Hyperbaric oxygen treatment for inflammatory bowel disease: a systematic review and analysis
Medical Gas Research volume 2, Article number: 6 (2012)
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.
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.
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.
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.
Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal (GI) tract characterized by chronic and recurrent ulcerations , and includes Crohn's disease and ulcerative colitis. IBD is usually accompanied by severe GI symptoms such as diarrhea, bleeding, abdominal pain, weight loss, and anemia. The symptoms of IBD can be intermittent, with periods of exacerbations and periods that may be relatively free of symptoms. Recent evidence suggests that the pathophysiology of IBD involves immune dysregulation, genetic susceptibilities, intestinal barrier dysfunction, and alterations in microbial flora . Activated macrophages appear to play a key role in the disease process and produce proinflammatory cytokines, including TNF-α and interleukins (IL-6 and IL-8) . Intestinal nitric oxide (NO) levels are also increased in some patients with IBD which may lead to increased intestinal tissue injury . Oxidative stress and mitochondrial dysfunction are also found in some patients with IBD [5, 6]. Some investigators have reported that certain infections such as Mycobacterium avium subspecies paratuberculosis may also play a role in IBD . Interestingly, decreased blood flow to the rectum has been reported in some individuals with ulcerative colitis .
Current medical treatments for IBD are aimed at maintaining clinical remission and include biologic therapies (e.g., monoclonal antibodies), immunomodulators, aminosalicylates, corticosteroids and other anti-inflammatory modalities . Several studies have reported improvements using hyperbaric oxygen treatment (HBOT) in some patients with IBD [10–12]. HBOT involves inhaling 100% oxygen at greater than one atmosphere absolute (ATA) in a pressurized chamber . HBOT has been used successfully in humans at varying pressures to treat a range of conditions. Many clinical applications of HBOT are at higher pressures (e.g., 2.0 ATA and above) including treatment of decompression sickness, arterial gas embolism, and carbon monoxide poisoning . HBOT has been shown to increase the oxygen content of plasma  and body tissues  and may normalize oxygen levels in ischemic tissues . Recently, evidence has accumulated that HBOT also has potent anti-inflammatory effects [18–20]. This manuscript is a systematic review and analysis of the medical literature concerning the use of HBOT in IBD.
A search of the Pubmed, EMBASE, Google Scholar, CINAHL, ERIC, AMED, PsychInfo, and Web of Science databases from their inception through December 31, 2011 was conducted to identify and collate pertinent publications using the search terms "hyperbaric oxygen", "HBOT", "hyperbaric" in all combinations with "IBD", "inflammatory bowel", "inflammatory bowel disease", "colitis", "ulcerative colitis", "Crohn", "Crohn's", "esophagitis", "gastritis", "duodenitis", "jejunitis", "ileitis", and "proctitis." Figure 1 demonstrates the flow chart of publications identified by the literature search.
Publications were initially included if they: (1) involved individuals or specimens from individuals with IBD (including Crohn's disease and ulcerative colitis) or were animal models of IBD, and (2) reported using HBOT. Abstracts of identified publications were reviewed to determine if a publication should be included. If the abstract was obscure or missing, the publication was reviewed to determine if inclusion was warranted. Publications of animal models were collated separately. Studies of gastrointestinal abnormalities caused exclusively by radiation treatment were excluded (36 studies). Studies not written in English (9 studies) [21–29] were excluded (unless an English abstract was available). Studies that were purely review articles (4 studies) [30–33] or letters to the editor (3 publications) [34–36] that did not present any new or unique data were also excluded. Finally, studies that published repeated data and not new or unique data (2 studies) [37, 38] were excluded.
Publications identified by the search
A total of 466 publications were identified. After 233 duplicates were removed, 233 publications were examined. Studies meeting inclusion criteria included 13 publications on the use of HBOT in Crohn's disease, 6 on ulcerative colitis and 12 on animal models of IBD.
Studies on Crohn's disease
Table 1 outlines the 13 studies [10, 11, 39–49] meeting inclusion criteria that reported the use of HBOT in Crohn's disease. Six studies were prospective [10, 41–43, 47, 49] and one contained a control group . In each of the 13 studies, the patients had severe Crohn's disease that was refractory to standard medical treatments, including, in some cases, corticosteroids, sulfasalazine, metronidazole, 6-mercaptopurine, and an elemental diet. One study reported improvements with a stay of up to 3 weeks at the Dead Sea (equivalent to 1.05 ATA) in 6 patients . Two studies contained patients from previous studies but reported new data on these patients [40, 49]. One study reported the effects of HBOT on flow-mediated vasodilation of the brachial artery in 2 patients with Crohn's disease, but did not report the clinical outcomes of HBOT on gastrointestinal inflammation in these patients . The remaining 9 studies [10, 11, 39, 41, 43–46, 48] totaled 40 unique patients with Crohn's disease who were treated with HBOT ranging from 2.0 to 2.8 ATA. Of these 40 patients, 31 (78%) had clinical improvements in Crohn's disease with HBOT. One study reported a significant decrease in proinflammatory cytokines (IL-1, IL-6 and TNF-α) after HBOT in 7 patients with Crohn's disease .
Studies on ulcerative colitis
Table 2 outlines the 6 studies [12, 50–54] meeting inclusion criteria that reported the use of HBOT in ulcerative colitis. In each study, the patients had severe ulcerative colitis that was refractory to standard medical treatments, including, in some cases, corticosteroids, 6-mercaptopurine, mesalamine, tetracycline, 5-amino salicylic acid, and azathioprine. One case series  reported two patients with ulcerative colitis who improved with HBOT; one of these patients had previously been reported . One study from Bulgaria was not published in English, except for the abstract which reported that 34 patients with chronic ulcerohemorrhagic colitis had improvements with HBOT ; however, since only the abstract was written in English, the strengths and weaknesses of this study could not be adequately assessed. The remaining 5 studies [12, 50–52, 54] totaled 5 unique patients with all 5 reported as having improvements in ulcerative colitis with HBOT; each patient was treated at 2.0 ATA. One study reported a decrease in the IL-6 concentration with HBOT .
