Hyperbaric Oxygen Therapy Counters Oxidative Stress/Inflammation-Driven Symptoms in Long COVID-19 Patients: Preliminary Outcomes

Abstract

Long COVID-19 patients show systemic inflammation and persistent symptoms such as fatigue and malaise, profoundly affecting their quality of life. Since improving oxygenation can oppose inflammation at multiple tissue levels, we hypothesized that hyperbaric oxygen therapy (HBOT) could arrest inflammation progression and thus relieve symptoms of COVID-19. We evaluated oxy-inflammation biomarkers in long COVID-19 subjects treated with HBOT and monitored with non-invasive methods. Five subjects (two athletes and three patients with other comorbidities) were assigned to receive HBOT: 100% inspired O₂ at 2.4 ATA in a multiplace hyperbaric chamber for 90 min (three athletes: 15 HBOT × 5 days/wk for 3 weeks; two patients affected by Idiopathic Sudden Sensorineural Hearing Loss: 30 HBOT × 5 days/wk for 6 weeks; and one patient with osteomyelitis: 30 HBOT × 5 days/wk for week for 6 weeks and, after a 30-day break, followed by a second cycle of 20 HBOT). Using saliva and/or urine samples, reactive oxygen species (ROS), antioxidant capacity, cytokines, lipids peroxidation, DNA damage, and renal status were assessed at T1_pre (basal level) and at T2_pre (basal level after treatment), and the results showed attenuated ROS production, lipid peroxidation, DNA damage, NO metabolites, and inflammation biomarker levels, especially in the athletes post-treatment. Thus, HBOT may represent an alternative non-invasive method for treating long COVID-19-induced long-lasting manifestations of oxy-inflammation.

Keywords: Electron Paramagnetic Resonance; HBOT; inflammation; long COVID-19; non-invasive methods; oxidative stress; reactive oxygen species; saliva; urine.

Figure 1

HBOT Experimental study design of working protocol with timeline of sample collection.

Figure 2

Effect of HBOT on oxidative stress in athletes and patients. Histogram plot (mean ± SD) and single plot of (A) ROS production (μmol.min⁻¹), (C) antioxidant capacity (TAC), (E) lipid peroxidation (8-iso PGF2α), and (G) DNA oxidation (8-OH-dG) in athletes (white and blue bars) and (B,D,F,H) patients (white and grey bars).

Figure 3

Effect of HBOT on NO metabolites (NOx) in (A) athletes (white and blue bars) and (B) patients (white and grey bars). Data are mean ± SD.

Figure 4

Effect of HBOT on inflammation in athletes and patients. Histogram plot (mean ± SD) and single plot of (A) IL-6, (C) TNF-α, and (E) IL-1β in athletes (white and blue bars) and (B,D,F) patients (white and gray bars).

Figure 5

Effect of HBOT on renal function in athletes and patients. Histogram plot (mean ± SD) and single plot of (A) creatinine, (C) neopterin, and (E) uric Acid in athletes (white and blue bars) and (B,D,F) patients (white and gray bars).

Figure 6

Significant effect of HBOT on biomarkers in all examined subjects. Histogram plot (mean ± SD) of (A) ROS production, (B) 8-iso PGF2α, and (C) NOx (collected at T1 and T2 pre-HBOT treatments). * p < 0.05 indicated a significant difference.