This trial showed that propranolol was effective at a dose of 3 mg per kilogram per day for 6 months in the treatment of infantile hemangioma. (Funded by Pierre Fabre Dermatologie; ClinicalTrials.gov number, NCT01056341.).

Objective-To evaluate the impact of childhood atopic eczema on families and assess the personal financial cost of its management. Design-Cross sectional survey. Setting-Paediatric dermatology and paediatric diabetology outpatient clinics. Patients-Parents of 48 randomly selected children with atopic eczema and 46 with insulin dependent diabetes mellitus. Main outcome measures-The impact on family score, the reported cost of relevant medical treatments, medical consultations, relevant hospitalisation, and income loss. Results-Families of children with moderate or severe atopic eczema had a significantly higher impact on family score than families of diabetic children. A conservative estimate of the annual personal financial cost of managing mild, moderate, and severe eczema was Aus$330, 818, and 1255, respectively. The financial cost to the community for the management of atopic eczema in the study groups was greater. The personal financial cost of managing eczema was greater than for asthma. Conclusion-Childhood atopic eczema has a profound impact on the social, personal, emotional, and financial perspectives of families. (Arch Dis Child 1997;76:159-162)

The decision to start systemic medication should include assessment of severity and quality of life while considering the individual's general health status, psychologic needs, and personal attitudes toward systemic therapies.

Many subjects with CARD14 mutations display characteristics of both psoriasis and PRP. We propose the term CARD14-associated papulosquamous eruption to describe this spectrum of disease. Subjects with clinical features suggestive of CAPE should undergo CARD14 sequencing and may benefit from treatment with ustekinumab.

No abstract

Although most infantile haemangiomas do not require treatment due to a natural history of spontaneous involution, some require early intervention. The Australasian Vascular Anomalies Network and the Australasian Paediatric Dermatology Network have developed a consensus statement for the treatment of infantile haemangiomas with oral propranolol. Infants with haemangiomas that are life threatening, at risk of ulceration, or at risk of causing a significant functional impairment, psychological impact or physical deformity should be treated early with oral propranolol. Oral propranolol is safe and effective and in most healthy infants oral propranolol can be started in an outpatient setting.

Patients with atopic dermatitis (AD) have an increased risk of bacterial skin infections, which cause significant morbidity and, if untreated, may become systemic. Staphylococcus aureus colonizes the skin of most patients with AD and is the most common organism to cause infections. Overt bacterial infection is easily recognized by the appearance of weeping lesions, honey-coloured crusts and pustules. However, the wide variability in clinical presentation of bacterial infection in AD and the inherent features of ADcutaneous erythema and warmth, oozing associated with oedema, and regional lymphadenopathyoverlap with those of infection, making clinical diagnosis challenging. Furthermore, some features may be masked because of anatomical site-and skin-type-specific features, and the high frequency of S. aureus colonization in AD makes positive skin swab culture of suspected infection unreliable as a diagnostic tool. The host mechanisms and microbial virulence factors that underlie S. aureus colonization and infection in AD are incompletely understood. The aim of this article is to present the latest evidence from animal and human studies, including recent microbiome research, to define the clinical features of bacterial infections in AD, and to summarize our current understanding of the host and bacterial factors that influence microbial colonization and virulence. The role of bacterial skin infections in atopic dermatitis, H. Alexander et al. 1335 Fig 6. Hypothetical damage-response framework for Staphylococcus aureus in atopic dermatitis (AD). 82 Different host-S. aureus interactions result in different damage-response relationships. Curves A and B represent the damage-response relationships of S. aureus with two different hosts or those of a single host with two different S. aureus strains. The outcome for the host depends on the strength of the host response to S. aureus or the virulence of S. aureus. During intermediate host responses neither interaction (A or B) causes clinical evidence of infection, as the amount of damage incurred by the host is insufficient (1). However, in the setting of weak or strong responses both interactions cause an AD flare (2) and interaction B causes overtly infected AD (3). The position of the curve is determined by multiple host and S. aureus factors.

Allergic diseases have increased dramatically in the developed world during the past few decades, yet the understanding of risk factors and effective prevention approaches remain limited. In this review, we summarize the evidence supporting the hypothesis that skin-barrier impairment and early-life atopic dermatitis (AD) could play a causal role in the development of sensitization and subsequent food allergies and allergic airways disease (allergic asthma and rhinitis). We further discuss the potential to target the skin barrier as a means to lower the incidence of allergic disease. Data Sources: Review of published literature. Study Selections: Narrative. Results: There is a strong link between AD and sensitization, food allergy, asthma, and allergic rhinitis, particularly AD that is severe and commences in the first 6 months of life. There also is emerging evidence that regular use of prophylactic emollients can significantly decrease the expression of AD, at least while treatment continues. Studies are exploring whether decreased AD expression might modulate the allergic response at a more fundamental level and potentially alter the association between early-life AD and subsequent development of food allergy and allergic airways disease.