Blistering skin diseases: a bridge between dermatopathology and molecular biology

Abstract

Although dermatopathology and molecular biology are often considered to be separate laboratory disciplines, the respective approaches are far from mutually exclusive. This is certainly the case for understanding the pathology of blistering skin diseases, both acquired and inherited. For example, in toxic epidermal necrolysis, dermatopathology in isolation may provide few clues to disease pathogenesis. There is widespread keratinocyte apoptosis and a variable infiltrate of cytotoxic T cells, but morphology alone offers little insight into what causes the epidermal destruction. In contrast, molecular biology studies have revealed several key processes that help explain the keratinocyte death, including increased expression of death receptors and their ligands on keratinocyte cell membranes as well as the presence of local or systemic immunocyte-derived cytolytic granules. For some inherited blistering diseases, however, such as epidermolysis bullosa, the molecular pathology is complex and difficult to unravel in isolation, yet the addition of dermatopathology is helpful in focusing molecular investigations. Notably, immunolabelling of cell adhesion proteins using specific antibody probes can identify reduced or absent immunoreactivity for candidate genes ⁄ proteins. Bridging dermatopathology and molecular biology investigations facilitates a greater understanding of disease processes, improves diagnostic accuracy, and provides a basis for the development and appraisal of new treatments.

Monitoring of the patient with toxic epidermal necrolysis in the intensive care unit

“…Albümin değerleri 30 mg/dL altına hiç inmedi. TEN'li olgularda mukozada deri değiştirme ve ödem sonucu solunum sıkıntısı görülebileceği ve bu durumda endotrakeal entübasyon ve ventilasyon gerekebileceği belirtilmektedir [27] . Ancak hastamızda invaziv yada non-invaziv ventilayon gereksinimi olmadı.…”

Genetic Analyses of Integrin Signaling

“…Interestingly, some of the EB patients also develop muscular dystrophy, underlining the pathophysiological link between these two diseases. As the histopathology of these diseases is very complex, the identification of the causative mutation has become a central diagnostic tool of EB (Nagy and McGrath 2010). Genetic mouse models for the different EB variants are available, and they have been used to work out therapeutic strategies for these diseases (Natsuga et al 2010).…”

A Case Report On Leptospirosis with secondary Steven Johnson Syndrome

“…The patient with an eruption resembling scalding of the skin called TEN [8]. It is mainly induced by the drugs or infection, environment chemicals, radiation &immunisation or sometimes it can be an idiopathic [9]. We report that the patient with Leptospirosis with SJS was treated with systemic steroidal therapy, Antibiotics, systemic supportive care & some topical creams for healing the fluid filled lesions on all over the body.…”