Socioeconomic inequality in catastrophic health expenditure in Brazil

OBJECTIVE

To analyze the evolution of catastrophic health expenditure and the inequalities in such expenses, according to the socioeconomic characteristics of Brazilian families.

METHODS

Data from the National Household Budget 2002-2003 (48,470 households) and 2008-2009 (55,970 households) were analyzed. Catastrophic health expenditure was defined as excess expenditure, considering different methods of calculation: 10.0% and 20.0% of total consumption and 40.0% of the family’s capacity to pay. The National Economic Indicator and schooling were considered as socioeconomic characteristics. Inequality measures utilized were the relative difference between rates, the rates ratio, and concentration index.

RESULTS

The catastrophic health expenditure varied between 0.7% and 21.0%, depending on the calculation method. The lowest prevalences were noted in relation to the capacity to pay, while the highest, in relation to total consumption. The prevalence of catastrophic health expenditure increased by 25.0% from 2002-2003 to 2008-2009 when the cutoff point of 20.0% relating to the total consumption was considered and by 100% when 40.0% or more of the capacity to pay was applied as the cut-off point. Socioeconomic inequalities in the catastrophic health expenditure in Brazil between 2002-2003 and 2008-2009 increased significantly, becoming 5.20 times higher among the poorest and 4.17 times higher among the least educated.

CONCLUSIONS

There was an increase in catastrophic health expenditure among Brazilian families, principally among the poorest and those headed by the least-educated individuals, contributing to an increase in social inequality.     

Association of cardiovascular risk factors with the different presentations of acute coronary syndrome

OBJECTIVE:

to identify the relationship between different presentations of acute coronary syndrome and cardiovascular risk factors among hospitalized individuals.

METHOD:

cross-sectional study performed in a teaching hospital in São Paulo, in the State of São Paulo (SP). Socio-demographic, clinical and anthropometric data of 150 individuals hospitalized due to acute coronary syndrome were collected through interviews and review of clinical charts. Association between these data and the presentation of the syndrome were investigated.

RESULTS:

there was a predominance of ST segment elevation acute myocardial infarction. There was significant association of systemic hypertension with unstable angina and high values of low density lipoprotein with infarction, without influence from socio-demographic characteristics.

CONCLUSION:

arterial hypertension and high levels of low-density lipoprotein were associated with different presentations of coronary syndrome. The results can provide support for health professionals for secondary prevention programs aimed at behavioural changing.     

Impaired brain energy metabolism in the BACHD mouse model of Huntington's disease: critical role of astrocyte–neuron interactions

Huntington''s disease (HD) is caused by cytosine-adenine-guanine (CAG) repeat expansions in the huntingtin (Htt) gene. Although early energy metabolic alterations in HD are likely to contribute to later neurodegenerative processes, the cellular and molecular mechanisms responsible for these metabolic alterations are not well characterized. Using the BACHD mice that express the full-length mutant huntingtin (mHtt) protein with 97 glutamine repeats, we first demonstrated localized in vivo changes in brain glucose use reminiscent of what is observed in premanifest HD carriers. Using biochemical, molecular, and functional analyses on different primary cell culture models from BACHD mice, we observed that mHtt does not directly affect metabolic activity in a cell autonomous manner. However, coculture of neurons with astrocytes from wild-type or BACHD mice identified mutant astrocytes as a source of adverse non-cell autonomous effects on neuron energy metabolism possibly by increasing oxidative stress. These results suggest that astrocyte-to-neuron signaling is involved in early energy metabolic alterations in HD.     

Evaluation of the Effect of Acute Sibutramine in Female Rats in the Elevated T‐Maze and Elevated Plus‐Maze Tests

Sibutramine is a serotonin and norepinephrine reuptake inhibitor indicated for the treatment of obesity. A pre‐clinical study showed that acute administration of sibutramine promoted anxiolytic‐ and panicolytic‐like effects in male rats. However, in clinical reports, sibutramine favoured the onset of panic attacks in women. In this study, the effect of sibutramine on experimental anxiety in females and the relevance of different oestrous cycle phases for this effect were analysed. In experiment 1, both male and female rats were submitted to acute intraperitoneal injection of sibutramine or vehicle 30 min. before testing in the elevated T‐maze (ETM) and in the open‐field test (OF). Females in the pro‐oestrus (P), oestrus (E), early dioestrus (ED) and late dioestrus (LD) phases were tested in the ETM and OF (experiment 2) or in the elevated plus‐maze (EPM) 30 min. after the injection of sibutramine. Sibutramine impaired the escape response in the ETM in both males and females. This effect was observed for P, E and ED, but not for LD females. Sibutramine altered neither the inhibitory avoidance in the ETM nor the behaviour of females in the EPM. Thus, sibutramine promoted a panicolytic‐like effect in female rats cycling at P, E and ED, but not in the LD phase and did not alter behaviours related to anxiety in both ETM and EPM. Considering that pre‐clinical studies aiming the screening of anxiolytic drugs employ male rodents, data here obtained reinforce the importance of better understanding the effects of drugs in females.     

Association of MASP2 polymorphisms and protein levels with rheumatic fever and rheumatic heart disease

MASP-2 is a key protein of the lectin pathway of complement system. Several MASP2 polymorphisms were associated with MASP-2 serum levels or functional activity. Here we investigated a possible association between MASP2 polymorphisms and MASP-2 serum levels with the susceptibility to rheumatic fever (RF) and rheumatic heart disease (RHD). We haplotyped 11 MASP2 polymorphisms with multiplex sequence-specific PCR in 145 patients with history of RF from south Brazil (103 with RHD and 42 without cardiac lesion [RFo]) and 342 healthy controls. MASP-2 levels were determined by ELISA. The low MASP-2 producing p.377A and p.439H variants were negatively associated with RF (P = 0.02, OR = 0.36) and RHD (P = 0.01, OR = 0.25). In contrast, haplotypes that share the intron 9 – exon 12 g.1961795C, p.371D, p.377V and p.439R polymorphisms increased the susceptibility to RHD (P = 0.02, OR = 4.9). MASP-2 levels were associated with MASP2 haplotypes and were lower in patients (P < 0.0001), which may reflect protein consumption due to complement activation. MASP2 gene polymorphisms and protein levels seem to play an important role in the development of RF and establishment of RHD.     

Increase in the Expression of CD4 + CD25+ Lymphocytic T Cells in the Indeterminate Clinical Form of Human Chagas Disease After Stimulation With Recombinant Antigens of Trypanosoma cruzi

Purpose

Regulatory T cells are involved in the clinical course of chronic Chagas disease, possibly because they exercise a control in the patient’s inflammatory response to Trypanosoma cruzi. This study analyzed the levels of CD4?+?CD25+ T cells in chronic Chagas disease patients after in vitro stimulation of the peripheral blood mononuclear cells with CRA (Cytoplasmic Repetitive Antigen) or FRA (Flagellar Repetitive Antigen) T. cruzi antigens.

Methods

Groups of patients with the cardiac form and indeterminate form; and non-infected individuals, were selected. The CD4?+?CD25+ T lymphocyte population, as well as the FoxP3 expression and the IL10 production, were evaluated by flow cytometry after stimulation with CRA or FRA.

Result

The IND group presented higher levels of CD4?+?CD25+ T cells than the CARD group. However, there was no evidence of a relationship between FoxP3 and IL10 with any of the chronic forms.

Conclusions

Our results suggest the possible involvement of CD4?+?CD25+ T cells specific to CRA and FRA in controlling the progression of clinical outcomes. Though, further studies are needed to define which mechanisms activate regulatory T cells and lead to pathology control in chronic human Chagas disease.