Abrams Burton
221 Linden Drive Elkins Park, PA 19027, USA.
Med Hypotheses. 2005;65(6):1024-7. doi: 10.1016/j.mehy.2005.05.046. Epub 2005 Aug 5.
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.
既往医学文献表明，缺氧所致的细胞损伤，如睡眠呼吸暂停引起的缺氧，会导致高尿酸血症。此外，最近一项研究显示，当高尿酸血症达到足够浓度以沉淀为尿酸钠时，会触发T细胞免疫反应。这种细胞损伤和免疫反应在较长时间内频繁重复出现，如长期睡眠呼吸暂停时发生的情况，可能会导致自身免疫性疾病的发生、持续或加重。
长期睡眠呼吸暂停被认为是细胞介导的自身免疫性疾病发生的致病因素。本一般假说还提出了几个推论。第一，一些与睡眠呼吸暂停相关的疾病可能有自身免疫病因。第二，一些通常不被认为与睡眠呼吸暂停相关的自身免疫性疾病可能确实存在这种关联。第三，在一些自身免疫性疾病患者中解决睡眠呼吸暂停以消除自身免疫刺激，可能有助于减缓、阻止甚至逆转自身免疫性疾病的进展。第四，由于尿酸钠在一些个体中也会导致痛风性关节炎，痛风的诊断可能使睡眠呼吸暂停得到足够早的解决，以预防自身免疫性疾病的发生。第五，抑制尿酸生成的别嘌醇可能是缓解或预防多种自身免疫性疾病的有效疗法。
这一假说通过一种先前未被认识的机制，即发生自身免疫性疾病的风险，强化了指向未解决的睡眠呼吸暂停危险性的证据。基于这一认识，可能会采用新的疗法来治疗和预防自身免疫性疾病，具体而言，解决睡眠呼吸暂停以及使用别嘌醇。
