Plasma Lactoferrin as a Marker of White Cell Degranulation in Venous Disease

1994 ◽  
Vol 9 (2) ◽  
pp. 55-58 ◽  
Author(s):  
D. A. Shields ◽  
S. Andaz ◽  
R. D. Abeysinghe ◽  
J. B. Porter ◽  
J. H. Scurr ◽  
...  
Keyword(s):  
Neutrophil Count ◽  
Varicose Veins ◽  
Cell Activity ◽  
Arterial Disease ◽  
White Cell ◽  
Venous Disease ◽  
Venous Ulceration ◽  
Control Subjects ◽  
Middlesex Hospital ◽  
Vascular Laboratory

Objective: To measure plasma lactoferrin as a marker of neutrophil degranulation in groups of patients with varying severity of venous disease and compare with age- and sex-matched control subjects. Design: Prospective study of patients with varicose veins compared with a group of control subjects with no history or clinical findings of varicose veins. Setting: The Middlesex Hospital Vascular Laboratory, Mortimer Street, London WIN 8AA, UK. Patients: Patients referred to the Middlesex Hospital Vascular Laboratory for investigation of venous disease. Control subjects were obtained from within the laboratory and hospital staff, and from a group of Patients attending the London Foot Hospital for routine chiropody. Neither group had arterial disease nor any other illness or medication known to alter white cell activity. Interventions: 10 ml of blood taken from an arm vein into EDTA for a neutrophil count and measurement of Plasma lactoferrin using an ELISA. Results: Significantly raised plasma lactoferrin was found in all four groups of patients compared with their controls ( p = 0.0156 for uncomplicated varicose veins, P = 0.01 for lipodermatosclerosis, p = 0.0413 for active venous ulceration, and p = 0.0005 for healed ulcers, Mann-Whitney U-test). Differences between medians (95% confidence interval) for the four groups were 269 (62–603), 199 (60–314), 133 (44–218) and 215 (98–349) ng/ml respectively. There was no difference in the neutrophil count between the patient and control groups, and correcting plasma lactoferrin for the neutrophil count did not remove significance in any group. Conclusions: This study shows evidence of increased neutrophil activation as shown by increased degranulation in patients with venous disease.

Soluble Markers of Leucocyte Adhesion in Patients with Venous Disease

1997 ◽  
Vol 12 (3) ◽  
pp. 82-85
Author(s):  
D. A. Shields ◽  
S. K. Andaz ◽  
J. B. Porter ◽  
J. H. Scurr ◽  
P. D. Coleridge Smith
Keyword(s):  
Neutrophil Count ◽  
Varicose Veins ◽  
Cell Activity ◽  
Arterial Disease ◽  
Clinical Findings ◽  
Venous Disease ◽  
Control Subjects ◽  
Middlesex Hospital ◽  
Neutrophil Degranulation ◽  
Vascular Laboratory

Objective: To measure soluble CD54 (ICAM-1) and CD62E (E-selectin) as markers of neutrophil adhesion in four groups of patients with varying severity of venous disease and compare the values obtained with those in age- and sex-matched control subjects. Design: Prospective study of patients with varicose veins compared with a group of control subjects with no history or clinical findings of varicose veins. Setting: The Middlesex Hospital Vascular Laboratory, London. Patients: Patients referred to the Middlesex Hospital Vascular Laboratory for investigation of venous disease. Neither patients nor controls had arterial disease, any other systemic illness, or were on any medication known to alter white cell activity. Interventions: Ten millimetres of blood taken from an arm vein into EDTA for a neutrophil count and soluble CD54 and CD62E, measured using an ELISA. Results: Similar levels of soluble CD54 and CD62E were found in all four groups of patients compared with their controls ( p = 0.71 for soluble CD54 for all patients compared with all controls, and p = 0.65 for soluble CD62E, Mann–Whitney U-test). There was no difference in the neutrophil count between the controls and patients in any group ( p = 0.74 for all subjects, Mann–Whitney U-test). Conclusion: This study shows no evidence of increased soluble CD54 or CD2E or CD62E in patients with venous disease, despite previous work showing increased CD54 and neutrophil degranulation in patients with venous disease. The reason for this is currently unknown.

