Sleep Impairment: A Trigger for Relapse in IBD?
Why is sleep aberration a problem?
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(Enlarge Slide)
Sleep deprivation and sleep interruption induce the upregulation of proinflammatory cytokines, such as tumor necrosis factor (TNF)-alpha and interleukins 1 and 6, and an elevation of C-reactive protein. With this in mind, think about what we do when we treat IBD. We use anti-TNF agents. We look at interleukin interruption, and modifiers of interleukin synthesis. We measure activity of IBD with C-reactive protein levels. All of these are upregulated in patients who have sleep deprivation.
Disruption of circadian rhythms allows the immunologic system to become dysfunctional. Evidence is clear from a number of studies that the prevalence of IBD may be increased in patients who are shift workers or have disruption of their circadian rhythms and normal sleep patterns.
Sleep deprivation increases the likelihood of drug-induced colitis in an animal model. Dextran sodium sulfate (DSS) is well accepted as a method of inducing IBD in mice. If the animals are sleep-deprived, they are more susceptible to DSS-induced colitis. The mediator for IBD is sleep deprivation.
Certain cytokines are known to interfere with sleep, and sleep deprivation results in upregulation of cytokines. Infusion of TNF-alpha or interleukin-1 disrupts standard sleep patterns, causing patients to become dysfunctional at night and more somnolent during the day.
Patients with IBD have many reasons to be up at night, such as disease activity, abdominal pain, and nocturnal stooling. The concomitant use of steroids and pain medications might disrupt their sleep. Not only might the symptoms of IBD create sleep problems, we may be perpetuating sleep deprivation by giving medications to these patients that further upregulate cytokines.
Sleep and Inflammation
Why is sleep aberration a problem?
[ CLOSE WINDOW ]
(Enlarge Slide)
Sleep deprivation and sleep interruption induce the upregulation of proinflammatory cytokines, such as tumor necrosis factor (TNF)-alpha and interleukins 1 and 6, and an elevation of C-reactive protein. With this in mind, think about what we do when we treat IBD. We use anti-TNF agents. We look at interleukin interruption, and modifiers of interleukin synthesis. We measure activity of IBD with C-reactive protein levels. All of these are upregulated in patients who have sleep deprivation.
Disruption of circadian rhythms allows the immunologic system to become dysfunctional. Evidence is clear from a number of studies that the prevalence of IBD may be increased in patients who are shift workers or have disruption of their circadian rhythms and normal sleep patterns.
Sleep deprivation increases the likelihood of drug-induced colitis in an animal model. Dextran sodium sulfate (DSS) is well accepted as a method of inducing IBD in mice. If the animals are sleep-deprived, they are more susceptible to DSS-induced colitis. The mediator for IBD is sleep deprivation.
Certain cytokines are known to interfere with sleep, and sleep deprivation results in upregulation of cytokines. Infusion of TNF-alpha or interleukin-1 disrupts standard sleep patterns, causing patients to become dysfunctional at night and more somnolent during the day.
Patients with IBD have many reasons to be up at night, such as disease activity, abdominal pain, and nocturnal stooling. The concomitant use of steroids and pain medications might disrupt their sleep. Not only might the symptoms of IBD create sleep problems, we may be perpetuating sleep deprivation by giving medications to these patients that further upregulate cytokines.
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