Background Osteoporosis is a common complication of ankylosing spondylitis (AS) even in the early stages of disease; however, previously published studies have demonstrated large discrepancies in the reported incidence of osteoporosis, based on measurement of bone mineral density (BMD). The aim of the present study was to compare bone quality using trabecular bone score (TBS) between AS patients and healthy controls and to evaluate factors associated with TBS in patients with AS. Results Ankylosing spondylitis patients had significantly lower BMD and T score at the neck of femur and lower total hip BMD than controls (BMD p = 0.010 and 0.032 respectively), (T score p = 0.006 and p = 0.025 respectively). The mean TBS was significantly lower in AS patients than in controls (p < 0.001). Lumbar spine TBS was directly correlated with BMI (p = 0.029) and BMD at the neck of femur (p = 0.016) and BMD of total hip (p = 0.007) while inversely correlated with the Bath AS Metrology Index (BASMI) (p = 0.026), the modified Stoke AS Spinal Score (mSASS) (p = 0.029), ESR (p = 0.031), and CRP (p = 0.033). Conclusion TBS evaluation detected lower bone quality in the lumbar spine in patients with AS when compared with matched controls, while lumbar BMD failed to identify it. These findings encourage the use of TBS as a beneficial tool to recognize the risk of axial osteoporosis as early as possible in AS patients. Also, we recommend its use for regular follow up of drug treatment for those patients.

Background Toll-like (TLRs) play a crucial role in both adaptive and innate immunity. The aim of the present study was to assess the association of TLR5-rs5744168, TLR9-rs187084, and TLR9-rs352140 single nucleotide polymorphisms (SNPs) with susceptibility to systemic lupus erythematosus (SLE) and lupus nephritis (LN) in Egyptian patients. Results The C allele and homozygous CC genotype of the TLR9-rs352140 in co-dominant and recessive models were more prevalent in SLE patients than controls (P = 0.047, P = 0.017, and P = 0.005 respectively). In contrast, allelic and genotyping distribution of TLR5-rs5744168 and TLR9-rs187084 SNPs showed no association with the risk of SLE. The T allele of the TLR5-rs5744168 was more prevalent in LN patients than controls (P = 0.021). The homozygous TT genotype of TLR5-rs5744168 SNP was more prevalent in LN patients in the co-dominant and the recessive models than controls (P = 0.036 and P = 0.011 respectively). The C allele of the TLR9-rs352140 was more prevalent in LN patients than controls (P = 0.015). The homozygous CC genotype of the TLR9-rs352140 SNP was more prevalent in LN than controls in co-dominant and recessive models (P = 0.002 and P < 0.001). In the recessive model of the TLR5-rs5744168 SNP, the TT genotype was found in 3.2% of the SLE patients while none of the SLE patients without LN or controls had TT genotype (P = 0.036). Also, in the recessive model of the TLR9-rs352140 SNP, the CC genotype was significantly more frequent in SLE patients with LN than without LN (44.4% vs 29.9%, P = 0.045). Conclusion Our results support the potential role of TLR5-rs5744168 SNP and TLR9-rs3532140 SNP not only in increasing the risk for development of SLE, but also in increasing the risk of LN in SLE patients among the Egyptian population.

Background A growing body of evidence suggested that uric acid (UA) may contribute in the pathways underlying osteoarthritis (OA) pathogenesis; however, studies that investigated the relationship between UA and OA emerged inconclusive results. The purpose of the study was to explore the association of serum uric acid (sUA) levels with clinical severity, radiological severity of knee osteoarthritis (KOA) based on Kellgren-Lawrence (KL) grading system, and MRI changes in non-gouty patients. Results WOMAC scores: pain, stiffness, function, and total score are significantly higher in H-sUA group than L-sUA group (p = 0.004, p = 0.019, p = 0.018, p = 0.008 respectively). Joint space width (JSW) is significantly narrower in H-sUA group than L-sUA group (p = 0.013). H-sUA group had more frequent KL grade 4 (p < 0.001), osteophytes grade 4 (p < 0.001), focal bone erosion (p < 0.001), bone marrow lesions (p = 0.023), and synovitis (p = 0.011) than L-sUA group. Female KOA patients in H-sUA group had significantly higher pain, stiffness, and function and total WOMAC scores than L-sUA group (p = 0.003, p = 0.015, p = 0.008, p = 0.004), more frequently had KL grade 4 and osteophytes grade 4 (p = 0.003, p < 0.001), significantly narrower JSW (p = 0.016), more frequently show focal bone erosion (p = 0.002), bone marrow lesions (p = 0.019), and synovitis (p = 0.004) than L-sUA group. In regression analysis, female sex (p = 0.035), duration of KOA (p = 0.031), and sUA level (p = 0.025) were associated with KL severity. For female patients with KOA, KL severity is associated with duration of KOA (p = 0.045) and sUA (p = 0.009). Conclusion Higher sUA level is associated with higher clinical severity, higher radiographic KL grades, and more frequent MRI findings in patients with primary KOA patients. Our results also indicated that sUA level was significantly associated with KOA severity in female patients, but not in male patients. More studies are warranted to explore whether the two conditions exist simultaneously or there is a direct causal relationship between the two conditions.