Neutrophil Activation in Experimental Venous Hypertension

1994 ◽  
Vol 9 (3) ◽  
pp. 119-124 ◽  
Author(s):  
D. A. Shields ◽  
S. Andaz ◽  
R. D. Abeysinghe ◽  
J. B. Porter ◽  
J. H. Scurr ◽  
...  
Keyword(s):  
Neutrophil Count ◽  
Venous Hypertension ◽  
White Cell ◽  
Venous Disease ◽  
Venous Ulceration ◽  
Cell Trapping ◽  
Normal Volunteers ◽  
Middlesex Hospital ◽  
Vascular Laboratory ◽  
The Right

Objective: To investigate the white cell trapping hypothesis of venous ulceration by measuring plasma lactoferrin as a marker of neutrophil degranulation in normal volunteers in two experimental models of venous hypertension. Design: A prospective study of volunteers with no history or clinical evidence of venous disease. Setting: The Middlesex Hospital Vascular Laboratory, Mortimer Street, London WIN 8AA, UK. Patients: Volunteers within the Middlesex Hospital Vascular Laboratory with no history or clinical findings of venous or arterial disease, no other systemic disease, on no medication known to alter white cell activity, and with no recent infection. Interventions: Venous blood was taken from cannulae in both feet and the right arm for a neutrophil count and Plasma lactoferrin, measured using an ELISA, during application of a tourniquet to 80 mmHG for 30 min to the right leg while supine, 5 min after release of tourniquet, and then during a 30 min period of standing. Results: During application of a tourniquet to the right leg there was a significant rise in plasma lactoferrin and in lactoferrin corrected for the neutrophil count ( p < 0.05, Wilcoxon). In the unoccluded leg, although Plasma lactoferrin rose, this was not significant when corrected for the rise in neutrophil count. After standing for 30 min, the lactoferrin and neutrophil count increased in all three limbs; corrected lactoferrin showed a significant increase in the legs ( p < 0.02), though not in the arm. Conclusion: Increased neutrolphil degranulation occurs during periods of short-term venous hypertension in normal volunteers, in keeping with the white cell trapping hypothesis.

Neutrophil CD11b Expression in Patients with Venous Disease

1996 ◽  
Vol 11 (2) ◽  
pp. 55-59 ◽  
Author(s):  
D. A. Shields ◽  
M. Saharay ◽  
C. Timothy-Antoine ◽  
J. B. Porter ◽  
J. H. Scurr ◽  
...  
Keyword(s):  
Confidence Interval ◽  
Varicose Veins ◽  
White Cell Count ◽  
Peripheral Circulation ◽  
White Cell ◽  
Venous Disease ◽  
Cd11b Expression ◽  
Control Subjects ◽  
Vascular Laboratory ◽  
Normal Controls

Objective: To determine whether neutrophil CD11b, a marker of neutrophil adhesion, differs in patients with varying degrees of severity of venous disease, and to compare the values obtained with those of age-matched normal control subjects. Design: Prospective study, measuring white cell count and neutrophil CD11b expression in whole blood using a fluorescent-labelled monoclonal antibody in a flow cytometer. Setting: The Middlesex Hospital Vascular Laboratory, a referral centre for the investigation of venous disease. Patients: Ten patients with uncomplicated varicose veins, 10 patients with skin changes of lipodermatosclerosis (LDS), and 20 age-matched control subjects with no history or clinical finding of venous disease. Results: Higher levels of CD11b were found in patients with uncomplicated varicose veins compared with their controls (median 4.6 cf. 1.43 for normal controls, P = 0.005, Mann-Whitney U-test, difference between medians 2.7, 95% confidence interval 1 to 4.6), and lower levels in patients with LDS (median 1.22 cf. 1.53 for normal controls, p = 0.028, Mann-Whitney U-test, difference between medians 0.45, 95% confidence interval 0.02 to 1.3). There was no difference in the white cell or neutrophil count between the patient and control groups. Conclusions: This study demonstrates increased neutrophil surface CD11b expression in patients with uncomplicated varicose veins, but decreased levels in patients with LDS. This might be due to up-regulation of CD11b in some neutrophils with subsequent adhesion, so that only those with low expression remained in the peripheral circulation. Alternatively, this might represent either down-regulation or chronic exhaustion of neutrophil CD11b in these patients.

Is the ‘Normal’ Limb Normal in Unilateral Varicose Veins?

