RESUMO
OBJECTIVES: Late-life depression (LLD) is the most common mental disorder among the elderly, but its clinical features remain unclear, especially among older adults. We sought to investigate if age, sex and education could influence the severity or frequency of LLD symptoms. METHODS: We evaluated 639 community-dwelling individuals aged 75+ years in Caeté (MG), Brazil. We used the Mini International Neuropsychiatric Interview to diagnose major depression according to DSM-IV criteria and the GDS-15 to measure depression severity. RESULTS: Excluding 174 individuals diagnosed with dementia, 54 (11.6%) of the remaining 457 individuals were diagnosed with LLD; 77.8% of which were female. On average, these participants were aged 81.0 ± 4.8 years and had 2.7 ± 3.3 years of schooling. Symptom severity was not influenced by sociodemographic variables. Death/suicidal ideation was more frequent among men, while psychomotor disturbance was more present in women (p = 0.04 and p = 0.042). More educated individuals (≥ 4 years) also reported a higher frequency of psychomotor disturbance (p = 0.039). CONCLUSIONS: Severity of depressive episode was not influenced by sociodemographic variables. Sex and educational level had a significant impact on symptom profiles.
Assuntos
Depressão , Transtorno Depressivo Maior , Idoso , Brasil/epidemiologia , Depressão/epidemiologia , Transtorno Depressivo Maior/diagnóstico , Transtorno Depressivo Maior/epidemiologia , Escolaridade , Feminino , Humanos , Masculino , Escalas de Graduação PsiquiátricaRESUMO
Hepatic fibrosis is considered a common response to many chronic hepatic injuries. It is a multifunctional process that involves several cell types, cytokines, chemokines and growth factors leading to a disruption of homeostatic mechanisms that maintain the liver ecosystem. In spite of many studies regarding the development of fibrosis, the understanding of the pathogenesis remains obscure. The hepatic tissue remodeling process is highly complex, resulting from the balance between collagen degradation and synthesis. Among the many mediators that take part in this process, the components of the Renin angiotensin system (RAS) have progressively assumed an important role. Angiotensin (Ang) II acts as a profibrotic mediator and Ang-(1-7), the newly recognized RAS component, appears to exert a counter-regulatory role in liver tissue. We briefly review the liver fibrosis process and current aspects of the RAS. This review also aims to discuss some experimental evidence regarding the participation of RAS mediators in the pathogenesis of liver fibrosis, focusing on the putative role of the ACE2-Ang-(1-7)-Mas receptor axis.
Assuntos
Cirrose Hepática/fisiopatologia , Sistema Renina-Angiotensina/fisiologia , Angiotensina II/metabolismo , Animais , Humanos , Cirrose Hepática/patologia , Fragmentos de Peptídeos/metabolismoRESUMO
BACKGROUND/AIMS: The circulating renin-angiotensin system (RAS) [plasma renin activity (PRA), Angiotensin (Ang) I, Ang II and Ang-(1-7)] was evaluated in a model of hepatic fibrosis in rats. To investigate the pathophysiological involvement of Ang-(1-7), animals were treated with the Ang-(1-7) Mas receptor antagonist, A-779. METHODS: RAS components, liver function and histology were examined in male Wistar rats (220-300 g). Animals were submitted to sham-surgery or ligature of the bile duct and evaluated 1, 2, 4 and 6 weeks later. Blood samples were obtained to determine biochemical parameters and RAS components. A second group was treated with A-779 or vehicle to measure liver hydroxyproline and total transforming growth factor beta-1 (TGFbeta1). RESULTS: PRA and Ang I were significantly elevated in rats at 4 and 6 weeks compared to sham-operated animals. Ang II and Ang-(1-7) progressively increased over the 6 weeks. Changes in RAS profile correlated with histological signs of fibrosis and deterioration in liver function. Pharmacological blockade of the Ang-(1-7) receptor aggravated liver fibrosis with a significant elevation in hydroxyproline and total TGFbeta(1). CONCLUSIONS: Hepatic fibrosis was associated with RAS activation in our model. Our data also suggested that Ang-(1-7) played a protective role in hepatic fibrosis.