Background/Objective: Ankylosing spondylitis (AS) is a common inflammatory rheumatic disease that affects the axial skeleton, causing characteristic inflammatory back pain. We aim to examine the genes FOXP3, RORγt, SOCS1, STAT3, STAT5, and SMAD3 in patients with ankylosing spondylitis who receive anti-TNF therapy to understand the progression of the disease in a clinically improved or failed response to anti-TNF treatment. Method: A prospective case-control study was conducted at Basrah Teaching Hospital in southern Iraq. Eighty-one AS patients were divided into two groups: 67 were treated with anti-TNF therapy; 14 were newly diagnosed patients as positive controls, and 65 were healthy individuals. Disease activity was assessed using the AS Bath Disease Activity Index (BASDAI). Conventional radiography and MRI are used to measure the severity of the disease. Blood samples were homogenized, and mRNA was isolated using a total RNA extraction kit. Reverse transcription (RT) was performed. The gene expression of RORγt, FOXP3, SOCS1, SAMD1, SMAD3, STAT3, and STAT5 was detected by implementing a real-timePCR system. Result: There was significant downregulation of the FOXP3 gene in anti-TNF-treated AS patients and biologically naïve AS patients compared to healthy control people, which may be due to how the disease affects the expression and activity of the FOXP3 gene, which does not change with the type of therapy (P = 0.001). RORγt expression was higher in both established and newly diagnosed AS patients (p 0.001) than in healthy controls. The SOCS1 gene was expressed at a low level in patients with AS and positive control patients compared to the SOCS1 gene in healthy control individuals (p 0.780). STAT3 expression was lower in established and biologically naïve AS patients than in healthy subjects. Simultaneously, biologically normal AS patients had higher levels of STAT5 in this group. SMAD3 was underexpressed in established and biologically naïve AS patients compared to healthy subjects. Conclusion: The progression of AS in patients treated with anti-TNF therapy is linked to a secondary change in the expression of the genes FOXP3, RORγt, SOCS1, STAT3, STAT5, and SMAD3 that leads to the induction of exTh17cells.
Aim of the work: This study analysed the prevalence of cervical spine instability in Rheumatoid Arthritis (RA) patients following at a single centre in Basrah. Patients and methods: Data were collected directly from patients through cervical spine examinations. Each patient was sent for dynamic (flexion and extension) lateral cervical radiographic imaging to assess the presence of atlantoaxial subluxation (AAS), superior migration of the odontoid (SMO) and sub-axial subluxation (SAS). Patients with positive radiographic findings were sent for MRI scans of the cervical spine to assess neurological compression. Results: The prevalence rate of cervical spine instability in RA was 15/203 (7.4%) of the total sample, occurring primarily in patients of 37e65 years old (mean: 48 ± 8.9 years), were 3/15 (20%) aymptomatic. The majority (60%) being at the moderate stage of the disease activity (using a Clinical Disease Activity Index [CDAI). In terms of type of cervical spine involvement, isolated AAS was found to have the highest occurrence (73.3%), followed by combined SAS and SMO (13.3%), combined AAS and SMO (6.7%), and combined AAS and SAS (6.7%). A significant relationship was found between the type of cervical spine involvement in RA and a disease onset duration, disease activity, body mass index and peripheral erosion with P value < 0.05. Conclusion: Cervical spine subluxation in RA patients may be asymptomatic It is therefore essential to obtain a dynamic radiographic image of the cervical spine in order to diagnose cervical spine involvement and protect the patient from severe outcomes. The clinical trial registration number included in a the official document from Ministry of Higher Ed-
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