Mapping the morbidity and mortality of Chagas disease in an endemic area in Brazil.

Chagas disease is among the 21 neglected diseases according to the World Health Organization. This study aimed to investigate the morbidity and mortality distribution of Chagas disease for identifying areas with greater prevalences and deaths of the disease in Northeast Brazil. A population-based ecological study was performed from 2016 to 2018 using data on acute Chagas disease patients from the Disease Notification Information System, chronic cases from the Chagas Disease and the referral Heart Failure Outpatient Clinic in Pernambuco, and Chagas disease-related mortality from the Mortality Information System. The unit of analysis were Pernambuco State mesoregions. The indicators were spatialized into thematic maps on the occurrence and mortality of the disease per 100,000 inhabitants. No cases of acute disease were reported in the period analyzed. Data on 801 chronic Chagas disease patients were analyzed. The population showed an average age of 62 years, with female predominance. The most prevalent comorbidity was systemic arterial hypertension and cardiologic involvement without ventricular dysfunction. The average chronic disease occurrence rate was 3.2/ 100,000 people/ year. As for deaths in the mortality system; in total, 350 deaths were recorded, showing male predominance, age ≥ 60 years, and chronic disease with cardiac involvement as the main mortality cause. The annual average mortality proportion was 1.6/100,000 people. The chronic case distribution showed spatial heterogeneity, with the highest rates of chronic disease and deaths observed in two mesoregions, with the main cause of death being heart-related. This highlights the need for more specialized services in areas with higher burden of the disease to avoid delay in the patients' care.

Mapping the morbidity and mortality of Chagas disease in an endemic area in Brazil

ABSTRACT Chagas disease is among the 21 neglected diseases according to the World Health Organization. This study aimed to investigate the morbidity and mortality distribution of Chagas disease for identifying areas with greater prevalences and deaths of the disease in Northeast Brazil. A population-based ecological study was performed from 2016 to 2018 using data on acute Chagas disease patients from the Disease Notification Information System, chronic cases from the Chagas Disease and the referral Heart Failure Outpatient Clinic in Pernambuco, and Chagas disease-related mortality from the Mortality Information System. The unit of analysis were Pernambuco State mesoregions. The indicators were spatialized into thematic maps on the occurrence and mortality of the disease per 100,000 inhabitants. No cases of acute disease were reported in the period analyzed. Data on 801 chronic Chagas disease patients were analyzed. The population showed an average age of 62 years, with female predominance. The most prevalent comorbidity was systemic arterial hypertension and cardiologic involvement without ventricular dysfunction. The average chronic disease occurrence rate was 3.2/ 100,000 people/ year. As for deaths in the mortality system; in total, 350 deaths were recorded, showing male predominance, age ≥ 60 years, and chronic disease with cardiac involvement as the main mortality cause. The annual average mortality proportion was 1.6/100,000 people. The chronic case distribution showed spatial heterogeneity, with the highest rates of chronic disease and deaths observed in two mesoregions, with the main cause of death being heart-related. This highlights the need for more specialized services in areas with higher burden of the disease to avoid delay in the patients' care.

Influence of Angiotensin-converting Enzyme Insertion/Deletion Gene Polymorphism in Progression of Chagas Heart Disease.

INTRODUCTION: Chagas disease (CD) is a neglected disease caused by the parasite Trypanosoma cruzi. One-third of infected patients will develop the cardiac form, which may progress to heart failure (HF). However, the factors that determine disease progression remain unclear. Increased angiotensin II activity is a key player in the pathophysiology of HF. A functional polymorphism of the angiotensin-converting enzyme (ACE) gene is associated with plasma enzyme activity. In CD, ACE inhibitors have beneficial effects supporting the use of this treatment in chagasic cardiomyopathy. METHODS: We evaluated the association of ACE I/D polymorphism with HF, performing a case-control study encompassing 343 patients with positive serology for CD staged as non-cardiomyopathy (stage A; 100), mild (stage B1; 144), and severe (stage C; 99) forms of Chagas heart disease. For ACE I/D genotyping by PCR, groups were compared using unconditional logistic regression analysis and adjusted for nongenetic covariates: age, sex, and trypanocidal treatment. RESULTS: A marginal, but not significant (p=0.06) higher prevalence of ACE I/D polymorphism was observed in patients in stage C compared with patients in stage A. Patients in stage C (CD with HF), were compared with patients in stages A and B1 combined into one group (CD without HF); DD genotype/D carriers were prevalent in the HF patients (OR = 2; CI = 1.013.96; p = 0.04). CONCLUSIONS: Our results of this cohort study, comprising a population from the Northeast region of Brazil, suggest that ACE I/D polymorphism is more prevalent in the cardiac form of Chagas disease with HF.

Influence of Angiotensin-converting Enzyme Insertion/Deletion Gene Polymorphism in Progression of Chagas Heart Disease

Abstract INTRODUCTION: Chagas disease (CD) is a neglected disease caused by the parasite Trypanosoma cruzi. One-third of infected patients will develop the cardiac form, which may progress to heart failure (HF). However, the factors that determine disease progression remain unclear. Increased angiotensin II activity is a key player in the pathophysiology of HF. A functional polymorphism of the angiotensin-converting enzyme (ACE) gene is associated with plasma enzyme activity. In CD, ACE inhibitors have beneficial effects supporting the use of this treatment in chagasic cardiomyopathy. METHODS: We evaluated the association of ACE I/D polymorphism with HF, performing a case-control study encompassing 343 patients with positive serology for CD staged as non-cardiomyopathy (stage A; 100), mild (stage B1; 144), and severe (stage C; 99) forms of Chagas heart disease. For ACE I/D genotyping by PCR, groups were compared using unconditional logistic regression analysis and adjusted for nongenetic covariates: age, sex, and trypanocidal treatment. RESULTS: A marginal, but not significant (p=0.06) higher prevalence of ACE I/D polymorphism was observed in patients in stage C compared with patients in stage A. Patients in stage C (CD with HF), were compared with patients in stages A and B1 combined into one group (CD without HF); DD genotype/D carriers were prevalent in the HF patients (OR = 2; CI = 1.013.96; p = 0.04). CONCLUSIONS: Our results of this cohort study, comprising a population from the Northeast region of Brazil, suggest that ACE I/D polymorphism is more prevalent in the cardiac form of Chagas disease with HF.

Expression of co-stimulatory molecules CD80 and CD86 is altered in CD14 + HLA-DR + monocytes from patients with Chagas disease following induction by Trypanosoma cruzi recombinant antigens.

INTRODUCTION: The relationships between monocytes and lymphocytes through MHC class II molecules and costimulatory, are of utmost importance for the production of an efficient immune response. In this work, we assessed the expression of surface molecules CD80 and CD86 on CD14+HLA-DR+ monocytes from patients with Chagas disease. METHODS:: The study population consisted of 31 patients with chronic clinical forms of Chagas disease. Patient blood samples were cultured in the presence of recombinant cytoplasmic repetitive antigen (CRA) and flagellar repetitive antigen (FRA). RESULTS:: We found considerable differences in the expression profile of surface molecules involved in antigen presentation. CONCLUSIONS:: CRA and FRA may contribute to host immune response evasion by Trypanozoma cruzi.