Explore the vast range of titles available.

BackgroundData regarding the relation between serum myostatin level, type I interferon-inducible gene expression and insulin resistance in dermatomyositis patients are limited. This study aimed to assess serum myostatin level, homeostatic model assessment of insulin resistance (HOMA-IR) and type I interferon-inducible gene expression in dermatomyositis patients. We evaluated the role of serum myostatin level, and type I interferon-inducible gene expression in the pathogenesis of dermatomyositis as well as the relation of serum myostatin level and type I interferon-inducible gene expression to the occurrence of insulin resistance. We evaluated serum levels of myostatin and HOMA-IR utilizing ELISA as well as IFIT1 and Mx1(MxA) gene expression with RT-PCR in 25 dermatomyositis patients (group A) and 25 obviously sound subjects as controls (group B).ResultsAmong group A, body mass index, serum levels of myostatin, fasting insulin, HOMA-IR, IFN-inducible genes Mx1 and IFIT1 were more significantly increased as well as; serum level of myostatin was positively correlated with age, gender, fasting insulin level, body mass index, and HOMA-IR.ConclusionsSerum level of myostatin, Mx1 and IFIT1 gene expression act as hazard factors of insulin resistance in group A.

Objectives: The objective of this study was to evaluate the relationship between interleukin-17 (IL-17) serum levels, musculoskeletal ultrasound (MSUS) observations, and clinical disease activity in patients with rheumatoid arthritis (RA) and hand osteoarthritis (OA). Methods: This case–control study involved 120 participants, with 40 individuals assigned to each of the three groups: RA, OA, and control. IL-17 serum levels were quantified in all participants. MSUS of the hand joints was performed on all RA and OA patients. Disease activity in patients with RA was assessed using the Clinical Disease Activity Score (CDAS). Both RA and OA patients completed a Visual Analog Scale (VAS) to evaluate pain intensity. Functional status was evaluated using the Health Assessment Questionnaire (HAQ) for RA patients, while the Australian/Canadian (AUSCAN) Osteoarthritis Hand Index was utilized for OA patients. Results: Serum levels of IL-17 were significantly higher in both the RA and OA groups compared to the control group. Among RA patients, a positive correlation was identified between the CDAS and the VAS for pain. In OA patients, a significant correlation was observed between VAS scores and serum IL-17 levels. Additionally, serum IL-17 levels were associated with the presence of synovitis in both RA and OA groups; however, no significant association was found between IL-17 levels and bony changes such as erosions or osteophytes. In terms of functional evaluation, serum IL-17 levels correlated with HAQ in the RA group, but not with AUSCAN in the OA group. Conclusions: Elevated IL-17 serum levels are linked to inflammatory changes identified by MSUS but not to bony changes. These findings suggest that the rise in IL-17 levels in both OA and RA is primarily driven by underlying inflammatory processes, positioning IL-17 as a potential therapeutic target for both conditions.

ObjectivesTo measure the expression level of the vacuolar protein sorting 13 (VPS13) gene and stimulator of interferon genes (STING) in patients with SLE with and without reported neuropsychiatric symptoms to establish their possible role in the pathogenesis of neuropsychiatric SLE (NPSLE).MethodsThis study included 100 subjects: 50 patients diagnosed with SLE and 50 age-matched and sex-matched healthy participants as the control group. The patients with SLE were further subdivided into NPSLE and non-NPSLE groups. All the subjects underwent rheumatological, neurological and psychological evaluation, MRI, VPS13C gene and STING expression assessment via quantitative real-time PCR.ResultsSeventy-eight per cent of the SLE group were classified as non-NPSLE, and 22% were classified as NPSLE. Positive MRI results were found in 55% of the patients with NPSLE and 7.7% of the patients without NPSLE.VPS13C expression levels were decreased in the patients with SLE compared with the control (p<0.001), while STING expression levels showed higher levels in the patients in comparison with the control (p<0.001). Both markers showed significant differences between the MRI-positive and MRI-negative groups.At a cut-off value of 0.225 for the VPS13C assessment and a cut-off value of 3.15 for STING expression, both markers were able to distinguish patients with NPSLE from those who were non-NPSLE; however, VPS13C performed better.ConclusionThe VPS13C expression levels were decreased in patients with NPSLE compared with patients without NPSLE, while STING expression levels showed higher levels in NPSLE. Both were associated with the MRI findings. To distinguish patients with NPSLE from those without it, the VPS13C assessment performed better.

