Siobhan Sutcliffe1, Thomas Jemielita2, H Henry Lai3, Gerald L Andriole4, Catherine S Bradley5, J Quentin Clemens6, Robert Gallop2, Thomas M Hooton7, Karl J Kreder8, John N Krieger9, John W Kusek10, Jennifer Labus11, M Scott Lucia12, Sean Mackey13, Bruce D Naliboff14, Nancy A Robinson2, Larissa V Rodriguez15, Alisa Stephens-Shields2, Adrie van Bokhoven12, Kathleen Y Wolin16, Yan Yan17, Claire C Yang9, J Richard Landis2, Graham A Colditz17. 1. Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri. Electronic address: sutcliffes@wustl.edu. 2. Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. 3. Division of Urologic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri; Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri. 4. Division of Urologic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri. 5. Department of Obstetrics and Gynecology, University of Iowa, Iowa City, Iowa. 6. Division of Neurology and Pelvic Reconstructive Surgery, Department of Urology, University of Michigan, Ann Arbor, Michigan. 7. Division of Infectious Diseases, Department of Medicine, University of Miami School of Medicine, Miami, Florida. 8. Department of Urology, University of Iowa, Iowa City, Iowa. 9. Department of Urology, University of Washington, Seattle, Washington. 10. National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. 11. Oppenheimer Center for Neurobiology of Stress and Resilience, Division of Digestive Diseases, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California. 12. Department of Pathology, University of Colorado, Aurora, Colorado. 13. Division of Pain Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Palo Alto, California. 14. Departments of Medicine and Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California. 15. Institute of Urology, University of Southern California, Beverly Hills, California. 16. ScaleDown, Chicago, Illinois. 17. Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri.
Abstract
PURPOSE: Although many factors have been proposed to trigger symptom exacerbations (flares) in patients with interstitial cystitis/bladder pain syndrome and chronic prostatitis/chronic pelvic pain syndrome, few studies have investigated these factors empirically. Therefore, we embedded a case-crossover study in the Multidisciplinary Approach to the Study of Chronic Pelvic Pain longitudinal study to evaluate a range of patient reported triggers. MATERIALS AND METHODS: We assessed exposure to proposed triggers, including diet, physical activities, sedentary behaviors, stress, sexual activities, infection-like symptoms and allergies, by questionnaire a maximum of 3 times when participants reported flares and at 3 randomly selected times. We compared participant preflare to nonflare exposures by conditional logistic regression. RESULTS: In our full analytical sample of 292 participants only 2 factors, including recent sexual activity (OR 1.44, 95% CI 1.06-1.96) and urinary tract infection symptoms (OR 3.39, 95% CI 2.02-5.68), which may overlap with those of flares, were associated with flare onset. On subanalyses restricted to flares with specific suspected triggers additional positive associations were observed for some factors such as certain dietary factors, abdominal muscle exercises, and vaginal infection-like symptoms and fever, but not for other factors (eg stress). CONCLUSIONS: Except for sexual activity our findings suggest that patient reported triggers may be individual or group specific, or they may not contribute to flares. These findings suggest caution in following rigid, global flare prevention strategies and support additional research to develop evidence-based strategies.
PURPOSE: Although many factors have been proposed to trigger symptom exacerbations (flares) in patients with interstitial cystitis/bladder pain syndrome and chronic prostatitis/chronic pelvic pain syndrome, few studies have investigated these factors empirically. Therefore, we embedded a case-crossover study in the Multidisciplinary Approach to the Study of Chronic Pelvic Pain longitudinal study to evaluate a range of patient reported triggers. MATERIALS AND METHODS: We assessed exposure to proposed triggers, including diet, physical activities, sedentary behaviors, stress, sexual activities, infection-like symptoms and allergies, by questionnaire a maximum of 3 times when participants reported flares and at 3 randomly selected times. We compared participant preflare to nonflare exposures by conditional logistic regression. RESULTS: In our full analytical sample of 292 participants only 2 factors, including recent sexual activity (OR 1.44, 95% CI 1.06-1.96) and urinary tract infection symptoms (OR 3.39, 95% CI 2.02-5.68), which may overlap with those of flares, were associated with flare onset. On subanalyses restricted to flares with specific suspected triggers additional positive associations were observed for some factors such as certain dietary factors, abdominal muscle exercises, and vaginal infection-like symptoms and fever, but not for other factors (eg stress). CONCLUSIONS: Except for sexual activity our findings suggest that patient reported triggers may be individual or group specific, or they may not contribute to flares. These findings suggest caution in following rigid, global flare prevention strategies and support additional research to develop evidence-based strategies.
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