4 research outputs found

    Association of cortisol serum levels as a prognostic factor in threat of pre-term birth

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    Background: Prematurity is one of the leading causes of death in children. In Mexico there is a frequency of 12% of preterm birth and this leads to significant maternal-fetal complications comprising 31.5% of neonatal morbidity and mortality. The patient who receives obstetric care in the gynecology service at the naval medical center requires prevention, diagnosis and treatment of threat of preterm birth to reduce perinatal and neonatal complications. Serum cortisol levels was determined as a prognostic factor for the threat of preterm birth in patients with obstetric care at the Naval Medical Center, it is a relatively easy parameter to obtain and would support a timely treatment.Methods: We used a quantitative, non-experimental, retrospective descriptive study of 30 patients with risk factors to develop preterm birth threats in gynecology service of the naval medical center from January to December 2018, which were taken 3 milliliters of peripheral blood to measure serum cortisol concentrations for later analysis. For statistical analysis of the present study, it was used Shapiro Wilk test. Likewise, Pearson's test was performed to measure the degree of association between the dependent and independent variable. Student's t-test was implemented to compare cortisol levels of pregnant women.Results: A total of 30 patients of these were analyzed, the mean age was 30.4 years (SD±5.184). The gestation weeks the average value was 30.63 weeks (SD±4.781). A student t test was performed where the cortisol values of pregnant women were compared with an average value of 2,586 (95% CI 0.45-472) and a t value=2,476 and a p=0.019 lower value of the significance value of 0.05 rejecting the null hypothesis. Which indicates that cortisol levels can be used as a predictive marker of the threat of preterm birth, considering it as an independent factor for this situation to occur in pregnant patients. The variables of the cortisol level and the weeks of gestation Pearson=-0.061 and a significance of p=0.747 were correlated (there being no strong enough relationship between the study variables). Regarding the triggers, it is observed that the highest factor was for urinary tract infection 40% n=12, abnormal uterine activity 20% n=6, followed by premature membrane rupture 16.7% n=5.Conclusions: The risk factors associated with the threat of preterm birth can be multiple, encompassing them in three important areas such as socioeconomic, psycho-emotional and clinicopathological, of the latter, nine of which are most frequent in our population are urinary infection, abnormal uterine activity and premature rupture of membranes. Regarding the association of cortisol levels as a prognostic factor for the threat of preterm birth taking it into account as an independent factor, it can be concluded that it is not statistically significant, however, according to what is reported in the literature, It should be considered as one of the multiple risk factors, considering this timely premise to boost the development of new research in the field

    Canagliflozin and renal outcomes in type 2 diabetes and nephropathy

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    BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to <90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], >300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years

    Effect of SGLT2 Inhibitors on Stroke and Atrial Fibrillation in Diabetic Kidney Disease: Results From the CREDENCE Trial and Meta-Analysis

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    BACKGROUND AND PURPOSE: Chronic kidney disease with reduced estimated glomerular filtration rate or elevated albuminuria increases risk for ischemic and hemorrhagic stroke. This study assessed the effects of sodium glucose cotransporter 2 inhibitors (SGLT2i) on stroke and atrial fibrillation/flutter (AF/AFL) from CREDENCE (Canagliflozin and Renal Events in Diabetes With Established Nephropathy Clinical Evaluation) and a meta-analysis of large cardiovascular outcome trials (CVOTs) of SGLT2i in type 2 diabetes mellitus.METHODS: CREDENCE randomized 4401 participants with type 2 diabetes mellitus and chronic kidney disease to canagliflozin or placebo. Post hoc, we estimated effects on fatal or nonfatal stroke, stroke subtypes, and intermediate markers of stroke risk including AF/AFL. Stroke and AF/AFL data from 3 other completed large CVOTs and CREDENCE were pooled using random-effects meta-analysis.RESULTS: In CREDENCE, 142 participants experienced a stroke during follow-up (10.9/1000 patient-years with canagliflozin, 14.2/1000 patient-years with placebo; hazard ratio [HR], 0.77 [95% CI, 0.55-1.08]). Effects by stroke subtypes were: ischemic (HR, 0.88 [95% CI, 0.61-1.28]; n=111), hemorrhagic (HR, 0.50 [95% CI, 0.19-1.32]; n=18), and undetermined (HR, 0.54 [95% CI, 0.20-1.46]; n=17). There was no clear effect on AF/AFL (HR, 0.76 [95% CI, 0.53-1.10]; n=115). The overall effects in the 4 CVOTs combined were: total stroke (HRpooled, 0.96 [95% CI, 0.82-1.12]), ischemic stroke (HRpooled, 1.01 [95% CI, 0.89-1.14]), hemorrhagic stroke (HRpooled, 0.50 [95% CI, 0.30-0.83]), undetermined stroke (HRpooled, 0.86 [95% CI, 0.49-1.51]), and AF/AFL (HRpooled, 0.81 [95% CI, 0.71-0.93]). There was evidence that SGLT2i effects on total stroke varied by baseline estimated glomerular filtration rate (P=0.01), with protection in the lowest estimated glomerular filtration rate (<45 mL/min/1.73 m2]) subgroup (HRpooled, 0.50 [95% CI, 0.31-0.79]).CONCLUSIONS: Although we found no clear effect of SGLT2i on total stroke in CREDENCE or across trials combined, there was some evidence of benefit in preventing hemorrhagic stroke and AF/AFL, as well as total stroke for those with lowest estimated glomerular filtration rate. Future research should focus on confirming these data and exploring potential mechanisms. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02065791
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