Obstructive Sleep Apnea Syndrome as a Potential Cause of Nocturia in Younger Adults.

OBJECTIVES: To investigate the impact of age on the relationship between obstructive sleep apnea syndrome (OSAS), nocturia, and other lower urinary tract symptoms (LUTSs). METHODS: This was a secondary analysis study based on data derived from a previously conducted prospective observational cohort study on OSAS and nocturia. We analyzed 90 subjects who were suspected of having OSAS. Prior to polysomnography, we assessed International Prostate Symptom Score-Quality of Life scores, Overactive Bladder Symptom Scores, and International Consultation on Incontinence Modular Questionnaire-Nocturia Quality of Life scores to evaluate LUTSs. Nocturnal urine volume, night-time frequency, and night-time urine electrolyte content were measured during polysomnography. Patients were divided into groups according to age and OSAS severity determined using apnea-hypopnea index (AHI) scores. Young patients were those aged <65 years and elderly patients, ≥65 years. A multiple linear regression with multiple imputations was performed to examine the association of night-time frequency with demographic, polysomnographic, and clinical characteristics. RESULTS: In young patients, night-time frequency was significantly associated with nocturnal urine volume, AHI score, and total IPSS. However, night-time frequency in elderly subjects was not associated with demographic and polysomnographic characteristics. In order to compare the severity of OSAS, night-time frequency and urinary sodium content significantly increased only in young patients (P = .007 and .004, respectively). CONCLUSION: OSAS is a strong candidate of causative factor for nocturia in younger individuals. When a younger patient complains nocturia without any urological disorders, OSAS should be kept in mind as a potential cause of nocturia.

Non-cardiogenic pulmonary oedema induced by salazosulfapyridine.

A 25-year-old woman received oral salazosulfapyridine, 4 g/day, for treatment of ulcerative colitis. At 10 days later, she presented with fever and respiratory symptoms. Based on physical, laboratory and radiological findings, bacterial pneumonia and non-cardiogenic pulmonary oedema was suspected. Salazosulfapyridine was immediately halted and antibiotic therapy started. Two days later, her symptoms and abnormal findings had improved rapidly. Bacteriological studies were negative. Salazosulfapyridine-induced non-cardiogenic pulmonary oedema was diagnosed. Non-cardiogenic pulmonary oedema should be considered as one of several salazosulfapyridine- induced pulmonary diseases in patients who are receiving salazosulfapyridine and who develop respiratory symptoms and an abnormal CXR.