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

Polycythemia vera (PV) is one of the myeloproliferative diseases, and, as such, is an example of clonal hematopoiesis. The progeny of a single, abnormal, hematopoietic stem cell gain a growth advantage over their normal counterparts resulting in overproduction of red cells generally accompanied by overproduction of granulocytes and platelets as well. There are a variety of nonspecific symptoms at onset related to the increased red cell mass and hematocrit accompanied by the more specific manifestations of pruritus, erythromelalgia, and hepatic, portal, and mesenteric vein thrombosis. Splenomegaly and hypertension are common. The laboratory hallmark is an increased red cell mass. There is also often an increase in white cell count, platelet count, and leukocyte alkaline phosphatase along with other findings reflecting the increased rate of turnover of hematopoietic cells. The bone marrow biopsy generally displays hypercellularity involving all three cell lines and absent iron stores. The diagnosis of PV depends on excluding spurious polycythemia in which there is a high hematocrit but a normal red cell mass and secondary polycythemia in which there is an increased red cell mass in response to tissue hypoxia or the inappropriate production of erythropoietin, generally by a tumor. In addition, one should try to establish the diagnosis in a positive fashion by a combination of studies of the blood and bone marrow. Phlebotomy and occasionally plateletpheresis should be used as acute therapy. Chronic therapy is guided by the knowledge that patients treated with phlebotomy alone have an increased rate of thrombotic complications particularly in older patients and those with previous thrombotic disease. Myelosuppressive therapy can reduce the incidence of these complications, but is commonly associated with an increased incidence of second malignancies, particularly acute leukemia. At present, hydroxyurea is the myelosuppressive agent of choice. Antiplatelet agents have a limited role except in the palliation of the syndrome of erythromelalgia. Median survival is approximately 10 years. As implied above, the causes of morbidity and mortality vary with the mode of chronic therapy which has been employed, leukemia being more common after myelosuppressive therapy and thrombotic complications being more common after therapy with phlebotomy alone. Ten percent to 50% of patients move into a spent phase followed by postpolycythemic myeloid metaplasia, irrespective of previous therapy employed. Eventually, the major problems may be cytopenias and massive splenomegaly.
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PMID:Polycythemia vera. 158 7

Conventional risk factors predict only about 30-50% of incidental cases in cardiovascular diseases, which are still the leading cause of death in western societies. During the last decade, the importance of thrombosis as an essential mechanism in acute myocardial infarction (AMI) and stroke has been established. The introduction of thrombolysis has led to an impressive reduction in AMI case fatality and possibly also to a substantial amelioration of its prognosis. Evidence from experimental, clinical and epidemiological studies suggest, that several hemostatic and hemorheological factors (e.g., fibrinogen, Factor VII, plasma viscosity, hematocrit, red blood cell aggregation, total white cell count) might not only play an important role in the evolution of acute thrombotic events, but may also take part in the pathophysiology of atherosclerosis. An increasing number of studies reports altered hemostatic and hemorheological parameters to be associated with smoking, hyperlipoproteinemia, and high blood pressure, as well as with adverse dietary habits and other life-style factors. To date, their way of interaction with the atherosclerotic process is poorly understood. Hemorheological or hemostatic mechanisms that might promote thromboatherogenesis include the predisposition to thrombosis via a hypercoagulable state, the enhancement of atherosclerosis by fibrinogen and its metabolites, and finally the reduction of blood flow through various rheological effects (e.g., increase in plasma viscosity and red cell aggregation, or leukocyte activation). Future research should focus in more detail on the interrelationship between accepted risk factors and the hemostatic system as well as hemorheological parameters. Deeper insight into the mechanisms involved might lead to new preventive strategies as well as to therapeutic procedures in the management of atherosclerosis and associated thrombotic events.
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PMID:The possible role of hemorheology in atherothrombogenesis. 163 76

Interest in white cell (WBC) rheology has largely been directed towards hypotensive conditions. However, as capillary flow is dependent on the relative arteriovenous pressure gradient, we investigated the dynamics of WBC flow in patients with venous hypertension. Three groups of matched subjects were studied: normal controls, patients with primary varicose veins, and patients with deep venous insufficiency confirmed by foot volumetry and Doppler studies. A venous cannula inserted at the level of the medial malleolus allowed blood samples to be taken at time 0 (supine) and then at 15, 30, 45, and 60 minutes after sitting up. Further samples were taken after subjects resumed a supine position. After 60 minutes sitting the haematocrit of blood leaving the foot increased by 9.6% in controls and 25.6% in patients with venous insufficiency. The difference in the behaviour of WBC was more marked. Controls showed a 5.0% decrease in the relative number of WBC after 60 minutes sitting compared to 28% decrease in patients with venous insufficiency. On resuming a supine position there was a significant increase in the number of WBC leaving the foot and this "wash-out" appeared to be delayed in the two patient groups. Platelets showed a corresponding fall when the foot was dependent but there appeared to be no washout after elevation.
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PMID:Increased white cell trapping in the dependent legs of patients with chronic venous insufficiency. 201 Jul 4

