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170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Venous ulcers are common in clinical practice. They are due to end stage skin and subcutaneous damage from sustained venous hypertension. The common cause may be post thrombotic syndrome or primary superficial venous insufficiency. This case illustrates the need to think of inherited thrombophilia as a primary cause.
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PMID:A straightforward venous ulcer. Or is it? 950 10

Growth factors produced by a variety of cells act as signalling peptides through specific cell surface receptor pathways. Functions such as cell proliferation, migration and differentiation have been assigned to each of them. Here, we report alterations of platelet-derived growth factor receptor alpha (PDGFR-alpha) and beta (PDGFR-beta) and vascular endothelial growth factor (VEGF) expression patterns in the progressive clinical stages of chronic venous insufficiency (CVI). A total of 30 punch biopsies were taken from patients with CVI, and VEGF and PDGFR were detected by indirect immunofluorescence and immunoperoxidase techniques. PDGFR-alpha and PDGFR-beta expression was strongly increased in endothelial cells of capillaries, pericapillary cells and connective tissue cells in the stroma of the skin of venous eczema and venous leg ulcer patients, and to a smaller extend in the dermis of those with lipodermatosclerosis. VEGF staining showed a similar expression pattern in the progressive CVI stages. However, staining of vessels in particular might simply reflect binding of VEGF, secreted by keratinocytes or fibroblasts, to its receptors. Growth factor and receptor expression in specimens from telangiectases and reticular veins, and from pigmented areas, resembled that of normal skin. We conclude that PDGFR-alpha, PDGFR-beta and VEGF play an important role in mediating inflammation and epithelial hyperproliferation in venous eczema, inducing connective tissue sclerosis in lipodermatosclerosis, and causing the reduced reepithelialization tendency in venous ulcers. We speculate that endothelial proliferation with chronic venous hypertension might be mediated by these growth factors.
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PMID:Increased expression of platelet-derived growth factor receptor alpha and beta and vascular endothelial growth factor in the skin of patients with chronic venous insufficiency. 970 59

The purpose of this review is to define animal models of chronic venous disease and to demonstrate how animal studies can impact our understanding and treatment of this disorder. To this end an extensive literature search was conducted highlighting potential animal models of chronic lower extremity venous disease. Scientific investigations using animals to study particular aspects of this disease are also reviewed. This review was conducted by members of the Committee on Research of the American Venous Forum to help provide direction for future venous research endeavors. Useful models of chronic venous occlusive disease involve controlled ligation of a major lower limb vein and multiple tributaries. Such a model can provide sustained venous hypertension and studies using this model have confirmed that an isodiametric graft can provide early hemodynamic relief. Models of primary, postphlebitic, and isolated chronic deep venous insufficiency are available for study. Valve repair or transplantation can positively impact the insufficiency observed in these models. Investigations into valve substitutes have generally been disappointing or are undergoing early evaluation. In conclusion, animal models for the study of some aspects of chronic venous disease do exist and have already affected our clinical approach to patients. The scientific study of basic pathophysiology, diagnostics, end-organ response, and long-term surgical treatments of this disorder in well-controlled animal experiments have not been conducted.
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PMID:Animal models for the study of lower extremity chronic venous disease: lessons learned and future needs. 973 30

The venoarteriolar response (VAR) of the skin in legs caused by experimental venous hypertension was measured using a new, double-wavelength laser Doppler probe technique (543 nm and 780 nm). This enables the measurement of the laser Doppler flux in the superficial and deep layers of the skin simultaneously. The recordings were obtained from the leg with the patient in a recumbent position with a sphygmomanometer cuff around the thigh. The VAR was recorded at the cuff pressures of 30 mmHg and 60 mmHg. Ten patients with chronic venous insufficiency (CVI) and 20 control subjects with healthy legs were investigated. The VAR increased in relation to the increase of cuff pressure at both wavelengths. There were no significant differences in the VAR between the cuff pressures within or between the legs with CVI and healthy legs. The VAR measured at 780 nm was very significantly greater than the VAR measured at 543 nm in legs with CVI (p<0.005), as well as in healthy legs (p<0.001). The VAR depends both on the wavelength of the laser Doppler light used and on the degree of venous hypertension. The VAR is not impaired in legs with CVI compared with healthy legs.
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PMID:Venoarteriolar response to experimental venous hypertension in legs with chronic venous insufficiency and in healthy legs, measured using a double-wavelength laser Doppler technique. 975 24

