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Background: Adenosine deaminase (ADA) is an enzyme involved in purine metabolism and it is a marker of nonspecific T-cell activation. Few studies have shown high levels of ADA in the epidermis and sera of psoriatic patients. Other inflammatory markers such as high-sensitive C-reactive protein (hsCRP), erythrocyte sedimentation rate (ESR), and serum uric acid (SUA) have shown correlations with psoriasis area severity index (PASI) score. The correlation between ADA and PASI score is still a matter of debate. Aims: The aim of this study was to evaluate serum ADA, hsCRP, SUA, and ESR in psoriatic patients and their correlation with PASI score. Patients and Methods: This study included 60 psoriatic patients divided according to PASI score into three groups (mild, moderate, and severe) each containing 20 patients. PASI score <10 was defined as mild, (10–20) moderate, and >20 severe. Twenty healthy subjects of matched age and sex were included as control. Serum ADA, hsCRP, SUA, and ESR were evaluated for patients and controls. Correlations of ADA, hsCRP, SUA, and ESR with PASI scores were done. Results: While ADA, hsCRP, SUA, and ESR showed a significant increase in psoriatic patients compared with that of the controls (P<001), they showed no significant difference between different psoriatic groups (P>0.05) and no correlations with PASI score (P>0.05). The frequency of joint affection increased with increasing severity of psoriasis (5%, 10%, and 25% in mild, moderate, and severe psoriasis, respectively). Conclusion: Serum ADA, hsCRP, SUA, and ESR showed higher levels among psoriatic patients than in controls. The increased ADA in psoriatic patients supports the role of T-cell activation and proliferative disorder in the pathogenesis of psoriasis. No significant correlations were found between these biomarkers and PASI score. Further studies are needed to validate these biomarkers as diagnostic and prognostic factors in psoriasis.

Background: Nephrotic syndrome is the most frequent kidney-related condition in the United States today, providing a severe health risk. The cornerstone of therapy is still corticosteroids. Protein deficiency was a major cause of linear growth retardation in nephrotic individuals before steroids were administered. The goal of our research was to see how corticosteroids affected growth hormone in children with nephrotic syndrome. Methodologies: From February to December 2020, a cross-sectional research was conducted on children with nephrotic syndrome who visited the Benha University Nephrology clinic. After receiving written agreement from the patients' parents, the research included 36 patients with nephritic syndrome of both sexes, divided into two groups: corticosteroid response group and corticosteroid plus other immunosuppressive medications group. The following conditions were applied to all of the instances in the study: Growth hormone level in blood was measured after a thorough history, full clinical examination, and laboratory testing. Results: The majority of our NS patients (66.7%) were on corticosteroid medication, while 33.3 percent were on corticosteroid plus immunosuppressive medication, according to our research. Complete remission was 1 (2.8%), steroid dependent was 20 (55.5%), rare recurrence was 3 (8.4%), and corticosteroid resistant was 12 in our research (33.3). According to the findings of the present research, small stature accounted for 15 percent of the cases analysed (41.7 percent ). The G.H distribution in the examined cases was found to vary between 0.04 and 2.80ng/ml, with a mean of 0.76 0.86. The distribution of elicited growth hormone in the examined patients varied from 1.17 to 14.60 (ng/ml), with a mean of 5.28 2.81. According to this research, the distribution of activated growth hormone categories among the analysed patients was as follows: borderline (10.78%), normal (6.17%), and subnormal (20%). (55.6 percent ). There was a statistically significant negative connection between cumulative steroid dosage and mortality in the present trial (growth hormone and provocated Growth hormone). Conclusion: The majority of children with nephrotic syndrome exhibited a height disadvantage. Children with nephrotic syndrome may have growth retardation as a result of chronic steroid therapy. In most instances of NS, growth hormone levels are below normal. Corticosteroid cumulative doses have a negative impact on linear growth.

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Background: Systemic sclerosis (SSc) is an autoimmune connective tissue disorder characterized by sclerotic changes which affect the skin and internal organs. is a newly reported cytokine of the IL-1 family. Objective: The aim of this work was to determine serum levels of IL-33 in SSc patients and evaluate its association with clinical manifestations and disease subset. Methodology: The study included two groups. Group A included 40 adult patients diagnosed asSSc, these were subdivided into diffuse systemic sclerosis (dSSc) and limited systemic sclerosis (lSSc) groups. All patients were diagnosed according to the ACR criteria for SSc. Group B included 20 healthy adult persons (age and sex matched) as the control group. All patients were selected from the Rheumatology department Benha University Hospital. Serum IL-33 levels were examined by means of enzyme-linked immunosorbent assay. Result: mean serum level of IL-33 were highly significant in SS patients in comparison to control groups [p<0.0001]. The levels of IL-33 were significantly higher in the dSSc subset compared with the lSSc subset. Also there was a statistically significant correlation between disease activity and serum levels of IL33. Conclusion: IL-33 may have a significant role in the pathogenesis of SSc. IL-33 serum levels paralleled the severity of the disease subset. Understanding of IL-33 functions is important for the development of new therapeutic approaches including IL-33 inhibitors and IL-33 receptor blockers as a therapeutic target.