ABSTRACT
Background: Chronic obstructive pulmonary disease is a multisystem disease with multiple comorbidities. Hearing is dependent on the cochlear functions that may be affected by oxygenation. Affection of hearing is problematic and represents a major concern that should be seriously investigated as an important comorbidity in chronic obstructive pulmonary disease patients. Objective: To assess auditory status among chronic obstructive pulmonary disease patients. Methodology: The current study was carried out at Al-Azhar University Hospitals, Cairo, from 1 August 2021 to 2022, including 120 participants. In addition to the control group (60 healthy participants), there were two study groups: chronic obstructive pulmonary disease patients with respiratory failure group (30 patients) and non-respiratory failure group (30 patients). Hearing functions were studied using pure tone audiometry, and auditory brain stem response. Results: There was statistically significant hearing impairment in chronic obstructive pulmonary disease patients in comparison to control group. The hearing impairment was more significant in chronic obstructive pulmonary disease with respiratory failure group in comparison to chronic obstructive pulmonary disease without respiratory failure group. The auditory impairment shows a negative interrelationship with oxygen tension (PaO2) and a positive interrelationship with the smoking index. Conclusion: Hearing affection was meaningfully higher among chronic obstructive pulmonary disease patients and more prominent in patients with respiratory failure. Hypoxia results in deterioration of pure tone audiometry and increased absolute and interpeak latencies in auditory brain stem response. At every frequency, the mean pure tone audiometry thresholds were higher for chronic obstructive pulmonary disease groups than control group albeit remaining in the mild to moderate area of hearing loss. Retro-cochlear affection was suggested among patients with chronic obstructive pulmonary disease as evidenced with the prolongation of auditory brain stem response waves latencies.
ABSTRACT
BACKGROUND: Immune dysregulation plays an important role in the pathogenesis of rheumatoid arthritis (RA). The CD4+CD25 high FoxP3+ subset of regulatory T cells plays an essential role in preventing autoimmunity and maintaining immune homeostasis. Negative regulation of JAK/STAT signaling is controlled by Suppressor of Cytokine Signaling (SOCs3) proteins. SOCs is produced at lower levels in RA. Our aim was to evaluate the expressional dysregulation of SOCs3 and FoxP3 genes in RA patients in relation to disease activity. METHODS: We have recruited 90 patients with RA and 60 healthy controls in case control study. Whole blood samples were collected from RA patients and healthy subjects. The measurement of FoxP3 and SOCs3 gene expression was performed by real-time PCR (qPCR). RESULTS: Patients with RA had significantly decreased expression levels of FoxP3 and SOCs3 genes in comparison with controls (P<0.001), in addition to the insignificance correlation of both genes with disease activity in RA patients. CONCLUSION: FoxP3 and SOCs3 genes showed significant defects in rheumatoid arthritis patients with no significant difference in disease activity.
Subject(s)
Arthritis, Rheumatoid , T-Lymphocytes, Regulatory , Humans , Case-Control Studies , Gene Expression , Suppressor of Cytokine Signaling 3 Protein/genetics , Suppressor of Cytokine Signaling 3 Protein/metabolism , Forkhead Transcription Factors/genetics , Forkhead Transcription Factors/metabolismABSTRACT
Renal dysfunction is a key risk factor for all-cause mortality in patients with type 2 diabetes (T2D). Special attention has been raised regarding the role of soluble tumor necrosis factor receptor1 (sTNFR1) and brain natriuretic peptide (BNP) in diabetic nephropathy (DN) since they play a crucial role in the pathogenesis of T2D complications. Elevated concentrations of sTNFR1and BNP were found to be associated with progression to end stage renal disease (ESRD) in T2D. We determined serum levels of sTNFR1 and BNP in T2D patients and correlated them with various clinical variables especially kidney function and urinary albumin creatinine ratio (UACR). This study included 30 patients with T2D who were divided into two groups according to estimated glomerular filtration rate (eGFR): group 1with (eGFR < 60 mL/min/1.73m²) and group 2 with (eGFR > 60 mL/min/1.73 m²). They were compared with 15 sexes and age matched healthy individuals as a control group. Serum levels of sTNFR1 and BNP were determined using ELISA. Serum levels of sTNFR1 and BNP were significantly higher in group1when compared with group 2 (P= 0.000, P= 0.000) and they were significantly higher in both group1 and group 2 as compared with control (P= 0.000, P= 0.000); (P= 0.000, P = 0.000) respectively. Both sTNFR1 and BNP levels showed significant negative correlation with eGFR (r = - 0.58, P = 0.000); (r= - 0.77, P= 0.000) respectively, and significant positive correlation with UACR (r= 0.84, P= 0.000); (r=0.80, P= 0.000) respectively. In conclusion, increased circulating levels of sTNFR1 and BNP were associated with loss of kidney function in T2D patients.
