La enfermedad inflamatoria intestinal y los riesgos de enfermedad cardiovascular

La enfermedad inflamatoria intestinal (EII), comprende tanto a la colitis ulcerosa como a la enfermedad de Crohn, entidades consideradas enfermedades inmunomediadas, sistémicas y de curso crónico que conllevan a menudo el desarrollo de manifestaciones extraintestinales. A pesar de que el estudio de las comorbilidades haya sido desarrollado tradicionalmente en contexto de otras enfermedades inflamatorias sistémicas, este concepto está emergiendo también en la EII. Multitud de patologías han sido vinculadas a la EII, entre las que destaca la enfermedad cardiovascular, la primera causa de muerte en los países desarrollados. Los pacientes con EII están expuestos a un mayor riesgo de entidades tales como arterosclerosis precoz e infarto de miocardio, o trombosis venosas y tromboembolismo pulmonar. El objetivo de esta revisión es hacer una aproximación a la fisiopatología de las diferentes manifestaciones de la enfermedad cardiovascular en los pacientes con EII y de cómo prevenirlas. Inflammatory bowel disease (IBD) includes both ulcerative colitis and Crohn's disease, which are well recognised as chronic systemic and immune-mediated conditions that frequently involve extraintestinal manifestations. Although comorbidities have long been the subject of research in other chronic inflammatory diseases, this concept is also emerging in IBD. Many pathologies have been linked to IBD, including cardiovascular disease, which is the main cause of death in developed countries. IBD patients are at increased risk of conditions such as early atherosclerosis and myocardial infarction or venous thrombosis and pulmonary thromboembolism. The aim of this review is to make an approximation of the physiopathology of the different manifestations of cardiovascular disease in patients with IBD and how to prevent them

A functional IL1RL1 variant regulates corticosteroid-induced sST2 expression in ulcerative colitis

Indexación: Web of Science; Scopus.The ST2/IL33 signalling pathway has been associated with ulcerative colitis (UC). ST2, encoded by the IL1RL1 gene, is expressed as both a membrane-anchored receptor (ST2L) activated by IL33 and as a soluble receptor (sST2) with anti-inflammatory properties. In UC patients, sST2 is further increased by corticosteroid treatment; however, the glucocorticoid-mediated molecular regulation remains unknown. We therefore tested whether genetic variants in the IL1RL1 distal promoter are involved in UC and affect glucocorticoid-mediated ST2 expression. Serum ST2 levels and genetic variants in the IL1RL1 distal promoter were examined by ELISA and PCR sequencing in UC patients receiving corticosteroids. Glucocorticoid-mediated ST2 production was evaluated in intestinal mucosa cultures. Molecular regulation of glucocorticoid-mediated ST2 was assessed by RT-qPCR, ChIP assay and luciferase reporter assay. Dexamethasone effect on ST2 transcript expression was analyzed in leukocytes and related to IL1RL1 variants. Sequencing of a distal IL1RL1 promoter region demonstrated that SNPs rs6543115(C) and rs6543116(A) are associated with increased sST2 in UC patients on corticosteroids. Dexamethasone up-regulated sST2 transcription through interaction with the glucocorticoid-response element (GRE) carrying rs6543115(C) variant. Our data indicate that IL1RL1 SNPs rs6543115(C) confer susceptibility to UC and is contained in the GRE, which may modulate glucocorticoid-induced sST2 expression.https://www.nature.com/articles/s41598-017-10465-

Psychiatric and cognitive phenotype in children and adolescents with myotonic dystrophy

Myotonic dystrophy type 1 (DM1) is the most frequent inherited neuromuscular disorder. The juvenile form has been associated with cognitive and psychiatric dysfunction, but the phenotype remains unclear. We reviewed the literature to examine the psychiatric phenotype of juvenile DM1 and performed an admixture analysis of the IQ distribution of our own patients, as we hypothesised a bimodal distribution. Two-thirds of the patients had at least one DSM-IV diagnosis, mainly attention deficit/ hyperactivity disorder and anxiety disorder. Two-thirds had learning disabilities comorbid with mental retardation on one hand, but also attention deficit, low cognitive speed and visual spatial impairment on the other. IQ showed a bi-modal distribution and was associated with parental transmission. The psychiatric phenotype in juvenile DM1 is complex. We distinguished two different phenotypic subtypes: one group characterised by mental retardation, severe developmental delay and maternal transmission; and another group characterised by borderline full scale IQ, subnormal development and paternal transmission

Is there a role for melatonin in fibromyalgia?

Fibromyalgia, characterised by persistent pain, fatigue, sleep disturbance and cognitive dysfunction, is a central sensitivity syndrome that also involves abnormality in peripheral generators and in the hypothalamic pituitary adrenal axis. Heterogeneity of clinical expression of fibromyalgia with a multifactorial aetiology has made the development of effective therapeutic strategies challenging. Physiological properties of the neurohormone melatonin appear related to the symptom profile exhibited by patients with fibromyalgia and thus disturbance of it’s production would be compatible with the pathophysiology. Altered levels of melatonin have been observed in patients with fibromyalgia which are associated with lower secretion during dark hours and higher secretion during daytime. However, inconsistencies of available clinical evidence limit conclusion of a relationship between levels of melatonin and symptom profiles in patients with fibromyalgia. Administration of melatonin to patients with fibromyalgia has demonstrated suppression of many symptoms and an improved quality of life consistent with benefit as a therapy for the management of this condition. Further studies with larger samples, however, are required to explore the potential role of melatonin in the pathophysiology of fibromyalgia and determine the optimal dosing regimen of melatonin for the management of fibromyalgia

Gastrointestinal microbiome, what is behind faecal microbiota transplantation?

The intestinal microbiota is made up of billions of microorganisms that coexist in an organised ecosystem, where strict and facultative anaerobic bacteria predominate. The alteration or imbalance of these microorganisms, known as dysbiosis, can be associated with both gastrointestinal and extraintestinal diseases.Based on a review of the literature, the intestinal microbiota is described in its state of health, the changes associated with some gastrointestinal diseases and the potential role that faecal microbiota transplantation has in the reestablishment of an altered ecosystem. Undoubtedly, the information revealed makes us reflect on the indication of faecal microbiota transplantation in various pathologies of intestinal origin. However, to ensure the efficacy and safety of this therapy, more studies are needed to obtain more evidence

Possible association between mycobacterium avium subsp paratuberculosis infection and crohn's disease Mycobacterium avium subsp paratuberculosis y enfermedad de crohn: Evidencias de una zoonosis

Paratuberculosis is a chronic intestinal disease of animals caused by Mycobacterium avium subsp. paratuberculosis (MAP), which has some pathological features similar to Crohn's disease (CD) in humans. The presence of MAP in food for human consumption and in affected tissues of patients with CD has been detected. Therefore, a causal association between this microorganism and the disease in humans, has been postulated. However, several related studies have failed to confirm this hypothesis and the scientific acceptance of MAP as a zoonotic agent remains controversial. This review presents the main findings related to this issue, contrasting evidences for and against an association between MAP and CD. The need to promote national studies focusing on this area is suggested