RESUMEN
BACKGROUND: The aim of this study was to systematically assess the efficacy and safety of mineralocorticoid receptor antagonists (MRAs) for patients with heart failure (HF) and diabetes mellitus (DM). METHODS: We conducted a comprehensive search for controlled studies that evaluated the efficacy and safety of MRAs in patients with DM and HF. Medline, Embase and Cochrane databases were searched. Two reviewers independently identified citations, extracted data and evaluated quality. Risk estimations were abstracted and pooled where appropriate. RESULTS: Four observational studies were included. MRAs use was associated with reduced mortality compared with controls (RR = 0.78; 95% CI: 0.69-0.88; I(2) = 0%; P < 0.001). Increased risk of developing hyperkalaemia was observed in those patients taking MRAs (RR = 1.74; 95% CI: 1.27-2.38; I(2) = 0%; P = 0.0005). CONCLUSIONS: The current cumulative evidence suggests that MRAs can improve clinical outcomes but increase the risk of hyperkalaemia in patients with DM and HF. TRIAL REGISTRATION: PROSPERO CRD42015025690 .
Asunto(s)
Diabetes Mellitus Tipo 2/epidemiología , Insuficiencia Cardíaca/tratamiento farmacológico , Hiperpotasemia/epidemiología , Comorbilidad , Insuficiencia Cardíaca/epidemiología , Humanos , Antagonistas de Receptores de Mineralocorticoides , Mortalidad , Factores de Riesgo , Resultado del TratamientoRESUMEN
INTRODUCTION: Mature cystic teratoma originating in the pancreas is very unusual, often observed as an incidental finding during routine examinations or recognized perioperatively as the patients present with very unspecific clinical symptoms. The confirmatory diagnosis of a pancreatic cystic teratoma is generally made by histopathology after surgical excision. So, the preoperative diagnosis is very challenging, especially differentiation from the other pancreatic pathologies. PATIENT CONCERNS: A 23-year-old woman was admitted to our hospital with a complaint of mild grade periumbilical abdominal pain. A pancreatic mass was revealed on a preliminary abdominal ultrasound examination. Her medical history was unremarkable with no long-standing illness or malignancy. DIAGNOSIS: Mature cystic teratoma in the head of the pancreas. INTERVENTIONS: Roux-enY choledochojejunostomy with gastrojejunostomy was performed, excising the tumor from the pancreatic head. OUTCOMES: The postoperative course was uneventful; the patient was asymptomatic and has no evidence of recurrence on a 2-year follow up. CONCLUSIONS: Pancreatic cystic teratoma is a benign, well-differentiated, and extremely rare congenital tumor. MRI is the choice of imaging modality and phase-GRE or fat suppression is the best technique for pre-operative diagnosis.
Asunto(s)
Neoplasias Pancreáticas/diagnóstico , Teratoma/diagnóstico , Diagnóstico Diferencial , Femenino , Humanos , Adulto JovenRESUMEN
BACKGROUND Sodium glucose transporter-2 inhibitors are the newest antidiabetic drugs that seem to be cardioprotective and can prevent type 2 diabetes in patients with high cardiovascular risks. Previous clinical trials have shown that these inhibitors can alleviate endothelial dysfunction, but the mechanism of action remains unknown. How SGLT inhibitor influences the release of NO in PA-induced HUVECs has never been reported. MATERIAL AND METHODS To explore the potential effects of the endothelial-protective mechanism of phlorizin and its impact on nitric oxide (NO), human umbilical vein endothelial cells (HUVECs) were incubated with palmitic acid (PA) and then treated with phlorizin. Western blotting was performed to assess the phosphorylation of AKT, eNOS, and IRS-1. To further explore potential targets, siRNA transfection was used to demonstrate the role of SGLT1 and SGLT2. RESULTS Phlorizin suppressed the expression of SGLT1 and SGLT2, activated the PI3K/AKT/eNOS signaling pathway, increased the output of NO, and promoted the consumption of glucose in PA-induced HUVECs. Through demonstrating siRNA suppression of the expression of SGLT1 and SGLT2 in PA-induced HUVECs, this study provides a new understanding of the mechanism behind SGLT1 and SGLT2. CONCLUSIONS Our data demonstrate that phlorizin ameliorates the endothelial dysfunction link with the activation of the PI3K/AKT/eNOS signaling pathway and augmentation of the release of NO, partially through suppressing the expression of SGLT1 and SGLT2 in PA-induced HUVECS.