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-
1.
Rassi A, Marin-Neto JA, 2010. Chagas disease. Lancet 375: 1388–1402.
-
2.
Moncayo A, 2003. Chagas disease: current epidemiological trends after the interruption of vectorial and transfusional transmission in the Southern Cone countries. Mem Inst Oswaldo Cruz 98: 577–591.
-
3.
Luz PR, Miyazaki MI, Chiminacio Neto N, Padeski MC, Barros ACM, Boldt ABW, Messias-Reason IJ, 2016. Genetically determined MBL deficiency is associated with protection against chronic cardiomyopathy in Chagas disease. PLoS Negl Trop Dis 10: e0004257.
-
4.
Turner M, 2003. The role of mannose-binding lectin in health and disease. Mol Immunol 40: 423–429.
-
5.
Jack DL, Klein NJ, Turner MW, 2001. Mannose-binding lectin: targeting the microbial world for complement attack and opsonophagocytosis. Immunol Rev 180: 86–99.
-
6.
Jensenius H, Klein DCG, van Hecke M, Oosterkamp TH, Schmidt T, Jensenius JC, 2009. Mannan-binding lectin: structure, oligomerization, and flexibility studied by atomic force microscopy. J Mol Biol 391: 246–259.
-
7.
Rassi A, Marcondes de Rezende J, 2012. American trypanosomiasis (Chagas disease). Infect Dis Clin North Am 26: 275–291.
-
8.
WHO. Chagas Disease (American trypanosomiasis). Geneva, Switzerland: World Health Organization. Available at: http://www.who.int/mediacentre/factsheets/fs340/en/. Accessed June 13, 2015.
-
9.
Pereira KS, Schmidt FL, Guaraldo AMA, Franco RMB, Dias VL, Passos LAC, 2009. Chagas’ disease as a foodborne illness. J Food Prot 72: 441–446.
-
10.
Malik LH, Singh GD, Amsterdam EA, 2015. Chagas heart disease: an update. Am J Med 128: 1251.e7–1251.e9.
-
11.
Moncayo A, Silveira AC, 2009. Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy. Mem Inst Oswaldo Cruz 104 (Suppl): 17–30.
-
12.
Bern C, Montgomery SP, 2009. An estimate of the burden of Chagas disease in the United States. Clin Infect Dis 49: e52–e54.
-
13.
Benziger CP, do Carmo GAL, Ribeiro ALP, 2017. Chagas cardiomyopathy. Cardiol Clin 35: 31–47.
-
14.
Cantey PT et al. 2012. The United States Trypanosoma cruzi Infection Study: evidence for vector-borne transmission of the parasite that causes Chagas disease among United States blood donors. Transfusion 52: 1922–1930.
-
15.
Ribeiro AL, Nunes MP, Teixeira MM, Rocha MOC, 2012. Diagnosis and management of Chagas disease and cardiomyopathy. Nat Rev Cardiol 9: 576–589.
-
16.
Rassi A, Little WC, 2000. Chagas’ heart disease. Clin Cardiol 23: 883–889.
-
17.
Malik LH, Singh GD, Amsterdam EA, 2015. The epidemiology, clinical manifestations, and management of Chagas heart disease. Clin Cardiol 38: 565–569.
-
18.
Roberts A, Kemp C, 2005. Chagas’ disease (American trypanosomiasis). J Am Acad Nurse Pract 13: 152–153.
-
19.
Luz PR, Miyazaki MI, Neto NC, Nisihara RM, Messias-Reason IJ, 2010. High levels of mannose-binding lectin are associated with the risk of severe cardiomyopathy in chronic Chagas Disease. Int J Cardiol 143: 448–450.
-
20.
Cestari I dos S, Krarup A, Sim RB, Inal JM, Ramirez MI, 2009. Role of early lectin pathway activation in the complement-mediated killing of Trypanosoma cruzi. Mol Immunol 47: 426–437.
-
21.
Beltrame MH, Boldt ABW, Catarino SJ, Mendes HC, Boschmann SE, Goeldner I, Messias-Reason I, 2015. MBL-associated serine proteases (MASPs) and infectious diseases. Mol Immunol 67: 85–100.
-
22.
Dutra WO, Rocha MOC, Teixeira MM, 2005. The clinical immunology of human Chagas disease. Trends Parasitol 21: 581–587.
-
23.