Background Diabetic neuropathy is one of the commonest chronic complications of diabetes seen in routine healthcare and considered the most common cause of peripheral neuropathy all over the world. Vitamin D (VD) deficiency is now recognized as a pandemic disease. This study was designed to explore the levels of 25-hydroxycholecalciferol [25(OH) D] in patients with type 2 diabetes mellitus (T2DM) with peripheral neuropathy. We also aimed to clarify the effect of VD supplementation on cardiometabolic status and electrophysiological pattern of peripheral neuropathy. Patients and methods This clinical trial enrolled 95 patients with T2DM with peripheral neuropathy. The enrolled patients were divided into three groups according to serum 25(OH) D levels. VD deficiency and insufficiency groups received VD supplements (42,000 IU oral VD per week and 500-mg calcium carbonate per day for 12 weeks). Clinical, electrophysiological pattern, and laboratory parameters were evaluated at baseline and after 12 weeks of intervention. Serum 25(OH) D levels were measured by using a competitive enzyme-linked immunosorbent assay kit. Results Our results revealed that, among 95 patients with T2DM with peripheral neuropathy, 32 patients had VD insufficiency [20 ng/ml <25(OH) D <30 ng/ml], 50 patients had VD deficiency [25(OH) D < 20 ng/ml], and 13 patients had VD sufficiency [25(OH) D >30 ng/ml]. Our results reported that 25(OH) D levels were negatively correlated with cardiometabolic risk factors and Toronto Clinical Scoring System. On the contrary, 25(OH) D levels were positively correlated with nerve conduction velocities (NCV). Stepwise multiple linear regression analysis revealed that glycated hemoglobin and Toronto Clinical Scoring System were the main predictors of 25(OH) D levels among other clinical and laboratory biomarkers. Logistic regression analysis observed that motor NCV and sensory NCV of median nerve and glycated hemoglobin were independent predictors of response to VD supplementation. NCV in studied groups showed that motor NCV and sensory NCV in the median, posterior tibial, and ulnar nerves were significantly decreased in both VD deficiency and insufficiency groups compared with VD sufficiency groups, and supplementation with 42 000 IU oral VD per week and 500-mg calcium carbonate per day for 12 weeks improved cardiometabolic risk factors and electrophysiological pattern of peripheral neuropathy. Conclusion The supplementation of VD for 12 weeks to VD deficiency and insufficiency groups improved the cardiometabolic and electrophysiological pattern of peripheral neuropathy.

Background Premature atherosclerosis has been recognized as a major co-morbid condition in systemic lupus erythematosus (SLE). Glucose-dependent insulinotropic polypeptide (GIP) is closely related to cardiovascular (CV) risk factors. We aimed to evaluate GIP expression level in SLE and to explore the possible associations of GIP expression profile with carotid intima-media thickness and insulin resistance (IR). Patients and methods A cross-sectional controlled study was conducted, comprising 170 patients with SLE and 120 controls. GIP expression level was measured by multiplex polymerase chain reaction. The carotid intimamedia thickness was measured. Serum GIP levels, homeostasis model assessments (HOMA-IR and HOMA-b), fibrinogen, and homocysteine were measured. Results In the patients with SLE with IR, there were significantly higher values of serum GIP (37.99±13.64) compared with patients with SLE without IR (24.61±10.74), as well as the control group (21.7±3.46). In addition, there were significant positive correlations between GIP serum level and cardiovascular risks. Regarding GIP gene expression levels, there were significantly lower levels of GIP gene expression in patients with SLE with IR (1.29±0.72) compared with patients with SLE without IR (2.43±0.61) as well as the control group. Receiver operating characteristic analysis revealed that the diagnostic power of GIP expression was stronger than GIP serum levels in differentiating SLE from control. In conclusion, in the SLE group, there were lower GIP expression and higher serum levels than control, especially in IR subgroup. GIP expression and serum levels were associated with cardiovascular disease pathogenesis and progression.

This study was established to assess the effects of IRF5 rs10488631 and CD28 rs1980422 single-nucleotide polymorphisms (SNPs) and HLA-DRB1 shared epitope (SE) allele on the prognosis and disease activity of rheumatoid arthritis (RA) patients. A total of 150 RA patients and 150 healthy controls were genotyped for the selected SNPs by real-time PCR. HLA-DRB1 SE was determined using LAB Type SSO Class II DRB1 typing. Our results suggest that HLA-DRB1, CD28, and IRF5 significantly discriminated (p < 0.001) RA patients and healthy controls (OR of single HLA-DRB1 SE allele = 2.431, CI = 1.467–4.027, OR of two SE alleles = 11.152, CI = 2.479–50.159), (OR of CD28 risk allele C = 2.794, 95% CI = 1.973–3.956) and (OR of IRF5 risk allele C = 4.925, CI = 3.26–7.439). Rheumatoid factor (RF) seropositivity was associated with HLA-DRB1 SE (p < 0.001) and IRF5 risk allele (p < 0.001). ACPA was significantly associated only with IRF5 risk allele (p < 0.001). A better response to methotrexate therapy was found in HLA-DRB1 SE non-carriers, and CD28 TT patients. This study demonstrated associations of HLA-DRB1 SE, CD28, and IRF5 with the risk of RA. HLA-DRB1 SE and CD28 rs1980422 can be used as predictors of methotrexate therapy response.

Ankylosing spondylitis (AS) is a chronic inflammatory disease that results in severe pain and stiffness in the joints. The causes and pathophysiology of AS are still largely unknown. The lncRNA H19 plays key roles in the pathogenesis of AS by mediating inflammatory progression by acting in the axis of IL-17A/IL-23. The aims of this study were determining the role of lncRNA H19 in AS and assessing its clinical correlation. A case–control study was conducted and qRT-PCR was utilized to measure H19 expression. Comparing AS cases to healthy controls, it was found that H19 expression was significantly upregulated. For AS prediction, H19 demonstrated a 81.1% sensitivity, 100% specificity, and 90.6% diagnostic accuracy at a lncRNA H19 expression value of 1.41. lncRNA H19 had a significantly positive correlation with AS activity, MRI results, and inflammatory markers. lncRNA H19 seemed to be an independent predictor of AS (adjusted OR of 211 (95% CI: 4.7–939; p = 0.025)). After 3 months of clinical follow-up, seventeen patients (32.1%) showed minimal clinical improvement and fifteen patients (28.3%) showed major improvement. AS activity scores were significantly decreased in patients with high H19 expression. A significantly elevated lncRNA H19 expression was observed in AS cases compared with that in healthy controls. These results suggest that upregulation of lncRNA H19 expression may be involved in the pathogenesis of AS. The expression of the lncRNA H19 is related to the duration and activity of the disease. LncRNA H19 expression seems to be an independent predictor of AS.