Adverse events in Crohn's disease and ulcerative colitis
Of the 13 studies in Crohn's disease, 10 did not report if there were any adverse events [11, 40, 42–49]. One study reported that one patient had a bilateral ear drum perforation and another had psychological intolerance; both patients had to stop HBOT after a few sessions . It should be noted that ear drum perforation and psychological intolerance are related to changes in pressure and confinement and not side effects of the oxygen being administered. Another study reported blurred vision in one patient which resolved spontaneously . The final study in Crohn's disease specifically reported that there were no adverse events . Of the 6 studies in ulcerative colitis, 3 studies did not report if there were any adverse events [12, 51, 53] while 3 studies specifically reported that there were no adverse events [50, 52, 54].
Studies of animal models of IBD
Table 3 outlines the 12 studies [55–66] meeting inclusion criteria that reported the use of HBOT in experimentally-induced colitis in an animal model of IBD. All 12 studies used rats as the animal model. One study was published only in abstract form  and another study was not published in English except for the abstract . Most studies were published in Turkey except for two studies published in the United States [63, 66] and one in Israel . Several studies reported that HBOT reduced markers of inflammation, including TNF-alpha [61, 63, 66], IL-1β [63, 66] and neopterin levels . HBOT also decreased edema or colonic tissue weight in 4 studies [56, 57, 62, 64]. One study reported HBOT was equivalent in anti-inflammatory effect to dexamethasone . Myeloperoxidase activity (an index of the accumulation of neutrophils) was reduced after HBOT in 5 studies [55, 57, 63, 64, 66]. Some studies reported that HBOT lowered markers of oxidative stress, including malondialdehyde [56, 60, 61] and plasma carbonyl content [55, 61], except for one study that reported HBOT increased protein carbonyl content . Two studies reported HBOT significantly increased glutathione peroxidase and superoxide dismutase levels [60, 61]. HBOT also decreased nitric oxide [58, 61, 63] and nitric oxide synthase levels [63, 64, 66]. Finally, in one study, HBOT decreased prostaglandin E2 levels . Nine studies used histopathology scores to document changes with HBOT [55–61, 64, 65] and 8 reported microscopic improvements [56–61, 64, 65].
Crohn's disease and ulcerative colitis are forms of IBD which have a limited repertoire of treatment options. Management consists of maintaining clinical remission. In the reviewed studies, HBOT was associated with improvements in most treated patients. Of note, all of the patients in these studies had IBD that was refractory to standard medical treatments and HBOT was essentially used as a treatment of last resort. Adverse events were minimal in most studies. Several animal studies reported that HBOT decreased inflammation and oxidative stress markers and led to improvements in IBD on both a microscopic and macroscopic level.
Effects of HBOT on inflammation and immune dysregulation in IBD
IBD is characterized by inflammation, ulcerations and the accumulation of neutrophils. Many of the reviewed animal models replicated IBD by inducing colitis which was accompanied by intestinal edema, ulcerations, accumulation of neutrophils, increased nitric oxide levels and elevated cytokines. Therefore, these animal models appeared effective at reproducing the pathophysiology of IBD.
HBOT has been shown to possess potent anti-inflammatory properties in both animal [55, 67, 68] and human studies [10, 11, 20, 46, 69] and has been reported to decrease the production of pro-inflammatory cytokines (such as TNF-alpha, interferon-gamma, IL-1 and IL-6) in both animal [66, 70] and human studies [20, 49] as well as increase IL-10 levels . Several of the reviewed studies (including human studies and animal models) reported a decrease in inflammation as measured by reduced tissue edema and histopathological changes, as well as a decrease in TNF-alpha, IL-1 and IL-6 with HBOT [49, 54, 61, 63, 66]. Some of these effects may have been mediated, to some degree, by the activity of stem cells . Stem cells have been shown to migrate to the sites of inflammation and damage . Several studies have reported that HBOT can stimulate the growth and differentiation of stem cells [74–78] as well as mobilize stem cells into the circulation from bone marrow [79, 80]. A number of studies have reported improvements using stem cells in some patients with Crohn's disease [81–86] or ulcerative colitis . Interestingly, some animal studies report that the use of HBOT combined with stem cells was more effective than stem cells alone [87–90]. Therefore, HBOT may help lower inflammation in patients with IBD through the increased mobilization of stem cells.
Animal models of IBD demonstrate that the GI mucosa develops hypoxia . Hypoxia has been reported to increase oxidative stress and inhibit mitochondrial function  as well as increase inflammation . Chronic inflammation can lead to tissue edema and impaired oxygen extraction from the blood into tissue  and a vicious cycle between hypoxia and inflammation can therefore ensue . Hypoxia also causes an increase in hypoxia-inducible transcription factor (HIF) which, in turn, can initiate an inflammatory cascade [96, 97]. In fact, HIF is essential for inflammation mediated by myeloid cells  and rats null for HIF demonstrate almost complete inhibition of the inflammatory response . Furthermore, intestinal biopsies from patients with IBD show elevated levels of HIF in the mucosa . Hypoxia and increased levels of HIF can then activate nuclear factor κB (NF-κB) which subsequently stimulates the production of TNF-alpha . HBOT has been shown to inhibit the expression of HIF and its target genes . Therefore, another method whereby HBOT may lower inflammation in patients with IBD is by the relief of hypoxia and the inhibition of HIF expression . Interestingly, decreased blood flow to the rectum has been reported in some individuals with ulcerative colitis . A reduction in tissue edema with the use of HBOT might lead to improved blood supply and relief of hypoxia. Therefore, HBOT may also ameliorate hypoxia and inflammation in individuals with IBD by reducing tissue edema.
Finally, the inflammation found in IBD could be secondary to an infectious agent. Since some investigators have reported that Mycobacterium avium subspecies paratuberculosis may play a role in IBD , it is possible the HBOT may be beneficial as it has been reported to kill Mycobacterium species [103, 104]. Additional studies investigating the effects of HBOT on inflammation and biomarkers of inflammation in individuals with IBD are warranted.
Effects of HBOT on oxidative stress in IBD
Some studies have reported evidence of oxidative stress and mitochondrial dysfunction in individuals with IBD. Several of the animal models of IBD reported a reduction in oxidative stress markers with HBOT. It should be noted that, theoretically, HBOT might increase oxidative stress through the augmented production of reactive oxygen species (ROS) from the high concentration of oxygen . This may occur because increased oxygen delivery to mitochondria can increase ROS production. However, HBOT has also been shown to upregulate the production of antioxidant enzymes such as superoxide dismutase [106, 107], glutathione peroxidase , catalase , paraoxonase  and heme-oxygenase 1 [110, 111]. This increase in antioxidant enzyme levels has been termed "conditioning" and can protect against damage caused by ROS [95, 112]. Two animal models of IBD reported a significant increase in glutathione peroxidase and superoxide dismutase levels with HBOT [60, 61], suggesting that the increased production of antioxidant enzymes may have limited or lowered oxidative stress in these studies. Although none of the reviewed studies measured changes in mitochondrial function with HBOT, it is possible that HBOT may have led to some improvements by augmenting mitochondrial function as reported in previous studies [113–116]. Further studies examining the effects of HBOT on oxidative stress and mitochondrial dysfunction in individuals with IBD are needed.
