الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Systemic lupus erythematosus (SLE) is a systemic multiorgan autoimmune disease with a wide range of symptoms. Pathologically, the disease is generally associated with a lack of immunological tolerance as well as aberrant B- and T-cell function. A combination of genetic, epigenetic, and environmental factors induces it. Genetic factors alone are insufficient to explain the development of SLE, and the disease is likely to emerge in a genetically vulnerable individual as a result of an interaction with environmental parameters. New understanding of disease modulators, such as symbiotic bacteria, may allow fine-tuning of immune system components. Autoimmune diseases are exacerbated by dysbiosis of the gut microbiota.
Mucocutaneous, musculoskeletal, hematological, cardiac, renal, and central nervous system symptoms are among the numerous clinical manifestations. Lupus nephritis is one of the most severe varieties of organ involvement, and it can shorten one’s life expectancy dramatically. 60 percent of lupus patients will develop clinically significant nephritis at some point throughout their disease, according to the general consensus. Renal impairment should be detected and treated as soon as possible, since an early response to medication is linked to a better consequence.
The gut microbiota’s potential importance as a crucial aspect in the development of autoimmune disorders has lately attracted considerable attention. There are 100 trillion bacteria, protozoa, fungus, and viruses in the human microbiome. It is significant in contributing to health through a variety of biological processes such as energy extraction, metabolic regulation, protection from harmful microorganisms, vitamin generation, and lastly immune system modulation.
Changes in the composition of the gut microbiota are supposed to be participating in the etiopathogenesis of SLE, and several studies have been carried out in mice and human to prove that gut microbiota dysbiosis affects the onset and development of SLE. Modulation of the gut microbiota constitutes a potential clinical therapy.
In our study, we aimed to evaluate the changes in Lactobacilli and Lactobacillus reuteri in the gut of a cohort of Egyptian patients with SLE with and without nephritis and how these changes affected the state of SLE disease activity.
This study included 40 patients with SLE fulfilling the SLICC criteria, they were divided into 2 groups (group I) those SLE patient without lupus nephritis and (group II) those SLE patients with lupus nephritis. 20 age and sex-matched healthy subjects were taken as the control group (group III).
All patients were subjected to: detailed history taking with special stress on symptoms related to SLE and renal affection and a complete clinical examination. Also the SLE disease activity index (SLEDAI) was applied for every lupus patient of the studied group and the scores were estimated.
Comprehensive blood count, erythrocyte sedimentation rate (ESR), renal function tests (blood urea, serum creatinine, and protein: creatinine ratio), complete urine analysis, anti-ds-DNA titre, and lactobacilli and Lreuteri microbiome studies were among the tests performed on the patients. In some SLE patients with clinical and laboratory signs of renal involvement, a renal biopsy was done. The activity and chronicity indices were calculated using the International Society of Nephrology/Renal Pathology Society (ISN/RPS) 2003 lupus nephritis categorization scheme.