BackgroundMaternal stress in early life has been associated with the development of asthma in children, although it is unclear whether there are any critical periods of exposure. The association of asthma with prenatal exposure to maternal stress has not been reported.ObjectiveWe tested whether prenatal and postnatal anxiety and/or depression in pregnant women predicted the risk of their offspring developing asthma in childhood.MethodsThe Avon Longitudinal Study of Parents and Children is a population-based birth cohort recruited during pregnancy. Data were available on maternal anxiety scores and asthma at age 7½ years in 5810 children. Anxiety was assessed at 18 and 32 weeks of gestation by using the validated Crown-Crisp Experiential Index. Asthma was defined at age 7½ years as doctor-diagnosed asthma with current symptoms or treatment in the previous 12 months. Multivariable logistic regression was used to determine the association of prenatal anxiety with asthma (odds ratio; 95% CI).ResultsIndependent of postnatal anxiety and adjusted for a number of likely confounders, there was a higher likelihood of asthma at age 7½ years (odds ratio, 1.64; 95% CI, 1.25-2.17) in children of mothers in the highest compared with lowest quartile of anxiety scores at 32 weeks of gestation, with evidence for a dose-response (P value for trend <0.001).ConclusionsMaternal anxiety symptoms as an indicator of stress during fetal life may program the development of asthma during childhood.

Disorders of mast cell activation can be classified as primary (mastocytosis), secondary (reactive) or idiopathic. This article discusses how to recognise and approach the diagnosis of patients suspected to have symptoms of abnormal mast cell activation. Given the highly varied and often complex symptomatology of such patients, we advocate applying a logical step-wise approach to investigating these patients to ensure the correct diagnosis is made. Treatments of mast cell activation disorders are discussed, dividing them into those that ameliorate the effects of mast cell mediators and those that act to stabilise the mast cell. IntroductionThe mast cell is a tissue resident granulocyte, active in the allergic response but also playing a vital role in immune tolerance, wound healing, angiogenesis and the innate immune response. It may be activated by the binding of allergens to receptor-bound specific IgE or by multiple other non-specific stimuli. Once activated, it releases histamine and other pro-inflammatory mediators (Fig 1 ). Disorders of mast cell activation can be highly varied in their presentation. The symptoms the patient experiences are caused by the excessive release of mast cell mediators, most notably histamine. The symptoms experienced depend on the affected organ, eg wheals, redness and itching in the skin or cramps and diarrhoea in the gastrointestinal tract. Sometimes patients will present with an isolated finding, such as the rash of cutaneous mastocytosis; other patients will present with a broad constellation of symptoms, eg flushing, pre-syncope, diarrhoea and cramps. The symptoms may be vague, subtle recurrent episodes or more immediate presentations, such as anaphylaxis or life threatening hypotension (Table 1 ). This article will discuss how to approach the diagnosis and treatment of a patient you suspect to have symptoms linked to abnormal mast cell activation.In order to encompass the wide range of conditions that may present with symptoms of mast cell activation, the umbrella term mast cell activation disorders (MCAD) has been proposed. Within this heterogeneous group of conditions, ABSTRACTAn update on mast cell disorders Akin 1 proposes stratifying them into primary (clonal), secondary (or reactive) and idiopathic (of unknown cause).

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Coxsackievirus A6 (CV-A6) is an emerging pathogen that has in recent years been associated with atypical hand, foot and mouth disease. This manifests as a generalized papular or vesicular eruption, which may be associated with fever and systemic disturbance. We report a series of six children presenting to a single centre in the UK with disseminated CV-A6 infection on a background of atopic dermatitis (AD). Our patients exhibited a widespread papular or vesicular eruption in association with exacerbation of AD. Several of our cases mimicked eczema herpeticum, but the extent was more generalized, and individual lesions were discrete rather than clustered and were less circumscribed in character. This series highlights that CV-A6 infection may be encountered in the UK, and should be considered in the differential diagnosis of an acute exacerbation of AD, particularly in children.