The development of cutaneous trophic changes in chronic venous insufficiency is linked to a complex microangiopathy whose central pathogenic event is subepidermal capillary destruction. Numerous studies, particularly those using classical and fluorescence cutaneous capillary microscopy, have demonstrated the causal effect of the microangiopathy. On a macrovascular point of view, it has been shown that ambulatory venous hypertension, linked to varicose veins or to postthrombotic disease, is the main pathogenic factor leading to this microangiopathy and its clinical consequences. The mechanism leading from macro--to microangiopathy remains, however, unknown. To date, the most plausible explanation of the skin capillary loss is the activation of leukocytes sequestrated in the cutaneous microcirculation during venous stasis. Several facts have been evidenced in this respect: the existence of a transient sequestration of leukocytes in the microcirculation of the lower limbs during orthostatic stasis; an increase of adhesion markers both on leukocytes and endothelial cells; and an increased production of leukocyte degranulation enzymes and oxygen free radicals. Although these data are consistent, experimental evidence is still required for decisive proof for the leukocyte hypothesis.
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PMID:[Role of leukocytes in the pathogenesis of trophic venous disorders]. 982 7

A significant number of patients with chronic venous insufficiency, venous hypertension, and venous ulceration are cared for by WOC nurses and other health care practitioners in the hospital, at home, or in an office setting. Although chronic and complicated in nature, all 3 of these disease processes may be successfully treated with gradient compression therapy. Many practitioners, however, are unaware that compression is the treatment of choice for venous ulceration, venous insufficiency, and venous hypertension. Instead, they rely primarily or exclusively on topical treatments to promote ulcer healing, and frequently become frustrated when such treatments fail or when ulceration recurs. The purpose of this article is to present an evidence-based rationale for the use of gradient compression therapy as the mainstay of venous ulcer treatment.
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PMID:Venous ulceration: compression as the mainstay of therapy. 1003 23

Lower limbs chronic venous insufficiency (CVI) is a widespread pathologic condition. Prevalence of venous ulcer in Europe ranges between 0.5% and 1.0%. Venous ulceration can be due to insufficiency of the superficial system, although deep venous insufficiency is responsible for 75% of the cases. Morbidity and socio-economic costs are exceedingly high especially because of frequent recurrences. CVI recognises mainly two causes: 1) increased influx, due to arteriovenous fistulas; 2) difficult outflow usually secondary to postphlebitic or primitive valvular incompetence. The prevalence of CVI and venous ulceration is difficult to assess. Surgical treatment tends to cure the underlying hemodynamic problem. Homans in 1916 first introduced surgical treatment of CVI and venous ulceration: excision of the cutaneous lesion and ligature suprafascial of the communicating veins. Since then different various techniques have been introduced in the clinical practice: Linton in 1938 supported subfascial interruption of the perforating veins but still reported a recurrence rate of 47%. Stripping of internal saphenous vein associated with division of perforating veins is still controversial, because lacks evidence of its real effectiveness in preventing recurrences. Felder's surgical technique is preferred by some authors to Linton's technique, because of the possibility to divide and section incompetent perforating veins without a cutaneous incision in the severely diseased postphlebitic tissues. In personal experience (56 patients) treated by Felder's techniques, we reached a cutaneous ulceration healing rate of 36% has been obtained. Subfascial interruption of perforating veins under endoscopic vision associated to the stripping of the internal saphenous vein could be a valuable option in the treatment of CVI because of the shorter duration of the operation and hospital stay and lesser postoperative complications. Repair and/or replacement of deep venous valves, originally described by Kistner in 1968, could be curative of venous hypertension due to primitive valvular insufficiency (primitive or postphlebitic): the same author in 1975 reported positive results (80% at 5 years). Major advantages of indirect valvuloplastic surgical technique are: 1) venotomy is not necessary; 2) it does not introduce extraneous material in the vasal lumen; 3) clamping of the vein is avoided; 4) heparine or other antithrombotic measures are usually not necessary. Although preliminary encouraging results, subsequent clinical experiences have demonstrated that correction of the reflux of the main axial venous system alone is not curative and durable resolution of venous symptoms also depends on the concomitant correction of all incompetent perforating veins. Venous valves transplantation is theoretically good to correct the deep long reflux and to improve calf pump function, although clinical results are still limited and follow-up not prolonged enough in terms of symptoms resolution and complete ulcer healing.
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PMID:[Deep venous insufficiency of the lower extremities]. 1020 91

