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

In this study we analysed blood samples taken from the dorsalis pedis vein and a brachial vein of 11 healthy test persons and 8 patients with venous leg ulcer under experimental venous hypertension in order to examine changes in the expression of leukocyte adhesion molecules (LFA-1 (CD11a), Mac-1 (CD11b), p150,95 (CD11c), CD18, VLA-4 (CD49d) and L-selectin (CD62L)) which are involved in the adhesion steps of leukocytes to endothelial cells for transmigration into tissues. Under orthostatic stress, lymphocytes in controls collected at the foot level showed a significant reduction in the expression of L-selectin (p=0.002), compared to those of patients. This finding suggests that venous stasis negatively influences the expression of L-selectin on leukocytes only in healthy volunteers. Patients with chronic venous insufficiency seem to suffer from a specific defect in the regulation of L-selectin shedding under orthostatic stress.
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PMID:Dysregulated L-selectin expression on lymphocytes in patients with chronic venous insufficiency. 1179 Aug 67

Many articles have been published on assessing and treating chronic venous insufficiency and venous leg ulcers; most recommend correcting the underlying cause. These same articles often fail to examine and address a common factor or cofactor of venous hypertension--musculoskeletal changes. Frequently, these changes accompany major injuries, neurological disease, vascular insufficiency, debilitating diseases, myositis, and bone and joint pain and can adversely affect the dynamics of the calf muscle pump. The calf muscles rapidly waste and weaken with disuse--even a change in gait related to a painful ulcer can exacerbate venous hypertension and cause calf muscle disuse atrophy. This article reviews the cause and effect of musculoskeletal changes on the hemodynamics of the calf muscle pump. Recommendations for changes in practice will be based on the identification of the underlying cause of chronic venous insufficiency related to these musculoskeletal changes.
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PMID:The impact of musculoskeletal changes on the dynamics of the calf muscle pump. 1189 75

We present a young male patient referred to our hospital with leg ulcers on both legs that were more than 3 years refractory to standard treatment with compression therapy. By thrombophilia screening factor V Leiden mutation, hyperhomocysteinemia and evidence for impaired fibrinolysis were found. Treatment with folic acid in combination with long-term oral anticoagulant therapy was added to non-elastic compression therapy. The leg ulcers showed slow improvement and complete healing within 3 years. During a 6-year follow-up period neither new thrombo-embolic events occurred nor recurrence of ulcerations. This case suggests a potential synergistic pathogenic role of factor V Leiden, hyperhomocysteinemia and impaired fibrinolysis in the development of postthrombotic syndrome and his sequelae. We postulate that increased formation of thrombi in the microcirculation of the skin in combination with ambulatory venous hypertension due to recurrent deep venous thrombosis might explain our observation.
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PMID:Recurrent leg ulcers in a young man with hyperhomocysteinemia, factor V Leiden and impaired fibrinolysis. 1201

Chronic leg ulceration is a common cause of morbidity in Jamaican patients with homozygous sickle cell (SS) disease. Ulcers heal more rapidly on bed rest and deteriorate on prolonged standing, suggesting a role of venous hypertension in their persistence. This hypothesis has been tested by Doppler detection of venous competence in SS patients and in matched controls with a normal haemoglobin (AA) genotype in the Jamaican Cohort Study. Venous incompetence was significantly more frequent in SS disease [137/183 (75%)] than in non-pregnant AA controls [53/137 (39%)]. Past or present ulceration occurred in 78 (43%) SS patients, with a highly significant association between leg ulceration and venous incompetence in the same leg (P < 0.001). Prominence and/or varicosities of the veins and spontaneous leg ulcers were more common among patients with multiple sites of incompetence. The association of venous incompetence with chronic leg ulceration identifies a further pathological mechanism contributing to the morbidity of SS disease. The cause of venous incompetence is unknown but the sluggish circulation associated with dependency, turbidity and impaired linear flow at venous valves, hypoxia-induced sickling, the rheological effects of high white cell counts, and activation of components of the coagulation system may all contribute. Venous hypertension in SS patients with leg ulceration suggests that firm elastic supportive dressings might promote healing of chronic leg ulcers.
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PMID:Chronic leg ulceration in homozygous sickle cell disease: the role of venous incompetence. 1240 2