1992 ◽  
Vol 7 (2) ◽  
pp. 75-77 ◽  
Author(s):  
S. Sarin ◽  
D. A. Shields ◽  
A. Abu-Own ◽  
J. H. Scurr ◽  
P. D. Coleridge Smith
Keyword(s):  
Prospective Study ◽  
Teaching Hospital ◽  
Varicose Veins ◽  
Duplex Scanning ◽  
Venous Disease ◽  
Clinically Normal ◽  
Middlesex Hospital ◽  
Vascular Laboratory ◽  
Primary Varicose Veins ◽  
Venous Function

Objective: To define venous function in the clinically normal limb of patients with unilateral primary varicose veins. Design: Prospective study using duplex scanning and photoplethysmography (PPG) as objective criteria of venous function. Setting: The Middlesex Hospital Vascular Laboratory, a teaching hospital centre of referral for the investigation of venous disease. Patients: Thirty patients with clinical unilateral primary varicose veins. Results: All clinically abnormal limbs had abnormalities on investigation. However, four of 30 patients (13%) also had abnormal duplex findings on the contralateral clinically normal limb, and six (20%) had abnormal PPG refilling times. A total of 26% clinically normal limbs could be demonstrated to have some abnormality of venous function using these two tests. Conclusions: We have shown that the contralateral, clinically normal limb cannot be assumed to be normal without full formal venous assessment.

Is arteriovenous shunting involved in the development of varicosities? A study of the intraluminal pressure and oxygen content in varicose veins

2008 ◽  
Vol 23 (3) ◽  
pp. 137-141 ◽  
Author(s):  
M A Murphy ◽  
L Hands
Keyword(s):  
Oxygen Content ◽  
Supine Position ◽  
Varicose Veins ◽  
Causative Factor ◽  
Intraluminal Pressure ◽  
Control Group ◽  
Venous Disease ◽  
Control Subjects ◽  
Pulsatile Pressure ◽  
Primary Varicose Veins

Objectives Arteriovenous (AV) shunting has been postulated as the underlying cause of varicose veins. The aim of this study was to analyse pressure and oxygen content in primary varicose veins in order to determine evidence of arterial shunting. Methods Thirty-nine patients with varicose veins underwent cannulation of varicosities. The pressure and the blood oxygen content within varicosities were measured in different positions and during exercise. Similar measurements were made in the long saphenous veins of 10 control subjects without venous disease. Results Mean pressure in varicose veins in the supine position was 12.3 mmHg (Standard deviation [SD] 3.6 mmHg). Control subjects had similar pressures measured in the long saphenous vein. No pulsatile pressure tracings were obtained. Varicosity pressures in the erect position averaged 66 mmHg (SD 9 mmHg). In all cases, the pressure correlated with the distance of the varicosity from the heart. Pressure reduction in varicosities after exercise was significantly less than that in control subjects. Recovery time (RT 90) was also significantly shorter than in the control group. Mean venous pO2 in varicosities was 4.5 kPa (SD 1.0) in the supine position dropping to 3.9 kPa (SD 0.9) on standing; these values were not significantly different to samples from control subjects. Conclusions AV shunting is unlikely to be a causative factor in the development of primary varicose veins.

Predicted burden of venous disease

2016 ◽  
Vol 31 (1_suppl) ◽  
pp. 74-79 ◽  
Author(s):  
Sarah Onida ◽  
Alun Huw Davies
Keyword(s):  
Varicose Veins ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Chronic Venous Disease ◽  
Venous Disease ◽  
Venous Ulceration ◽  
Increased Risk ◽  
Future Burden ◽  
Clinical Signs And Symptoms

Chronic venous disease is a common condition with clinical signs and symptoms ranging from spider veins, to varicose veins, to active venous ulceration. Both superficial and deep venous dysfunction may be implicated in the development of this disease. Socio-economic factors are shaping our population, with increasing age and body mass index resulting in significant pressure on healthcare systems worldwide. These risk factors also lead to an increased risk of developing superficial and/or deep venous insufficiency, increasing disease prevalence and morbidity. In this chapter, the authors review the current and future burden of chronic venous disease from an epidemiological, quality of life and economic perspective.

Epidemiology of chronic venous disease

2008 ◽  
Vol 23 (3) ◽  
pp. 103-111 ◽  
Author(s):  
L Robertson ◽  
C Evans ◽  
F G R Fowkes
Keyword(s):  
Risk Factors ◽  
Varicose Veins ◽  
Adult Population ◽  
Chronic Venous Disease ◽  
Western World ◽  
Venous Disease ◽  
Venous Ulceration ◽  
Prolonged Standing ◽  
True Incidence ◽  
Disease Definition

