Subclinical neuropsychiatric dysfunctions in female patients with systemic lupus erythematosus

الملخص EN

Objective To examine for presence of subclinical neuropsychiatric lupus and cerebral atherosclerosis and their correlation with MRI/magnetic resonance angiography (MRA) findings and disease activity and to find if these radiological changes compared with laboratory parameters could be predictive of the early NP affection aiming for early management of these dysfunctions.

Patients and methods Thirty adult female patients with systemic lupus erythematosus (SLE) were enrolled, with assessment of SLE disease activity using Systemic Lupus Erythematosus Disease Activity Index; psychometric evaluations using the Modified Mini-Mental State Examination to assess for cognitive dysfunction; Hamilton Depression Rating Scale andHamilton Anxiety Scale to assess for depression and anxiety, respectively; and brain MRI/MRA to detect any changes in subclinical cases.

Results The mean age was 31.7 years.

Twelve (40%) patients had positive antiphospholipid (aPL) antibodies with or without clinically evident antiphospholipid syndrome, 22 (73.33%) had different NP manifestations, 13 (43.3%) depression, 15 (50%) anxiety, and 16 (53.3%) cognitive dysfunction.

All patients with depression and anxiety and 87.5% of patients with dementia showed abnormalities on MRI.

All patients with positive aPL showed abnormalities on MRI, whereas abnormalities on MRI were found in only eight patients with SLE with negative aPL (100 vs.

44.4%).

There was a significant correlation between SLE disease activity and both NP manifestations and abnormalities on MRI/MRA, and also between aPL antibodies and NP manifestations.

Abnormalities on MRI included discrete white matter lesions, cortical atrophy, and gross infarctions.

Conclusion Significant number of patients with SLE without overt NP manifestations had subclinical cerebrovascular and cognitive dysfunctions, depression, and anxiety by simple bedside questionnaires.

SLE disease activity positively correlates with NP manifestations.

The presence of aPL antibodies is a strong risk factor for developing NP SLE.

Several distinct brain MRI patterns were observed in patients with active NP SLE, suggestive of different pathogenic mechanisms