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1.
Curr Rheumatol Rev ; 20(5): 534-543, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38299415

RESUMO

INTRODUCTION: Systemic lupus erythematosus (SLE) is a chronic idiopathic systemic autoimmune disorder with dysregulation of adaptive and innate immune systems. Interleukin (IL)-17 is the prototypical pro-inflammatory cytokine of T helper 17 (Th17) cells. Therefore, it contributes to the pathogenesis of human SLE. AIM: The aim of the research paper was the evaluation of IL-17 level as a biomarker in the SLE cohort and its relation to disease activity and analysis of IL-17 concentration in patients with lupus nephritis and non-lupus nephritis. METHODS: The research enrolled 45 SLE patients according to Systemic Lupus International Collaborating Clinics Classification Criteria (SLICC), and age and sex-matched. The patients underwent full history, clinical examination, laboratory investigation, and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) calculation. RESULTS: The mean age ± SD of the participants equaled 32 ± 11 years, and serum IL-17 in SLE cases was statistically significantly high (p < 0.001). No statistically significant correlations were reported between disease activity according to SLEDAI and IL-17. In addition, a statistically significant positive correlation was reported between IL-17 and ESR, and a high statistically significant negative correlation was reported between IL-17 and C3 and C4 (P < 0.001). A statistically significant positive correlation was reported between IL-17 and 24-hour urinary proteins with a Pvalue of 0.01. CONCLUSION: SLE cases demonstrated higher levels of serum IL-17, contributing to SLE pathogenesis. However, no statistically significant difference was reported between IL-17 and Lupus nephritis. IL-17 and SLE activity (SLEDAI) did not correlate. A statistically significant positive relation was reported between IL-17 and 24-hour urinary proteins. Additionally, a high statistically significant negative correlation was reported between IL-17 and C3 and C4.


Assuntos
Biomarcadores , Interleucina-17 , Lúpus Eritematoso Sistêmico , Humanos , Interleucina-17/sangue , Adulto , Feminino , Biomarcadores/sangue , Lúpus Eritematoso Sistêmico/sangue , Masculino , Egito , Adulto Jovem , Índice de Gravidade de Doença , Nefrite Lúpica/sangue , Nefrite Lúpica/urina , Pessoa de Meia-Idade
2.
Curr Rheumatol Rev ; 19(4): 463-469, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-36999177

RESUMO

OBJECTIVE: One of the potential factors that cause systemic lupus erythematosus (SLE) development is autophagy. Immunity-related GTPase family M protein (IRGM) has been shown to be linked to immune-mediated diseases. The aim of the current study was to assess the role of the IRGM-autophagy gene in SLE susceptibility in an Egyptian population and its relation to lupus nephritis. METHODS: A case-control study was conducted in which a total of 200 subjects (100SLE and 100 healthy controls) were enrolled. Two single-nucleotide polymorphisms (SNPs) (rs10065172 and rs4958847) were genotyped. Genotypes and alleles analysis was conducted to compare between cases and controls, as well as a stratification analysis was conducted on the presence or absence of lupus nephritis. RESULTS: Among selected SNPs of IRGM, no association was found between both SNPs and SLE susceptibility. For rs10065172, the major expressed genotype was CC (61% and 71%) (Adj OR= 2.9, 95%= 0.545-15.5), followed by TC (34% and 27%) (Adj OR= 1.985, 95% = 0.357-11.041) in cases and controls, respectively. For rs4958847, AA and AG were comparably expressed in case [(43% and 39%) (Adj OR= 1.073, 95% = 0.483-2.382)] and control [(41% and 43%) (Adj OR= 1.24, 95% = 0.557- 2.763)], respectively. Additionally, no relationship among both SNPs and gender, lupus nephritis, disease activity, or disease duration, was observed. CONCLUSION: IRGM SNPs (rs10065172 and rs4958847) expression was comparable among SLE patients and controls of the Egyptian cohort. Genotype and allele frequency of IRGM SNPs did not differ in lupus nephritis and non-lupus nephritis patients.


Assuntos
Doença de Crohn , Lúpus Eritematoso Sistêmico , Nefrite Lúpica , Humanos , Polimorfismo de Nucleotídeo Único , Predisposição Genética para Doença , Doença de Crohn/epidemiologia , Doença de Crohn/genética , Estudos de Casos e Controles , Egito , Proteínas de Ligação ao GTP/genética , Lúpus Eritematoso Sistêmico/genética , Nefrite Lúpica/genética
3.
Egypt J Intern Med ; 34(1): 49, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35754946

RESUMO

The outbreak of coronavirus disease 2019 (COVID-19), which is caused by the highly contagious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was announced a pandemic in March 2020 by the World Health Organization. The disease can be diagnosed on the basis of clinical symptoms, polymerase chain reaction positivity, and the presence of ground-glass opacities on computed tomography (CT) scans. Recent studies have focused on the role of serum inflammatory markers that predict COVID-19, such as lymphocyte counts and C-reactive protein (CRP), homocysteine, and D-dimer levels. Vitamin D is thought to reduce the risk of viral infections through several mechanisms. Our aim was to evaluate the correlation between serum vitamin D level and inflammatory markers and severity in Egyptian patients with COVID-19 infection. Serum vitamin D level had a positive correlation with hemoglobin level and lymphocytes. As results, serum vitamin D had a negative correlation with serum ferritin, CRP, and D-dimer and was not correlated with CORAD scoring in the CT chest. In conclusion, serum vitamin D was inversely correlated with inflammatory markers (ferritin, CRP, and D-dimer) which mean that participants with symptoms of COVID-19 had a high level of inflammatory markers and a low level of vitamin D. Participants without symptoms of COVID-19 had normal inflammatory markers and normal vitamin D level.

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