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New Onset Diabetes After Transplantation (NODAT) is a serious metabolic complication. While β-cell dysfunction is considered the main contributing factor in the development of NODAT, the precise pathogenesis is not well understood. Cytokines are thought to be involved in the inflammation of islet β-cells in diabetes; however, few studies have investigated this hypothesis in NODAT. A total of 309 kidney transplant recipients (KTRs) were included in this study. An association between kidney transplants, and the development of diabetes after transplant (NODAT) was investigated. Comparison was made between KTRs who develop diabetes (NODAT cases) or did not develop diabetes (control), using key cytokines, IL-6 G (− 174)C, macrophage mediator; IL-4 C (− 490)T, T helper (Th)-2 cytokine profile initiator; Th-1 cytokine profile initiator interferon-γ T (+ 874) A gene and TGF β1 C (+ 869) T gene polymorphisms were investigated. The genes were amplified using well-established polymerase chain reaction (PCR) techniques in our laboratory. Compared to the AA and AT genotypes of interferon gamma (IFNG), there was a strong association between the TT genotype of IFNG and NODAT kidney transplant recipients (KTRs) versus non-NODAT KTRs ( p  = 0.005). The AA genotype of IFNG was found to be predominant in the control group ( p  = 0.004). Also, significant variations of IL6 G (− 174) C, IL-4 C (− 590) T, interferon-γ T (+ 874) A gene and transforming growth factor β1 C (+ 869) T may contribute to NODAT. Our data is consistent with theTh-1/T-reg pathway of immunity. Further larger pan Arab studies are required to confirm our findings.

Objectives:To describe primary Sjögren’s syndrome (pSS) cohort in Saudi Arabiain view in of clinical/serological/histopathological phentotype, and, diagnostic delay.Methods:A cross-sectional study conducted between October 2018 and May 2019. Diagnostic delay was calculated from symptoms onset to clinical diagnosis. The European League Against Rheumatism (EULAR) Sjögren’s Syndrome Disease Activity Index (ESSDAI) and EULAR Sjogren’s Syndrome Patient Reported Index (ESSPRI) were calculated.Results:Forty-one patients were included in the study. There were predominantly females (78%) with a mean (±SD) age of 58.76±12.7 and disease duration of 4.6±2.28 years. The mean diagnostic delay was 2.2±2.4 (range 1-11) years. Minor salivary gland biopsy was performed on 38 (92.7%) patients with a mean focus score of 2.3± 1.2 points. Interstitial lung disease and arthritis were the most common extra-glandular manifestations (EGM) affecting 27 (65.9%) patients for both. The mean ESSDAI was 9.95±7.73 and ESSPRI was 5.17±2.4.Conclusion:Saudi primary Sjogren’s syndrome patients have a high prevalence of EGM predominantly arthritis and ILD. The diagnostic delay is variable in our cohort.

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease that causes multi-articular synovitis. The illness is characterized by worsening inflammatory synovitis, which causes joint swelling and pain. Synovitis erodes articular cartilage and marginal bone, resulting in joint deterioration. This bone injury is expected to be permanent. Cytokines play a prominent role in the etiology of RA and could be useful as early diagnostic biomarkers. This research was carried out at Riyadh’s King Khalid University Hospital (KKUH). Patients were enrolled from the Rheumatology unit. Seventy-eight RA patients were recruited (67 (85.9%) females and 11 (14.1%) males). Patients were selected for participation by convenience sampling. Demographic data were collected, and disease activity measurements at 28 joints were recorded using the disease activity score (DAS-28). Age- and sex-matched controls from the general population were included in the study. A panel of 27 cytokines, chemokines, and growth factors was determined in patient and control sera. Binary logistic regression (BLR) and discriminant analysis (DA) were used to analyze the data. We show that multiple cytokine biomarker profiles successfully distinguished RA patients from healthy controls. IL-17, IL-4, and RANTES were among the most predictive variables and were the only biomarkers incorporated into both BLR and DA predictive models for pooled participants (men and women). In the women-only models, the significant cytokines incorporated in the model were IL-4, IL-17, MIP-1b, and RANTES for the BLR model and IL-4, IL-1Ra, GM-CSF, IL-17, and eotaxin for the DA model. The BLR and DA men-only models contained one cytokine each, eotaxin for BLR and platelet-derived growth factor-bb (PDGF-BB) for DA. We show that BLR has a higher fidelity in identifying RA patients than DA. We also found that the use of gender-specific models marginally improves detection fidelity, indicating a possible benefit in clinical diagnosis. More research is needed to determine whether this conclusion will hold true in various and larger patient populations.

