The results presented here demonstrate the effectiveness of HBO2 in alleviating signs and symptoms of psoriasis in two patients. No adverse effects were reported during or after treatment with HBO2.
Leukocytes, cytokines, and keratinocyte growth or differentiation abnormalities are involved in psoriatic skin lesions. Psoriasis vulgaris is a T-cell-driven disease, with type I (interferon-γ-producing) T cells predominating in skin lesions [10
]. A lymphocytic infiltrate in psoriasis plaques consists of a mixture of activated CD4+
T cells; the latter predominate in lesional epidermis and CD4+
cells in the dermis [12
]. The therapeutic benefit of immunosuppressive drugs supports the view that activated T cells are pathogenic effectors of psoriasis [10
]. Dendritic cells are found in psoriatic skin lesions, producing interleukin (IL)-12 and IL-23. Cytokine changes in psoriatic lesions consist of elevated levels of interferon-γ, tumor necrosis factor (TNF)-α, numerous interleukins (such as IL-1, IL-2, IL-6, IL-8, IL-12, IL-17, and IL-19), and multiple chemokines (MIG/CXCL9, IP-10/CXCL10, I-TAC/CXCL11, and MIP3α/CCL20) [11
]. IL-12 p40 mRNA and expression of interferon-γ, inducible nitric oxide synthase, B7-1, and TNF-α are elevated in psoriatic tissue [11
]. A rheumatoid-like pattern has been identified as one of the most common types of psoriatic arthritis. Autoantibodies directed against nuclear antigens, cytokeratins, epidermal keratins, and heat shock proteins have also been reported in psoriatic arthritis.
suppresses the proliferation of macrophages and the formation of foam cells in atherosclerotic lesions [12
also intensifies the suppressive function of T lymphocytes, normalizes cell-bound immunity, and decreases the serum concentration in immune complexes [13
]. The immunosuppressive effects of HBO2
include suppression of autoimmune symptoms, decreased production of IL-1 and CD4+
cells, and increased percentage and absolute number of CD8+
]. In addition, long-term HBO2
exposure suppresses development of autoimmune symptoms such as proteinuria, facial erythema, and lymphadenopathy. HBO2
decreases the CD4:CD8 ratio and proliferation of lymphocytes, and activates neutrophils to migrate to regions of high oxygen tension [14
suppresses TNF-α production induced by lipopolysaccharide, lipid A, and phytohemagglutinin A [15
]. A marked decrease in IL-1 and IL-2 production, and a significant decrease in prostaglandin E2
production have been observed.
The positive clinical effects that HBO2
has in the treatment of chronic inflammation may relate to its effects on secretion of IL-1, IL-6, and TNF-α. The effects of HBO2
on prostaglandin, nitric oxide, and cytokines involved in wound pathophysiology and inflammation in particular were recently reviewed [8
]. That review indicates that HBO2
has important effects on the biology of cytokines and other mediators of inflammation. HBO2
causes downregulation of cytokines and upregulation of growth factors. It transiently suppresses stimulus-induced proinflammatory cytokine production and affects the liberation of TNF-α and endothelins. Vascular endothelial growth factor levels are significantly increased with HBO2
therapy, whereas levels of prostaglandin E2
and cyclo-oxygenase-2 mRNA are markedly reduced. Therefore, the anti-inflammatory and immunosuppressive properties of HBO2
might account for its efficacy in the cases presented here.
Patient 2 before treatment with hyperbaric oxygen (Side View Torso).
Patient 2 after treatment with hyperbaric oxygen (Side View Torso).
Patient 2 before treatment with hyperbaric oxygen (Side View Legs).
Patient 2 after treatment with hyperbaric oxygen (Side View Legs).