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Venous Disease (venous + disease)
Kinds of Venous Disease Selected AbstractsSerum Iron and Matrix Metalloproteinase-9 Variations in Limbs Affected by Chronic Venous Disease and Venous Leg UlcersDERMATOLOGIC SURGERY, Issue 6 2005Paolo Zamboni MD Background. Severe chronic venous disease (CVD) is characterized by both dermal hemosiderin accumulation and matrix metalloproteinase (MMP) hyperactivation. The iron-driven pathway is one of the recognized mechanisms of MMP hyperactivation. Objective. To investigate the potential consequences of leg hemosiderin deposits on both iron metabolism and activation of MMPs. Methods. We contemporaneously assessed the following in the serum of the arm and ankle veins of 30 patients (C4,6) with CVD and 14 normal subjects: ferritin, transferrin, iron, percentage of transferrin iron binding capacity (%TIBC), and MMP-9. Optical microscopy examinations with Perls' staining of chronic wounds were also performed. Results. Histology consistently revealed iron deposits. Serum ferritin, iron, and %TIBC were significantly increased in the legs affected by severe CVD compared with the arm of the same subjects or the controls. In addition, iron and %TIBC were significantly elevated in the legs of ulcer patients. The rate of activation of MMP-9 was significantly elevated in CVD. Conclusions. The increased iron deposition in legs affected by CVD seems to be more instable in ulcer patients, leading to iron release in the serum of the affected leg. Our data suggest the iron-driven pathway as a further mechanism for MMP hyperexpression leading to tissue lesion. [source] The Impact of Duplex Scanning in PhlebologyDERMATOLOGIC SURGERY, Issue 1 2002Nicos Labropoulos PhD Chronic venous disease (CVD) is a tremendous medical and economic burden on society. In the past two decades the use of duplex ultrasound has emerged as the diagnostic method of choice for the diagnosis and management of CVD. In this article, we describe the specific techniques used in the assessment of the superficial, perforating, and deep venous systems. We also discuss the methods of ulcer bed and chronic obstruction evaluation. The contributions of the duplex ultrasound to the understanding of the pathophysiology and improvement of treatments for chronic venous disease are reviewed. [source] Hemochromatosis genotypes and risk of 31 disease endpoints: Meta-analyses including 66,000 cases and 226,000 controls,HEPATOLOGY, Issue 4 2007Christina Ellervik Hemochromatosis genotypes have been associated with liver disease, diabetes mellitus, heart disease, arthritis, porphyria cutanea tarda, stroke, neurodegenerative disorders, cancer, and venous disease. We performed meta-analyses including 202 studies with 66,263 cases and 226,515 controls to examine associations between hemochromatosis genotypes C282Y/C282Y, C282Y/H63D, C282Y/wild type, H63D/H63D, and H63D/wild type versus wild type/wild type and 9 overall endpoints and 22 endpoint subgroups. We also explored potential sources of heterogeneity. For liver disease, the odds ratio for C282Y/C282Y versus wild type/wild type was 3.9 (99% confidence interval: 1.9,8.1) overall, 11 (3.7,34) for hepatocellular carcinoma, 4.1 (1.2,14) for hepatitis C, and 10 (2.1,53) for nonalcoholic steatohepatitis. For porphyria cutanea tarda, the odds ratios were 48 (24,95) for C282Y/C282Y, 8.1 (3.9,17) for C282Y/H63D, 3.6 (1.8,7.3) for C282Y/wild type, 3.0 (1.6,5.6) for H63D/H63D, and 1.7 (1.0,3.1) for H63D/wild type versus wild type/wild type. Finally, for amyotrophic lateral sclerosis, the odds ratio was 3.9 (1.2,13) for H63D/H63D versus wild type/wild type. These findings were consistent across individual studies. The hemochromatosis genotypes were not associated with risk for diabetes mellitus, heart disease, arthritis, stroke, cancer, or venous disease in the overall analyses; however, the odds ratio for C282Y/C282Y versus wild type/wild type was 3.4 (1.1,11) for diabetes mellitus among North Europeans. Conclusion: In aggregate, clinically ascertained cases who are homozygous for the C282Y mutation are associated with a 4,11,fold risk of liver disease, whereas all 5 hemochromatosis genotypes are associated with a 2,48,fold risk of porphyria cutanea tarda, and H63D/H63D is associated with a 4-fold risk of amyotrophic lateral sclerosis. These results, mainly from case-control studies, cannot necessarily be extrapolated to the general population. (HEPATOLOGY 2007.) [source] Air pollution and hospitalization for venous thromboembolic disease in ChileJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2010R. E. DALES See also Mannucci PM. Fine particulate: it matters. This issue, pp 659,61; Bonzini M, Tripodi A, Artoni A, Tarantini L, Marinelli B, Bertazzi PA, Apostoli P, Baccarelli A. Effects of inhalable particulate matter on blood coagulation. This issue, pp 662,8. Summary.,Background:,Ambient air pollution is a risk factor for stroke and myocardial infarction, possibly because of alterations in coagulation that influence the arterial circulation. Whether air pollution influences diseases associated with peripheral venous thrombogenesis remains largely unknown. Objectives: To determine the association between air pollution and venous thromboembolic disease (VTE) in a sample of the general population. Methods: A time-series analysis was used to test the association between daily air pollution and VTE hospitalizations in Santiago between 2001 and 2005. Results were adjusted for long-term trends, day of the week and average daily humidex. Results: