Severe fingolimod rebound syndrome after switching to cladribine treatment.

We present the clinical and imaging characteristics of a patient whom presented with rebound syndrome after switching from fingolimod to cladribine treatment due to hematologic toxicity. Previous imaging studies had shown a non-aggressive phenotype of the disease, however multiple active tumefactive lesions became evident after beginning treatment with cladribine. The patient responded well to plasmapheresis.

Adipose Tissue in Metabolic Syndrome: Onset and Progression of Atherosclerosis.

Metabolic syndrome (MetS) should be considered a clinical entity when its different symptoms share a common etiology: obesity/insulin resistance as a result of a multi-organ dysfunction. The main interest in treating MetS as a clinical entity is that the addition of its components drastically increases the risk of atherosclerosis. In MetS, the adipose tissue plays a central role along with an unbalanced gut microbiome, which has become relevant in recent years. Once visceral adipose tissue (VAT) increases, dyslipidemia and endothelial dysfunction follow as additive risk factors. However, when the nonalcoholic fatty liver is present, risk of a cardiovascular event is highly augmented. Epicardial adipose tissue (EAT) seems to increase simultaneously with the VAT. In this context, the former may play a more important role in the development of the atherosclerotic plaque than the latter. Hence, EAT may act as a paracrine tissue vis-à-vis the coronary arteries favoring the local inflammation and the atheroma calcification.