Effects of HBOT on IBD in human studies
The total number of identified publications utilizing HBOT in Crohn's disease was about twice the number of studies in ulcerative colitis. In these studies, the number of patients treated in both diseases was similar, although one study in ulcerative colitis reported improvements in 34 patients, but this finding was only reported in an English abstract, and therefore the strengths and weaknesses of this study could not be adequately assessed . The remaining 5 studies in ulcerative colitis only totaled 5 patients. Therefore, the evidence in the reviewed studies for a positive effect of HBOT is stronger for Crohn's disease than for ulcerative colitis.
In the studies of Crohn's disease, 78% of treated patients had an improvement with HBOT at a pressure ranging from 2.0 to 2.8 ATA. In the studies of ulcerative colitis, all treated patients showed improvements with a pressure delivered at 2.0 ATA. These studies suggest that a higher pressure may be needed to achieve these improvements. However, because none of these studies utilized a lower pressure of HBOT, it is not known if a lower pressure or oxygen level would be beneficial in IBD. However, some investigators have reported improvements in GI function in some children with autism using HBOT at 1.3 to 1.5 ATA [117, 118]. Furthermore, previous studies have reported improvements in certain neurological conditions using hyperbaric treatment at lower pressures and/or oxygen levels [119–122]. Additional studies using HBOT at varying oxygen concentrations and atmospheric pressures would be helpful in determining optimal treatment protocols.
It is especially noteworthy that all of the studies on Crohn's disease and ulcerative colitis used HBOT in patients who were refractory to multiple medical treatments, including, in some cases, corticosteroids, 6-mercaptopurine, mesalamine, tetracycline, 5-amino salicylic acid, azathioprine, sulfasalazine, metronidazole, and an elemental diet. It is possible that earlier treatment with HBOT in individuals with IBD before severe symptoms develop would be even more effective in ameliorating the condition. Additional studies examining the clinical effects of HBOT in individuals with IBD would be helpful in assessing this possibility.
Many of the reviewed studies suffered from limitations, including the lack of a control group, the open-label nature and the small number of participants. Some of the studies were retrospective while only a few were prospective [10, 41–43, 47, 49]. Most of the reviewed studies did not report if HBOT was supplied in a monoplace or multiplace chamber, and whether or not masks or hood systems were used, and therefore the ability to determine the effects of different types of chambers or oxygen delivery systems in these studies could not be adequately assessed. Most studies did not specifically report if there were any adverse events. Presumably, if there had been any adverse events, the investigators would have reported them. Therefore, the adverse events in these studies were most likely minimal, but since most studies did not report this, a full assessment cannot be performed. Some of the studies may have been limited by referral bias; for example, none of the studies were population-based which could have reduced potential referral bias. Another limitation of the studies may have been publication bias where only cases that had improvements with HBOT were published, and cases of IBD that were treated with HBOT that did not improve may not have been published. However, it should be noted that for a new treatment to be recognized, it is common for case reports to first be published to introduce and confirm a new treatment before sufficient interest is generated to commit resources to completing larger high-quality, stronger studies. Since most reviewed studies had limitations, larger studies examining the effects of HBOT in individuals with IBD are warranted.
HBOT ameliorated symptoms of IBD in both human studies and animal models. HBOT also lowered pro-inflammatory cytokine concentrations and lowered biomarkers of inflammation and oxidative stress. Adverse events were minimal. Many 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. Additional studies are warranted to investigate both the effects of HBOT on biomarkers of oxidative stress and inflammation as well as clinical outcomes in individuals with IBD.
Hyperbaric oxygen treatment
Inflammatory bowel disease
Fiocchi C: Inflammatory bowel disease: etiology and pathogenesis. Gastroenterology. 1998, 115 (1): 182-205. 10.1016/S0016-5085(98)70381-6.
Kucharzik T, Maaser C, Lugering A, Kagnoff M, Mayer L, Targan S, Domschke W: Recent understanding of IBD pathogenesis: implications for future therapies. Inflamm Bowel Dis. 2006, 12 (11): 1068-1083. 10.1097/01.mib.0000235827.21778.d5.
Papadakis KA, Targan SR: The role of chemokines and chemokine receptors in mucosal inflammation. Inflamm Bowel Dis. 2000, 6 (4): 303-313. 10.1002/ibd.3780060408.
Rachmilewitz D, Stamler JS, Bachwich D, Karmeli F, Ackerman Z, Podolsky DK: Enhanced colonic nitric oxide generation and nitric oxide synthase activity in ulcerative colitis and Crohn's disease. Gut. 1995, 36 (5): 718-723. 10.1136/gut.36.5.718.
Beltran B, Nos P, Dasi F, Iborra M, Bastida G, Martinez M, O'Connor JE, Saez G, Moret I, Ponce J: Mitochondrial dysfunction, persistent oxidative damage, and catalase inhibition in immune cells of naive and treated Crohn's disease. Inflamm Bowel Dis. 2010, 16 (1): 76-86.
Iborra M, Moret I, Rausell F, Bastida G, Aguas M, Cerrillo E, Nos P, Beltran B: Role of oxidative stress and antioxidant enzymes in Crohn's disease. Biochem Soc Trans. 2011, 39 (4): 1102-1106. 10.1042/BST0391102.
Hermon-Taylor J, Bull TJ, Sheridan JM, Cheng J, Stellakis ML, Sumar N: Causation of Crohn's disease by Mycobacterium avium subspecies paratuberculosis. Can J Gastroenterol. 2000, 14 (6): 521-539.
McLeod RS, Churchill DN, Lock AM, Vanderburgh S, Cohen Z: Quality of life of patients with ulcerative colitis preoperatively and postoperatively. Gastroenterology. 1991, 101 (5): 1307-1313.
Pithadia AB, Jain S: Treatment of inflammatory bowel disease (IBD). Pharmacol Rep. 2011, 63 (3): 629-642.
