Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four-compartment fasciotomies used to relieve abnormally high compartment pressures necessitate interruption of the ensheathing fascial membrane. In the calf, this is considered an important component in maintaining a viable musculovenous pump and preventing venous hypertension, a leading cause of venous insufficiency. Through postoperative physical examination and photoplethysmography evaluation of 47 patients who underwent this procedure, no indication exists that division of the fascial component leads to calf pump dysfunction and chronic venous insufficiency. Of the patients studied, 92 per cent had unchanged musculovenous pump function upon photoplethysmography reevaluation at 19 weeks compared with the initial values recorded 6 weeks postoperatively; 6 per cent had improved venous flow, while only one of the 47 (2%) had venous recovery measurements consistent with diminished venous flow.
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PMID:Venous insufficiency: a late sequelae of four-compartment fasciotomy in the lower extremity? 836 63

Microlymphatics of human skin form two superposed networks. The superficial one located at the level of dermal papillae may be visualized by fluorescence microlymphography. Microlymphatics fill from a subepidermal depot of minute amounts of FITC-dextran 150,000. In primary lymphedema with late onset the depicted network with vessels of normal size is significantly larger than in healthy controls, whereas in congenital lymphedema (Milroy's disease) microlymphatics are aplastic or ectatic (diameter > 90 microns). Lymphatic microangiopathy with obliterations of microvessels develops in chronic venous insufficiency, in lipedema (preliminary results) and after recurrent erysipelata. In healthy controls microlymphatics are permeable to FITC-dextran 40,000 and impermeable to the larger molecule 150,000. Preserved fragments of the network in chronic venous insufficiency exhibit increased permeability to FITC-dextran 150,000. After visualization of the vessels by the fluorescent dye microlymphatic pressure may be measured by the servo-nulling technique. First results indicate that microlymphatic hypertension contributes to edema formation in patients with primary lymphedema.
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PMID:Microlymphatics of human skin. 847 66

The effect of nifedipine in the treatment of hypertensive venous leg ulcers was studied on 30 outpatients in a double-blind placebo-controlled trail over a period of 2 months. The dose of nifedipine or the matching placebo was 10 mg 3 times daily. Most of the subjective symptoms such as pain, paraesthesia and cramps at night considerably improved during the treatment with nifedipine and were slightly affected in the placebo group. The ulcer surface area decreased after 2 months treatment with nifedipine by 26.9% (p < 0.05), and after treatment with placebo by 8.6% (p > 0.05). An improvement of the photopletysmographic record of the lower legs in the nifedipine group was observed, demonstrated by an increase of the index recovery time (by 36.1%, p < 0.05), while there were no significant changes in the placebo group. The results show favorable effect of nifedipine in the treatment of hypertensive venous leg ulcers which might be due to a great extent to improvement of the subcutaneous circulation of the lower legs. Nifedipine may be an important adjunct to the conservative management of the complications caused by chronic venous insufficiency and hypertension.
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PMID:Treatment of hypertensive venous leg ulcers with nifedipine. 874 28

The present paper is an overview taking into account the four most important etiological factors which can be involved in the development of chronic venous insufficiency (CVI): (1) weakness of the vascular wall including connective tissue and smooth muscle, (2) dysfunction and damage of the venous endothelium, (3) damage of the venous valves and (4) disturbancies of the microcirculation. The first three can be implicated in the development of reflux and venous hypertension and it is difficult to pin-point one single factor as being the most important. Disturbancies of the microcirculation eventually lead to the typical complications of CVI. With better understanding of the disease process it is possible to attack the causative factors leading to CVI and prevent and heal complications.
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PMID:The venous wall and valvular function in chronic venous insufficiency. 880 34

At the core of chronic venous insufficiency (CVI) is valvular incompetence affecting the large veins, which results in ambulatory venous hypertension. Recent research has revealed the pathophysiological stages involved: damage to the endothelium of the vein, leukocyte trapping and, finally, inflammatory reconstruction of the vessel wall. Lymphangiopathy involving the small and large lymph vessels is always present. One of the measures capable of influencing elevated venous pressure is compression therapy, which is discussed in detail in the present article. Drug treatment is a rational supplement to curative therapeutic approaches to chronic venous insufficiency that in mild-to-moderate cases, can result in an alleviation of symptoms similar to that achieved with compression therapy.
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PMID:[Chronic venous insufficiency--from pathophysiology to therapy. 1: Pathophysiology--compression treatment--systemic pharmacotherapy]. 899 1

