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

Histologic and morphologic methods were employed to study the influence of chronic hemodialysis on kidney vessels in chronic renal insufficiency. Arteries of contracted kidneys from patients with and without hemodialysis treatment were investigated. The dialysis group was made up of 33 patients, 28 having undergone bilateral nephrectomy and 5 having died. The control group consisted of 21 patients with chronic renal insufficiency, who died in uremic coma without prior hemodialysis. A statistical evaluation was done by comparing measurements from corresponding arteries in the dialysis- and control groups. The correlation pattern from a BMD 03D-program, in which each group was separately assessed for the possible influence of various clinical findings, was determined. Clinical influences taken into account included the course of the kidney disease, grade of renal insufficiency, duration and degree of hypertension as affecting the renal arteries. The statistical results showed that hemodialysis treatment, even taking clinical data into consideration, influenced the development of intimal fibrosis in the arteries of contracted kidneys in an increasing positive manner. Decreased perfusion of the kidneys during hemodialysis suggested as a possible cause. The examination of early lesions in renal arteries following short-term dialysis treatment lends support to this possibility. Here edema and proliferation of the intimal cells in the arteries, similar to that in vessels having a reduced blood flow, is observed.
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PMID:[Obliterative intimofibrosis of the renal arteries under the influence of hemodialysis in patients with chronic renal insufficiency (author's transl)]. 81 4

32 patients with different histologically proven forms of glomerulonephritis were treated with heparin for an average of 31 days. A dosage of heparin was chosen, which allowed an increase in thrombin time to 20-40 seconds. Histological findings alone do not allow any prediction concerning the therapeutic success of heparin treatment in glomerulonephritis. According to our results and comparable information given in the literature, the following therapeutic scheme can be recommended: Best results are seen in patients with a slow decrease of GFR (i.e. less than 30 ml/min) during the year preceding the beginning of the treatment. In rapid progredient glomerulonephritis, however, as in patients without any changes of GFR during this time, predictions as to the course of illness cannot be made. A high level of fibrin split products in serum may be expected to be the most valuable sign of therapeutic effect, as could be documented in 7 out of 8 successfully treated patients. Hypertension and proteinuria were not influenced by the treatment. Because of severe side effects the heparin treatment of glomerulonephritis should not be initiated in patients with severe hypertension.
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PMID:[Treatment of glomerulonephritis with heparin (author's transl)]. 87 75

To test conditions under which thyroid hormone might be deleterious to bone, we studied a group of 58 patients who had undergone thyroidectomy because of thyroid cancer 1 to 21 years previously and were treated with steady doses of exogenous thyroid hormone. Vertebral bone density (BMD Z-score) was significantly reduced and biochemical indices of bone resorption (urinary hydroxyproline and plasma tartrate-resistant acid phosphatase activity) and of osteoblastic activity (plasma osteocalcin and bone isoenzyme of serum alkaline phosphatase) as well as the calculated prevalence of bone resorption relative to osteoblastic activity (HBP) were significantly increased in thyroid hormone-treated post-menopausal women but not in men and premenopausal women. The HBP as well as the biochemical indices of bone remodeling were significantly negatively correlated with serum TSH levels. In treated patients, BMD Z-score was significantly dependent on the HBP, menopausal state, duration of treatment and serum TSH levels. In conclusion, the further increase in bone resorption by thyroid hormone is predisposed by menopausal changes in bone turnover. The simultaneous evaluation of biochemical indices of bone resorption and formation improves the assessment of bone loss in patients treated with thyroid hormone in a suppressive dose.
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PMID:Biochemical assessment of bone loss in patients on long-term thyroid hormone treatment. 162 31

In a retrospective study of 632 patients with pituitary disease we diagnosed pituitary insufficiency without hypersecretion of any pituitary hormone in 122 patients. Patients were substituted with sex hormones (76%), hydrocortisone (74%) and/or L-thyroxine (77%). 76% had additional growth hormone deficiency, as shown by an increase of growth hormone of less than 5 ng/ml after i.v. administration of L-arginine. In 17% of all patients the diagnosis of osteoporosis was proven or suspected radiologically. 57% had low bone mass of lumbar spine (dualphotonabsorptiometry) and 73% had low bone mass of the proximal forearm (singlephotonabsorptiometry). BMD values of pituitary insufficient patients were in the same range as those of patients with established osteoporosis. More than half of all patients (53%) complained of tiredness, exhaustion and muscle weakness. 40% suffered from adipositas. 77% had hyperlipidemia (68% hypertriglyceridemia and 42% hypercholesterinemia), 18% had hypertension. 14% of the patients had arteriosclerotic events in their history (myocardial infarction or stroke). These figures are higher than incidences shown in the German PROCAM-study. These data show an increased prevalence of osteoporosis and vascular diseases. This is in contrast to the general opinion, that patients with pituitary insufficiency are adequately treated by substitution with adrenal, thyroid and sex hormones. Whether other factors such as the additional growth hormone deficiency are responsible for these diseases has to be examined in prospective studies.
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PMID:[Increased prevalence of osteoporosis and arteriosclerosis in conventionally substituted anterior pituitary insufficiency: need for additional growth hormone substitution?]. 176 81