From a population of 5.4 million, there were, on average, 2.3 admissions for VTE per day. Pooled estimates of relative risk (RR) [95% confidence interval (CI)] of hospitalization for venous disease were: 1.07 (1.05, 1.09) for a 58.4 p.p.b. increase in ozone (O3); 1.06 (1.02, 1.09) for a 5.85 p.p.b. increase in sulphur dioxide (SO2); 1.08 (1.03, 1.12) for a 29.25 ,g/m3 increase in nitrogen dioxide (NO2); and 1.05 (1.03, 1.06) for a 20.02 ,g/m3 increase in particulate matter , 2.5 ,m in mean aerodynamic diameter (PM2.5). For pulmonary embolism (PE) results were: 1.10 (1.07, 1.13) for O3; 1.05 (1.02, 1.08) for SO2; 1.07 (1.04, 1.09) for NO2; and 1.05(1.03, 1.06) for PM2.5, respectively. Conclusion: Air pollution appears to be a risk factor for venous thrombosis and PE, a disease with a significant fatality rate. [source] Experimental Models To Investigate Inflammatory Processes in Chronic Venous InsufficiencyMICROCIRCULATION, Issue S1 2000RONALD J. KORTHUIS ABSTRACT Chronic venous insufficiency (CVI) is characterized by leukocyte adhesion and infiltration, venous hypertension and dilatation, and valvular dysfunction. The fact that activated white cells can direct a powerful cytotoxic arsenal at parenchymal cells following their extravasation into the tissues led to the original proposal that leukocytes may play a causative role in the pathogenesis of venous disease. A large body of subsequent work indicates that white blood cells are indeed activated in CVI. However, identification of the factors responsible for initiating leukosequestration and activation in such disorders and determination of whether these activated cells then contribute to the progression of venous disease have been hampered by the lack of appropriate animal models that accurately mimic the human condition. Tantalizing evidence suggesting that cyclical periods of ischemia and reperfusion (I/R) may occur in diseased regions of the skin is beginning to accumulate. As is the case with CVI, leukocyte infiltration is a prominent feature in I/R and activated neutrophils play a causative role in the reperfusion component of tissue injury via the targeted release of reactive oxygen metabolites and hydrolytic enzymes. In light of these considerations, many investigators have suggested that examining the mechanisms of I/R injury in skin and skeletal muscle, where ischemia is produced by arterial occlusion, may provide a relevant model for studying the pathogenesis of CVI. Others have suggested that venous occlusion may represent a more appropriate model, as this approach also produces the venous hypertension that is characteristic of the disease. The purpose of this review is to summarize the evidence pointing to the involvement of I/R and venous hypertension as causative factors in CVI-induced leukocyte recruitment. In addition, we will describe the evidence in favor of the view that white blood cells contribute to the pathogenesis of CVI. Finally, we will describe several different experimental models that have been used to examine the role of I/R-induced microvascular dysfunction as it may pertain to the development of CVI, together with a discussion of the relative advantages and limitations of the various models. [source] Lymphatic microsurgery for the treatment of lymphedemaMICROSURGERY, Issue 1 2006C. Campisi M.D. One of the main problems of microsurgery for lymphedema consists of the discrepancy between the excellent technical possibilities and the subsequently insufficient reduction of the lymphoedematous tissue fibrosis and sclerosis. Appropriate treatment based on pathologic study and surgical outcome have not been adequately documented. Over the past 25 years, more than 1000 patients with peripheral lymphedema have been treated with microsurgical techniques. Derivative lymphatic micro-vascular procedures has today its most exemplary application in multiple lymphatic-venous anastomoses (LVA). For those cases where a venous disease is associated to more or less latent or manifest lymphostatic pathology of such severity to contraindicate a lymphatic-venous shunt, reconstructive lymphatic microsurgery techniques have been developed (autologous venous grafts or lymphatic-venous-Iymphatic-plasty - LVLA). Objective assessment was undertaken by water volumetry and lymphoscintigraphy. Subjective improvement was noted in 87% of patients. Objectively, volume changes showed a significant improvement in 83%, with an average reduction of 67% of the excess volume. Of those patients followed-up, 85% have been able to discontinue the use of conservative measures, with an average follow-up of more than 7 years and average reduction in excess volume of 69%. There was a 87% reduction in the incidence of cellulitis after microsurgery. Microsurgical lymphatic-venous anastomoses have a place in the treatment of peripheral lymphedema and should be the therapy of choice in patients who are not sufficiently responsive to nonsurgical treatment. Improved results can be expected with operations performed earlier at the very first stages of lymphedema. © 2006 Wiley-Liss, Inc. Microsurgery 26: 65,69, 2006. [source] Minimally Invasive Vein Surgery: Latest Options for Vein DiseaseMOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 3 2010FACPhArticle first published online: 20 MAY 2010, Steven Elias MD Abstract The goal of treatment for venous disease is to decrease ambulatory venous hypertension. Various strategies are employed. These can be divided into exogenous and endogenous treatments. Exogenous methods concern those employed from the outside of