Background/ObjectiveA search for the ideal biomarker for lupus nephritis (LN) is still underway, one that can be used for early detection and correlate with the class and activity of LN. Urine is normally devoid of leukocytes; however, it has been observed that macrophages and T lymphocytes are routinely present in the urine of LN patients and those with other proliferative renal diseases. This provides the idea for their potential use as biomarkers for proliferative LN. Here, we measured the urinary CD4+, CD8+ T lymphocytes, and CD14+ monocytes in patients with systemic lupus erythematosus (SLE) as potential biomarkers for LN.MethodsA longitudinal case-control study included 30 SLE patients with LN, 30 SLE patients without past or current LN, and 20 healthy subjects as a control group. The flow cytometric analysis was done using BD FACS Calibur multiparameter flow cytometer equipped with BD CellQuest Pro software for data analysis.ResultsCD14+ cells were the most abundant cells in the urine of LN patients. The mean numbers of urinary CD8+, CD4+, and CD14+ cells/mL were significantly higher in patients with LN than in those without. The cell counts correlated significantly with proteinuria. Urinary CD14+ cells seem to occur in much higher counts in class IV than class III LN.ConclusionsUrinary CD8+, CD4+, and CD14+ cells are highly sensitive and specific markers for detecting proliferative LN. A low CD4:CD8 ratio provides a further clue. Urinary CD14 cell counts may be a potential biomarker to differentiate between the different classes of proliferative LN.

Background:literature suggests that smoking is one of the crucial triggering factors of rheumatological diseases.(1) In axial Spondyloarthritis (axSpA), classified into radiographic SpA (AS) and non-radiographic SpA (nrSpA), smoking associated with disease activity and extra-articular manifestation. (2) The relationship between smoking and HLAB-27 as well as MRI inflammation in axSpA patients and the difference between nrSpA and AS regarding smoking have not been studied to date in details.Objectives: to investigate the influence of smoking on disease activity and MRI inflammation in axSpA patients (AS and nrSpA).Methods:sixty Egyptian patients (42 males and 18 females) with the mean age (31.33 ± 7.02), with early active axial spondyloarthritis (49 AS and 11 non-radiographic SpA) within two years disease duration, diagnosed based on ASAS classification criteria. All clinical indices (BASDI, BASFI, BASMI, ASDAS-CRP) were applied to all patients. HLA-B27 and the inflammatory markers (ESR, CRP) was done. MRI of sacroiliac joints was performed in a standard protocol using short tau inversion recovery and T1 sequences (slice thickness 3-4mm, both semi-coronal and semi-axial orientations), and scored by the Berlin method. Smoking use assessed by smoking pack-year index.Results:of all 60 patients, 38 smokers and 22 non-smokers. No significant difference regarding smoking packs index between nrSpA and AS. (p=0.822) There was a robust correlation between smoking packing index and the Berlin score of MRI in all axSpA patients (rs=0.631) (p=<0.001). Moreover, there was a significant correlation between smoking and C-reactive protein (rs=0.952) as well as HLA-B27. (rs=0.340) (p<0.001) Furthermore, a significant relationship between smoking and activity indices (BASDI (rs=0.961) and ASDAS-CRP (rs=0.938)). Otherwise, no significant correlation among smoking, BASMI, and BASFI as well as ESR.Table (1): Correlation between smoking pack index and different parameters Disease activity Smoking pack index Non radiographic SpA (n = 11) Radiographic SpA (n = 49) Total (n = 60) rs p rs p rs p BASDI 0.986* <0.001* 0.224<0.001* 0.204<0.001* ASDAS-CRP 0.981* <0.001* 0.969* <0.001* 0.938* <0.001* rs: Spearman coefficient*: Statistically significant at p ≤ 0.05Table (2): Correlation between smoking pack index and HLAB27, inflammatory marker (CRP) and Berlin score of MRISmoking pack index Non radiographic SPA (n = 11) Radiographic SPA (n = 49) Total (n = 60) rs P rs p rs p HLAB27 0.602* 0.049* 0.293* 0.041* 0.340* 0.008* Berlin score of MRI 0.687* 0.020* 0.742* <0.001* 0.631* <0.001* CRP 0.991* <0.001* 0.970* <0.001* 0.952* <0.001* rs: Spearman coefficient*: Statistically significant at p ≤ 0.05Conclusion:Smoking has no significant difference between AS and nrSpA. Smoking has a significant association with HLA-B27, the inflammatory lesions of MRI, and clinical indices (BASDI, ASDAS-CRP) as well as C reactive protein in AS and non-radiographic SpA patients while it has no association with the other clinical in...