An abnormality in platelet aggregability or fibrinolysis, namely elevated activity of plasminogen activator inhibitor-1 (PAI-1), has been recently documented in patients suffering from Klinefelter's syndrome associated with leg ulceration without underlying venous insufficiency. To determine whether increased PAI-1 activity is a general feature of Klinefelter's syndrome, or more specifically associated with leg ulceration, we investigated PAI-1 influencing parameters and PAI-1 activity in two groups of patients: (i) Klinefelter patients suffering from leg ulceration (n = 7); and (ii) Klinefelter patients without leg ulceration (n = 6). On analysing PAI-1 influencing parameters such as age, body mass index, triglycerides, C-reactive protein, testosterone, smoking behaviour, the presence of diabetes mellitus, and arterial hypertension, respectively, we found no statistically significant differences between the two groups. However, PAI-1 activity in group 1 was highly significantly elevated compared with that in group two patients (P < 0.005). We conclude that (i) PAI-1 activity is not elevated in Klinefelter's syndrome in general; (ii) elevation of PAI-1 activity in patients suffering from Klinefelter's syndrome does not appear to be secondary to PAI-1 influencing parameters; and (iii) elevation of PAI-1 activity may play a crucial role in the pathogenesis of leg ulceration in Klinefelter's syndrome. Therefore, a therapy for leg ulceration in Klinefelter's syndrome that aims to return the elevated PAI-1 activity to normal should be explored.
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PMID:Leg ulcers in Klinefelter's syndrome--further evidence for an involvement of plasminogen activator inhibitor-1. 911 12

The non-healing leg ulcer is examined by discussing three disease processes: peripheral vascular occlusive disease (PVOD), chronic venous insufficiency (CVI), and vasculitis. For PVOD, management decisions are based on risk factors and disease history. Comprehensive management includes the discontinuation of smoking, exercise conditioning and regulation of diabetes, hyperlipidemia, hypertension, and the appropriate application of anticoagulant/antiplatelet drugs. Methods of surgical management include bypass with autogenous or synthetic material in addition to reconstructive surgery with patch angioplasty or extra-anatomic bypass, amputation, percutaneous transluminal angioplasty/stents, thrombolytic infusion, atherectomy, intraluminal ultrasound, and angioscopy. The optimal healing environment for all ulcers prevents contamination, pain, and fluid loss. In CVI, higher venous pressure in the veins of the lower limb during exercise results in ambulatory venous hypertension and ulceration. Various theories are associated with the disease and ulceration process; the classic treatment of elevation, ambulation, and compression for venous disease remains unchallenged. Diagnosis is based on history, physical examination, invasive venography, and/or non-invasive studies. Two groups of vasculitic disorders that share varying degrees of vascular inflammation and necrosis are arteritis (lupus, erythematosus, periarteritis nodosa, dermatomyositis) and blood dyscrasias (sickle cell disease, thalassemia). Leg ulcers associated with vasculitis are due to inadequate tissue oxygenation at the local level, are typically chronic, slow to heal, and commonly recur.
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PMID:The non-healing leg ulcer: peripheral vascular disease, chronic venous insufficiency, and ischemic vasculitis. 939 80

We report a 29-year follow-up of a high-velocity superficial femoral vein injury sustained during the Vietnam War that was treated by emergent ligation. After years of suffering recurrent ulceration from chronic venous insufficiency, this patient underwent axillary vein valve transfer with improvement in his venous hypertension. Long-term follow-up of patients with deep venous injuries is necessary to avoid complications from chronic venous insufficiency.
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PMID:Long-term follow-up of a superficial femoral vein injury: a case report from the Vietnam Vascular Registry. 946 76