Lavy A, Weisz G, Adir Y, Ramon Y, Melamed Y, Eidelman S: Hyperbaric oxygen for perianal Crohn's disease. J Clin Gastroenterol. 1994, 19 (3): 202-205. 10.1097/00004836-199410000-00006.
Takeshima F, Makiyama K, Doi T: Hyperbaric oxygen as adjunct therapy for Crohn's intractable enteric ulcer. Am J Gastroenterol. 1999, 94 (11): 3374-3375.
Buchman AL, Fife C, Torres C, Smith L, Aristizibal J: Hyperbaric oxygen therapy for severe ulcerative colitis. J Clin Gastroenterol. 2001, 33 (4): 337-339. 10.1097/00004836-200110000-00018.
Feldmeier JJ, Chairman and Editor: Hyperbaric oxygen 2003: indications and results: the hyperbaric oxygen therapy committee report. 2003, Kensington: Undersea and Hyperbaric Medicine Society
Leach RM, Rees PJ, Wilmshurst P: Hyperbaric oxygen therapy. BMJ. 1998, 317 (7166): 1140-1143. 10.1136/bmj.317.7166.1140.
Shandling AH, Ellestad MH, Hart GB, Crump R, Marlow D, Van Natta B, Messenger JC, Strauss M, Stavitsky Y: Hyperbaric oxygen and thrombolysis in myocardial infarction: the "HOT MI" pilot study. Am Heart J. 1997, 134 (3): 544-550. 10.1016/S0002-8703(97)70093-0.
Gill AL, Bell CN: Hyperbaric oxygen: its uses, mechanisms of action and outcomes. QJM. 2004, 97 (7): 385-395.
Ackerman NB, Brinkley FB: Oxygen tensions in normal and ischemic tissues during hyperbaric therapy. Studies in rabbits. JAMA. 1966, 198 (12): 1280-1283.
Al-Waili NS, Butler GJ: Effects of hyperbaric oxygen on inflammatory response to wound and trauma: possible mechanism of action. ScientificWorldJournal. 2006, 6: 425-441.
Benson RM, Minter LM, Osborne BA, Granowitz EV: Hyperbaric oxygen inhibits stimulus-induced proinflammatory cytokine synthesis by human blood-derived monocyte-macrophages. Clin Exp Immunol. 2003, 134 (1): 57-62. 10.1046/j.1365-2249.2003.02248.x.
Granowitz EV, Skulsky EJ, Benson RM, Wright J, Garb JL, Cohen ER, Smithline EC, Brown RB: Exposure to increased pressure or hyperbaric oxygen suppresses interferon-gamma secretion in whole blood cultures of healthy humans. Undersea Hyperb Med. 2002, 29 (3): 216-225.
Atienza P: Refractory perineal fistulas in Crohn's disease. Gastroenterol Clin Biol. 2007, 31 (4): 404-411. 10.1016/S0399-8320(07)89400-0.
Ben Bouali A, Burtin P, Delaby J, Alquier P, Bouachour G, Joubaud F: Indications of hyperbaric oxygen for the treatment of severe ulcerative colitis?. Medecine et Chirurgie Digestives. 1990, 19 (6): 340-
Ermakov EV, Orlov AV, Barskii RL: Effect of hyperbaric oxygenation on the secretory and motor functions of the stomach in peptic ulcer and chronic gastritis with secretory insufficiency. Klin Med (Mosk). 1981, 59 (8): 67-71.
Grigoryeva GA: Non-specific ulcerative colitis and Crohn's disease. Klin Med (Mosk). 1991, 69 (11): 108-115.
Kameyama K, Noguchi Y, Matsumoto T, Takenawa H, Fujigasaki H, Kanda T, Mizusawa H: Pneumatosis intestinalis in a patient of myasthenia gravis treated with high-dose corticosteroid. Rinsho Shinkeigaku. 2003, 43 (5): 277-280.
Komarov FI, Efuni SN, Pogromov AP, Egorov AP, Narula R: Effect of hyperbaric oxygenation on gastric acid-forming function in chronic gastritis and peptic ulcer patients. Voen Med Zh. 1984, 6: 18-22.
Poliakova LV, Lukich VL, Grigor'eva GA: Hyperbaric oxygenation and drug therapy in treatment of nonspecific ulcerative colitis and Crohn's disease. Fiziol Zh. 1991, 37 (5): 120-123.
Teixeira MG, Habr-Gama A, Takiguti CK, Rocha ME, dos Santos HA, de Oliveira AL: Perianal manifestations in Crohn's disease. Rev Hosp Clin Fac Med Sao Paulo. 1996, 51 (4): 125-130.
Vasil'ev VA: The effect of oxygen barotherapy on gastric secretion in patients with chronic gastritis. Vrach Delo. 1990, 4: 20-21.
Bouguen G, Siproudhis L, Bretagne JF, Bigard MA, Peyrin-Biroulet L: Nonfistulizing perianal Crohn's disease: clinical features, epidemiology, and treatment. Inflammatory Bowel Diseases. 2010, 16 (8): 1431-1442.
Dolezal V: Hyperbaric oxygen therapy in gastroenterology. Prakticky Lekar. 2000, 80 (2): 79-81.
Noyer CM, Brandt LJ: Hyperbaric oxygen therapy for perineal Crohn's disease. Am J Gastroenterol. 1999, 94 (2): 318-321. 10.1111/j.1572-0241.1999.00848.x.
Odes SH, Odes LR: Clinical and epidemiological data on inflammatory bowel disease, colorectal cancer and helicobacter pylori infection in Israel. Ann Gastroenterol. 2002, 15 (4): 355-359.
Buchman AL: Therapeutic efficacy of hyperbaric oxygenation in ulcerative colitis refractory to medical treatment - Response. J Clin Gastroenterol. 2002, 35 (3): 287-288. 10.1097/00004836-200209000-00022.
Connor DJ, Bennett M: Response to article by Buchman et al. Use of hyperbaric oxygenation in the treatment of ulcerative colitis. J Clin Gastroenterol. 2002, 35 (1): 98-author reply 98
Welfare MR, Barton JR, Cobden I, Kuroki K: Hyperbaric oxygen for toxic megacolon (multiple letters) . Lancet. 1999, 353 (9146): 70-71.
