Kaplan E L
Department of Pediatrics, University of Minnesota Medical School, Minneapolis 55455.
Postgrad Med J. 1992;68 Suppl 1:S21-3.
Although the relationship between group A streptococcal upper respiratory tract infection and the development of acute rheumatic fever has been known for many years, the pathogenetic mechanism(s) have never been defined. Thus, the mechanism of damage to the valves and to the myocardium in patients with rheumatic fever remains unexplained. Traditionally, emphasis has been placed on the valvular damage in rheumatic heart disease, but there is considerable evidence for myocardial involvement. An abnormal immune response to some as yet unrecognized somatic or extracellular antigen of the group A streptococcus is probably related to the cardiomyopathy. This abnormal immune response is supported by considerable clinical and experimental evidence. Recent studies have suggested other mechanism to explain the myocardial damage including the influx of lymphocytes into the area as well as the possibility of damage relating to generation of oxygen-free radicals. As more sophisticated molecular biological studies of the group A streptococcus become available, perhaps the mystery of this very unique and common cardiomyopathy can be resolved.
虽然A组链球菌引起的上呼吸道感染与急性风湿热的发展之间的关系已为人所知多年，但其发病机制尚未明确。因此，风湿热患者心脏瓣膜和心肌受损的机制仍无法解释。传统上，人们一直将重点放在风湿性心脏病的瓣膜损害上，但有大量证据表明心肌也会受累。对A组链球菌某些尚未识别的体细胞或细胞外抗原的异常免疫反应可能与心肌病有关。大量临床和实验证据支持这种异常免疫反应。最近的研究提出了其他机制来解释心肌损伤，包括淋巴细胞流入该区域以及与氧自由基产生相关的损伤可能性。随着对A组链球菌更复杂的分子生物学研究的开展，也许这种非常独特且常见的心肌病之谜能够得到解决。
