INTRODUCTION
Atopic dermatitis (AD), or atopic eczema, is a chronic skin
disorder with a high prevalence in children. According
to the National Institute of Arthritis and Musculoskeletal
and Skin Diseases (NIAMS), 10% to 20% of all children suffer
from AD. In many children, AD tends to resolve by 2 years
of age, but in 60% of them some symptoms will continue into
adulthood.1 About 65% of patients develop AD within the first 12
months of life and 90% within the first 5 years. In 2004, approximately
15 million patients in the United States were affected by
AD; this accounted for $154 million in AD prescription drugs or
15% of total direct costs, which is over $1 billion per year.1
Atopic dermatitis has a complex pathogenesis but there is increased
evidence that a genetically-impaired skin barrier plays a
primary role in its development.2,3 Mutations in the filaggrin gene,
in particular, are strongly associated with AD (42% of FLG heterozygotes
develop the disease).2 The protein filaggrin is important for
the correct formation of the stratum corneum barrier and filaggrin
deficiency produces increased barrier permeability and other stratum
corneum abnormalities.3 Indeed, several clinical studies have
found skin barrier defects and dry skin in both lesional and clinically
normal skin of AD patients: increased transepidermal water
loss (TEWL) and pH,4 and decreased skin hydration.4,5 A reduced
content of ceramides in the stratum corneum has also been shown
in both lesional and nonlesional skin.6
The defective barrier allows penetration of irritants and antigens,
which lead to the release of cytokines, causing secondary
skin inflammation.7 Skin inflammation can also derive in part from decreased stratum corneum hydration (xerosis).8 These
biological changes ultimately lead to the clinical manifestations
of pruritus and eczema, which are key diagnostic criteria for AD.
Intense pruritus is an initial symptom; this triggers scratching,
which in turns generates an increased immune response that
leads to the development of eczematous lesions.9
Thus, soothing of pruritus, restoration of skin barrier and stratum
corneum hydration, and reduction of inflammation are
critical for the amelioration of AD and for an improved quality
of life. Moisturization and barrier protection are paramount
to prevent entrance of noxious agents into the skin, and to
reduce pruritus and thus scratching.10,11 In fact, the Consensus
Conference on Pediatric Atopic Dermatitis suggested that
emollients (ointments and creams in particular) can be used as
first-line agents in the management of AD12 and can be steroidsparing.10,11
The regular use of emollients in AD has also been
recommended by the PRACTALL consensus report.13
Oatmeal Properties
Colloidal oatmeal is approved by the Food and Drug Administration
(FDA) as a skin protectant drug for over-the-counter
(OTC) use. One of its approved labelings is that it can "temporarily
protect and help relieve minor skin irritation and itching
due to eczema."14 Colloidal oatmeal is produced as a fine powder
from the grinding and processing of whole oat grains and it
contains various dermatological active compounds with moisturizing,
protective, anti-inflammatory, antioxidant, soothing,
buffering, and cleansing properties.15,16
