Mielolipoma suprarrenal atípico en paciente con hipertensión arterial resistente

Adrenal myelolipoma is a slow-growing tumour, composed of fatty tissue and haematopoietic elements, typically non-secretory, although a low percentage is associated with endocrine pathology. We present the case of a 35-year-old man who, during the study of resistant arterial hypertension, was diagnosed with a large adrenal incidentaloma with an image congruent with adrenal myelolipoma, whose analytical determinations were anodyne, suggesting a non-functioning adenoma. After surgical resection, the anatomopathological study of the mass revealed pheochromocytoma cells, which produce catecholamines and are responsible for the patient's high blood pressure resistance.El mielolipoma suprarrenal es un tumor de lento crecimiento, compuesto por tejido graso y elementos hematopoyéticos, típicamente no secretor, aunque un bajo porcentaje asocia coexistencia con patología endócrina. Presentamos el caso de un varón de 35 años al que, durante el estudio de hipertensión arterial resistente, se le diagnostica de incidentaloma suprarrenal de gran tamaño con imagen congruente con mielolipoma suprarrenal, cuyas determinaciones analíticas eran anodinas sugiriendo un adenoma no funcionante. Tras la resección quirúrgica, el estudio anatomopatológico de dicha masa reveló células de feocromocitoma, productor de catecolaminas, que condiciona la resistencia de la hipertensión arterial del paciente

Reelin is overexpressed in the liver and plasma of bile duct ligated rats and its levels and glycosylation are altered in plasma of humans with cirrhosis

Reelin is an extracellular matrix protein secreted by a variety of cell types in both embryonic and adult tissues, including the liver. However, the physiological significance of Reelin in normal and cirrhotic liver has thus far not been elucidated. We have investigated Reelin levels in the liver and plasma of bile duct ligated (BDL) rats. We observe a 115% increase in full-length Reelin and its 310- and 180-kDa fragments in liver extracts from BDL rats, compared to sham-operated controls (p = 0.005). The overall increase in protein levels was associated with a 30% increase of Reelin transcripts (p = 0.03). Immunohistochemical analysis demonstrated that hepatic stellate cells are the major source of Reelin in the injured liver. Increased liver Reelin in BDL rats leads to a pronounced 165% increase in the plasma levels (p < 0.001), particularly in the less abundant 180-kDa fragment (300% increase; p < 0.001). The data provides evidence that a fraction of plasma Reelin is synthesized in the liver. In human subjects suffering liver cirrhosis the level of the 180-kDa fragment was also increased by 140% in the plasma (p < 0.001). Analysis of Reelin glycosylation by lectin binding demonstrated that the 180- and predominant 310-kDa Reelin fragments in the plasma of cirrhotic patients are differentially glycosylated compared to non-diseased control subjects. The data show that Reelin is up-regulated in experimental liver cirrhosis and that its levels and glycosylation are altered in plasma from patients with cirrhosis, thereby supporting that Reelin is involved in the pathogenesis of liver disease. © 2007 Elsevier Ltd. All rights reserved.This work was supported by grants from Generalitat Valenciana (GV04B-664) and Instituto de Salud Carlos III (PI05/1269 & PI06/0181, and CIBERNED) from Spain.Peer Reviewe

Portal hypertension increases the risk of hepatic decompensation after 90Yttrium radioembolization in patients with hepatocellular carcinoma: a cohort study

Background: Transarterial radioembolization (TARE) is increasingly used in patients with hepatocellular carcinoma (HCC). This treatment can induce or impair portal hypertension, leading to hepatic decompensation. TARE also promotes changes in liver and spleen volumes that may modify therapeutic decisions and outcomes after therapy. Objectives: We aimed to investigate the impact of TARE on the incidence of decompensation events and its predictive factors. Design: In all, 63 consecutive patients treated with TARE between February 2012 and December 2018 were retrospectively included. Methods: We assessed clinical (including Barcelona Clinic Liver Cancer stage, portal hypertension assessment, and liver decompensation), laboratory parameters, and liver and spleen volumes before and 6 and 12 weeks after treatment. A multivariate analysis was performed. Results: In total, 18 out of 63 (28.6%) patients had liver decompensation (ascites, variceal bleeding, jaundice, or encephalopathy) within the first 3 months after therapy, not associated with tumor progression. Clinically significant portal hypertension (CSPH) and bilobar treatment independently predicted the development of liver decompensation after TARE. A significant volume increase in the non-treated hemi-liver was observed only in patients with unilobar treatment (median volume increase of 20.2% in patients with right lobe TARE; p  = 0.007), especially in those without CSPH. Spleen volume also increased after TARE (median volume increase of 16.1%; p  = 0.0001) and was associated with worsening liver function scores and decreased platelet count. Conclusion: Bilobar TARE and CSPH may be associated with an increased risk of liver decompensation in patients with intermediate or advanced HCC. A careful assessment considering these variables before therapy may optimize candidate selection and improve treatment planning

Rationale, design, and baseline characteristics in Evaluation of LIXisenatide in Acute Coronary Syndrome, a long-term cardiovascular end point trial of lixisenatide versus placebo

BACKGROUND: Cardiovascular (CV) disease is the leading cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). Furthermore, patients with T2DM and acute coronary syndrome (ACS) have a particularly high risk of CV events. The glucagon-like peptide 1 receptor agonist, lixisenatide, improves glycemia, but its effects on CV events have not been thoroughly evaluated. METHODS: ELIXA (www.clinicaltrials.gov no. NCT01147250) is a randomized, double-blind, placebo-controlled, parallel-group, multicenter study of lixisenatide in patients with T2DM and a recent ACS event. The primary aim is to evaluate the effects of lixisenatide on CV morbidity and mortality in a population at high CV risk. The primary efficacy end point is a composite of time to CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina. Data are systematically collected for safety outcomes, including hypoglycemia, pancreatitis, and malignancy. RESULTS: Enrollment began in July 2010 and ended in August 2013; 6,068 patients from 49 countries were randomized. Of these, 69% are men and 75% are white; at baseline, the mean ± SD age was 60.3 ± 9.7 years, body mass index was 30.2 ± 5.7 kg/m(2), and duration of T2DM was 9.3 ± 8.2 years. The qualifying ACS was a myocardial infarction in 83% and unstable angina in 17%. The study will continue until the positive adjudication of the protocol-specified number of primary CV events. CONCLUSION: ELIXA will be the first trial to report the safety and efficacy of a glucagon-like peptide 1 receptor agonist in people with T2DM and high CV event risk