Long-term sleep apnea as a pathogenic factor for cell-mediated autoimmune disease

Previous medical literature has shown that cell injury from hypoxia, such as that induced by sleep apnea, leads to hyperuricemia. Furthermore, a recent study has shown that when hyperuricemia reaches sufficient concentration to precipitate as monosodium urate, a T-cell immune response is triggered. The frequent repetition of this cell injury and immune response over a prolonged time, as would occur with long-term sleep apnea, may lead to the development, continuation, or aggravation of autoimmune disease.

Long-term sleep apnea is hypothesized to be a pathogenic factor in the development of cell-mediated autoimmune disease. Several corollaries are presented along with this general hypothesis. First, some of the diseases associated with sleep apnea may have an autoimmune etiology. Second, some autoimmune diseases not usually recognized to be associated with sleep apnea may indeed have that association. Third, resolving sleep apnea in some patients with autoimmune disease to remove that autoimmune stimulus may aid in deceleration, halt, or even reversal of the progress of the autoimmune disease. Fourth, because monosodium urate also causes gouty arthritis in some individuals, diagnosis of gout may allow for resolution of sleep apnea early enough to prevent autoimmune development. Fifth, allopurinol, which suppresses uric acid generation, may be an effective therapy for the remission or prevention of a number of autoimmune diseases.

This hypothesis strengthens the evidence pointing to the danger of unresolved sleep apnea by a mechanism previously unrecognized, namely the risk of developing an autoimmune disease. As a result of this realization, new therapies may be adopted for the treatment and prevention of autoimmune disease, specifically, resolving sleep apnea and the use of allopurinol.