place when the urinary-tract infections occurred within 15 days of delivery. Death rates were highest when the urinary-tract infections coexisted with maternal hypertension and acetonuria.Hydramnios, amniotic-fluid bacterial infections and abruptio placentae were responsible for two thirds of the more frequent preterm deliveries in the pregnancies complicated by urinary-tract infections.
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PMID:Causes of the excessive rates of perinatal mortality and prematurity in pregnancies complicated by maternal urinary-tract infections. 37 May 93

Very fat people die earlier than people of normal weight because hypertension, diabetes and coronary disease are more frequent among the markedly obese. Most obese subjects, however, are only slightly overweight and their mortality is not elevated. Reasons for dieting are more often psychological than somatic. 2. Reducing diets are ineffective because the obese rarely follow them. Total fasting and intestinal bypass may provide better results, but are more dangerous. 3. Atkins' diet eliminates carbohydrates from food without restricting protein and fat intake. Deprived of carbohydrates, the body uses fat for fuel. A small part of metabolized fat is eliminated in the urine as ketone bodies, and this is why such diets are called "ketogenic". They have been known at least since 1863. 4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the non-diabetic. It is maximal during total fasting and cannot be increased by a ketogenic diet. 5. In the short run, such diets produce rapid weight loss due to polyuria. On the other hand, refeeding carbohydrates causes water retention and weight gain. 6. The diet decreases appetite: patients eat less without feeling severe hunger and without measuring their food intake. 7. Orthostatic hypotension, fatigue, and nausea are frequent, despite what Dr. ATKINS claims. 8. The diet increases plasma cholesterol and uric acid. It may be dangerous in diabetes (anorexia, acidosis) and in heart or kidney failure (hypokalemia). 9. The diet, though far from good, is better than the book. ATKINS' theories are at best half-truths, and the results he claims lack credibility. The obese subject's disappointment with traditional reducing diets and the book's hard-sell style account for ATKINS' success.
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PMID:[Dr. Atkins' dietetic revolution: a critique]. 89 45

907 consecutive patients, (456 Asian and 451 Caucasian) were assessed, employing a similar methodology to the multi-centre WHO study. The Asians were older at diagnosis (46.5 years compared with 40.6 years, P less than 0.01); they had a shorter duration of diabetes (6.3 years versus 11.4 years, P less than 0.1), a higher rate of diabetes in the first degree relatives (29.5% compared with 16%, P less than 0.1), less ketonuria at presentation (85.3% compared with 47.8%, P less than 0.1), and fewer were treated with insulin (31.4% compared with 68.7%). Comparing the prevalence of complications between Asians and Caucasians, the ischaemic heart disease rate was similar; peripheral vascular disease was less (3.7% Asian, 9.3% Caucasian, P less than 0.05); retinopathy was less (11.6% Asian, 32.3% Caucasian, P less than 0.01) but renal disease was more (22.3% Asian, 12.6% Caucasian, P less than 0.01). After adjusting for age, sex, duration of diabetes, age at diagnosis, hypertension, smoking and treatment with or without insulin, these differences remained significant. Multivariate logistic regression failed to reveal a significant contribution due to any of the above variables, or due to body mass index (BMI), haemoglobin A (HbA1), or physical activity in the prevalence of complications in Asians compared with Caucasians. Marked heterogeneity in the complications of diabetes in the two ethnic groups studied was found, but must be confirmed from population-based studies.
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PMID:A comparison of the clinical features and vascular complications of diabetes between migrant Asians and Caucasians in Leicester, U.K. 177 13

Selected hemodynamic, renal, and biochemical parameters were assessed in chronically instrumented third-trimester pregnant ewes and in the same ewes after induction of pregnancy toxemia. Ewes with induced pregnancy toxemia developed hypertension, proteinuria, ketonuria, decreased glomerular filtration rate, decreased cardiac output, and decreased left uterine artery blood flow. Histological and transmission electron microscopy revealed the development of renal morphologic changes consistent with those observed in human pregnancy-induced hypertension. These studies have elucidated that pregnancy-induced hypertension can be produced experimentally in the pregnant ewe. Furthermore, the pathophysiologic features of ovine pregnancy toxemia are similar to those of human preeclampsia, and therefore the sheep provides a suitable animal model to study the human condition, which still remains a major complication of pregnancy, jeopardizing both mother and fetus.
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PMID:Pregnancy-induced hypertension: development of a model in the pregnant sheep. 372 88

Diabetic ketoacidosis is usually associated with marked secondary hyperaldosteronism. Plasma levels of renin, angiotensin II, and aldosterone are markedly raised before treatment in most patients, with values falling rapidly toward normal as metabolic control is restored. In a few patients, mostly those with long-term complications of diabetes, plasma levels of renin, angiotensin II, and aldosterone before treatment remain within the normal range. In moderately hyperglycemic patients who have glycosuria but not ketonuria, plasma levels of all three substances are significantly higher than when control is improved. Occasionally, moderately hyperglycemic patients have mild secondary hyperaldosteronism. Improved metabolic control in such patients causes a rise in plasma volume and a rise in total exchangeable sodium, the latter to levels significantly above normal. Plasma catecholamine levels are markedly elevated in diabetic ketoacidosis, probably as a consequence of the ketoacidotic state. In nonketotic patients with moderate hyperglycemia, basal plasma norepinephrine levels are normal; catecholamine responses to exercise may be exaggerated, however. Epidemiological and animal studies suggest a relationship between blood pressure and blood glucose levels. There are few clinical studies of the effects of altering metabolic control of diabetes on blood pressure, and this is an important area for further study.
Hypertension
PMID:Diabetic control and the renin-angiotensin system, catecholamines, and blood pressure. 393 82

