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Egyptian Rheumatologist [The]. 2009; 31 (2): 111-119
in English | IMEMR | ID: emr-150758

ABSTRACT

Cardiovascular disease has recently been acknowledged as a primary cause of morbidity and mortality in SLE. There are conflicting reports about CRP values in different spectrum of disease activity in SLE. Though CRP values are higher in active disease compared to inactive disease, its value may or may not correlate with disease activity. Elevated basal CRP has been associated with increased cardiovascular risk, while CRP dysregulation may be a feature of SLE. The aim of the present study was to assess the CRP level in SLE patients asymptomatic for any cardiac involvement especially pericardial effusion and find its relation with clinical and laboratory findings as well as the disease activity and damage indices. Correlation with antiphospholipid antibodies was also considered a point of interest. Thirty female SLE patients were recruited from the Rheumatology department and out patient clinic, Cairo University Hospitals. Patients were asymptomatic for any cardiac involvement. Full history taking, thorough examination, laboratory and relevant radiological investigations were performed for all the patients. Echocardiography was performed to detect pericardial effusion [PE]. Quantitative CRP level was assessed as well as the autoantibodies including anti cardiolipin antibodies [IgG and IgM], anti Ro [SSA] and Anti La [SSB] were detected by ELISA. Disease activity and damage were assessed for all the patients using the SLEDAI and SLICC/ ACR DI. Fifteen age matched female healthy subjects were considered as a control group for the corresponding patients. The mean age of patients was 28.53 +/- 6.77 years, age at disease onset was 24.51 +/- 7.05 years and disease duration was 4.02 +/- 2.57 years. There were 7 patients [23.33%] with pericardial effusion as detected by echocardiography. There was no significant difference in the mean age and disease duration between those with and those with out PE, although there was a tendency to blood pressure elevation in those with PE. Three SLE patients had secondary antiphospholipid syndrome [SAPS]. None of the patients had myocardial infarctions. The mean CRP level in SLE patients with PE was significantly higher than in those with out [33.71 +/- 33.22 and 13.57 +/- 11.51 mg/L, respectively, p 0.017]. Pericardial effusion and serositis may be responsible for the marked elevation of the CRP level in this subset of SLE patients. Those without PE, although active, only had modest CRP elevation. A muted CRP response is seen in the majority of patients with active SLE; levels achieved are generally low. SLE subset with pericardial serositis show marked CRP response, perhaps reflecting the likelihood that SLE is not a single disease entity


Subject(s)
Humans , Female , Pericardial Effusion , C-Reactive Protein , Antibodies, Antiphospholipid/blood , Disease Progression
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