Abstract
BACKGROUND: Traditionally, hyperbaric oxygen treatment (HBOT) has been used to treat a limited repertoire of disease, including decompression sickness and healing of problem wounds. However, some investigators have used HBOT to treat inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis. METHODS: Comprehensive searches were conducted in 8 scientific databases through 2011 to identify publications using HBOT in IBD. Human studies and animal models were collated separately. RESULTS: Thirteen studies of HBOT in Crohn's disease and 6 studies in ulcerative colitis were identified. In all studies, participants had severe disease refractory to standard medical treatments, including corticosteroids, immunomodulators and anti-inflammatory medications. In patients with Crohn's disease, 31/40 (78%) had clinical improvements with HBOT, while all 39 patients with ulcerative colitis improved. One study in Crohn's disease reported a significant decrease in proinflammatory cytokines (IL-1, IL-6 and TNF-alpha) and one study in ulcerative colitis reported a decrease in IL-6 with HBOT. Adverse events were minimal. Twelve publications reported using HBOT in animal models of experimentally-induced IBD, including several studies reporting decreased markers of inflammation or immune dysregulation, including TNF-alpha (3 studies), IL-1beta (2 studies), neopterin (1 study) and myeloperoxidase activity (5 studies). HBOT also decreased oxidative stress markers including malondialdehyde (3 studies) and plasma carbonyl content (2 studies), except for one study that reported increased plasma carbonyl content. Several studies reported HBOT lowered nitric oxide (3 studies) and nitric oxide synthase (3 studies) and one study reported a decrease in prostaglandin E2 levels. Four animal studies reported decreased edema or colonic tissue weight with HBOT, and 8 studies reported microscopic improvements on histopathological examination. Although most publications reported improvements with HBOT, some studies suffered from limitations, including possible publication and referral biases, the lack of a control group, the retrospective nature and a small number of participants. CONCLUSIONS: HBOT lowered markers of inflammation and oxidative stress and ameliorated IBD in both human and animal studies. Most treated patients were refractory to standard medical treatments. Additional studies are warranted to investigate the effects of HBOT on biomarkers of oxidative stress and inflammation as well as clinical outcomes in individuals with IBD.