We previously found mild hypothermia (34-36 degrees C), induced before cardiac arrest, to improve neurologic outcome. In this study we used a reproducible dog model to evaluate mild hypothermia by head cooling during arrest, continued with systemic cooling (34 degrees C) during recirculation and for 1 h after arrest. In four groups of dogs, ventricular fibrillation (no flow) of 12.5 min at 37.5 degrees C was reversed with cardiopulmonary bypass and defibrillation in less than or equal to 5 min, and followed by controlled ventilation to 20 h and intensive care to 96 h. In Study A we resuscitated with normotension and normal hematocrit; Control Group A-I (n = 12) was maintained normothermic, while Treatment Group A-II (n = 10) was treated with hypothermia. In Study B we resuscitated with hypertension and hemodilution. Control Group B-I (n = 12) was maintained normothermic (6 of 12 were not hemodiluted), while Treatment Group B-II (n = 10) was treated with hypothermia. Best overall performance categories (OPCs) achieved between 24 and 96 h postarrest were in Group A-I: OPC 1 (normal) in 0 of 12 dogs, OPC 2 (moderate disability) in 2, OPC 3 (severe disability) in 7, and OPC 4 (coma) in 3 dogs. In Group A-II, OPC 1 was achieved in 5 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.001), OPC 3 in 1, and OPC 4 in 0 dogs. In Group B-I, OPC 1 was achieved in 0 of 12 dogs, OPC 2 in 6, OPC 3 in 5, and OPC 4 in 1 dog. In Group B-II, OPC 1 was achieved in 6 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.05), and OPC 3 or 4 in 0 dogs. Mean neurologic deficit and brain histopathologic damage scores showed similar significant group differences. Morphologic myocardial damage scores were the same in all four groups. We conclude that mild brain cooling during and after insult improves neurologic outcome after cardiac arrest.
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PMID:Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs. 229 37

The effect of cyclosporin A in acute and chronically active inflammatory bowel disease was tested in 11 patients with Crohn's disease and two with ulcerative colitis who had exhibited a poor response to at least eight weeks of conventional therapy. Trough levels of the drug in the therapeutic range were obtained in 12 of 13 patients. Cyclosporin A, which was usually added to the continued previous medication, including corticosteroids (11 of 13) or metronidazol (1 of 13), prompted an apparent clinical improvement in all but one patient. In six of the nine Crohn's disease patients with an initial Best index of greater than 150, a definite fall by at least 100 points was observed after 2-10 weeks of treatment, but the van Hees index declined only in two patients. All four patients with chronic perineal fistulation experienced symptomatic relief. Both patients with ulcerative colitis had a clinical remission. Erythrocyte sedimentation rate or serum albumin improved in eight of 13 patients. However, two of the nine responders with Crohn's disease relapsed during cyclosporin A therapy and three immediately after the medication was discontinued. Common side effects included hypertrichosis, tremor, and hyperesthesia; hypertension and epigastric pain each occurred only in one patient.
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PMID:Cyclosporin A treatment in inflammatory bowel disease. 276 6

A 16 year old girl with the rare syndrome characterised by hypertension, hyperkalemia, and acidosis was treated with a range of drugs, including thiazides, frusemide, and beta-adrenoceptor antagonists. None of the agents normalised the hypertension and biochemical abnormalities. Best results were obtained with methyclothiazide in full dosage, which normalised the blood pressure, serum potassium level, and bicarbonate level in the face of increased plasma renin activity. Empirical treatment with thiazides is the most satisfactory method for long term management.
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PMID:Treatment of mineralocorticoid-resistant renal hyperkalemia with hypertension (type II pseudohypoaldosteronism). 346 75

