PDF(Pubmed)
Abstract：
Leprosy is a chronic infectious disease caused by the bacillus Mycobacterium leprae. The disease may evolve for inflammatory reactions, reversal reaction (RR) and erythema nodosum leprosum (ENL), the major cause of irreversible neuropathy in leprosy, which occur in 1 in 3 people with leprosy, even with effective treatment of M. leprae. Leprosy remains persistently endemic in our region where it predominantly affects lowest socioeconomic conditions people, as Toxoplasma gondii infection in the municipality studied. Previously, we have shown T. gondii coinfection as a risk marker for leprosy, mainly in its severe form. This present study assessed whether T. gondii infection is also a risk factor for leprosy reactions and the predictive value of immunoglobulin production prior to development of leprosy reactions. Patients with leprosy (n = 180), co-infected or not with T. gondii, had their serum investigated for levels of IgA, IgE, IgG1, IgG2, IgG3 and IgG4 anti-PGL-1 by ELISA prior to development of leprosy reactions. The serologic prevalence for T. gondii infection was 87.7% in leprosy reaction patients reaching 90.9% in those with ENL. The leprosy reaction risk increased in T. gondii seropositive individuals was two-fold ([OR] = 2.366; 95% confidence interval [CI 95%]: 1.024-5.469) higher than those seronegative, and considering the risk of ENL, this increase was even more evident (OR = 6.753; 95% CI: 1.050-72.85) in coinfected individuals. When evaluated the prediction of anti-PGL-1 immunoglobulin levels for development of leprosy reactions in patients coinfected or not with T. gondii, only the increase IgE levels were associated to occurrence of reactional episodes of leprosy, specifically ENL type, in patients coinfected with T. gondii, compared to those not coinfected or no reaction. Thus, the immunomodulation in co-parasitism T. gondii-M. leprae suggest increased levels of IgE as a biomarker for early detection of these acute inflammatory episodes and thereby help prevent permanent neuropathy and disability in leprosy patients.
摘要：
麻风病是由麻风分枝杆菌引起的慢性传染病。这种疾病可能演变为炎症反应，逆转反应（RR）和结节性麻风红斑（ENL），麻风病不可逆神经病的主要原因，发生在三分之一的麻风病患者中，即使是麻风分枝杆菌的有效治疗。麻风病在我们地区仍然持续流行，主要影响社会经济状况最低的人，作为该市弓形虫感染的研究。以前,我们已经证明弓形虫共感染是麻风病的风险标志，主要是严重的形式。本研究评估了弓形虫感染是否也是麻风病反应的危险因素，以及在麻风病反应发展之前免疫球蛋白产生的预测价值。麻风病患者（n=180），是否与弓形虫共感染，对他们的血清进行了IgA水平的调查，IgE,在麻风反应发生之前通过ELISA测定IgG1、IgG2、IgG3和IgG4抗PGL-1。麻风反应患者弓形虫感染的血清学患病率为87.7％，ENL患者为90.9％。弓形虫血清阳性个体的麻风病反应风险比血清阴性者高两倍（[OR]=2.366；95％置信区间[CI95％]：1.024-5.469），考虑到ENL的风险，在合并感染的个体中,这种增加更为明显(OR=6.753;95%CI:1.050-72.85).当评估抗PGL-1免疫球蛋白水平对合并感染或未感染弓形虫的患者麻风反应发展的预测时，只有IgE水平的升高与麻风病反应性发作的发生有关，特别是ENL类型，同时感染弓形虫的患者，与没有共感染或没有反应的人相比。因此，共寄生T.gondii-M.的免疫调节麻风病提示IgE水平升高可作为早期发现这些急性炎症发作的生物标志物,从而有助于预防麻风病患者的永久性神经病变和残疾.