A 44-year-old woman who weighed 130 kg (height 158 cm, BMI 52) with a complicated psychiatric history was referred for obesity surgery because of severe sleep apnea, obesity hypoventilation syndrome with frequent pneumonias, arterial hypertension, diabetes mellitus, polyarthralgia and back pain, venous insufficiency, dysmenorrhea, severe heartburn, and incisional hernia. From childhood until 1983, she had undergone 106 operations, mainly for septic/pyemic and intra-abdominal abscesses, 86 of them under general anesthesia. In the 4 years before undergoing bariatric surgery, she had gained 40 kg, nonoperative attempts at weight reduction had failed. Some months before obesity surgery she could fall asleep while standing, and she noticed an entire loss of capacity for work. Respiratory disturbance index measured during sleep by Mesam-4 device was 68 events per hour. Preoperative controlled positive airway pressure (C-PAP) therapy was used. Vital indications for weight reduction were established. Bariatric surgical steps included six operations: (1) vertical banded gastroplasty (VBG); (2) relaparotomy with suspicion of peritonitis, no complications found; (3) hernioplasty simultaneously with panniculectomy; (4) revision and removal of additional flap because of marginal skin necrosis; (5) bilateral thigh dermatolipectomy simultaneously with right-side saphenectomy; and (6) removal of intramammary abscess. Twenty-four months after VBG, she had lost 39 kg (56.5 % EWL) and was doing rather well. Obesity-related diseases except back pain were relieved.
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PMID:Successful bariatric surgery in a patient who underwent more than 100 various operations. 1048 18

Subfascial endoscopic perforator surgery (SEPS) is a new, minimally invasive technique performed in patients with advanced chronic venous insufficiency. The objective of the operation is to interrupt incompetent medial calf perforating veins to decrease venous reflux and reduce ambulatory venous hypertension in critical areas above the ankle where venous ulcers most frequently develop. Patients with stasis skin changes and healed or active venous ulcerations are potential candidates for the operation. Preoperative evaluation is performed with duplex scanning of the superficial, deep and perforator system, to diagnose both obstruction and valvular incompetence. Results of the North American SEPS Registry (NASEPS) as well as experience in several individual centers confirmed that the operation has significantly fewer wound complications than the classic open surgical techniques, and that rapid ulcer healing can be achieved. At the Mayo Clinic an ulcer recurrence rate of 12% was observed, with recurrence significantly more frequent in post-thrombotic limbs than in patients with primary venous valvular incompetence. The NASEPS Registry report confirmed a 2-year cumulative ulcer recurrence rate of 28%; ulcer recurrence was significantly more frequent in post-thrombotic limbs, especially in those with deep venous obstruction. SEPS is a new, low-risk, outpatient procedure that effectively decreases perforator reflux in patients with venous ulcerations, and should be added to our armamentarium to treat patients with advanced chronic venous disease. Long-term prospective and randomized studies are, however, still required to provide level I evidence of late efficacy.
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PMID:Subfascial endoscopic perforator vein surgery: indications and results. 1051 97

Knowledge of the pathophysiology of the venous circulation and its evaluation before treatment determines not only the best therapeutic plan, but at the same time makes it possible to avoid operations which are not necessary and a priori doomed to lead to a relapse. The basic therapeutic principles in the treatment of chronic venous insufficiency after evaluation and localization of the functional disorder by an objective examination method (duplex sonography, phlebography ...) are: a) compression, b) severing of pathological points of insufficient perforators, orifices of both saphenous veins, c) antireflux operation of the deep veins with preference of the popliteal vein. Any therapeutic procedure which does not have the aim to reduce venous hypertension is a priori doomed to failure and very soon a relapse develops. From this aspect it is not important to remove chaotically and extensively superficial varicosities (surgically or by sclerotherapy) but to severe the insufficient perforators and the insufficient orifices of saphenous veins surgically or by sclerotherapy.
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PMID:[Pathophysiologic aspects of chronic venous insufficiency]. 1059 65


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