4.5 Article

Symptoms of chronic venous disease and association with systemic inflammatory markers

Journal

JOURNAL OF VASCULAR SURGERY
Volume 38, Issue 5, Pages 950-954

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/S0741-5214(03)00600-1

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Purpose: We recorded symptoms reported by patients with chronic venous disease (CVD) of the leg and correlated these with systemic inflammatory markers. Methods: This was an observational study in a cohort of 132 adult patients with CVD attending the vascular clinic of a teaching hospital. Patients were excluded in whom recent surgery, illness, or concomitant medication may have influenced measurements of systemic inflammatory mediators. Patients with CEAP clinical stages C-2 to C-5 only were considered for inclusion in the study. CEAP clinical stage was established for each patient, and duplex ultrasound scanning was used to assess extent of venous disease in the lower limbs. Blood was taken from a foot vein, and the following inflammatory mediators were measured with enzyme-linked immunosorbent assay: von Willebrand factor, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, soluble (s)E-selectin, sP-selectin, L-selectin, VEGF, and cytokines interleukin (IL)-1alpha, IL-1beta, IL-6, and tumor necrosis factor-alpha. Symptoms were recorded by patients using a visual analog scale (VAS) for the symptoms of pain, cramps, heaviness, paresthesia, and feeling of swelling. Results: The greatest VAS symptom scores were observed in the less severe disease stages: C-2 median pain score, 2.8 units (interquartile range [IQR], 0.1-5); C-3, 4.5 (IQR, 3.4-5.5), C-4, 0.5 (IQR, 0-3.0); C-5, 0 (IQR, 0-4). Symptom scores were similar in patients with primary and recurrent venous disease after previous surgery and in patients with superficial venous reflux and deep venous reflux. No correlation was found between the measurements of inflammatory mediators and the symptoms assessed with the VAS. Conclusion: We found no correlation between symptoms reported by patients and the internationally agreed clinical stages of venous disease of C-2 to C-5. Neither was there any correlation between levels of inflammatory mediators and patient symptoms. Symptoms reported by patients with CVD cannot be explained by anatomic distribution of venous disease in the lower limb veins or by the systemic inflammatory response in venous disease.

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