Luz PR, Boldt ABW, Grisbach C, Kun JFJ, Velavan TP, Messias-Reason IJT, 2013. Association of L-ficolin levels and FCN2 genotypes with chronic Chagas disease. PLoS One 8: e60237.
-
24.
Boldt ABW, Luz PR, Messias-Reason IJT, 2011. MASP2 haplotypes are associated with high risk of cardiomyopathy in chronic Chagas disease. Clin Immunol 140: 63–70.
-
25.
Lidani KCF, Beltrame MH, Luz PR, Sandri TL, Nisihara RM, de Messias-Reaso IJ, 2015. Is pentraxin 3 a cardiovascular marker in patients with chronic Chagas disease? Int J Cardiol 190: 233–235.
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Case Report: High Mannose-Binding Lectin Serum Determined by MBL2 Genotype and Risk for Clinical Progression to Chagasic Cardiomyopathy: A Case Report of Three Patients
Kárita Cláudia Freitas Lidani
Kárita Cláudia Freitas Lidani
Laboratory of Molecular Immunopathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil
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Fabiana Antunes Andrade
Fabiana Antunes Andrade
Laboratory of Molecular Immunopathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil
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Ronaldo Kiviatcoski Kozlowski
Ronaldo Kiviatcoski Kozlowski
Laboratory of Molecular Immunopathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil
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Paola Rosa Luz
Paola Rosa Luz
Laboratory of Molecular Immunopathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil
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Iara J. Messias-Reason
Iara J. Messias-Reason
Laboratory of Molecular Immunopathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil
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Chagas disease (CD), caused by infection with the parasite Trypanosoma cruzi, leads to severe cardiomyopathy in 20–30% of patients, whereas the remainder may stay asymptomatic and never develop cardiomyopathy or other clinical manifestations. The underlying cause for this variable outcome is not fully characterized, although previous studies have found high levels of circulating mannose-binding lectin (MBL) to be associated with cardiac failure echocardiographic changes. We report three indeterminate (asymptomatic) chronic Chagas patients who were followed up for 10 years. Two of these patients developed chronic chagasic cardiomyopathy (CCC) during this follow-up period and, when genotyped, were found to be carriers of the high MBL producer HYPA/HYPA genotype, suggesting that genetically determined high MBL serum might be associated with the risk of CCC development. These results suggest the use of MBL quantification and MBL2 genotyping as tools for clinical assessment in patients with chronic CD.
Author Notes
These authors contributed equally to this work.
Financial support: This work was supported by research grants from Coordenação de Aperfeiçoamento de Pessoal Superior (CAPES Edital Parasitologia Básica 32/2010) and Fundação Araucária (PPSUS-01/2016).
Conflict of interest: All authors read and approved the final version of the manuscript and declare that they have no conflicts of interest. Written consent was obtained from the patients to publish their cases.
Authors’ addresses: Kárita Cláudia Freitas Lidani, Fabiana Antunes Andrade, Ronaldo Kiviatcoski Kozlowski, and Paola Rosa Luz, Department of Medical Pathology, Universidade Federal do Parana Hospital de Clinicas, Curitiba, Brazil, E-mails: kari.lidani@gmail.com, fabiana.una@gmail.com, ronaldo.koki@gmail.com, and pazinha.bio@gmail.com. Iara J. Messias-Reason, Department of Immunopathology, Hospital de Clinicas, Curitiba, Brazil, E-mail: iaramessias@yahoo.com.br.
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
EndNote
-
1.
Rassi A, Marin-Neto JA, 2010. Chagas disease. Lancet 375: 1388–1402.
-
2.
Moncayo A, 2003. Chagas disease: current epidemiological trends after the interruption of vectorial and transfusional transmission in the Southern Cone countries. Mem Inst Oswaldo Cruz 98: 577–591.
-
3.
Luz PR, Miyazaki MI, Chiminacio Neto N, Padeski MC, Barros ACM, Boldt ABW, Messias-Reason IJ, 2016. Genetically determined MBL deficiency is associated with protection against chronic cardiomyopathy in Chagas disease. PLoS Negl Trop Dis 10: e0004257.
-
4.
Turner M, 2003. The role of mannose-binding lectin in health and disease. Mol Immunol 40: 423–429.
-
5.