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Background Rheumatoid arthritis (RA) is an autoimmune inflammatory disease. It is characterized by an inflammatory polyarthritis that preferentially affects the small joints leading to joint damage and eventual deformity and disability, and can also present with extra-articular manifestations. Micro RNA (miRNA) is a class of non-coding RNAs which negatively regulate messenger RNA (mRNA) expression. Several studies had shown that miRNA-23b has a close relationship with inflammation and autoimmune diseases. An increasing evidence has suggested that miRNA-23b is closely associated with many inflammatory and autoimmune diseases. The current study aimed to evaluate the plasma expression of miRNA-23b in rheumatoid arthritis (RA) patients and to explore its potential association with diseases activity. Results RA patients had a significantly higher plasma miRNA-23b expression than controls (P < 0.001). The miRNA-23b plasma expression was significantly associated with the clinical and laboratory indices of RA activity as well as with the DAS28-ESR score (P = 0.009) and grades (P < 0.001). The miRNA-23b plasma expression was significantly correlated with the radiological severity of RA (P = 0.002). Conclusions Plasma expression of miRNA-23b is significantly increased in patients with RA than controls. In RA patients, plasma expression of miRNA-23b was significantly correlated with the activity and radiological severity of RA. miRNA-23b may represent a potential therapeutic target that can retard progression of RA.

Introduction: There are debates about the role of the X-ray repair cross-complementation group 1 (XRCC1) Arg399Gln gene in the pathogenesis of Systemic Lupus Erythematosus (SLE). Methods: The study was a case-control study carried out on 100 recently diagnosed SLE patients compared to 100 control subjects. The study of XRCC1 Arg399Gln polymorphism was performed by a polymerase chain reaction and restriction fragment length polymorphism. Results and Discussion: A higher frequency of ‘G’ allele in SLE (38.5%) versus control (32%) was noticed; however, this difference was not statistically significant (p = 0.174). Besides, a slightly higher frequency of G/G genotype was found in SLE (22%) vs. control (12%); again, this difference was not statistically significant (p = 0.157). A statistically significantly higher proportion of arthritis, serositis, and thrombocytopenia was observed in the A/A genotype (p = 0.010, 0.032, and 0.036, respectively). Furthermore, we noticed a statistically significant lower hemoglobin level in G/G genotype (p = 0.027). Otherwise, there was no statistically significant difference between the three genotypes regarding other parameters: photosensitivity, malar rash, oral ulceration, ANA, anti-dsDNA antibody, anemia, leucopenia, neurologic manifestations, and all lab parameters except hemoglobin level. Similar results were reported previously. According to genotype, in the study of Clinical and laboratory parameters in SLE patients, a statistically significantly higher proportion of arthritis, serositis, and thrombocytopenia was observed in the A/A genotype (p =0 .01, 0.032, and 0.036 respectively). Furthermore, we noticed a statistically significant lower hemoglobin level in G/G genotype (p = 0.027). These findings suggest a pathogenic connection between the seriousness of the defective DNA repair and the autoimmune severity; such connection is consistent with that found in several murine models. Additionally, negative regulation of the genes encoding the proteins involved in the NER pathway in SLE patients, specifically and XPC, has been found previously. Conclusion: The present study highlights the higher insignificant increase of G allele and GG genotype of XRCC1 399 gene in patients with SLE compared to healthy control. This increase was significantly associated with anemia in patients, which may reflect the aggravation of environmental risk factors to SLE associated with the reduced repair of DNA. Further longitudinal studies are required to validate the present findings.