CASE 1: A 65-year-old woman with essential thrombocythemia (ET) had been taking oral hydroxyurea (HU), 1,000 mg daily, for 7 years. Six months ago, she developed an ulcer on the outer part of her left ankle, which healed spontaneously within 2 months. She presented with a new, tender, shallow ulcer, 2 cm x 2 cm in size, at the same site. Doppler examination revealed thrombosis of the left common femoral vein and a calcified atheroma plaque of the left common femoral artery. The dosage of HU was decreased to 500 mg daily when the platelet counts were found to be within normal levels. The ulcer completely healed within 2 months with occlusive wound dressings, and has not recurred within the follow-up period of 1 year. CASE 2: A 56-year-old women presented with multiple, painful, leg ulcers of 1 year duration. She had been diagnosed as having ET and had been on HU therapy, 1,500 mg/day, for the past 5 years. Interferon-alpha-2b was started 3 months ago, in addition to HU, which was tapered to 1,000 mg daily. She had suffered from hypertension for 20 years treated with nifedipine and enalapril, and had recently been diagnosed with diabetes mellitus which was controlled by diet. Examination revealed three ulcers located on the lateral aspects of both ankles and right distal toe. Arterial and venous Doppler examinations were within normal limits. Histopathology of the ulcer revealed nonspecific changes with a mixed inflammatory cell infiltrate around dermal vessels. The ulcers completely healed within 10 weeks with topical hydrocolloid dressings. After healing, she was lost to follow-up. A year later, it was learned that she had developed a new ulcer at her right heel, 3 months after her last visit (by phone call). This ulcer persisted for 8 months until HU was withdrawn. CASE 3: A 64-year-old woman with ET presented with a painful leg ulcer of 6 months' duration. She had been taking oral HU for 5 years. She had a 20-year history of hypertension treated with lisinopril. Examination revealed a punched-out ulcer of 2 cm x 2 cm over the right lateral malleolus. Doppler examination of the veins revealed insufficiency of the right greater saphenous and femoral veins. Angiography showed multiple stenoses of the right popliteal and femoral arteries. As her platelet count remained high, HU was continued. During the follow-up period of 13 months, the ulcer showed only partial improvement with local wound care.
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PMID:Leg ulcers and hydroxyurea: report of three cases with essential thrombocythemia. 1249 73

Venous ulceration remains a common problem and a significant challenge to the physicians treating it. Many theories have been advanced in the past to explain its causes but there is little evidence to support tissue hypoxia as the main factor, as was once thought. In recent years attention has focussed on the inflammatory events which attend venous disease and the development of venous ulceration. It has been proposed that these form a major contribution to the development of venous leg ulcers. In the arterial system an analogous series of events appears to cause damage following severe ischemia. Massive neutrophil activation in the microcirculation following reperfusion of a tissue results in severe, ischemic damage to that tissue. A similar series of events is proposed to explain venous disease. During venous hypertension leukocytes are sequestrated in the microcirculation of the lower limb. It has been shown that these undergo activation whilst they are in the leg. The exact location of leukocyte sequestration is unclear but it is suggested that this may occur in the skin. The damage caused to the lower limb skin components can be identified by measuring plasma levels of endothelial adhesion molecules, which are shed into the circulation following a period of venous hypertension. In the long term this leads to a chronic inflammatory state in the skin in some patients where venous hypertension is sustained or there is susceptibility to venous hypertension. The resulting inflammatory process is referred to as "lipodermatosclerosis" and has a number of well known clinical features. There is proliferation of the dermal capillaries eventually leading to a "glomerulus" like appearance. In the skin and subcutaneous tissues there is fibrosis. The microcirculation in the papillary dermis is surrounded by an inflammatory cellular infiltrate. The importance of understanding the mechanisms of the development of venous ulceration is in creating new treatments for this problem. Compression treatment has been effective in healing leg ulcers for thousands of years. Surgical treatment offers a possible cure in patients where superficial venous reflux is the main problem. Deep vein reconstruction is only suitable for a few patients. Many venous ulcers can be healed by compression, only to recur within a few months. Pharmacological treatments may offer the possibility of more rapid ulcer healing and the maintenance of an ulcer-free state if the correct pathophysiological mechanisms can be identified and addressed.
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PMID:Deleterious effects of white cells in the course of skin damage in CVI. 1251 77

Within the organization of national health care based on the DRG/ROD system, angiology services provided in "day hospital" play not only a large social role in the life of the community and the patient but also an economic one in hospital administration as there facilities allow continuation of inpatient care. Many diseases can be managed in an outpatient setting, both in diagnosis and treatment, particularly arterial hypertension, chronic obliterating arteriopathies of the lower extremities, microcirculatory and collagen disorders, VTE, and leg ulcers. A review of case records from the recent past confirms the importance of the role of the Angiology Outpatient Services plays within the Polyclinic of the University of Palermo. The exponential growth in the services provided by our facility has led to a twofold increase in the number of outpatient admissions over the past two years. This growth has produced a wider impact on the service area and allowed the introduction of angiology services that are economically profitable, while avoiding unprofitable services, through effective service management recognization. Our study results show that, where possible, outpatient care should be increasingly used. We believe that an optimal model for angiology services permits the integration of the two types of hospital care, with short stays on an inpatient basis, especially for the treatment of more severe or acute disease, and greater outpatient service utilization in ambulatory care.
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PMID:[The role of the ambulatory care center in angiology services]. 1265 67

