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
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 , 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 . The aim of our observation is to prove that HBOT therapy may be an effective adjuvant therapy for fistulising Crohn's Disease (CD).
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.
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.
Patient No. Age/Sex CDAI CRP (mg/l) Fecal calprotectin (μg/g) MRI E I E IV E I E IV E I E IV E I E IV 1 26/M 71 31 15.4 37.3 119 179 Active Active/Regression 2* 40/W 179 110 1 1.1 >1800 964 Active Active 3* 31/M 40 78 1 $<1.6$ 227 63 Active Active/Regression 4 36/W 60 94 4 4 880 121 Active Active/Regression 5 21/W 169 113 19.9 15.7 614 275 Active Active 6* 28/M 352 78 51.8 1.4 831 429 Active active/Regression 7 19/M 340 97 5.4 7.3 831 >1000 Active Active/Regression
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.
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