Plasmapheresis for Chagas’ diseaseChagas' disease is a chronic disease of the heart, struck more than 16 million people in the Americas and the resulting infection of the protozoan parasite Trypanosoma cruzi. After the acute phase of the disease, which is manifested esophageal bleeding, often 20-30 years revealed lesions of the esophagus (dilatation), colon (megacolon) and hearts with the development of inflammatory cardiomyopathy with severe dilatation of the cavities of the heart, congestive heart failure and death.
Histological examination revealed a diffuse myocarditis with degeneration of cardiomyocytes, combined with fibrosis, mononuclear infiltration and damage elements of the conduction system of the heart in the absence of parasites themselves [Mirkin GA et al., 1997]. These data suggest a large percentage of the probability of an autoimmune pathogenesis of this disease. Autoantibodies effect on G-protein receptors of the myocardium such as b-adrenoceptors and M2 acetylcholine receptor.
There is evidence of structural (antigen) closeness of immunodominant ribosomal protein of the parasite and b1 -adrenoceptor, indicating the potential for cross-molecular mimicry of the two proteins that make antibodies, naturally raised against this parasite, to respond in the future also the ownership structure of the heart muscle tissue [Elies R. et al., 1996; Engman D.M., Leon J.S., 2002; Leon J.S., Engman D.M., 2003; Cunha-Neto E. et al., 2006]. Thus, in addition to the myocardium, the antibodies developed against antigens of T. cruzi, is cross-react with antigens endothelium, neurons of the brain and cerebellum, peripheral nerve trunks.
This suggests that such "autoantibodies" actually have a heterogeneous nature, but react with autoantigens due to the proximity of the antigenic structure of the parasite and host. In this case, the usual "triple" therapy (azathioprine, prednisone and cyclosporine) is able to reactivate this chronic parasitic infection [Brener Z., Gazzinelli RT, 1997].
Keep in mind that the pathogen can be transmitted from mother to fetus, and in blood transfusions from infected donors. And, even in non-endemic regions of Ecuador and Bolivia, about one quarter of donors positive for the presence of T. cruzi. This parasite can be very long in human blood, regardless of their clinical condition, especially since the majority of those infected – are asymptomatic and may be in the ranks of donors. The incubation period of the disease lasts up to 114 days.
This disease can not be attributed only to the exotic species that infects people distant continents. Sick as a disease can our domestic tourists when visiting countries located between 400 North latitude (Texas) and 430 South latitude (Argentina) and immigrants from these regions, which in Italy alone there are about 80,000 people, and potentially infected with can be from 20.000 to 40.000 [Crovato F., Rebora A., 1997].
With so many details in favor of the autoimmune nature of myocardial lesion in Chagas' disease, can be considered as indication for plasmapheresis, because only in this case can be removed and autoantibodies, and a variety of toxic cytokines.