Epidermal barrier function is abnormal in individuals with atopic dermatitis (AD). It is
controversial whether primary epidermal barrier abnormalities alone account for the physiological
and clinical abnormalities found in those persons with AD or whether the observed
barrier dysfunction is a consequence of primary immunologic abnormalities. Recent evidence
is strengthening the argument for the former hypothesis. Attention to epidermal
barrier care (ie, gentle skin care) has long been an important part of the therapy of AD.
Advances in our understanding of the biology of the epidermal barrier and how this relates
to the clinical manifestations of this disease has important consequences for new therapeutic
approaches in the management of AD.
Semin Cutan Med Surg 27:108-114 © 2008 Elsevier Inc. All rights reserved.
Atopic dermatitis is a common, complex disease that frequently follows a chronic, relapsing
course. The disease can impact the quality of life (QOL) of patients and families to a
significant degree. Patients and caregivers may focus on unproven triggers at the expense
of proper skin care. A multidisciplinary approach is needed to comprehensively evaluate
triggers and response to treatment, address confounding factors including sleep disruption,
and educate patients and caregivers.
Semin Cutan Med Surg 27:115-127 © 2008 Elsevier Inc. All rights reserved.
The discovery that null mutations in the filaggrin gene (FLG) are associated with atopic
eczema represents the single most significant breakthrough in understanding the genetic
basis of this complex disorder. The association has been replicated in multiple independent
studies during the past 2 years with the use of various methodologies, from populations in
Europe, the United States, and Japan. Filaggrin plays a key role in epidermal barrier
function, and its association with atopic eczema emphasizes the importance of barrier
dysfunction in eczema pathogenesis. This review aims to summarize the current state of
knowledge regarding the role of FLG mutations in ichthyosis vulgaris, atopic eczema, and
other skin disorders, with an emphasis on potential clinical applications. Further research
is needed to clarify the precise role of filaggrin in skin and systemic atopic disease, to pave
the way for novel therapeutic interventions.
Semin Cutan Med Surg 27:128-137 © 2008 Elsevier Inc. All rights reserved.
Atopic dermatitis (AD) is a chronic inflammatory skin disease with a complex pathogenesis.
It is clinically well-defined and represents one manifestation of the atopic state, along with
asthma, food allergy and/or allergic rhinitis. Within the last several decades, there has been
much evidence to support the contribution of immune mechanisms in the pathogenesis of
AD. It has also been documented that the prevalence of all atopic disease, including AD,
has been increasing, although the environmental factors that may be contributing to this
increase are not clearly defined. A better understanding of the underlying immunopathogenesis
of AD should aid in better clinical management and development of new treatment
Semin Cutan Med Surg 27:138-143 © 2008 Elsevier Inc. All rights reserved
The innate immune system evolved more than 2 billion years ago to first recognize
pathogens then eradicate them. Several distinct defects in this ancient but rapidly responsive
element of human immune defense account for the increased incidence of skin
infections in atopics. These defects include abnormalities in the physical barrier of the
epidermis, alterations in microbial pattern recognition receptors such as toll receptors and
nucleotide binding oligomerization domains, and a diminished capacity to increase the
expression of antimicrobial peptides during inflammation. Several antimicrobial peptides
are affected including; cathelicidin, HBD-2, and HBD-3, which are lower in lesional skin of
atopics compared with other inflammatory skin diseases, and dermcidin, which is decreased
in sweat. Other defects in the immune defense barrier of atopics include a relative
deficiency in plasmacytoid dendritic cells. In the future, understanding the cause of these
defects may allow therapeutic intervention to reduce the incidence of infection in atopic
individuals and potentially decrease the severity of this disorder.
Semin Cutan Med Surg 27:144-150 © 2008 Elsevier Inc. All rights reserved.