Cerebral metabolic disturbance as detected with magnetic resonance spectroscopy in neuropsychiatric systemic lupus erythematosus

To evaluate the spectral brain changes using 1H-MR spectroscopy in Neuropsychiatric Systemic Lupus Erythematosus [NPSLE] patients: and, to correlate their neuropsychiatric clinical data with MRI and 1 PI-MRS abnormalities. Twenty three NPSLE patients and 8 age and sex matched control volunteers were included. Disease activity was measured by SLE Disease Activity Index [SEEDAI]. Patients were classified into two groups; the first included NPSEE patients with normal MRI, and the second included those with abnormal MRI. Single voxel proton MRS was evaluated in the parieto-occipital white matter in all patients and volunteers and in areas of MRI abnormal lesions. The metabolic peaks were fitted at known frequencies where N-acetylaspartate [NAA] at 2.02 ppm, creatine [Cr] at 3.02 ppm, and choline [Cho] at 3.22 ppm. The relative ratios of NAA to Cr and of Cho to Cr we measured. the most common neuropsychiatric features were headache and cognitive impairment with 39.1% for each of them, 9 patients had abnormal MRI imaging, while spectral changes were present in 20 patients. MRS changes were in agreement and statistically significant [P=0.001] with the neuropsychiatric manifestations, compared with MRI changes [P=0.8]. Neuropsychological tests were significantly affected in patients with abnormal MRI versus those with normal ones. In patients with abnormal MRI, the NAA/Cr ratio was significantly lower than those with normal MRL while the Cho/Cr ratio was significantly higher. In patients with NPSLE, 1H-MR spectroscopic findings seem to reflect the cerebral metabolic disturbances as functional abnormalities, related to the neuropsychiatric symptoms. It is a complementary tool to MRI in diagnosing the CNS involvement

Antikeratin antibodies [AKAS]: Usefulness in differentiation between rheumatoid arthritis and hepatitis C virus associated arthritis

Among the different clinical disorders associated with hepatitis C virus [HCV] infection, articular involvement is a frequent complication. Symmetric polyarthritis associated with HCV infection frequently displays a rheumatoid arthritis [RA] like clinical picture. Thus, differentiating patients with HCV related symmetric polyarthritis from patients with RA represents both a diagnostic and a therapeutic challenge. Our aim was to investigate whether antikeratin antibodies [AKAs] could be useful markers in differentiating patients with rheumatoid arthritis [RA]; from patients with hepatitis C virus [HCV,] associated polyarthritis who are seropositive for rheumatoid factor [RF]. Serum AKAs were determined in two groups of patients; all were RF seropositive. Group [I]: 25 patients with HCV associated symmetric polyarthralgia or arthritis: Group [II]: 25 patients with RA [ACR revised criteria for diagnosis of RA, 1988]. Fifteen healthy individuals, age and sex matched, served as controls. AKAs were tested using an indirect immunofluorescence technique with 1:10 serum dilution. The study revealed that AKAs were detected in 15/25 [60%] patients with true RA and in only 3/25 [12%] patients with HCV associated arthritis [p<0.0001]. AKAs were not found in the sera of the healthy controls. AKAs can be useful markers in differentiating patients with true RA from those with HCV arthritis

Serum vascular endothelial growth factor in rheumatoid arthritis: a relationship to disease activity and pathogenesis

This study aims to determine the serum level of vascular endothelial growth factor [VEGF] in rheumatoid arthritis [RA] patients and to search for a relationship between serum VEGF level and clinical, laboratory, and radiological variables of the disease in an attempt to provide more insight regarding its role in disease activity and pathogenesis. 75 RA patients, diagnosed according to the American College of Rheumatology [ACR] criteria and 20 control subjects were included in this study. RA patients were divided into active group [38 patients] and non-active group [37 patients] as assessed clinically by using modified disease activity score [DAS-28] and laboratory by using erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP]. All patients included in this study were subjected to full history taking, thorough clinical examination and laboratory investigations including ESR, CRP, complete blood picture, rheumatoid factor, and serum VEGF assay using ELISA technique. Assessment of radiological severity by Larsen's score was done by using plain X-ray for both hands and wrists joints. We found that serum VEGF level was higher in RA patients group than control subjects and in the active group than non-active one. In RA patients, the serum level of VEGF was positively correlated to DAS-28, ESR and CRP. Also, the levels of serum VEGF were higher in patients with early grades of Larsen's score than those with late grades. Also, RA patients with early disease duration [<2 years] had higher serum VEGF levels than those of late disease duration [>3 years]. We suggest that VEGF may be involved in the pathogenesis of RA, and serum VEGF is a non-invasive useful method for monitoring the disease activity of RA, although this is not a specific marker for RA. Anti-VEGF strategies should largely be confined to modulating angiogenesis in RA