Ulcerative colitis (UC) is a chronic inflammatory bowel disease associated with recurrent
mucosal inflammation. Clinically, the disease is characterized by bloody diarrhea, abdominal
pain, and constitutional symptoms such as fever and weight loss. Treatment strategies vary
based on disease activity and target various aspects of the inflammatory cascade. Options
include: anti-inflammatory drugs (mesalamine), immunosuppressive or modulatory medications
(corticosteroids, thiopurines, cyclosporine) and biologic agents (Anti-TNF). Disease severity
can be wide ranging, and nearly 25% of UC patients are hospitalized for acute severe disease.
Of these patients, 30% will undergo colectomy after the acute episode, a quarter of which
will experience post-operative complications. Although there has been great progress in
treatment of UC over the past decade, even with the anti-TNF agent infliximab, the one-year
remission rate for patients not responding to conservative management is barely 20%.
Furthermore, corticosteroids have significant long-term consequences and immune suppressive
drugs such as 6-mercaptopurine, azathioprine and infliximab have been associated with serious
adverse events including life-threatening infections and lymphomas. With growing evidence
that the pathogenesis of UC is multi-factorial and involves a complex interaction of genetic
and environmental factors, newer treatment modalities are being evaluated to target the
mucosal immune response and mucosal inflammatory regulatory system.

Hyperbaric oxygen offers a promising new treatment option since it targets both tissue
hypoxia and inflammation. Recent small scales studies evaluating the impact of hyperbaric
oxygen treatment in acute ulcerative colitis flares demonstrated improved outcomes. The
mechanisms underlying the improvement are not known. In this study, we will treat ulcerative
colitis flares with hyperbaric oxygen and measure changes in both markers of tissue hypoxia
and inflammation. We hypothesize that hyperbaric oxygen will (a) improve outcomes, and (b)
show reductions in markers of both tissue hypoxia and inflammation.