A Kallick Charles
Rush University Medical Center, Chicago, Illinois, USA.
Med Hypothesis Discov Innov Ophthalmol. 2012 Summer;1(2):33-6.
In the United States, 20,000 patients each year lose their sight from diabetic retinopathy. The cause has been attributed to a failure of control of glucose levels. Recent studies have challenged this, and have suggested that there is no evidence for a consistent glycemic threshold in various populations relating to the incidence of retinopathy. The Ehrlichia have been recently suggested as having a role in diabetes. The action of this obligate parasitic bacterium which often affects the cells involved in immunity has the potential of affecting various tissues randomly. This includes self-reactive T or B cells which may be erroneously altered or released from the marrow because of infection of marrow precursors by an Ehrlichia. The discovery of a gene obtained by molecular methodology from a leukemia patient, has given us a tool to identify by molecular methods, the presence of this gene and assumed bacterium in the blood of patients with various syndromes that includes diabetes. Because of the inconsistent evidence of a uniform glycemic threshold in retinopathy and the failure of its control, this hypothesis raises the question of something else that might be causing this damage. The suspected bacterium in diabetes may have as a significant side effect of its infection of the immune system, specifically the site of action of damage to the small vessels of the retina which could lead to what is regularly described in retinopathy; further, and that may include damage to other vessels seen in peripheral and coronary arteries. The availability of a molecular test in whole blood specimens from diabetics suggests a survey for the gene of the bacterium described in diabetic patients and matched controls. Such an investigation could lead to other therapies directed against the bacterium's presence in the marrow if discovered, and strategies to eliminate the harmful self-reactive T or B cells, if found in diabetes.
在美国,每年有2万名患者因糖尿病性视网膜病变而失明。病因一直被归咎于血糖水平控制不佳。最近的研究对此提出了质疑,并表明没有证据表明在不同人群中存在与视网膜病变发病率相关的一致血糖阈值。最近有人提出埃立克体在糖尿病中起作用。这种专性寄生细菌的作用通常会影响参与免疫的细胞,有可能随机影响各种组织。这包括自身反应性T细胞或B细胞,由于骨髓前体细胞被埃立克体感染,它们可能会被错误地改变或从骨髓中释放出来。通过分子方法从一名白血病患者身上获得的一种基因的发现,为我们提供了一种通过分子方法来识别该基因以及假定细菌在包括糖尿病在内的各种综合征患者血液中存在情况的工具。由于视网膜病变中血糖阈值统一的证据不一致以及血糖控制不佳,这一假说提出了可能导致这种损害的其他因素的问题。糖尿病中疑似的细菌可能因其对免疫系统的感染而产生重大副作用,特别是对视网膜小血管的损伤作用部位,这可能导致视网膜病变中经常描述的情况;此外,这可能还包括对在周围动脉和冠状动脉中看到的其他血管的损伤。对糖尿病患者全血标本进行分子检测的可行性表明,应对糖尿病患者和匹配对照组中所述细菌的基因进行调查。这样的调查可能会导致针对如果发现细菌在骨髓中的存在而采取的其他治疗方法,以及如果在糖尿病中发现有害的自身反应性T细胞或B细胞则采取消除它们的策略。