Chapters authored
Asthma-COPD Overlap Syndrome (ACOS): Current Understanding and Future Perspectives
This chapter resumes our current understanding of asthma–chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS), pretending to offer a comprehensive approach for the practicing physician, and provides some future perspectives on this entity.
Part of the book: Asthma
Current and Future Asthma Treatments: Phenotypical Approach on the Path to Personalized Medicine in Asthma
Despite widely available and effective treatments, achieving asthma control is still an unmet need for many patients. One of the explanations resides perhaps in the heterogeneity of the disease. Asthma is in fact, as we understand it today, a complex syndrome made up of numerous disease variants or asthma phenotypes; when the different underlying mechanisms are identified, the more ambitious term “endotype” is used, with consequent therapeutic implications. Remarkable efforts have been made to identify the features of difficult-to-control (usually severe) asthma, which are different from those described for mild-to-moderate asthma, setting the stage for the development of new and even individualized therapies. As different drugs target different pathways, it is necessary to determine the individual profile of pathophysiological abnormalities for each patient. The most fascinating options of the new asthma treatments are the monoclonal antibodies targeted against key inflammatory cytokines, and the most proximately available treatments within the next years are discussed here. Also, current evidence and understanding of somehow older therapeutic options, such as anticholinergics, thermoplasty, or omalizumab, are reviewed from a phenotypical approach.
Part of the book: Asthma
Bradykinin-Mediated Angioedema Across the History
The origins of the discovery of the “Complement System” date from the second half of the nineteenth century. The official paternity of the Complement System is attributed to Jules Bordet. The complement system can be activated through three major pathways. The classical pathway, the alternative pathway, and the lectin pathway converge in a common final lytic pathway. Hereditary angioedema (HAE) due to C1-inhibitor (C1-INH) deficiency (C1-INH-HAE) was first described by Robert Graves in his clinical lectures. The autosomal dominant pattern of HAE was recognized by Sir William Osler. The pathophysiologic basis of C1-INH-HAE as a deficiency of a plasma inhibitor was discovered in the early 1960s. In 1986, the C1NH gene was identified, which encodes the C1-INH protein. Although the possible relationship between angioedema and estrogens in women was described as early as 1986, it was not until the first decade of the twenty-first century when several series of patients with HAE were described with normal levels of the fractions of the complement system. In the last decade, several drugs have been approved and marketed in Europe, in the United States, and in other countries, contributing to the improved management of C1-INH-HAE and patient’s quality of life.
Part of the book: Urticaria and Angioedema