RESUMEN
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.
RESUMEN
Background: Cigarette smoking is an important modifiable risk factor in kidney disease progression. Although long-term smoking has been associated with chronic kidney disease (CKD), its effect on kidney function in early stages has not been clarified. Objective: To detect the early effects of smoking either active or passive on kidney functions. Methodology: The current study was comparative cross sectional study conducted on 280 participants, 140 were nonsmokers and 140 were smokers (70 passive smokers and 70 active smokers). The two groups were comparable in terms of all parameters. We investigated the possible effects of smoking on kidney functions using both serum kidney function tests especially; serum urea, serum creatinine, serum cotinine levels and detection of albumin in urine. Smoking history, full Laboratory investigations, Ventilatory function test including (FEV1/FVC, FEV1, FEF 25-75%, VC and FVC) were done. Results: Serum urea, serum creatinine, serum cotinine levels and urinary albumin were statistically significant higher in smokers group in comparison to nonsmokers, also the serum cotinine levels and urinary albumin were statistically significant in active smokers in comparison to passive smokers. There were positive correlations between the level of urinary albumin and pack/year (r = 0.9, p<0.05), smoking index (r = 0.9, p<0.05), smoking duration (r = 0.4, p<0.05), and serum cotinine (r = 0.6, p<0.050) with good statistical significance. The most significant predictive risk factors of microalbuminuria among smokers group in descending orders were active smoking, passive smoking, age and serum cotinine level. Conclusion: Both active and passive smoking, especially among heavy smokers, is a significant risk factor for microalbuminuria. This finding increase the importance of early cessation of smoking in order to minimize early renal affection among healthy smokers that may not be discovered by routine renal function tests.