[Immunoglobulin E (IgE) plays a central role in the pathogenesis of the inflammation of the bronchial mucosa and airway hyperreactivity, which in turn produces the symptoms of allergic bronchial asthma. Omalizumab, the recently developed anti-IgE monoclonal antibody binds to the Cε3 region of the IgE molecule and thus prevents binding of the IgE to the surface of FCεRI receptor bearing cells (mast cells, basophils and antigen presenting dendritic cells). In the absence of cell-bound IgE, these cells are not activated and thus do not release inflammatory mediators and proinflammatory cytokines upon allergen exposition. Treatment with omalizumab significantly decreases the number of bronchial mucosal eosinophils and FCεRI positive cells, and the FCεRI receptor expression of the latter. Double blind controlled clinical studies have demonstrated that omalizumab treatment reduces the number of exacerbations and emergency room visits, the β2-agonist requirement and the dose of inhaled steroids, improves exspiratory airflow limitation, asthmatic symptoms and asthma-related quality of life in patients with moderate to severe allergic asthma. Low baseline FEV1, the use of high dose inhaled corticosteroids and a history of emergency asthma treatment in the past year are significant predictors of a better response to omalizumab. Omalizumab is tolerated well by patients. With the exception of local skin reactions, no significant difference in adverse events between patients taking omalizumab and control groups have been reported. According to the GINA (Global Initiative for Asthma) stepwise therapy protocol of asthma, omalizumab is indicated for severe asthmatics whose symptoms can not be controlled by inhaled corticosteroids and long-acting β2 agonists.]

[Obesity affects a significant proportion of the population in Western countries. Metabolic changes that are associated with obesity lead to metabolic syndrome, a significant risk factor of cardiovascular mortality. Body mass index, which is used to describe the extent of obesity, is not suitable on its own to predict cardiovascular risk or assess metabolic changes, because it doesn't provide information on the distribution of accumulated fat within the body. Several studies have shown that it is the central/abdominal/visceral type of obesity that significantly increases cardiovascular morbidity and mortality. Visceral and subcutaneous fat tissue differ both in their function and the biological effects of adipocytokines secreted by them. Apart from the known effects of free fatty acids on insulin resistance and consequently to other metabolic parameters, adipocyte-derived adipokines have been shown to have a beneficial, antiatherosclerotic effect. In order to precisely estimate the obesity-related cardiovascular risk in everyday practice, not only body mass index, but waist circumference, a marker of visceral obesity, should also be measured.]