Altinel O, Demirbas S, Cayci T, Akgul EO, Ozerhan IH, Duran E, Uysal B, Kurt B, Ersoz N, Yaman H, et al: Comparsion of hyperbaric oxygen and medical ozone therapies in a rat model of experimental distal colitis. Turk J Biochem. 2010, 35:
Gurbuz AK, Elbuken E, Yazgan Y, Yildiz S: A different therapeutic approach in severe ulcerative hyperbaric oxygen treatment. Rom J Gastroenterol. 2003, 12 (2): 170-171.
Brady CE, Cooley BJ, Davis JC: Healing of severe perineal and cutaneous Crohn's disease with hyperbaric oxygen. Gastroenterology. 1989, 97 (3): 756-760.
Brady CE: Hyperbaric oxygen and perineal Crohn's disease: a follow-up. Gastroenterology. 1993, 105 (4): 1264-
Colombel JF, Mathieu D, Bouault JM, Lesage X, Zavadil P, Quandalle P, Cortot A: Hyperbaric oxygenation in severe perineal Crohn's disease. Dis Colon Rectum. 1995, 38 (6): 609-614. 10.1007/BF02054120.
Fraser GM, Niv Y: Six patients whose perianal and ileocolic Crohn's disease improved in the Dead Sea environment. J Clin Gastroenterol. 1995, 21 (3): 217-219. 10.1097/00004836-199510000-00010.
Iezzi LE, Feitosa MR, Medeiros BA, Aquino JC, Almeida AL, Parra RS, Rocha JJ, Feres O: Crohn's disease and hyperbaric oxygen therapy. Acta Cir Bras. 2011, 26 (Suppl 2): 129-132.
Jiang T, Covington JA, Haile CA, Murphy JB, Rotolo FS, Lake AM: Fournier gangrene associated with Crohn disease. Mayo Clin Proc. 2000, 75 (6): 647-649. 10.4065/75.6.647.
Kiel N, Ho V, Pascoe A: A case of gas gangrene in an immunosuppressed Crohn's patient. World J Gastroenterol. 2011, 17 (33): 3856-3858. 10.3748/wjg.v17.i33.3856.
Nelson EW, Bright DE, Villar LF: Closure of refractory perineal Crohn's lesion. Integration of hyperbaric oxygen into case management. Dig Dis Sci. 1990, 35 (12): 1561-1565. 10.1007/BF01540577.
Saglam M, Bozlar U, Kantarci F, Ay H, Battal B, Coskun U: Effect of hyperbaric oxygen on flow-mediated vasodilation: an ultrasound study. J Ultrasound Med. 2008, 27 (2): 209-214.
Sipahi AM, Damiao AO, de Sousa MM, Barbutti RC, Trivellato S, Esteves C, D'Agostino M, Laudanna AA: Hyperbaric oxygen: a new alternative in the treatment of perianal Crohn's disease. Rev Hosp Clin Fac Med Sao Paulo. 1996, 51 (5): 189-191.
Weisz G, Lavy A, Adir Y, Melamed Y, Rubin D, Eidelman S, Pollack S: Modification of in vivo and in vitro TNF-alpha, IL-1, and IL-6 secretion by circulating monocytes during hyperbaric oxygen treatment in patients with perianal Crohn's disease. J Clin Immunol. 1997, 17 (2): 154-159. 10.1023/A:1027378532003.
Demirturk L, Ozel M, Yazgan Y, Buchman AL: Therapeutic efficacy of hyperbaric oxygenation in ulcerative colitis refractory to medical treatment. J Clin Gastroenterol. 2002, 35 (3): 286-287. 10.1097/00004836-200209000-00021. author reply 287-288
Gurbuz AK, Elbuken E, Yazgan Y, Yildiz S: A different therapeutic approach in patients with severe ulcerative colitis: hyperbaric oxygen treatment. South Med J. 2003, 96 (6): 632-633. 10.1097/01.SMJ.0000074507.31006.79.
Hulagu S, Demirturk L, Ozel M, Dundar K, Altin M: Therapeutic experience of hyperbaric oxygenation in ulcerative colitis refractory to medical treatment (Case report). Turk J Gastroenterol. 1997, 8 (1): 109-111.
Karkumov M, Nikolov N, Georgiev L, Mitreva D, Uzunova A: Hyperbaric oxygenation as a part of the treatment of chronic ulcerohemorrhagic colitis. Vutr Boles. 1991, 30 (2): 78-80.
Kuroki K, Masuda A, Uehara H, Kuroki A: A new treatment for toxic megacolon. Lancet. 1998, 352 (9130): 782-10.1016/S0140-6736(98)95043-7.
Akin ML, Gulluoglu BM, Uluutku H, Erenoglu C, Elbuken E, Yildirim S, Celenk T: Hyperbaric oxygen improves healing in experimental rat colitis. Undersea Hyperb Med. 2002, 29 (4): 279-285.
Altinel O, Demirbas S, Cakir E, Yaman H, Ozerhan IH, Duran E, Cayci T, Akgul EO, Ersoz N, Uysal B, et al: Comparison of hyperbaric oxygen and medical ozone therapies in a rat model of experimental distal colitis. Scand J Clin Lab Invest. 2011, 71 (3): 185-192. 10.3109/00365513.2010.548875.
Atug O, Hamzaoglu H, Tahan V, Alican I, Kurtkaya O, Elbuken E, Ozdogan O, Tozun N: Hyperbaric oxygen therapy is as effective as dexamethasone in the treatment of TNBS-E-induced experimental colitis. Dig Dis Sci. 2008, 53 (2): 481-485. 10.1007/s10620-007-9956-4.
Ercin CN, Yesilova Z, Korkmaz A, Ozcan A, Oktenli C, Uygun A: The effect of iNOS inhibitors and hyperbaric oxygen treatment in a rat model of experimental colitis. Dig Dis Sci. 2009, 54 (1): 75-79. 10.1007/s10620-008-0498-1.
Gorgulu S, Yagci G, Kaymakcioglu N, Ozkara M, Kurt B, Ozcan A, Kaya O, Sadir S, Tufan T: Hyperbaric oxygen enhances the efficiency of 5-aminosalicylic acid in acetic acid-induced colitis in rats. Dig Dis Sci. 2006, 51 (3): 480-487. 10.1007/s10620-006-3159-2.
Gulec B, Yasar M, Yildiz S, Oter S, Akay C, Deveci S, Sen D: Effect of hyperbaric oxygen on experimental acute distal colitis. Physiol Res. 2004, 53 (5): 493-499.