To describe primary Sjögren's syndrome (pSS) cohort in Saudi Arabiain view in of clinical/serological/histopathological phentotype, and, diagnostic delay. A cross-sectional study conducted between October 2018 and May 2019. Diagnostic delay was calculated from symptoms onset to clinical diagnosis. The European League Against Rheumatism (EULAR) Sjögren's Syndrome Disease Activity Index (ESSDAI) and EULAR Sjogren's Syndrome Patient Reported Index (ESSPRI) were calculated. Forty-one patients were included in the study. There were predominantly females (78%) with a mean (±SD) age of 58.76±12.7 and disease duration of 4.6±2.28 years. The mean diagnostic delay was 2.2±2.4 (range 1-11) years. Minor salivary gland biopsy was performed on 38 (92.7%) patients with a mean focus score of 2.3± 1.2 points. Interstitial lung disease and arthritis were the most common extra-glandular manifestations (EGM) affecting 27 (65.9%) patients for both. The mean ESSDAI was 9.95±7.73 and ESSPRI was 5.17±2.4. Saudi primary Sjogren's syndrome patients have a high prevalence of EGM predominantly arthritis and ILD. The diagnostic delay is variable in our cohort.

Background: Primary Sjögren’s syndrome (pSS) is an autoimmune disease that can cause fatigue and extraglandular manifestations (EGMs). pSS is associated with cytokine network dysregulation, which may be related to the immune-mediated destruction of exocrine glands. Objective: We determined cytokine levels and their relationship to EGMs, the European League Against Rheumatism (EULAR) Sjögren’s syndrome disease activity index (ESSDAI), and fatigue in Saudi patients with pSS. Methods: This study was a cross-sectional, single-center study. We included forty-one patients and 71 controls. Serum samples were collected from random healthy people and pSS patients who were followed in the rheumatology and pulmonary clinics of King Saud University Medical City in Riyadh, Saudi Arabia. Levels of the frequently studied cytokines were measured using Luminex xMAP technology. Each ESSDAI score and EGM were recorded, and the Arabic version of the fatigue severity scale (FSS) was applied to assess fatigue. The main outcome measures were cytokine levels in pSS Saudi patients using/not using immune-suppressive medications (ISMs). Results: Thirty-six (87.8%) patients had one or more EGMs, and the mean ESSDAI score was 9.95 ± 7.73. There was a significant decrease in TNFα and IL-21 levels in the pSS group compared to those in the control group (p = 0.034 and p < 0.001, respectively), whereas IL-12 levels were significantly elevated in the pSS group (p = 0.002). Cytokine levels in patients who used ISMs were the same as those in patients who did not use medications. Decreased IL-1β (p = 0.014), IL-2 (p = 0.035), IL-6 (p = 0.014), and IL-35 (p = 0.010) levels were observed in patients who had EGMs. Patients who had low disease activity exhibited low IL-10 (p = 0.018) and high IFN-α (p = 0.049), IFN-β (p = 0.049), IL-1β (p = 0.006), and IL-35 (p = 0.032) levels compared to patients with high disease activity. A negative association between a positive fatigue score and IL-1β (p = 0.010), IL-2 (p = 0.037), IFN-α (p = 0.025), TNFα (p = 0.030), IL-17 (p = 0.029), IL-12 (p = 0.046), and IL-21 (p = 0.005) levels was found. Conclusions: Cytokine profiles correlate with EGMs, ESSDAI, and fatigue. Patients with controlled disease activity have a normal cytokine profile that is similar to that of controls.

Kidney transplantation is the optimal treatment choice for end stage renal disease; this option needs a major change in the recipients' lifestyle and requires strict adherence to medications. The study aim was to assess the compliance of renal transplant patients to medications and lifestyle modifications in the Hamed Al-Essa Organ Transplant Center in Kuwait. One-hundred and twenty renal transplant patients were interviewed for their lifestyle behaviors after transplantation, including transplant adherence to their medications, healthy meals, personal hygiene, physical activity, regular out-patient follow up visits, and preventive measures against infection and cancer, in addition to sexual function. The questionnaire used was created by staff of the Faculty of Medicine, Mansura University, Egypt. Sixty percent of the renal transplant patients were compliant with medications and lifestyle. Risk factors associated with poor medication compliance were being Kuwaiti citizens, women, and having had unrelated living donors ( <0.05). Compliance with medications was associated with less transplant related complications ( =0.003). Only 15% of the participants were compliant with low-salt diet, 8% with low-fat, and 11% with low-carb. One fourth of patients were compliant with a daily shower and 20% were physically active. More than 70% of the patients were regularly visiting the out-patient clinic. Compliance to preventive measures against infection was observed in 85% of patients but only 5% were avoiding direct sun exposure. Half of the male patients had sexual dysfunction but only half of them were consulting their nephrologists about it. Kidney transplant patients in Kuwait had moderate compliance with medications and lifestyle modifications. Closer assessment is needed to identify the risk factors before and after transplantation to avoid any complications associated with non-compliance.