A survey of 67 pregnancies in 51 professional women (physicians, psychologists, nurses, administrators, etc.) revealed the occurrence of symptoms of cognitive dysfunction such as forgetfulness, disorientation, confusion and reading difficulties in 28 pregnancies occurring in 21 women. These were unrelated to such factors as age of delivery, percentage weight gain, the baby's sex or birth weight, alcohol consumption, smoking, a history of migraine or allergy or other symptoms occurring during pregnancy such as sleepiness and lack of concentration, irritability, loss of interest in job or nightmares. Nor was there any correlation with hypertension, proteinuria, glycosuria, ketonuria, anemia, or morning sickness. Furthermore, these cognitive disturbances were not related to depression or sleep deprivation. Despite these symptoms, none of the women suffering from them were forced to interrupt their professional activities during pregnancy. The syndrome of benign encephalopathy of pregnancy should be recognized so that simple precautions can be taken to prevent any interference with professional or other activities. The etiology of the syndrome is unknown.
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PMID:Benign encephalopathy of pregnancy. Preliminary clinical observations. 395 58

To delineate the hormonal mechanism of dietary-induced changes in sodium balance, the role of insulin and glucagon in natriuresis of fast was evaluated in obese subjects submitted to a total starvation and given either glucagon or somatostatin infusion on day 4 of fast. While large amounts of glucagon (1 mg over 6 h) stimulated concomitantly ketonaemia, ketonuria and renal sodium losses, the ten-times lower amounts of glucagon induced an increase in renal ketone body and sodium excretion without any significant change in ketonaemia. It was concluded, therefore, that elevated plasma glucagon level may enhance renal sodium loss in ketotic states, through a direct renal effect reducing tubular ketone body reabsorption, hence increased ketonuria and natriuresis. It appears nevertheless that decreased insulin secretion, rather than an increase in plasma glucagon level must be considered as a key hormonal factor responsible for natriuresis attending starvation. Indeed, the concomitant reduction in plasma glucagon and insulin levels, resulting from somatostatin infusion on day 4 of fast, was followed by significant increase in natriuresis. The latter observation supports several previous studies indicating that insulin stimulates sodium reabsorption by the kidney and that the reduction in insulin secretion may induce an increase in renal sodium excretion. It was concluded, therefore, that not only sodium intake but also the carbohydrate content of the diet should be reduced in an attempt to induce a negative sodium balance and to correct hypertension in obese subjects.
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PMID:Influence of insulin and glucagon on sodium balance in obese subjects during fasting and refeeding. 611 18

A 300 kcal (1.25 MJ) diet of conventional food is described, which has been studied under in-patient conditions for four to six weeks. It contained 22.6 g protein, 34 g CHO and 6.9 g fat but not the full RDA of vitamins and minerals since this is impossible without supplementation. Hunger disappeared after the third day. Patients developed ketonuria and hyperuricemia; serum lipids were normalised and hypertension disappeared. The diet offers advantages in that it induces better nutritional knowledge and habits.
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PMID:A 300 kcal (1.2 MJ) diet using conventional food. 727 57

Data were analyzed from 36,068 U.S. pregnancies to determine whether any of the more frequent maternal risk factors are associated with seasonal variations in perinatal mortality rates. These mortality rates decreased below the yearly mean in January and rose sharply above the mean during the spring. The perinatal mortality rate in May/June was 30% above the rate in January/February (P less than 0.001). This and other variations in perinatal mortality rates closely followed changes in maternal coital activity. The proportion of women having coitus was 26% greater in May/June than in January/February (P less than 0.001). Seasonal variations in the frequencies of maternal hypertension, acetonuria and low pregnancy weight gain did not correlate with changes in perinatal mortality rates.
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PMID:Seasonal variations in coitus and other risk factors, and the outcome of pregnancy. 738 28

Severe ketonuria developed during sedation with propofol in a 12 year old girl with brain injury. Deep sedation with propofol (5.1 mg/kg/h) was required because of agitation and severe intracranial hypertension; as a part of our management protocol, glucose intake was restricted to 5 Kcal/h. After 18 hours of propofol infusion there was intense ketonuria (8+ by Ketostix) without any evidence of metabolic acidosis (pH, HCO3- and anion gap were within normal values). At this time, indirect calorimetry (Deltatrac) confirmed that energy expenditure was principally based on fat consumption (70% of energy expenditure). Lowering the propofol infusion rate and increasing glucose intake reduced fat consumption to 39% within 8 hours: at this time, Ketostix was negative for ketone bodies. This case illustrates a potential risk of ketonuria during prolonged sedation with propofol (a 10% solution of intralipid), particularly if glucose intake is restricted. Monitoring urinary ketone bodies is recommended under these circumstances.
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PMID:Massive ketonuria during sedation with propofol in a 12 year old girl with severe head trauma. 820 21


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