Aim of the work: to evaluate urinary CD163 as a possible biomarker indicating activity of lupus nephritis (LN). This retrospective, cross-sectional study evaluated 68 patients diagnosed with systemic lupus erythematosus (SLE) over a year, focusing on different states of lupus nephritis (LN). Participants included 38 with active LN, 15 with a history of LN in a non-active phase, and 15 without kidney involvement. The study utilized the SLEDAI index to classify disease activity, with active LN identified through specific urinary parameters. Renal biopsies were performed for those with active disease, following established classification criteria. Comprehensive assessments included blood tests, urinary protein levels, and measurement of urinary sCD163 using ELISA. Statistical analyses employed SPSS, utilizing various tests to compare groups and assess relationships between urinary sCD163 levels and clinical characteristics, establishing significance at p < 0.05. The findings contribute to the understanding of renal manifestations in SLE and the potential role of urinary biomarkers in monitoring disease progression and activity. Laboratory data from 68 participants were analyzed, focusing on correlations among active LN, inactive LN, and SLE without renal involvement. Significant correlations (p < 0.05) were observed in CD163, C3, C4, hemoglobin, platelets, serum creatinine, proteinuria, and BUN, while WBC count, serum albumin, and ESR showed no significant correlation. Notably, 98.5% of patients had positive anti-ds-DNA antibodies. Urinary sCD163 levels were highest in active LN patients. Linear regression showed that serum albumin and ESR significantly predicted urinary sCD163 levels. The optimal cut-off for urinary sCD163 to predict renal activity was > 4.2, with 60.5% sensitivity and 66.7% specificity. However, sCD163 levels did not correlate with renal histopathological classifications. Integration of urinary sCD163 as a biological marker for evaluating the activity of LN together with accurately distinguishing between histopathological classes mostly needs to be further evaluated. To this point of the study, sCD163 can be a good indicator of LN activity, sCD163 still can’t substitute for renal biopsy in differentiation of LN classes as it would not provide the comprehensive understanding necessary for effective management of LN.

Bladder cancer is the 7th most commonly diagnosed cancer in males worldwide and the 11th when both genders are considered. Seventy five per cent of bladder cancer cases are non-muscle invasive bladder cancer (NMIBC). Bacillus Calmette–Gu rin (BCG) immunotherapy remains the standard intravesical agent for NMIBC. The exact mechanism by which BCG prevents recurrence is unknown. The aim of this study was to evaluate NLR4 gene expression and IL-1β as possible prognostic indicators for NMIBC recurrence and BCG treatment failure, and to detect the difference in their levels among muscle invasive bladder cancer (MIBC) and NMIBC that may aid in primary differentiation between cases. This study was conducted in 30 patients who had NMIBC and 17 patients who had MIBC. Urine samples were obtained in sterile cups before operation. From NMIBC cases, four more samples were obtained as mentioned below. Evaluation of NLR4 gene expression was performed in pre-surgical sample for MIBC and in 4 samples for NMIBC: pre-surgical sample, sample collected 4 hours after the 3rd dose of BCG instillation, and samples collected during follow up (3 and 6 months post-surgically). There was statistical significant increase in NLRP4 expression levels in NMIBC (CT=0.87±1.48) compared to MIBC (CT=2.82±2.07). As far as we searched, no published results were found regarding comparative gene expression levels between NMIBC and MIBC cases. Gene expression in recurrent cases was higher in pre-surgical urine samples than in non-recurrent cases. The expression level further increased up to 21 fold than the pre-surgical level in the sample taken after injection of the 3rd dose of BCG. This level decreased distinctly to become 1-fold increase over pre-surgical level at the 3rd month follow up then to only 0.9-fold at the 6th month. In non- recurrent cases, gene expression level started pre-surgically in much lower levels than those encountered in recurrent cases. There were 11-fold increase in expression level after 3rd dose of BCG instillation and then decreased to be 5.6 folds higher in the sample taken at 3rd month follow up than in presurgical samples. Gene expression further decreased to become 4.1 fold higher in samples taken at 6 month follow up than the pre-surgical levels. IL-1β levels were estimated for NMIBC and MIBC cases in urine samples pre-surgically and during BCG therapy in case of NMIBC before and 4 hours after the 3rd dose and during 3rd month follow-up of those cases for searching its possible use of for primary differentiation between NMIBC and MIBC, and also as a prognostic factor for possible recurrence in case of NMIBC cases. The level of IL-1β was generally higher in pre-surgical samples (0.62±0.12 pg/ml) when compared to its level before the 3rd dose of BCG induction therapy (0.53±0.13 pg/ml). Its level was distinctly higher four hours after administration of the 3rd dose BCG (1.96±0.62 pg/ml) than both previous levels. Levels decreased bellow pre-surgical level at 3rd month follow up (0.57±0.099 pg/ml). The levels of IL-1β estimated in samples collected four hours after the 3rd dose BCG was higher in cases that showed recurrence later on than non-recurrent cases. The levels decreased in both cases and became higher in non-recurrent cases (0.64±0.05 pg/ml) than in cases already developed recurrence at the 3rd month diagnosed during follow-up (0.45±0.05 pg/ml). To conclude, on following NLRP4 gene expression and IL-1β levels during BCG administration among recurrent and non-recurrent cases of thirty NMIBC cases, there was a significant statistical difference in both levels for the samples collected after the third dose BCG, being higher in patients who showed subsequent recurrence at the 3rd and 6th month of follow-up. If these preliminary reported findings will be confirmed in upcoming larger cohort’s studies, it could be promising in prognosis of such cases, with the possibility of early manipulation of individualized treatment schedule, keeping patients most probably prone to encounter recurrence safe from possible side effects of BCG therapy. The assessment of NLRP4 expression and IL-1β levels could help predict failure of BCG therapy, playing an appreciable role in early deciding radical surgery. When comparing NLRP4 expression and IL-1β levels between MIBC and NMIBC cases, increased values were noted among non-invasive ones. This finding may serve as a possible diagnostic tool, which represents a challenging issue. Hence, cut-off values for gene expression and cytokine level are to be specified.

