Systemic lupus erythematosus (SLE) is a connective tissue disease characterized by the formation of autoantibodies and immune complexes. Lupus nephritis is one of the hallmark features of SLE. CXCL10 is a chemokine secreted by IFNg- stimulated endothelial cells and has been shown to be involved in the pathological processes of autoimmune diseases. The objective was to measure urinary CXCL10 in SLE patients, to compare levels between nephritis and non-nephritis groups and to study its correlation with other variables. Sixty lupus patients were enrolled in our trial. Thirty patients had lupus nephritis and the other 30 were without evidence of lupus nephritis. Thirty healthy subjects were willing to participate as a healthy control group. Renal biopsy was performed for lupus nephritis group. Urinary CXCL10 was measured using the ELISA technique. Serum creatinine, C3, C4 and 24 h urinary proteins were measured. Lupus activity was assessed using systemic lupus erythematosus disease activity index (SLEDAI) scoring system. Renal activity was measured using renal activity scoring system. CXCL10 was significantly higher in lupus nephritis patients than in lupus patients without nephritis. CXCL10 was significantly correlated with renal activity score, 24 hours urinary proteins and the SLEDAI score. It is highly valid predictor of SLE nephritis with high sensitivity and specificity. CXCL 10 a highly sensitive and specific non-invasive diagnostic tool for lupus nephritis patients.
Methylenetetrahydrofolate reductase (MTHFR) gene plays a pivotal role in folate metabolism. Several genetic variations in MTHFR gene as MTHFR-C677T and MTHFR-A1298C result in decreased MTHFR activity, which could influence efficient DNA methylation and explain susceptibility to different cancers. The etiology of chronic myeloid leukemia (CML) is obscure and little is known about individual's susceptibility to CML. In order to assess the influence of these genetic polymorphisms on the susceptibility to CML and its effect on the course of the disease among Egyptians, we performed an age-gender-ethnic matched case-control study. The study included 97 CML patients and 130 healthy controls. Genotyping of MTHFR-C677T and -A1298C was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. The results showed no statistical difference in the distribution of MTHFR-C677T and -A1298C polymorphic genotypes between CML patients and controls. The frequency of MTHFR 677-TT homozygous variant was significantly higher in patients with accelerated/blastic transformation phase when compared to those in the chronic phase of the disease. In conclusion, our study revealed that MTHFR-C677T and -A1298C polymorphisms could not be considered as genetic risk factors for CML in Egyptians. However, MTHFR 677-TT homozygous variant might be considered as a molecular predictor for disease progression.
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