New onset diabetes after transplantation (NODAT) is a serious metabolic complication following kidney transplantation. Although beta-cell dysfunction is considered the main contributing factor in the development of this complication, its exact etiology is yet to be identified. We aimed to investigate NODAT among kidney transplant cohort in Kuwait with special stress on correlation between its risk factors and interferon gamma genotyping. We surveyed 309 kidney transplant recipients from Hamed Al Essa Transplantation Centre, Kuwait. The participants were categorized into cohorts according to the development of NODAT diagnosed based on the American Diabetes Association guidelines. Statistical analyses were performed using SPSS software. We genotyped interferon gamma as the leading immunosignature for T lymphocyte. No relationship between ethnicity and the development of NODAT was identified. However, there was a significant difference in age between cohorts. Younger patients demonstrated a lower rate of NODAT while, NODAT reached its maximum in 40-60-year age group. IFNG TT genotype was significantly associated with NODAT ( =0.005), while IFNG AA was considerably higher in the non-NODAT group. Beside the conventional contributing factors of NODAT, our results might represent a suitable platform for a larger cytokine and chemokine spectrum genotyping.

Fatigue is a prevalent symptom affecting primary Sjögren's syndrome (pSS) patients. The purpose of this study is to determine the prevalence of fatigue in Saudi pSS patients and its correlation with disease features and outcome measures using a validated tool. This is a cross-sectional study evaluating fatigue in pSS using the Arabic version of the fatigue severity scale (FSS). The EULAR Sjögren's syndrome disease activity index (ESSDAI) and EULAR Sjögren's syndrome patient reported index (ESSPRI) were calculated. Forty-one patients met the sample criteria and were involved in the final report. There were predominantly females (78%) with a mean (±SD) age and disease duration of 58.76±12.7 and 4.6±2.28 years, respectively. Based on the FSS, 18 (43.9%) patients had a positive test with a mean score of 5.43±0.76. The mean ESSDAI was 9.95±7.73, while the mean EESPRI was 5.17±2.4 with individual component scores were dryness (5.23±2.62), fatigue (5.4±2.88), and pain (4.88±3.31). The FSS had a significant correlation with PGA (r=0.559; <0.001), PhGA (r=0.671; <0.001), ESSDAI (r=0.402; =0.01), ESSPRI fatigue component (r=0.0.621; <0.001), ESSPRI pain component (r=0.558; <0.001), and missed significance for the ESSPRI dryness component (r=0.289; =0.071). There was no correlation between the total ESSPRI score and presence of fatigue (r=-0.261; =0.104) nor the FSS score (r=-0.136; =0.409). Fatigue is prevalent in Saudi pSS patients. FSS correlated with ESSDAI and ESSPRI components but not its total score signaling other unmeasured factors contributing to fatigue development.

Rheumatoid arthritis (RA) is a complex, multifactorial disorder with an autoimmune etiology. RA is highly heritable and is associated with both human leucocyte antigen (HLA) and non-HLA genes. We investigated the associations of 33 single nucleotide polymorphisms (SNPs) with RA in the Saudi population. Methods: This study included 105 patients with RA and an equal number of age- and sex-matched controls. The patients with RA attended outpatient clinics at King Khalid University Hospital in Riyadh, Saudi Arabia. Blood samples were collected, and DNA was extracted using Qiagen kits. Primers were designed for the 33 selected SNPs using the MassEXTEND primers program, and samples were genotyped on the Sequenom MassARRAY iPLEX platform. The allele frequencies and genotypes were determined for each SNP, and the results obtained for the patients were compared to those for the controls. Results: The allele and genotype frequencies of six SNPs were significantly associated with RA: rs1188934, rs10919563, rs3087243, rs1980422, rs10499194, and rs629326. The minor alleles of rs1188934, rs10919563, rs10499194, and rs629326 were protective, with odds ratios of 0.542, 0.597, 0.589, and 0.625, and p-values of 0.002, 0.023, 0.013 and 0.036, respectively. In addition, the heterozygote frequencies of two SNPs (rs6859219 and rs11586238) were significantly higher in the controls than in the patients. Conclusions: There is considerable heterogeneity in the genetics of RA in different populations, and the SNPs that are associated with RA in some populations are not in others. We studied 33 SNPs and only eight were associated with RA. The remaining SNPs showed no allelic or genotypic associations with RA.