Minoxidil in combination with propranolol and diuretics was used in the treatment of 41 patients with severe refractory hypertension due to a spectrum of causes. These etiologies included essential hypertension, advanced renal failure, renovascular hypertension, and kidney transplant rejection. All patients had evidence of renal and cardiac damage prior to therapy and had failed to respond to all standard medications. The study included patients treated for periods of 3--42 months. Forty of the 41 patients responded most impressively to this therapy. Minoxidil was given in a dose of 7.5--40 mg daily. No tolerance to minoxidil was observed. Side effects were minimal. Three myocardial infarcts were observed. Two of these patients had had previous infarcts. One patient suffered a fatal cerebrovascular accident after he had deliberately stopped all medications. Nine patients showed sodium retention, which was easily controlled in 8 cases. Mild hirsutism was occasionally seen. Mean serum creatinine levels showed a slight decrease in the essential hypertension group after treatment. Best long-term results were seen in the essential hypertension and renovascular groups, although several cases with advanced renal disease and with kidney transplant rejection hypertension showed very impressive and encouraging outcomes.
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PMID:Minoxidil in the treatment of refractory hypertension due to a spectrum of causes. 615 48

Diabetes, known since antiquity, has been defined by glycosuria. In 1886, when Minkowski demonstrated that pancreatectomized dogs developed diabetes, the islets of Langerhans became a focus of the search for an active principle culminating in the discovery and the isolation of insulin in 1921 by Banting, Best and Collip. In 1959, the radioimmunoassay of Yalow and Berson solidified the concept of insulin resistance in non-insulin dependent diabetes (NIDDM). In 1971, the insulin receptor was defined as a cell surface protein that initiated the insulin signal transduction cascade. Today, we know that NIDDM accounts for at least 90% of all diabetes worldwide and involves approximately 100 million people. The microvascular complications of NIDDM are the same as for insulin dependent diabetes (IDDM) and are related to the intensity and duration of hyperglycaemia. Further, it is clear from the Diabetes Control and Complications Trial (DCCT) that all microvascular complications can be reduced with intensive control of the blood glucose. Macrovascular disease is also accelerated in NIDDM, including both hypertension and dyslipidemia. The major risk factor for NIDDM are age, obesity, physical inactivity, and genetic background. The earliest features seen in individuals destined to develop NIDDM is insulin resistance, but for hyperglycaemia to ensure there must be a defect in insulin secretion. Thus, insulin resistance defines the prehyperglycaemic phase of NIDDM, but varying degrees of insulin secretory deficiency define the hyperglycaemic phase. Macrovascular risk occurs throughout the lifetime of the individual, whereas microvascular risk ensues with the inception of hyperglycaemia. Tomorrow, we will understand more clearly whether lifestyle changes, such as diet and exercise, or new classes of drugs, can delay or prevent NIDDM. Clinical trials are now beginning to test whether impaired glucose tolerance (IGT) can be delayed or prevented from moving to overt NIDDM. The genetics of NIDDM are under intense study. Mutations in the insulin receptor lead to NIDDM in a small number of patients, and mutations in the glucokinase gene lead to maturity onset diabetes of the young (MODY). Work is now underway to study other candidate genes as well as work on positional cloning techniques to identify diabetes genetic loci. The hormone Leptin has just been discovered and is a major regulator of body weight. In summary, the most important new emphasis on the treatment of NIDDM is the recognition of the importance of hyperglycaemia and our ability to both treat and possibly prevent this metabolic perturbation. This joins the longer-term emphasis on cardiovascular risk reduction from both treatment and prevention of hypertension and dyslipidemia.
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PMID:Non-insulin dependent diabetes--the past, present and future. 928 27

Mibefradil is a new T-channel selective calcium antagonist effective in the treatment of hypertension and chronic stable angina pectoris. In this study steady-state plasma mibefradil concentrations and pharmacodynamic measurements were obtained from American and European clinical studies and analyzed using NONMEM. Doses ranged from 12.5-200 mg orally once-daily. A linear one-compartment pharmacokinetic model with first-order absorption was employed. Best parameter estimates were as follows: absorption rate-constant = 2.7 hours-1, clearance = 5.7 L/hour, volume of distribution = 179 L. The bioavailability of the 25 mg oral dose relative to higher doses was 0.83. Conclusions based on the Emax model equations were that at average plasma concentrations achieved clinically (approximately 300 ng/ml and approximately 600 ng/ml for 50 and 100 mg/day, respectively) the effect on heart rate is near maximum, the effect on blood pressure is about 50% of maximum, and the effect on PQ interval is small. The model also predicts that diastolic blood pressure and heart rate reductions will tend to be greater in patients with higher baseline values and with increasing mibefradil plasma concentrations. The increase in PQ interval is strongly related to plasma mibefradil concentration. The population analysis shows that mibefradil pharmacokinetics and pharmacodynamics were not affected in a clinically relevant manner by demographic characteristics.
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PMID:Mibefradil pharmacokinetic and pharmacodynamic population analysis. 967 23


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