White, Bradley

AbstractSeveral environmental factors have been implicated in the pathogenesis of inflammatory bowel diseases (IBD); however, the evidence for alcohol is sparse, as is its implications on disease activity and overall management. Here, we examine the available evidence for the effect of alcohol on IBD, including its association with the development of IBD, role in exacerbations, and potential medication interactions. Several mechanisms have been demonstrated to mediate the effects of ethanol in the gastrointestinal tract. Alcohol has been shown to alter the gut microbiome, disrupt intestinal barrier, and increase intestinal permeability, directly and indirectly promoting immune activation. Conversely, specific alcoholic beverages, notably red wine, may have anti-inflammatory properties capable of assisting in disease control and affecting disease monitoring. Nonetheless, most alcohol-mediated effects seem to facilitate intestinal inflammation and consequently impact disease onset, recurrence, and symptom control. Furthermore, alcohol use interferes with the metabolism of several medications leading to increased side effect profiles or even loss of effect. Notably, mesalamine, azathioprine, methotrexate, and biologic medications can all be affected by concomitant alcohol intake via a variety of mechanisms.

INTRODUCTION: In younger men, in whom organic prostate disease is uncommon, the etiology of lower urinary tract symptoms (LUTS) is frequently unclear. Studies suggest that in this young cohort voiding phase dysfunction is more common than storage phase dysfunction or normal urodynamics. Abnormal pelvic floor muscle relaxation, which can result in constipation, could potentially result in voiding dysfunction also. To date, no studies have investigated the relationship between posterior pelvic floor dysfunction and LUTS in young men. METHODS: Men who had undergone both anorectal manometry and uroflowmetry (i.e. had lower gastrointestinal and urinary symptoms) between October 2012 and September 2018 were identified. Patients >40 years old were excluded to reduce the likelihood of prostate disease. Clinical data was extracted from the electronic health records. Descriptive and comparative analyses were performed. RESULTS: Of 47 identified patients, 13 were excluded due to a history of neurogenic bowel/bladder, urethral/anal surgery or significant neurological disease. The mean age and standard deviation (SD) of the 34 men analyzed was 30 ± 6 years. Twenty patients demonstrated an abnormal balloon expulsion test (BET). The median (and interquartile range [IQR]) number of LUTS was 1.5 (1-2). An abnormal BET was not associated with symptoms of nocturia, hesitancy, incomplete emptying or the total number of LUTS (2 vs 1, P = 0.6). An abnormal balloon expulsion test was associated with a lower maximum urinary flow rate (Qmax, 14 vs 29 mls/sec, P < 0.001) but not flow duration (34 vs. 27 seconds, P = 0.2), residual urine volume (55 vs. 43 mls, P = 0.7) or urine volume (300 vs. 301 mls, P = 0.5). No correlation was seen between anal pressures at rest or during simulated evacuation and maximum urinary flow rate. No correlation was found between functional constipation and Qmax, LUTS or abnormal uroflow. No relationship between rectal sensory thresholds and urinary symptoms was identified. CONCLUSION: In this study of young men undergoing both anorectal manometry and uroflow, pelvic floor dysfunction was not associated with specific LUTS but was associated with a clinically significant reduction in maximum urinary flow rate. However an objective diagnosis of functional constipation was not associated with urologic abnormalities. Further studies will be needed to prospectively characterize this cohort and to identify whether PFD-associated LUTS and reduced flow respond to biofeedback therapy.