RESUMO
BACKGROUND: Mothers of children with food allergy have increased anxiety, which may be influenced by healthcare professionals' communication of risk. OBJECTIVE: To evaluate a brief psychological intervention for reducing anxiety in mothers of children with food allergy. METHODS: Two hundred mothers of children with food allergy were recruited from allergy clinics. A computer-generated randomization list was used to allocate participants to a single-session cognitive behavioural therapy intervention including a risk communication module, or standard care. Anxiety and risk perception were assessed at 6 weeks and 1 year. Primary outcome was state anxiety at 6 weeks. Secondary outcomes included state anxiety at 1 year, risk perception at 6 weeks and 1 year, and salivary cortisol response to a simulated anaphylaxis scenario at 1 year. RESULTS: We found no significant difference in the primary outcome state anxiety at 6 weeks, with mean 31.9 (SD 10.2) intervention, 34.0 (10.2) control; mean difference 2.1 (95% CI -0.9, 5.0; P=.17). There was significantly reduced state anxiety at 6 weeks in the intervention group, in the subgroup of participants with moderate/high anxiety at enrolment (103/200, 52%), with mean 33.0 (SD 9.3) intervention, 37.8 (SD 10.0) control; mean difference 4.8 (95% CI 0.9, 8.7; P=.016; Cohen's d effect size 0.50). The psychological intervention also reduced risk perception and salivary cortisol response (P=.032; effect size 0.36). CONCLUSION: We found evidence that a brief psychological intervention which incorporates accurate risk information may impact on anxiety, risk perception and physiological stress response in mothers of children with food allergy.
Assuntos
Ansiedade/epidemiologia , Ansiedade/terapia , Terapia Cognitivo-Comportamental , Hipersensibilidade Alimentar/epidemiologia , Mães/psicologia , Percepção , Adulto , Criança , Pré-Escolar , Comorbidade , Feminino , Humanos , Lactente , Londres/epidemiologia , Masculino , Fatores de Risco , Estresse PsicológicoRESUMO
BACKGROUND: Previous work has shown patients commonly misuse adrenaline autoinjectors (AAI). It is unclear whether this is due to inadequate training, or poor device design. We undertook a prospective randomized controlled trial to evaluate ability to administer adrenaline using different AAI devices. METHODS: We allocated mothers of food-allergic children prescribed an AAI for the first time to Anapen or EpiPen using a computer-generated randomization list, with optimal training according to manufacturer's instructions. After one year, participants were randomly allocated a new device (EpiPen, Anapen, new EpiPen, JEXT or Auvi-Q), without device-specific training. We assessed ability to deliver adrenaline using their AAI in a simulated anaphylaxis scenario six weeks and one year after initial training, and following device switch. Primary outcome was successful adrenaline administration at six weeks, assessed by an independent expert. Secondary outcomes were success at one year, success after switching device, and adverse events. RESULTS: We randomized 158 participants. At six weeks, 30 of 71 (42%) participants allocated to Anapen and 31 of 73 (43%) participants allocated to EpiPen were successful - RR 1.00 (95% CI 0.68-1.46). Success rates at one year were also similar, but digital injection was more common at one year with EpiPen (8/59, 14%) than Anapen (0/51, 0%, P = 0.007). When switched to a new device without specific training, success rates were higher with Auvi-Q (26/28, 93%) than other devices (39/80, 49%; P < 0.001). CONCLUSIONS: AAI device design is a major determinant of successful adrenaline administration. Success rates were low with several devices, but were high using the audio-prompt device Auvi-Q.
Assuntos
Anafilaxia/tratamento farmacológico , Epinefrina/administração & dosagem , Vasoconstritores/administração & dosagem , Criança , Pré-Escolar , Feminino , Hipersensibilidade Alimentar/tratamento farmacológico , Humanos , Lactente , Injeções , Masculino , Glândulas Salivares/metabolismo , alfa-Amilases Salivares/metabolismo , Autoadministração , Resultado do Tratamento , alfa-AmilasesRESUMO
We have carried out a genome screen for atopic dermatitis (AD) and have identified linkage to AD on chromosomes 1q21, 17q25 and 20p. These regions correspond closely with known psoriasis loci, as does a previously identified AD locus on chromosome 3q21. The results indicate that AD is influenced by genes with general effects on dermal inflammation and immunity.
Assuntos
Dermatite Atópica/genética , Ligação Genética , Predisposição Genética para Doença , Psoríase/genética , Criança , HumanosRESUMO
A recent case of absence of a cervical pedicle in a traumatized patient is presented. An incorrect radiological interpretation of the patient's plain films resulted in inappropriate management. Further radiological investigation, including computed tomography, revealed the underlying abnormality, and prevented subsequent misadventure . A review of the literature on this interesting abnormality and a complete differential diagnosis are presented.
Assuntos
Vértebras Cervicais/anormalidades , Mielografia , Tomografia Computadorizada por Raios X , Adulto , Vértebras Cervicais/diagnóstico por imagem , Diagnóstico Diferencial , Erros de Diagnóstico , Humanos , MasculinoRESUMO
IgE dysregulation is a major pathogenic feature of atopic dermatitis and other IgE-mediated allergic diseases such as asthma and rhinitis. Allergen complexed to IgE binds to the high affinity receptor for IgE (Fc epsilon RI) on the surface of epidermal Langerhans cells, mast cells and basophils, triggering the release of inflammatory mediators. The beta subunit of Fc epsilon RI has been localized to human chromosome 11q12-13, and variants within this gene have been shown to associate with asthma and measures of atopy. We have tested several polymorphisms within Fc epsilon RI-beta for association to atopic dermatitis in a panel of 60 families (panel A), recruited through a proband with atopic dermatitis. The findings were tested in a second panel of families (panel B). Significant sharing of maternal alleles was seen for atopic dermatitis and allele 2 of RsaI intron 2 (RsaIvin2*2) (P = 0.0022) and allele 1 of RsaI exon 7 (RsaIvex7*1) (P = 0.0036) Fc epsilon RI-beta gene polymorphisms. These findings were replicated in Panel B, confirming the association of Fc epsilon RI-beta RsaI polymorphisms with atopic dermatitis. The combined significance of the association of atopic dermatitis to RsaI polymorphisms was P = 0.0002 (RsaIvin2*2) and P = 0.00034 (RsaIvex7*1). The polymorphisms also showed association with asthma: P = 0.0068 (RsaIvin2*2) and P = 0.018 (RsaIvex7*1). Polymorphisms within the Fc epsilon RI-beta gene are strongly associated with atopic dermatitis.