Jack DL, Klein NJ, Turner MW, 2001. Mannose-binding lectin: targeting the microbial world for complement attack and opsonophagocytosis. Immunol Rev 180: 86–99.
-
6.
Jensenius H, Klein DCG, van Hecke M, Oosterkamp TH, Schmidt T, Jensenius JC, 2009. Mannan-binding lectin: structure, oligomerization, and flexibility studied by atomic force microscopy. J Mol Biol 391: 246–259.
-
7.
Rassi A, Marcondes de Rezende J, 2012. American trypanosomiasis (Chagas disease). Infect Dis Clin North Am 26: 275–291.
-
8.
WHO. Chagas Disease (American trypanosomiasis). Geneva, Switzerland: World Health Organization. Available at: http://www.who.int/mediacentre/factsheets/fs340/en/. Accessed June 13, 2015.
-
9.
Pereira KS, Schmidt FL, Guaraldo AMA, Franco RMB, Dias VL, Passos LAC, 2009. Chagas’ disease as a foodborne illness. J Food Prot 72: 441–446.
-
10.
Malik LH, Singh GD, Amsterdam EA, 2015. Chagas heart disease: an update. Am J Med 128: 1251.e7–1251.e9.
-
11.
Moncayo A, Silveira AC, 2009. Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy. Mem Inst Oswaldo Cruz 104 (Suppl): 17–30.
-
12.
Bern C, Montgomery SP, 2009. An estimate of the burden of Chagas disease in the United States. Clin Infect Dis 49: e52–e54.
-
13.
Benziger CP, do Carmo GAL, Ribeiro ALP, 2017. Chagas cardiomyopathy. Cardiol Clin 35: 31–47.
-
14.
Cantey PT et al. 2012. The United States Trypanosoma cruzi Infection Study: evidence for vector-borne transmission of the parasite that causes Chagas disease among United States blood donors. Transfusion 52: 1922–1930.
-
15.
Ribeiro AL, Nunes MP, Teixeira MM, Rocha MOC, 2012. Diagnosis and management of Chagas disease and cardiomyopathy. Nat Rev Cardiol 9: 576–589.
-
16.
Rassi A, Little WC, 2000. Chagas’ heart disease. Clin Cardiol 23: 883–889.
-
17.
Malik LH, Singh GD, Amsterdam EA, 2015. The epidemiology, clinical manifestations, and management of Chagas heart disease. Clin Cardiol 38: 565–569.
-
18.
Roberts A, Kemp C, 2005. Chagas’ disease (American trypanosomiasis). J Am Acad Nurse Pract 13: 152–153.
-
19.
Luz PR, Miyazaki MI, Neto NC, Nisihara RM, Messias-Reason IJ, 2010. High levels of mannose-binding lectin are associated with the risk of severe cardiomyopathy in chronic Chagas Disease. Int J Cardiol 143: 448–450.
-
20.
Cestari I dos S, Krarup A, Sim RB, Inal JM, Ramirez MI, 2009. Role of early lectin pathway activation in the complement-mediated killing of Trypanosoma cruzi. Mol Immunol 47: 426–437.
-
21.
Beltrame MH, Boldt ABW, Catarino SJ, Mendes HC, Boschmann SE, Goeldner I, Messias-Reason I, 2015. MBL-associated serine proteases (MASPs) and infectious diseases. Mol Immunol 67: 85–100.
-
22.
Dutra WO, Rocha MOC, Teixeira MM, 2005. The clinical immunology of human Chagas disease. Trends Parasitol 21: 581–587.
-
23.
Luz PR, Boldt ABW, Grisbach C, Kun JFJ, Velavan TP, Messias-Reason IJT, 2013. Association of L-ficolin levels and FCN2 genotypes with chronic Chagas disease. PLoS One 8: e60237.
-
24.
Boldt ABW, Luz PR, Messias-Reason IJT, 2011. MASP2 haplotypes are associated with high risk of cardiomyopathy in chronic Chagas disease. Clin Immunol 140: 63–70.
-
25.
Lidani KCF, Beltrame MH, Luz PR, Sandri TL, Nisihara RM, de Messias-Reaso IJ, 2015. Is pentraxin 3 a cardiovascular marker in patients with chronic Chagas disease? Int J Cardiol 190: 233–235.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 605 | 535 | 23 |
| Full Text Views | 1024 | 8 | 0 |
| PDF Downloads | 117 | 10 | 0 |