Background: Psoriatic arthritis (PsA) is a chronic inflammatory arthropathy that gradually damages joints. The pathogenesis of PsA involves immune-mediated chronic inflammation, resulting in tissue damage. Calprotectin (S100A8/A9) (CLP) acts as a proinflammatory factor of innate immunity, thus contributing to chronic inflammatory conditions. Aim of the work: To evaluate whether serum CLP could reflect disease activity and pathological findings detected by musculoskeletal ultrasound in PsA patients receiving biological therapy. Patients and methods: There were 120 participants in this cohort study: 60 patients with PsA receiving biological therapy for more than three months and 60 healthy controls. The Disease Activity in Psoriatic Arthritis (DAPSA) and the Psoriasis Area and Severity Index (PASI) were used to assess patients with PsA. A human CLP ELISA kit was used to measure serum CLP. Musculoskeletal ultrasound was performed on the dominant site using the PsASon13 composite score to evaluate inflammatory and structural changes. Results: The median age of PsA patients was 35 years, and 68.3% of them were female. The PsASon13 imaging score had a median (IQR) of 7.0 (3.0–14.0). Median serum CLP levels were significantly higher in patients compared to controls (1468.4 vs. 1169.7 ng/mL, p < 0.001). ESR levels also revealed a significant difference among groups ( p = 0.005). DAPSA and PsASon13 scores showed a strong positive correlation, and both were significantly correlated with serum CLP ( p < 0.001). PASI score was correlated with DAPSA (rho = 0.494) and SON13 (rho = 0.435) scores ( p < 0.001). ROC curve analysis of serum CLP showed 73.3% sensitivity and 81.7% specificity in differentiating PsA patients from controls at an optimal cut-off value of 1285 ng/mL. Conclusions: Serum CLP is a promising biomarker for monitoring disease activity in PsA, reflecting both clinical and ultrasound-assessed inflammation, and may aid management of patients on biologic therapy.

Background/Objectives: Parkinson’s disease (PD) is a neurodegenerative disease with a heterogeneous nature. Many molecular pathways are engaged in PD pathogenesis. Granzyme B (GrB) is an enzyme released by CTLs and has roles in neuroinflammation, axonal degeneration, demyelination, and neuronal ischemic death. However, little is reported about its role in PD pathogenesis and deterioration. To evaluate the role of GrB in PD. Method: A total of 94 participants were recruited from outpatient neurology clinics (47 PD patients and 47 healthy controls). Serum GrB levels were measured using ELISA. Results: Among PD patients, the age of onset was 57.30 ± 4.92 years, and the duration of illness was 7.13 ± 4.20 years. Sociodemographic data revealed statistically significant associations between the development of PD and HCV infection (0.001*), family history of neuropsychiatric illness (0.004*), and/or PD (0.028*). MoCA TS showed a significant reduction in cognitive performance among PD patients even after correction (p < 0.001*). H_Y score showed that >50% of PD patients were clustered in stages 1 and 2, and motor scores showed a substantial reduction. GrB levels were markedly increased among PD patients compared with the control group (1721.4 ± 588.8 pg/mL vs. 418.4 ± 131.3 pg/mL) (p < 0.001*). This indicates a strong association between elevated granzyme B and PD. However, no statistically significant correlations were observed between GrB levels and the parameters studied. Conclusion: GrB levels are significantly elevated among PD patients. This reflects underlying immune activation or inflammatory processes associated with the progression of PD. GrB showed a promising diagnostic association with PD, but was not correlated with disease severity, activity, or duration in this cohort. Formal evaluation of GrB’s diagnostic accuracy in an independent, disease-control-inclusive cohort is warranted before it can be considered a diagnostic biomarker.