Evaluation of central and peripheral corneal thicknesses in patients with rheumatoid arthritis

ABSTRACTPurpose:To evaluate central corneal thickness (CCT) and peripheral corneal thickness (PCT) in patients with rheumatoid arthritis (RA) and to assess the relationships among the corneal parameters, dry eye disease, and clinical variables of RA.Methods:A total of 58 RA patients and 58 control subjects participated in this study. A detailed ophthalmological examination was performed on each subject. Dry eye evaluation was performed using Schirmer’s test, tear break-up time (TBUT), corneal fluorescein staining, and Ocular Surface Disease Index (OSDI). Corneal thickness at the apex point, the center of the pupil, the thinnest point, and PCT (3 mm from the apex to the superior, inferior, nasal, and temporal locations) were evaluated using Scheimpflug imaging (Pentacam®). Additionally, the relative peripheral index (RPI) was calculated by dividing the PCT by the CCT. The disease severity and quality of life were evaluated with DAS28 and HAQ, respectively. The laboratory evaluation comprised ESR and CRP.Results:The mean corneal thicknesses at the apex point, the center of the pupil, the thinnest point, and the superior, inferior, nasal, and temporal points were significantly thinner in RA patients than controls. Schirmer’s test scores and TBUT were significantly lower, and corneal staining and OSDI scores were significantly higher in RA patients. There were no significant correlations between the corneal parameters and the clinical variables of RA or dry eye tests.Conclusion:The CCT and PCT were thinner in RA patients compared to those in control subjects. However, there were no significant correlations between the corneal parameters and the clinical variables of RA or dry eye tests

Clinical significance of NCOA5 gene rs2903908 polymorphism in Behçet`s disease

Behçet’s disease (BD) is an autoimmune multisystemic disease. The precise etiology of BD is not fully understood; however, it is thought that interactions between genetic and environmental factors play an essential role in its pathogenesis. The nuclear receptor coactivator-5 (NCOA5) gene encodes a coregulator for nuclear receptor sub- family 1 group D member 2 (NR1D2) and estrogen receptor 1 and 2 (ESR1 and ESR2). Also, the NCOA5 gene insufficiency leads to an elevated expression of IL-6, and increased levels of IL-6 were found to be related to the pathogenesis of BD. In this study, we aimed to clarify the impact of the NCOA5 rs2903908 polymorphism on susceptibility and clinical findings of BD. This study included 671 participants (300 BD patients and 371 healthy controls). The analyses of NCOA5 rs2903908 polymorphism was performed by using the TaqMan allelic discrim- ination assay. The frequency of TT genotype of the NCOA5 rs2903908 polymorphism was found significantly higher in BD patients compared to those in healthy controls (p=0.016, OR=1.46, 95 % CI=1.08–1.99). Also, the frequencies of CT genotype was observed significantly higher in BD patients with genital ulceration and uveitis than without genital ulceration and uveitis (p=0.002 and p=0.005, respectively). The most significant association was found between C allele frequencies of BD patients with and without uveitis (p=0.0001). Our study represents e first time that the NCOA5 rs2903908 polymorphism seemed to be linked to BD susceptibility and clinical findings

Associations between polymorphisms of IL-17F and IL-17A genes with disease activity and clinical outcome of Ankylosing Spondylitis

Aims: In this study, we aimed to investigate the associations between the 7383A/G and 7488A/G polymorphisms of the interleukin (IL)-17F gene and the G197A polymorphism of the IL-17A gene with disease activity and clinical outcomes in Turkish patients with ankylosing spondylitis (AS). Methods: The study included 101 AS patients and 106 healthy controls. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels, in addition to scores of the Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Metrology Index and Bath Ankylosing Spondylitis Functional Index (BASFI) of the patients, were recorded. The frequencies of genotypes 7383A/G and 7488A/G of the IL-17F and G197A of IL-17A genes and alleles were compared between the patients and healthy controls. Results: There were significant differences in the allele frequencies and genotype distribution of IL-17F 7488A/G. There were also significant differences in the CRP levels and BASFI scores of patients due to the genotype distribution of the IL-17F 7488A/G polymorphism (p=0.029, 0.045, respectively). Conclusions: This study suggests that the IL-17F 7488A/G polymorphism may be associated with susceptibility to AS, disease activity and functional status in Turkish patients. Further studies with larger numbers of AS patients, with a long-term follow-up, are needed to elucidate the observed relations

Association of GSTM1, GSTT1, GSTP1-ILE105VAL and ACE I/D polymorphisms with ankylosing spondylitis

Ankylosing spondylitis (AS) is a chronic inflammatory disease of unknown origin. The aim of this study is to clarify the relationships between susceptibility and severity of AS and GST-mu1 (GSTM1), GST-theta1 (GSTT1), GST-pi1 (GSTP1)-Ile105Val and angiotensin-converting enzyme (ACE) I/D polymorphisms in AS patients. One hundred thirty-eight AS patients and seventy-one healthy controls were enrolled in this study. Erythrocyte sedimentation rate and C-reactive protein (CRP) levels of the AS patients were recorded. The scores of the numeric rating scale (NRS) pain, the Bath Ankylosing Spondylitis Activity Index, the Bath Ankylosing Spondylitis Metrology Index and the Bath Ankylosing Spondylitis Functional Index were calculated. The genotypes distributions and allele frequencies of GSTM1, GSTT1, GSTP1-Ile105Val and ACE I/D polymorphisms were compared between patients and healthy controls. The Multiplex polymerase chain reaction (PCR) and the PCR-restriction fragment length polymorphism methods were used to detect the polymorphisms of ACE I/D, the GSTT1 and GSTM1 genes and the GSTP1-Ile105Val polymorphism, respectively. There were significantly higher levels of the GSTT1 null and the ACE II genotypes in AS patients compared to those in healthy controls (p = 0.002 and 0.005, respectively). We found significantly higher levels of CRP and the NRS pain scores in the patients with ACE ID or DD genotypes compared to those in the patients with ACE II genotypes (p = 0.005 and 0.035, respectively). The present results showed that genes involved in protection from oxidative stress and ACE gene may influence disease development and course in AS