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P576 Could the hyperbaric oxygen therapy be an effective adjuvant therapy for fistulising Crohn's disease?

Piotrowicz G.*1, Kowerzanow J.2, Banaszkiewicz P.2, Babicki A.2, Kot J.3, Rydzewska G.4

1Self-Dependet Health Care Unit of Ministry of Iterior, Gastroenetrology, Gdansk, Poland 2Self-Dependent Health Care Unit of Ministry of Interior, Surgery, Gdansk, Poland 3UCMMiT, Clinic Hyperbaric Medicine and Sea Rescue, Gdynia, Poland 4Central Clinical Hospital of the Ministry of Interior of Warsaw, Gastroenterology, Warsaw, Poland

Background

Hyperbaric oxygen therapy (HBOT) is a treatment modality utilising 100% oxygen in a hyperbaric chamber, under increased pressure conditions. Blood hyperoxygenation provides better oxygen penetration into the tissues in accordance with the laws of physics [1], thereby reducing the inflammatory response by reducing the adhesion of leukocytes to the vascular endothelium of damaged tissues, reducing the production of Pro-Inflammatory Cytokines, stimulating angiogenesis, improving metabolism and antibacterial and antifungal action [2]. The aim of our observation is to prove that HBOT therapy may be an effective adjuvant therapy for fistulising Crohn's Disease (CD).

Methods

Observations were made in 7 patients with active perianal fistulising CD. Three patients (the first group) were in the course of biological therapy and immunomodulatory therapy, while the other four (the second group) were administered only standard immunomodulatory therapy. Both groups have undergone HBOT according to the following protocol: 30 session, 90 minutes each, with pressure of 2.5 standard atmosphere. Analysis of clinical disease activity was performed by means of CDAI scale, biomarkers (fecal calprotectin (FC), blood CRP) and imaging studies: endoscopy and magnetic resonance imaging (MRI) of the pelvis with contrast. Observational study was divided into 4 stages: stage I – prior to treatment, stage II-HBOT therapy, stage III-after completing the HBOT treatment, stage IV – 6 weeks after HBOT.

Regression of lesions confirmed in clinical evaluation and imaging studies was assigned as the end point.

Results

Analysis of the group of patients showed clinical improvement in CDAI in 2 out of 3 patients from the first group and in 3 out of 4 from the second group. Levels of FC decreased in all 3 patients form the first group and in 3 out of 4 from the second group, while the level of blood CRP decreased in one patient from the first group and one patient from the second group. Imaging studies (MRI, endoscopy) showed regression of lesions in 2 out of 3 patients from the first group and in 3 out of 4 patients from the the second group.

The summary of results is presented in Table 1.

Table 1

Patient No.Age/SexCDAICRP (mg/l)Fecal calprotectin (μg/g)MRI
E IE IVE IE IVE IE IVE IE IV
126/M713115.437.3119179ActiveActive/Regression
2*40/W17911011.1>1800964ActiveActive
3*31/M40781$<1.6$22763ActiveActive/Regression
436/W609444880121ActiveActive/Regression
521/W16911319.915.7614275ActiveActive
6*28/M3527851.81.4831429Activeactive/Regression
719/M340975.47.3831>1000ActiveActive/Regression

Conclusion

On the basis of the results recorded in both groups of assessed patients we can conclude that HBOT may be an effective way to support the treatment of CD by improving clinical improvement and significantly reducing the occurrence of inflammatory lesions in the imaging studies.

This is a preliminary report, as the study is ongoing.

References:

[1] Gow AJ et al. (2005), Nitric oxide, hemoglobin, and hypoxic vasodilation, Am J Respir Cell Mol Biol, 479–82

[2] Bismar K et al. (1997), Dose-dependent hyperbaric oxygen stimulation of human fibroblast proliferation, Wound Repair Regen, 147–50