Background: First-degree relatives (FDRs) of rheumatoid arthritis (RA) patients are known to have increased risk of developing the disease. The detection of altered bone metabolism in FDRs could be a predictor of the disease. Preclinical phase of RA is characterized by a state of autoimmunity and inflammation. Musculoskeletal ultrasound (MSUS) is known for its ability to detect subclinical joint inflammation in RA, but changes in FDRs are not yet described.Objectives: To study serum osteopontin (OPN) and osteoprotegerin (OPG) levels in first degree relatives (FDRs) of rheumatoid arthritis (RA) as markers of altered bone metabolism in relation to clinical, laboratory and musculoskeletal ultrasound (MSUS) findings. Methods: Fifty-five individuals were included, 20 had definite RA, 25 were FDRs of RA patients, and 10 healthy controls. Clinical evaluation for joint swelling/tenderness was performed for all. ESR, CRP, rheumatoid factor (RF), anti-citrullinated antibodies (ACPA), OPN, OPG, and MSUS by the US7 score were evaluated.Results: OPG was significantly higher in RA (143.89 pg/ml±365.47) than in FDRs (22.23 pg/ml±65.73; p=0.009) and controls (6.20 pg/ml±12.43; p=0.003). OPN was also higher in RA (3.66 ng/ml±4.20) than in FDRs (1.97 ng/ml±1.04) and controls (2.81 ng/ml±1.31), though not significant (p=0.102). Eight of 25 FDRs (32%) had arthralgia without clinical arthritis and 17/25 (68%) were asymptomatic. FDRs with arthralgia had significantly higher ESR and CRP levels than asymptomatic FDRs (9.82 mm/h±4.13; p=0.003, and 3.93 mg/l±3.58; p=0.003). OPG was higher in FDRs than in controls, and also in those with arthralgia (51.55 pg/ml±114.68) than in those without (8.44 pg/ml±9.67), though without significant difference. OPN was higher in FDRs with arthralgia (2.09 ng/ml±1.19) than in asymptomatics (1.70 ng/ml±0.55), also without significant difference. Pathologic findings by US7 were detected in 10/25 (40%) FDRs, of which three (12%) had arthralgia and seven (28%) were asymptomatic. Conclusions: The raised OPG and lower OPN in FDRs than in controls reflect an altered bone metabolism which could precede clinical disease phase. OPN and OPG could serve as markers of altered preclinical bone metabolism in FDRs of RA. US7 score might be a useful screening tool to identify ‘at-risk’ individuals.

ObjectiveTo measure the T-cell receptor-CD3 zeta chain (TCR-CD3ζ) gene expression profile in a cohort of patients with rheumatoid arthritis (RA). Patients and methodsA case-control study on 150 consecutive RA patients diagnosed according to 2010 ACR/EULAR criteria and 150 matched healthy controls without a family history of RA or other autoimmune diseases. RA patients with other autoimmune diseases, viral hepatitis B or C, malignancy or hematological disorders were excluded from the study. All participants were subjected to history taking, clinical examination, assessment of disease activity (in RA patients) using Disease Activity Score-28 and Health Assessment Questionnaire, routine laboratory investigations, inflammatory marker levels, serological tests, as well as molecular analysis for TCR-CD3ζ mRNA expression by quantitative real-time PCR. Results TCR-CD3ζ gene expression was significantly lower in RA cases than in controls (P<0.05). Expression of TCR-CD3ζ has shown a significant negative correlation with RA disease duration, rheumatoid factor, and erythrocyte sedimentation rate (P<0.05) in RA cases. The level of TCR-CD3ζ also showed a significantly less expression in patients with positive rheumatoid factor. ConclusionOur results demonstrated a lower expression of TCR-CD3ζ in RA patients than in healthy controls. We suggested that CD247 gene downregulation might contribute in the susceptibility to RA and help understanding the pathways responsible for deficient T-cell responses in RA patients.

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