Guven A, Gundogdu G, Uysal B, Cermik H, Kul M, Demirbag S, Ozturk H, Oter S: Hyperbaric oxygen therapy reduces the severity of necrotizing enterocolitis in a neonatal rat model. J Pediatr Surg. 2009, 44 (3): 534-540. 10.1016/j.jpedsurg.2008.06.008.
Guven A, Uysal B, Oztas E, Yasar M, Cayci T, Korkmaz A: The Comparison of the Effectiveness of Hyperbaric Oxygen and Medical Ozone Therapy Against Acute Distal Colitis in a Rat Model. Am J Gastroenterol. 2010, 105: S445-S446.
Nandi J, Saud B, Zinkievich JM, Yang ZJ, Levine RA: TNF-alpha modulates iNOS expression in an experimental rat model of indomethacin-induced jejunoileitis. Mol Cell Biochem. 2010, 336 (1-2): 17-24. 10.1007/s11010-009-0259-2.
Rachmilewitz D, Karmeli F, Okon E, Rubenstein I, Better OS: Hyperbaric oxygen: a novel modality to ameliorate experimental colitis. Gut. 1998, 43 (4): 512-518. 10.1136/gut.43.4.512.
Simsek D, Aydinoz S, Mutluoglu M, Ipcioglu OM, Cermik H, Kul M, Karademir F, Uzun G, Gocmen I: Effects of hyperbaric oxygen therapy on experimental necrotizing enterocolitis in newborn rats. Nobel Medicus. 2011, 7 (1): 12-16.
Yang Z, Nandi J, Wang J, Bosco G, Gregory M, Chung C, Xie Y, Yang X, Camporesi EM: Hyperbaric oxygenation ameliorates indomethacin-induced enteropathy in rats by modulating TNF-alpha and IL-1beta production. Dig Dis Sci. 2006, 51 (8): 1426-1433. 10.1007/s10620-006-9088-2.
Luongo C, Imperatore F, Cuzzocrea S, Filippelli A, Scafuro MA, Mangoni G, Portolano F, Rossi F: Effects of hyperbaric oxygen exposure on a zymosan-induced shock model. Crit Care Med. 1998, 26 (12): 1972-1976. 10.1097/00003246-199812000-00022.
Sumen G, Cimsit M, Eroglu L: Hyperbaric oxygen treatment reduces carrageenan-induced acute inflammation in rats. Eur J Pharmacol. 2001, 431 (2): 265-268. 10.1016/S0014-2999(01)01446-7.
Abbot NC, Beck JS, Carnochan FM, Gibbs JH, Harrison DK, James PB, Lowe JG: Effect of hyperoxia at 1 and 2 ATA on hypoxia and hypercapnia in human skin during experimental inflammation. J Appl Physiol. 1994, 77 (2): 767-773.
Inamoto Y, Okuno F, Saito K, Tanaka Y, Watanabe K, Morimoto I, Yamashita U, Eto S: Effect of hyperbaric oxygenation on macrophage function in mice. Biochem Biophys Res Commun. 1991, 179 (2): 886-891. 10.1016/0006-291X(91)91901-N.
Buras JA, Holt D, Orlow D, Belikoff B, Pavlides S, Reenstra WR: Hyperbaric oxygen protects from sepsis mortality via an interleukin-10-dependent mechanism. Crit Care Med. 2006, 34 (10): 2624-2629. 10.1097/01.CCM.0000239438.22758.E0.
Aggarwal S, Pittenger MF: Human mesenchymal stem cells modulate allogeneic immune cell responses. Blood. 2005, 105 (4): 1815-1822. 10.1182/blood-2004-04-1559.
Meier C, Middelanis J, Wasielewski B, Neuhoff S, Roth-Haerer A, Gantert M, Dinse HR, Dermietzel R, Jensen A: Spastic paresis after perinatal brain damage in rats is reduced by human cord blood mononuclear cells. Pediatr Res. 2006, 59 (2): 244-249. 10.1203/01.pdr.0000197309.08852.f5.
Wang XL, Yang YJ, Wang QH, Xie M, Yu XH, Liu CT, Wang X: Changes of Wnt-3 protein during the proliferation of endogenous neural stem cells in neonatal rats with hypoxic-ischemic brain damage after hyperbaric oxygen therapy. Zhongguo Dang Dai Er Ke Za Zhi. 2007, 9 (3): 241-246.
Milovanova TN, Bhopale VM, Sorokina EM, Moore JS, Hunt TK, Hauer-Jensen M, Velazquez OC, Thom SR: Hyperbaric oxygen stimulates vasculogenic stem cell growth and differentiation in vivo. J Appl Physiol. 2009, 106 (2): 711-728.
Yang YJ, Wang XL, Yu XH, Wang X, Xie M, Liu CT: Hyperbaric oxygen induces endogenous neural stem cells to proliferate and differentiate in hypoxic-ischemic brain damage in neonatal rats. Undersea Hyperb Med. 2008, 35 (2): 113-129.
Wang XL, Yang YJ, Xie M, Yu XH, Liu CT, Wang X: Proliferation of neural stem cells correlates with Wnt-3 protein in hypoxic-ischemic neonate rats after hyperbaric oxygen therapy. Neuroreport. 2007, 18 (16): 1753-1756. 10.1097/WNR.0b013e3282f0ec09.
Yu XH, Yang YJ, Wang X, Wang QH, Xie M, Qi BX, Liu CT, Wang XL, Jia YJ, Zhong L: Effect of hyperbaric oxygenation on neural stem cells and myelin in neonatal rats with hypoxic-ischemic brain damage. Zhongguo Dang Dai Er Ke Za Zhi. 2006, 8 (1): 33-37.
Thom SR, Milovanova TN, Yang M, Bhopale VM, Sorokina EM, Uzun G, Malay DS, Troiano MA, Hardy KR, Lambert DS, et al: Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. Wound Repair Regen. 2011, 19 (2): 149-161. 10.1111/j.1524-475X.2010.00660.x.
Thom SR, Bhopale VM, Velazquez OC, Goldstein LJ, Thom LH, Buerk DG: Stem cell mobilization by hyperbaric oxygen. Am J Physiol Heart Circ Physiol. 2006, 290 (4): H1378-1386.
