RESUMEN
Background:Despite progress in the health indexes in recent years, health inequalities remain as a global challenge within and between regions and countries. This study is the first to quantify the socioeconomic inequity in gastroesophageal reflux disease [GERD] using the concentration index
Methods: In this cross-sectional study, we used baseline data [7012 subjects] from the Fasa Cohort Study [the Southern Iran]. The principal component analysis was used to construct socioeconomic status of the participants. The concentration index and concentration curve were used to measure socioeconomic- related inequality in GERD. Decomposition of concentration index was also done to identify the contribution of each explanatory variable to the wealth-related inequality in GERD prevalence
Results: The prevalence of GERD was 16.9% [95% CI: 15.9-17.7%]. The overall concentration index for GERD was 0.093 [95% CI: 0.062-0.166]. Correspondingly, this figure for men and women were 0.116 [95% CI: 0.062-0.171%] and 0.091 [95% CI: 0.044-0.137%], respectively. The main contributors of socioeconomic-related inequality in GERD prevalence were socioeconomic status [64.4%], alcohol drinking [29%], and age [8.4%]
Conclusion: GERD is significantly more concentrated among richest people. There was significant socioeconomic inequality in GERD according to some individual factors. These inequalities need to be addressed by policy makers to identify the vulnerable subgroups and to reduce the disease burden in the community
RESUMEN
Evidences suggest that besides the neurotransmitters contributing to the development of depression, renin-angiotensin system [RAS] may also have a substantial role. Certain polymorphisms of RAS are associated with over activity of RAS and depression. Considering that antidepressants reduce the actions of angiotensin II, the main product of RAS, this may come into mind that genetic polymorphisms of the mentioned system may affect the outcome of therapy in depressed patients. In the present study, 100 newly diagnosed depressed patients, according to DSM-IV criteria, were treated with 20 mg of fluoxetine for 8-12 weeks. Patients were categorized into responsive and non-responsive groups according to 50% reduction in symptoms. Genotype frequencies of angiotensin-converting enzyme [ACE] gene [ACE [I/D, A-240T and A2350G]] were then determined in DNAs extracted from venous blood of the patients using polymerase chain reaction-restriction fragment length polymorphism [PCR- RFLP] and PCR. Results indicate that polymorphisms studied and their haplotypes were not associated with better response to fluoxetine. However, a strong association between age and treatment in depressed Iranian patients was observed [P=0.001]. In conclusion, unlike previous reports, this study does not support the hypothesis of special genotypes of RAS contributing to a better response to antidepressants in depressed patients