Fibrinogen in systemic lupus erythematosus: More than an acute phase reactant?

Citation
Prj. Ames et al., Fibrinogen in systemic lupus erythematosus: More than an acute phase reactant?, J RHEUMATOL, 27(5), 2000, pp. 1190-1195
Citations number
36
Categorie Soggetti
Rheumatology,"da verificare
Journal title
JOURNAL OF RHEUMATOLOGY
ISSN journal
0315162X → ACNP
Volume
27
Issue
5
Year of publication
2000
Pages
1190 - 1195
Database
ISI
SICI code
0315-162X(200005)27:5<1190:FISLEM>2.0.ZU;2-J
Abstract
Objective. To investigate whether plasma fibrinogen (FNG) measured longitud inally in a cohort of patients with systemic lupus erythematosus (SLE) incr eased over observational time faster than in a control group, and whether i ts increase might depend upon age, disease duration, disease activity, and medications. Methods. Hospital based retrospective study with repeated measurements of p lasma FNG and C-reactive protein (CRP) for patients and controls and erythr ocyte sedimentation rate (ESR) and lupus activity index (LAI) for patients only. Study groups included patients with SLE, n = 96 (95% female), and hea lthy controls: n = 39 (95% female). Of the patients, 42% had SLE only, 23% had SLE with antiphospholipid antibodies (aPL), and 34% had SLE with aPL re lated thrombosis. Results. Median baseline FNG was higher in patients (357 mg/dl; 95% CI 339- 375) than in controls (271 mg/dl; 95% CI 251-291) by 86 mg/dl (95% CI 56-11 5, p < 0.001); in older subjects than younger (in patients and in controls) ; in patients with thrombosis than in other patient groups (by an average o f 35 mg/dl; 95% CI 9-61 mg/dl), and in patients with longer disease duratio n (p = 0.05). Mean FNG increased faster in patients (19 mg/dl/year; 95% CI 12-26 mg/dl) than in controls (2.6 mg/dl/year; 95% CI 2.0-3.2 mg/dl). The i ncrease was faster than the age effect and independent of patient group and disease activity. Conclusion. Plasma FNG in patients with SLE increases throughout followup r egardless of disease activity, mimicking the age related increment observed in population based studies. The rapidity of the increment may reflect the prematurity of vascular disease typical of SLE.