The use of Daflon 500 mg has been shown to improve venous tone, microvascular permeability, lymphatic activity, and microcirculatory nutritive flow. This study aimed to assess the effects of Daflon 500 mg at a daily dose of 2 tab/day on microcirculatory, haemorheologic parameters, white blood cell counts and neutrophil activation in patients suffering from chronic venous insufficiency (CVI). This was a single-centre double-blind placebo-controlled study comparing two parallel groups of CVI patients who were treated for 2 months with Daflon 500 mg (n = 39) or placebo (n = 38). Evaluations were performed before treatment (D0) and at the end of treatment (D60). Blood samples were drawn from a foot vein before and at the end of a 15-min period of venous hypertension provoked by a cuff inflated to 100 mm Hg. Red blood cell (RBC) deformability was determined by the initial flow rate filtration technique using a Hanss haemorheometer. RBC aggregation was evaluated by a Myrenne aggregometer based on analysis of transmitted light through a blood sample during flow. RBC disaggregation was evaluated by Sefam erythro-aggregometer based on analysis of the backscattered light through a blood sample in a Couette flow. Microcirculatory parameters were assessed by means of laser Doppler fluxmetry and transcutaneous oxymetry measurements and consisted of continuous records of blood flux (BF) and TcPO2 before and during 15 min of venous hypertension. Results are expressed as absolute values at baseline (before stasis) and at the end of stasis, before and after 2 months of treatment. Univariate analysis showed a significant reduction of the stasis-induced RBC aggregation index (Daflon 500 mg: -0.07+/-0.20; placebo: 0.04+/-0.18; mean +/- SD; p = 0.03). Multivariate analysis identified a subset of 5 variables (RBC aggregation, RBC count, microcirculatory BF, amplitude and frequency of vasomotion) that produced a good discrimination model between the two treatments. Linear combination of these 5 variables in 48 patients with complete data showed a significant difference (p < 0.001) between the groups. These changes suggest a protective effect of Daflon 500 mg on the deleterious influence of stasis on microcirculatory (BF) and hemorheologic (RBC aggregation) parameters in CVI patients in comparison to patients receiving placebo.
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PMID:Evaluation of haemorheological and microcirculatory disturbances in chronic venous insufficiency: activity of Daflon 500 mg. 947 42

Venous valves are more frequent in distal veins and venulae, providing a protecting action against blood skin reflux. Structurally simple, collagen and endothelium, they allow a cavity to be formed by distension, when occlusion occurs. Venous angioscopy can distinguish bicuspid floating valves, reinforced, reinforcing valves with free edges and seat valves as well as the presence of apertures of small collateral vessels in the sinus, of which they play a role in the filling up. Valves are inefficient in supine and in standing among 20% of the adult population. Sinuses allow vortices to be created, low recirculating zones, where blood flow move slowly in niches, at a low shear rate, independently from the main stream. A deep vortex is located in sinus, usually empty, but likely to receive red cell aggregates and leukocytes in the condition of stasis and hyperviscosity. Such a vortex is hypoxic, cause of endothelial activation. In such areas fibrin-leucocytic nidus are created, histologically recognized, of which sub-endothelium has become thick and thrombogenic. Two stages characterized its progression: stage I: a few alteration in the valves, little thrombin generation, taken over by the coagulation inhibitors: AT III, APC and TFPI. Stage II: damaged valves, local consumption of the inhibitors and extended generation of thrombin over the platelets, through factor IXa. Hereditary inhibitor deficits increase the risk (frequent factor Leyden V). When the coagulation cascade is considered, VIIa-tissue factor complex appears to be the thrombotic pathway, leading first to wall linked thrombin, uneasily reached by AT III and facteur IXa non inhibited by TFPI, therefore explaining the platelet extension. Monocytes, which can bear tissue factor, may be "lodged" inside the niches. Besides this important role in deep venous thrombosis, incompetent venous valves are responsible for the skin venous hypertension, a subsequent ground for ulcers. Their role in chronic venous insufficiency is uncertain. In the near future, venous angioscopy will bring about new findings about the pathophysiology of venous valves.
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PMID:[Venous valves in the legs: hemodynamic and biological problems and relationship to physiopathology]. 948 Mar 31


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