Abd El-Moaty Ali Afifi1, Reham M Shaat2, Ola Mohamed Gharbia1, M Elhanafy3, Al Shimaa Goda Hasan1. 1. Faculty of Medicine, Department of Rheumatology and Rehabilitation, Mansoura University, El Gomhoria St., Mansoura, Egypt. 2. Faculty of Medicine, Department of Rheumatology and Rehabilitation, Mansoura University, El Gomhoria St., Mansoura, Egypt. reham1975@yahoo.com. 3. Faculty of Medicine, Department of Clinical Pathology, Mansoura University, El Gomhoria St., Mansoura, Egypt.
Abstract
BACKGROUND: Serum leptin and leptin receptor gene polymorphisms may play a role in the etiopathogenesis of SLE. OBJECTIVE: This study was undertaken to explore the relationship between serum leptin levels and leptin receptor (LEPR) gene polymorphisms with susceptibility to SLE in Egyptian population and to study their relationships with clinical, laboratory, radiographic findings, and disease activity of SLE (SLEDAI). MATERIALS AND METHODS: A total of 50 unrelated female patients, who met the SLICC classification criteria for SLE and fifty healthy blood donors, matched for age, sex, and BMI with SLE patients, serving as a control group, were included in this study. All participants had completed preliminary questionnaires and clinical, laboratory, and radiographic examinations. Serum leptin levels were measured by ELISA assays. LEPR genotyping was done by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method. We compared serum leptin levels and LEPR gene polymorphisms in SLE patients and controls, and we tested their relationships with clinical, laboratory, and radiographic findings and SLEDAI in SLE patients. RESULTS: The present study showed significant differences of serum leptin levels between SLE patients and controls (p < 0.001). Moreover, higher frequencies of variant genotype (AA) and (A) allele were found in SLE patients compared to controls (p = 0.008 and 0.001, respectively). No associations were observed between the serum leptin, various LEPR genotypes, and gene alleles and the development of clinical, laboratory, and radiological manifestations. Furthermore, no associations were observed between the various LEPR genotypes or gene alleles and leptin levels (p = 0.633 and 0.337 respectively) in SLE patients. Additionally, no correlations were observed between leptin levels, various genotypes, and alleles with SLEDAI (p = 0.244, 0.741, and 0.838 respectively) in SLE patients. CONCLUSION: Serum leptin and LEPR gene polymorphism increase risk of SLE in Egyptian population; however, they are not associated with the development of clinical, lab, and radiological findings. Disease activity is neither correlated with serum leptin level nor associated with LEPR gene polymorphism. Serum levels of leptin are not associated with LEPR gene polymorphism. Key Points • Serum leptin and LEPR gene polymorphism increase risk of SLE in Egyptian patients. • Serum leptin is not associated with SLE disease activity.
BACKGROUND: Serum leptin and leptin receptor gene polymorphisms may play a role in the etiopathogenesis of SLE. OBJECTIVE: This study was undertaken to explore the relationship between serum leptin levels and leptin receptor (LEPR) gene polymorphisms with susceptibility to SLE in Egyptian population and to study their relationships with clinical, laboratory, radiographic findings, and disease activity of SLE (SLEDAI). MATERIALS AND METHODS: A total of 50 unrelated female patients, who met the SLICC classification criteria for SLE and fifty healthy blood donors, matched for age, sex, and BMI with SLE patients, serving as a control group, were included in this study. All participants had completed preliminary questionnaires and clinical, laboratory, and radiographic examinations. Serum leptin levels were measured by ELISA assays. LEPR genotyping was done by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method. We compared serum leptin levels and LEPR gene polymorphisms in SLE patients and controls, and we tested their relationships with clinical, laboratory, and radiographic findings and SLEDAI in SLE patients. RESULTS: The present study showed significant differences of serum leptin levels between SLE patients and controls (p < 0.001). Moreover, higher frequencies of variant genotype (AA) and (A) allele were found in SLE patients compared to controls (p = 0.008 and 0.001, respectively). No associations were observed between the serum leptin, various LEPR genotypes, and gene alleles and the development of clinical, laboratory, and radiological manifestations. Furthermore, no associations were observed between the various LEPR genotypes or gene alleles and leptin levels (p = 0.633 and 0.337 respectively) in SLE patients. Additionally, no correlations were observed between leptin levels, various genotypes, and alleles with SLEDAI (p = 0.244, 0.741, and 0.838 respectively) in SLE patients. CONCLUSION: Serum leptin and LEPR gene polymorphism increase risk of SLE in Egyptian population; however, they are not associated with the development of clinical, lab, and radiological findings. Disease activity is neither correlated with serum leptin level nor associated with LEPR gene polymorphism. Serum levels of leptin are not associated with LEPR gene polymorphism. Key Points • Serum leptin and LEPR gene polymorphism increase risk of SLE in Egyptian patients. • Serum leptin is not associated with SLE disease activity.
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Authors: Alfonso Cordero-Barreal; María González-Rodríguez; Clara Ruiz-Fernández; Djedjiga Ait Eldjoudi; Yousof Ramadan Farrag AbdElHafez; Francisca Lago; Javier Conde; Rodolfo Gómez; Miguel Angel González-Gay; Ali Mobasheri; Jesus Pino; Oreste Gualillo Journal: Int J Mol Sci Date: 2021-02-27 Impact factor: 5.923