Garcia-Olmo D, Garcia-Arranz M, Garcia LG, Cuellar ES, Blanco IF, Prianes LA, Montes JA, Pinto FL, Marcos DH, Garcia-Sancho L: Autologous stem cell transplantation for treatment of rectovaginal fistula in perianal Crohn's disease: a new cell-based therapy. Int J Colorectal Dis. 2003, 18 (5): 451-454. 10.1007/s00384-003-0490-3.
Burt RK, Traynor A, Oyama Y, Craig R: High-dose immune suppression and autologous hematopoietic stem cell transplantation in refractory Crohn disease. Blood. 2003, 101 (5): 2064-2066. 10.1182/blood-2002-07-2122.
Garcia-Olmo D, Garcia-Arranz M, Herreros D: Expanded adipose-derived stem cells for the treatment of complex perianal fistula including Crohn's disease. Expert Opin Biol Ther. 2008, 8 (9): 1417-1423. 10.1517/147125220.127.116.117.
Ditschkowski M, Einsele H, Schwerdtfeger R, Bunjes D, Trenschel R, Beelen DW, Elmaagacli AH: Improvement of inflammatory bowel disease after allogeneic stem-cell transplantation. Transplantation. 2003, 75 (10): 1745-1747. 10.1097/01.TP.0000062540.29757.E9.
Garcia-Olmo D, Herreros D, Pascual I, Pascual JA, Del-Valle E, Zorrilla J, De-La-Quintana P, Garcia-Arranz M, Pascual M: Expanded adipose-derived stem cells for the treatment of complex perianal fistula: a phase II clinical trial. Dis Colon Rectum. 2009, 52 (1): 79-86. 10.1007/DCR.0b013e3181973487.
Oyama Y, Craig RM, Traynor AE, Quigley K, Statkute L, Halverson A, Brush M, Verda L, Kowalska B, Krosnjar N, et al: Autologous hematopoietic stem cell transplantation in patients with refractory Crohn's disease. Gastroenterology. 2005, 128 (3): 552-563. 10.1053/j.gastro.2004.11.051.
Pan HC, Chin CS, Yang DY, Ho SP, Chen CJ, Hwang SM, Chang MH, Cheng FC: Human amniotic fluid mesenchymal stem cells in combination with hyperbaric oxygen augment peripheral nerve regeneration. Neurochem Res. 2009, 34 (7): 1304-1316. 10.1007/s11064-008-9910-7.
Khan M, Meduru S, Pandian RP, Rivera BK, Kuppusamy P: Effect of oxygenation on stem-cell therapy for myocardial infarction. Adv Exp Med Biol. 2011, 701: 175-181. 10.1007/978-1-4419-7756-4_24.
Khan M, Meduru S, Gogna R, Madan E, Citro L, Kuppusamy ML, Sayyid M, Mostafa M, Hamlin RL, Kuppusamy P: Oxygen cycling in conjunction with stem cell transplantation induces NOS3 expression leading to attenuation of fibrosis and improved cardiac function. Cardiovasc Res. 2012, 93 (1): 89-99. 10.1093/cvr/cvr277.
Khan M, Meduru S, Mohan IK, Kuppusamy ML, Wisel S, Kulkarni A, Rivera BK, Hamlin RL, Kuppusamy P: Hyperbaric oxygenation enhances transplanted cell graft and functional recovery in the infarct heart. J Mol Cell Cardiol. 2009, 47 (2): 275-287. 10.1016/j.yjmcc.2009.04.005.
Karhausen J, Furuta GT, Tomaszewski JE, Johnson RS, Colgan SP, Haase VH: Epithelial hypoxia-inducible factor-1 is protective in murine experimental colitis. J Clin Invest. 2004, 114 (8): 1098-1106.
Magalhaes J, Ascensao A, Soares JM, Ferreira R, Neuparth MJ, Marques F, Duarte JA: Acute and severe hypobaric hypoxia increases oxidative stress and impairs mitochondrial function in mouse skeletal muscle. J Appl Physiol. 2005, 99 (4): 1247-1253. 10.1152/japplphysiol.01324.2004.
Eltzschig HK, Carmeliet P: Hypoxia and inflammation. N Engl J Med. 2011, 364 (7): 656-665. 10.1056/NEJMra0910283.
Harrison DK, Abbot NC, Carnochan FM, Beck JS, James PB, McCollum PT: Protective regulation of oxygen uptake as a result of reduced oxygen extraction during chronic inflammation. Adv Exp Med Biol. 1994, 345: 789-796. 10.1007/978-1-4615-2468-7_103.
Rossignol DA: Hyperbaric oxygen therapy might improve certain pathophysiological findings in autism. Med Hypotheses. 2007, 68 (6): 1208-1227. 10.1016/j.mehy.2006.09.064.
Semenza GL: Oxygen sensing, homeostasis, and disease. N Engl J Med. 2011, 365 (6): 537-547. 10.1056/NEJMra1011165.
Nathan C: Immunology: oxygen and the inflammatory cell. Nature. 2003, 422 (6933): 675-676. 10.1038/422675a.
Cramer T, Yamanishi Y, Clausen BE, Forster I, Pawlinski R, Mackman N, Haase VH, Jaenisch R, Corr M, Nizet V, et al: HIF-1alpha is essential for myeloid cell-mediated inflammation. Cell. 2003, 112 (5): 645-657. 10.1016/S0092-8674(03)00154-5.
Cramer T, Johnson RS: A novel role for the hypoxia inducible transcription factor HIF-1alpha: critical regulation of inflammatory cell function. Cell Cycle. 2003, 2 (3): 192-193.
Giatromanolaki A, Sivridis E, Maltezos E, Papazoglou D, Simopoulos C, Gatter KC, Harris AL, Koukourakis MI: Hypoxia inducible factor 1alpha and 2alpha overexpression in inflammatory bowel disease. J Clin Pathol. 2003, 56 (3): 209-213. 10.1136/jcp.56.3.209.
Chen LW, Egan L, Li ZW, Greten FR, Kagnoff MF, Karin M: The two faces of IKK and NF-kappaB inhibition: prevention of systemic inflammation but increased local injury following intestinal ischemia-reperfusion. Nat Med. 2003, 9 (5): 575-581. 10.1038/nm849.
Ostrowski RP, Colohan AR, Zhang JH: Mechanisms of hyperbaric oxygen-induced neuroprotection in a rat model of subarachnoid hemorrhage. J Cereb Blood Flow Metab. 2005, 25 (5): 554-571. 10.1038/sj.jcbfm.9600048.