the limb, such as compression and elevation. Endogenous modalities treat from inside the limb the underlying venous pathology due to venous valvular dysfunction or venous obstruction. Traditional endogenous procedures include stripping, ligation, and phlebectomy. All these procedures require incisions, anesthesia, and perhaps hospitalization, and involve significant discomfort. Newer minimally invasive vein surgery procedures now exist. These are all same-day, outpatient procedures, usually involving local anesthesia. Most can be performed percutaneously without incisions. Patients ambulate the day of the procedure. Morbidity is less than 1%. This article summarizes the concept of minimally invasive vein surgery and summarizes new technologies to manage all forms of venous disease. Mt Sinai J Med 77:270,278, 2010. © 2010 Mount Sinai School of Medicine [source] Asymptomatic lower extremity deep venous thrombosis resulting in fibula free flap failure,THE LARYNGOSCOPE, Issue 6 2009Adam S. Jacobson MD Abstract Objectives/Hypothesis: The successful harvest and transplant of a fibular flap depends on many factors, including healthy inflow and outflow systems. A contraindication to harvesting a fibular flap is disease of the lower extremity arterial system; therefore, preoperative evaluation of the arterial system is routine. Preoperative evaluation of the venous system is not routine, unless there is clinical suspicion of venous disease. Methods: Retrospective chart review. Results: Two cases of occult deep venous thrombosis (DVT) were encountered intraoperatively resulting in nontransplantable flaps. Conclusions: This finding represents a serious concern, and we believe that venous imaging should be considered in patients with significant risk factors for harboring an occult DVT. Laryngoscope, 2009 [source] Noninvasive bioengineering assessment of the skin barrier function in patients with chronic venous insufficiencyBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2010I. Angelova-Fischer Summary Background Chronic venous insufficiency (CVI) comprises all symptoms caused by permanent venous and capillary hypertension. While the clinical manifestations of the disease have been well characterized, there is little knowledge on the skin barrier function in the affected patients. Objectives The aim of the study was to assess noninvasively the barrier function in patients with CVI stage C2 and stage C4 according to the CEAP classification in comparison with healthy controls (stage C0). Methods Thirty patients with CVI without concomitant diseases and 15 healthy, aged-matched controls were recruited for the study. The skin barrier function was assessed by measuring transepidermal water loss (TEWL), capacitance and skin colour symmetrically on the calf, medial and lateral malleolus, posterior arch (arcus venosus) and volar forearm. Results Compared with the forearm, there was a tendency for increased TEWL and significant reduction of capacitance on all measurement sites on the lower limb. Compared with the control group, the patients with CVI had significantly higher TEWL values on all measurement sites on the lower extremities while no difference in capacitance between patients and controls was observed. Conclusions Changes in the epidermal barrier function in patients with CVI are readily detectable by bioengineering methods as early as stage C2 and are manifested by significantly increased TEWL. Our results suggest that the reduced stratum corneum hydration in patients with CVI is due to anatomical differences rather than venous disease. These findings may help better understand the factors contributing to disease progression and its complications. [source] Procollagen type I gene expression and cell proliferation are increased in lipodermatosclerosisBRITISH JOURNAL OF DERMATOLOGY, Issue 2 2005A.M. DeGiorgio-Miller Summary Background, Lipodermatosclerosis (LDS) is characterized by a hardening and hyperpigmentation of lower leg skin as a consequence of chronic venous insufficiency. The degree of skin hardening or fibrosis associated with LDS is proposed to relate directly to skin breakdown and venous ulcer formation as well as to a subsequent delay in ulcer healing. Objectives, To determine whether elevated procollagen type I gene expression and increased cell proliferation are responsible for the fibrotic changes associated with LDS. Methods, Skin biopsies were obtained from the legs of patients with varying degrees of chronic venous disease and were assessed for procollagen gene expression by in-situ hybridization and for cell proliferation by immunolocalization of proliferating cell nuclear antigen. Results, The number of cells expressing procollagen type I mRNA (COL1A1) was significantly higher in the dermis of LDS-affected skin compared with samples from the other patient groups. In addition, there was a significant increase in the number of dermal fibroblasts undergoing proliferation in both LDS samples and skin samples prior to LDS changes compared with control samples. However, there was no significant difference in level of inflammation in biopsy samples between patient classes. Conclusions, These results suggest that enhanced cell proliferation and procollagen gene expression are both involved in LDS development. Furthermore, fibrotic changes may occur in the absence of, or subsequent to, any significant inflammatory response, indicating that additional profibrotic factors produced in the skin as a consequence of chronic venous insufficiency may play a role in LDS formation. [source] | ||||||||||