The purpose of this study was to examine the effects on the skin microcirculation of a short period of venous hypertension. 34 subjects (17 patients with lipodermatosclerosis and 17 controls) were studied. Laser-Doppler flowmetry was used to assess the hyperaemic responsiveness of the skin following three minutes of ischaemia. This was done by measuring the ratio of peak to basal flow, and the time taken to reach 95% of peak flow. The limb was then subjected to 30 minutes of venous hypertension, following which the hyperaemic responses were repeated. Normal controls demonstrated a significant reduction in hyperaemic response after venous hypertension. Liposclerotic skin had a much less pronounced response to ischaemia which was not significantly affected by 30 minutes of venous hypertension. The clinically normal skin in venous patients showed intermediate values. The results suggest that a short period of venous hypertension causes an immediate deficit in microcirculatory function. This short time scale is consistent with the white cell activation theory of skin damage in venous disease. The loss of vasodilatory capacity by liposclerotic skin may reflect either the constricting effect of pericapillary fibrin cuffs or a fixed degree of capillary occlusion.
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PMID:Skin microcirculatory responses in chronic venous insufficiency: the effect of short-term venous hypertension. 203 3

CSF evaluation is the single most important aspect of the laboratory diagnosis of meningitis. Analysis of the CSF abnormalities produced by bacterial, mycobacterial, and fungal infections may greatly facilitate diagnosis and direct initial therapy. Basic studies of CSF that should be performed in all patients with meningitis include measurement of pressure, cell count and white cell differential; determination of glucose and protein levels; Gram's stain; and culture. In bacterial meningitis, Limulus lysate assay and tests to identify bacterial antigens may allow rapid diagnosis. Where there is strong suspicion of tuberculous or fungal meningitis, CSF should also be submitted for acid-fast stain, India ink preparation, and cryptococcal antigen; unless contraindicated by increased intracranial pressure, large volumes (up to 40-50 mL) should be obtained for culture. If a history of residence in the Southwest is elicited, complement-fixing antibodies to Coccidioides immitis should also be ordered. Newer tests based on immunologic methods or gene amplification techniques hold great promise for diagnosis of infections caused by organisms that are difficult to culture or present in small numbers. Despite the great value of lumbar puncture in the diagnosis of meningitis, injudicious use of the procedure may result in death from brain herniation. Lumbar puncture should be avoided if focal neurologic findings suggest concomitant mass lesion, as in brain abscess, and lumbar puncture should be approached with great caution if meningitis is accompanied by evidence of significant intracranial hypertension. Institution of antibiotic therapy for suspected meningitis should not be delayed while neuroradiologic studies are obtained to exclude abscess or while measures are instituted to reduce intracranial pressure.
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PMID:Approach to diagnosis of meningitis. Cerebrospinal fluid evaluation. 227 90

In previous studies, administration of adrenocorticotrophin (ACTH; 0.5 mg i.m. b.d. for 5 days) to normal subjects produced an adrenally dependent rise in blood pressure (BP) of some 20 mmHg, accompanied by an increase in cardiac output and an increase in plasma volume. The BP and metabolic effects of ACTH (increase in plasma glucose, fall in eosinophils, increase in body weight and urine sodium retention) were reproduced by infusion of the glucocorticoid (GC) cortisol at rates (6-8 mg/h) which reproduced the blood concentrations of the steroid achieved with ACTH administration. Oral administration (hydrocortisone 200 mg daily) produced similar changes qualitatively, although the cortisol concentrations and increase in pressure (12 mmHg) were less. Plasma volume was increased. To determine the role of urine sodium retention and plasma volume expansion in the hypertension, we gave synthetic steroids to six normal subjects for 5 days, at doses which were calculated to be similar for GC activity, but which had little or no mineralocorticoid (MC) activity. Prednisolone (40 mg/day), methylprednisolone (32 mg/day), triamcinolone (40 mg/day) and dexamethasone (8 mg/day) all produced equivalent GC effects (increase in plasma glucose, increase in total white cell count, fall in direct eosinophil count). There were no MC effects with any of the steroids. Body weight did not increase and urinary sodium excretion increased rather than decreased. Plasma volume (125I human serum albumin) and haematocrit were unchanged. BP rose with all four steroids: systolic BP rose by 13 mmHg with prednisolone, by 9 mmHg with methylprednisolone, by 10 mmHg with triamcinolone, and by 6 mmHg with dexamethasone. Diastolic BP increases were 8, 11, 8 and 7 mmHg, respectively. Thus, neither MC activity nor an increase in plasma volume is essential for steroids to induce an increase in blood pressure. Therefore, screening of synthetic GCs to minimize MC activity will not prevent hypertensive complications.
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PMID:The hypertensive effect of synthetic glucocorticoids in man: role of sodium and volume. 276 Apr 58