Chronic venous disease of the legs occurs commonly in the general population in the Western world. Estimates of the prevalence of varicose veins vary widely from 2–56% in men and from 1–60% in women. These variations reflect differences in variability of study populations including age, race and gender, methods of measurement and disease definition. Definitions of chronic venous disease may rely on reports of varicose veins by study participants, based on self-diagnosis or recall of a diagnosis, or on a standardized physical examination. Venous ulceration is less common, affecting approximately 0.3% of the adult population. Age and pregnancy have been established as risk factors for developing varicose veins. Evidence on other risk factors for venous disease is inconclusive. Prolonged standing has been proposed, but results of studies should be interpreted with caution given the difficulty in measuring levels of posture. Obesity has been suggested as a risk factor in women, but appears to be an aggravating factor rather than a primary cause. Other postulated risk factors include dietary intake and smoking, but evidence is lacking. Longitudinal studies using standardized methods of evaluation are required before the true incidence of chronic venous disease and associated risk factors can be determined.

Vascular surgery

2016 ◽  
Author(s):  
Suzanne Davies ◽  
Alison Kite ◽  
Annette Wye
Keyword(s):  
Nursing Care ◽  
Varicose Veins ◽  
Arterial Disease ◽  
Assessment Process ◽  
Treatment Modalities ◽  
Venous Disease ◽  
Carotid Disease ◽  
Anatomy And Physiology ◽  
Abdominal Aortic ◽  
Peripheral Ischaemia

Vascular conditions are common in surgical nursing care and range from varicose veins to more complex arterial disease. This chapter gives the nurse an understanding of the assessment process for vascular conditions, the associated anatomy and physiology, and treatment modalities. The chapter also focuses on specific conditions, including amputation, venous disease, ulcers, and arterial conditions such as abdominal aortic aneurysm, peripheral ischaemia, and carotid disease.

Genetic polymorphisms of vein wall remodeling in chronic venous disease: a narrative and systematic review

Blood ◽  
2014 ◽  
Vol 124 (8) ◽  
pp. 1242-1250 ◽  
Author(s):  
Vighnesh Bharath ◽  
Susan R. Kahn ◽  
Alejandro Lazo-Langner
Keyword(s):  
Systematic Review ◽  
Varicose Veins ◽  
Chronic Venous Disease ◽  
Current Evidence ◽  
Postthrombotic Syndrome ◽  
Venous Disease ◽  
Genetic Associations ◽  
Vein Wall ◽  
Venous Ulceration ◽  
Therapeutic Implications

Abstract Chronic venous disease encompasses a spectrum of disorders caused by an abnormal venous system. They include chronic venous insufficiency, varicose veins, lipodermatosclerosis, postthrombotic syndrome, and venous ulceration. Some evidence suggests a genetic predisposition to chronic venous disease from gene polymorphisms associated mainly with vein wall remodeling. The literature exploring these polymorphisms has not been reviewed and compiled thus far. In this narrative and systematic review, we present the current evidence available on the role of polymorphisms in genes involved in vein wall remodeling and other pathways as contributors to chronic venous disease. We searched the EMBASE, Medline, and PubMed databases from inception to 2013 for basic science or clinical studies relating to genetic associations in chronic venous disease and obtained 38 relevant studies for this review. Important candidate genes/proteins include the matrix metalloproteinases (extracellular matrix degradation), vascular endothelial growth factors (angiogenesis and vessel wall integrity), FOXC2 (vascular development), hemochromatosis (involved in venous ulceration and iron absorption), and various types of collagen (contributors to vein wall strength). The data on associations between these genes/proteins and the postthrombotic syndrome are limited and additional studies are required. These associations might have future prognostic and therapeutic implications.

An Overview of the Surgical Aspects of Lower Limb Venous Disease

2009 ◽  
Vol 54 (3) ◽  
pp. 30-35 ◽  
Author(s):  
Cn Parnaby ◽  
Gh Welch ◽  
Wp Stuart
Keyword(s):  
Lower Limb ◽  
Varicose Veins ◽  
Wide Spectrum ◽  
Healthcare Providers ◽  
Venous Disease ◽  
Venous Ulceration ◽  
Chronic Skin ◽  
Surgical Aspects ◽  
Invasive Techniques ◽  
High Degree

Summary Points Lower limb venous disease encompasses a wide spectrum of pathology, the importance of which relates to high prevalence rather than mortality. The complications of chronic venous insufficiency (CVI), namely lipodermatosclerosis and chronic venous ulceration, represent a major burden to healthcare providers and a high degree of personal morbidity for patients. Management is based upon accurate clinical diagnosis supported by non-invasive imaging. Open surgical and minimally invasive techniques are used to treat varicose veins. Chronic skin complications of CVI require a multi-disciplinary approach.

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