Krieg RE, Wolcott JH, Meyers WM: Mycobacterium ulcerans infection: treatment with rifampin, hyperbaric oxygenation, and heat. Aviat Space Environ Med. 1979, 50 (9): 888-892.
Krieg RE, Wolcott JH, Confer A: Treatment of Mycobacterium ulcerans infection by hyperbaric oxygenation. Aviat Space Environ Med. 1975, 46 (10): 1241-1245.
Alleva R, Nasole E, Di Donato F, Borghi B, Neuzil J, Tomasetti M: alpha-Lipoic acid supplementation inhibits oxidative damage, accelerating chronic wound healing in patients undergoing hyperbaric oxygen therapy. Biochem Biophys Res Commun. 2005, 333 (2): 404-410. 10.1016/j.bbrc.2005.05.119.
Ozden TA, Uzun H, Bohloli M, Toklu AS, Paksoy M, Simsek G, Durak H, Issever H, Ipek T: The effects of hyperbaric oxygen treatment on oxidant and antioxidants levels during liver regeneration in rats. Tohoku J Exp Med. 2004, 203 (4): 253-265. 10.1620/tjem.203.253.
Gregorevic P, Lynch GS, Williams DA: Hyperbaric oxygen modulates antioxidant enzyme activity in rat skeletal muscles. Eur J Appl Physiol. 2001, 86 (1): 24-27. 10.1007/s004210100503.
Nie H, Xiong L, Lao N, Chen S, Xu N, Zhu Z: Hyperbaric oxygen preconditioning induces tolerance against spinal cord ischemia by upregulation of antioxidant enzymes in rabbits. J Cereb Blood Flow Metab. 2006, 26 (5): 666-674. 10.1038/sj.jcbfm.9600221.
Sharifi M, Fares W, Abdel-Karim I, Koch JM, Sopko J, Adler D: Usefulness of hyperbaric oxygen therapy to inhibit restenosis after percutaneous coronary intervention for acute myocardial infarction or unstable angina pectoris. Am J Cardiol. 2004, 93 (12): 1533-1535. 10.1016/j.amjcard.2004.03.009.
Speit G, Dennog C, Eichhorn U, Rothfuss A, Kaina B: Induction of heme oxygenase-1 and adaptive protection against the induction of DNA damage after hyperbaric oxygen treatment. Carcinogenesis. 2000, 21 (10): 1795-1799. 10.1093/carcin/21.10.1795.
Rothfuss A, Radermacher P, Speit G: Involvement of heme oxygenase-1 (HO-1) in the adaptive protection of human lymphocytes after hyperbaric oxygen (HBO) treatment. Carcinogenesis. 2001, 22 (12): 1979-1985. 10.1093/carcin/22.12.1979.
Rothfuss A, Speit G: Investigations on the mechanism of hyperbaric oxygen (HBO)-induced adaptive protection against oxidative stress. Mutat Res. 2002, 508 (1-2): 157-165. 10.1016/S0027-5107(02)00213-0.
Rockswold SB, Rockswold GL, Zaun DA, Zhang X, Cerra CE, Bergman TA, Liu J: A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury. J Neurosurg. 2010, 112 (5): 1080-1094. 10.3171/2009.7.JNS09363.
Gutsaeva DR, Suliman HB, Carraway MS, Demchenko IT, Piantadosi CA: Oxygen-induced mitochondrial biogenesis in the rat hippocampus. Neuroscience. 2006, 137 (2): 493-504. 10.1016/j.neuroscience.2005.07.061.
Kurt B, Kurt Y, Karslioglu Y, Topal T, Erdamar H, Korkmaz A, Turkozkan N, Yaman H, Odabasi Z, Gunhan O: Effects of hyperbaric oxygen on energy production and xanthine oxidase levels in striated muscle tissue of healthy rats. J Clin Neurosci. 2008, 15 (4): 445-450. 10.1016/j.jocn.2007.01.010.
Calvert JW, Zhang JH: Oxygen treatment restores energy status following experimental neonatal hypoxia-ischemia. Pediatr Crit Care Med. 2007, 8 (2): 165-173. 10.1097/01.PCC.0000257113.75488.84.
Rossignol DA: The use of hyperbaric oxygen therapy in autism. Hyperbaric Oxygen For Neurological Disorders. Edited by: Zhang JH. 2008, Flagstaff: Best Publishing Company, 209-258.
Van Dyke K: Hyperbaric oxygen therapy (HBOT) for autism: an introduction. Autism File. 2009, 33: 5-6.
Harch PG, Andrews SR, Fogarty EF, Amen D, Pezzullo JC, Lucarini J, Aubrey C, Taylor DV, Staab PK, Van Meter KW: A phase I study of low-pressure hyperbaric oxygen therapy for blast-induced post-concussion syndrome and post-traumatic stress disorder. J Neurotrauma. 2012, 29 (1): 168-185. 10.1089/neu.2011.1895.
Rossignol DA, Rossignol LW, James SJ, Melnyk S, Mumper E: The effects of hyperbaric oxygen therapy on oxidative stress, inflammation, and symptoms in children with autism: an open-label pilot study. BMC Pediatr. 2007, 7 (1): 36-10.1186/1471-2431-7-36.
Rossignol DA, Rossignol LW, Smith S, Schneider C, Logerquist S, Usman A, Neubrander J, Madren EM, Hintz G, Grushkin B, et al: Hyperbaric treatment for children with autism: a multicenter, randomized, double-blind, controlled trial. BMC Pediatr. 2009, 9: 21-10.1186/1471-2431-9-21.
Stoller KP: Quantification of neurocognitive changes before, during, and after hyperbaric oxygen therapy in a case of fetal alcohol syndrome. Pediatrics. 2005, 116 (4): e586-591. 10.1542/peds.2004-2851.
The author treats individuals with HBOT in his clinical practice and derives revenue from this. He has previously received research funding from the International Hyperbarics Association (IHA) for two studies of hyperbaric treatment in children with autism [120, 121] and is a medical advisor (unpaid) for IHA.
Authors’ original submitted files for images
Below are the links to the authors’ original submitted files for images.
About this article
Cite this article
Rossignol, D.A. Hyperbaric oxygen treatment for inflammatory bowel disease: a systematic review and analysis. Med Gas Res 2, 6 (2012). https://doi.org/10.1186/2045-9912-2-6