The acute and long-term efficacy, tolerance and safety of two orally active angiotensin converting enzyme (ACE) inhibitors, captopril (C) and enalapril (E) were compared in patients on regular haemodialysis (RHD). C and E were successively administered for 6 months to 8 RHD patients with hypertension unresponsive to fluid withdrawal and conventional antihypertensive therapy. The fall in blood pressure after a starting dose of 25 mg C or 5 mg E was of the same magnitude. It was not correlated with the initial PRA levels, which were normal in all patients. The mean daily dose of ACE inhibitor was 45 +/- 28 mg during the C period and 19.4 +/- 17.6 mg at the end of the E period. Three patients required additional treatment, comprising beta-blockers and/or calcium antagonists. The individual daily dose of ACE inhibitor, the need for additional treatment and the antihypertensive response achieved were highly correlated during both study periods. During C administration 4 out of 8 patients presented a taste disturbance, which disappeared 2 weeks after substituting E for C. Serum electrolytes, liver enzymes, haemoglobin concentration and white cell and platelet counts remained unchanged throughout both study periods. It is concluded that RHD patients with hypertension are responsive to ACE inhibitors, C and E being equally effective.
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PMID:Intra-individual comparison of captopril and enalapril in patients undergoing regular haemodialysis. 301 37

One hundred and seventy-four patients who were receiving drug therapy for hypertension were asked to restrict their sodium intake for three months. At the end of that time their drug therapy was replaced with enalapril and the dose of the drug "titrated" to obtain a diastolic blood pressure of less than 90 mmHg. Sodium restriction caused a small fall in blood pressure and could be used as sole therapy in only 6% of patients. Enalapril therapy was instituted without problems and control of blood pressure below 90 mmHg was achieved in 62% of persons with monotherapy. The number of tablets of enalapril that were taken was reduced from 5.9 to 2.7; in most patients these were taken once a day. There were few side-effects and no depression of white cell count, no proteinuria and no deterioration of renal function. Seventy-six per cent of patients preferred the new regimen either because they felt better than with their previous therapy (52%) or because of the more simple regimen (24%). Enalapril was an effective, well tolerated antihypertensive agent and potentially has a major role to play in the management of patients with high blood pressure.
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PMID:Use of sodium restriction and enalapril in persons with moderate to severe hypertension. 303 55

Urinary tract infection is the commonest human bacterial infection. Bacteriuria alone does not appear to produce progressive renal damage or hypertension. However, it can produce considerable morbidity. Urinalysis is a simple, relatively sensitive, and reliable way of diagnosing urinary tract infection. It is not clear that routine screening should be performed in all patients, but pregnant females, patients with known anatomic abnormalities, and patients with recent genitourinary instrumentation should be screened. The major determinant of therapeutic success in patients with urinary tract infections is the anatomic site of infection. Superficial mucosal infection of the bladder is well treated with a single dose of an appropriate antibiotic, whereas deep tissue infection of the kidney or prostate should be treated with a prolonged and intensive course of therapy. Urinalysis is an insensitive tool in the localization of infection. However, the presence of white cell casts on the examination of the urinary sediment is pathognomonic of upper tract infection and would lead one to pursue an aggressive course of therapy. Examination of the concentrating ability is of limited help in this regard because of the wide range of overlap of concentrating ability in patients with upper and lower tract infections. In selected instances, urinalysis is of help in guiding therapy of urinary tract infections. This is particularly true of the patients with acute urethral syndrome where therapy is guided by the presence or absence of pyuria. Urinalysis, a simple front-line test, is of paramount importance in the evaluation and management of the patient with urinary tract infection.
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PMID:Urinalysis in the diagnosis of urinary tract infections. 304 58

The cause of venous ulceration remains unclear but recent evidence suggests that white cell trapping may play a significant role. In this study venous blood taken from the dependent leg of 15 normal subjects was compared to samples taken from a similar number of patients with deep venous insufficiency. About 25 p. cent fewer white cells and platelets left the dependent foot of the patients with venous hypertension. When the foot was elevated there was a significant washout of white cells but not platelets suggesting platelet consumption within the microcirculation of the dependent foot. In 8 of the patients these changes were reversed by external compression.
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PMID:White cell and platelet trapping in patients with chronic venous insufficiency. 324 94


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