The prevalence of leg ulcers is about 1%, approximately 75% of them are of venous origin. The precondition for the development of venous ulcers is ambulatory venous hypertension. It is assumed than a linear correlation exists between the severity of ambulatory venous hypertension and the incidence of venous ulcers. Venous ulcers caused by superficial vein reflux are called varicose ulcers and are more frequent than postthrombotic ones. Crossectomy removes the hemodynamic disorder responsible for the development of varicose ulcers and creates conditions for a quick and mostly definitive ulcer healing. In cases with simultaneous reflux in the saphenous and femoral veins the saphenous reflux is responsible for the severity of venous disorder, whereas femoral reflux is hemodynamically unimportant. Selective abolition of saphenous reflux restores normal hemodynamic conditions in such cases. Compressive therapy continues to be the most frequently used therapeutic procedure in the treatment of venous ulcers; it must be considered as a symptomatic measure, because it is not able to substantially affect the underlying venous disorder in spite of the fact that the correctly lying bandage positively influences venous hemodynamics. The diagnostic procedure in patients with leg ulcers should screen out cases with varicose ulcers; abolition of superficial vein reflux can deliver these patients from their annoying disease.
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PMID:[Hemodynamic basis for the development of varicose ulcers and their therapy]. 1465 57

A multicenter prospective randomized clinical trial was undertaken to compare a generic four-layer bandage system with a cohesive short-stretch system (Actico, Activa Healthcare) in the management of venous leg ulceration. Both systems are designed to produce sufficient pressure to counteract venous hypertension. Patients in leg ulcer services with leg ulceration were screened for inclusion in this trial. Patients with arterial disease (ankle brachial pressure index < 0.8) and causes of ulceration other than venous disease were excluded. For patients with bilateral ulceration, the limb with the larger area of ulceration was studied. Patients were randomized to receive either type of compression bandage and simultaneously randomized to one of two foam dressings that were changed weekly unless more frequent changes were clinically required. In all, 156 patients met entry criteria and were randomized from the 12 clinical centers with median (range) ulcer size of 4.33 (0.33-123.10) cm(2). Analysis revealed that after 24 weeks a total of 111 (71%) of patients had complete ulcer closure, 32 (21%) had withdrawn from the trial, 12 (8%) remained with open ulceration, and one patient had died. Of the 74 patients randomized to the four-layer bandage, 51(69%) had ulcer closure on treatment compared with 60/82 (73%) on the cohesive short-stretch system. Intention-to-treat analysis produced a hazard ratio for healing of 1.08 (95 percent CI 0.63-1.85, p= 0.79). Withdrawal rates were similar between groups (15, 20% four-layer bandage; 17, 21% cohesive short-stretch system). Ulcer closure rates for patients treated with the cohesive short-stretch system were similar to those for patients managed by the four-layer bandage system in this trial.
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PMID:Randomized trial of cohesive short-stretch versus four-layer bandaging in the management of venous ulceration. 1508 66

Venous reflux is the most common cause of venous hemodynamic disorders. In this paper 2 issues are discussed: how and where does reflux arise and what are the hemodynamic consequences of retrograde flow. Pressure gradient and incompetent vein connecting both poles of the gradient are the prerequisite for venous reflux to arise. Ambulatory pressure gradient occurs during the activity of the calf muscle venous pump between deep veins of the thigh and the lower leg. Thus the incompetent reflux-carrying vein must connect the popliteal, femoral, profunda femoris, or iliac vein with 1 of the deep veins of the lower leg. Reflux can be considered as shunting of blood from thigh veins into the lower leg veins. The most frequently found incompetent veins are the long and short saphenous veins and perforators communicating with deep veins of the thigh. On the other hand, calf perforators emptying into the deep veins of the lower leg, where the lower pole of the pressure gradient is located, cannot be the feeding source of reflux. A physiological bidirectional flow takes place in calf perforators connecting superficial and deep veins of the lower leg and making them conjoined vessels. Venous reflux produces ambulatory venous hypertension. The quantity of reflux volume and not the localization of retrograde flow in superficial or deep veins is the most important hemodynamic factor. Reflux in superficial veins, when large enough, can cause the most serious symptoms of chronic venous insufficiency including leg ulcers. Plethysmographic findings have shown that incompetence of the femoral and calf perforating veins is hemodynamically unimportant. Large incompetent calf perforators are not the cause of venous abnormality but are the consequence of saphenous retrograde flow.
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PMID:The venous reflux. 1537 17


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