Manejo dermatitis marcha atópica
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Platicas par uso en el consultorio, para discutir con la familia de niñas y niños atopicos. La marcha atopica : se entiendo la manifestaciones clinicas que se maproducen de manera diacrona. Inician con alergia alimenticia y eczema de pañal, luego se manifiestan cuadros respiratorios, rinitis y se evoluciona asma alérgico. Las estrategias evitativas, surten efecto , igualmente la terapia con inmunomodulardores,antihistaminicos... ver recomendaciones prácticas,,,.
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Manejo dermatitis marcha atópica
- 1. New !
- 2. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 2
- 3. Managua , Nicaragua Email: juanherrera salazar@hotmail.com Llámenos: 22781169 2270-3359 , 89465022 claro › 84311649 claro, 88825513 mov 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 3
- 4. Atopic Dermatitis Author: Bernice R Krafchik, MBChB, FRCPC; Chief Editor: Dirk M Elston, MD more... Atopic Dermatitis Author: Brian S Kim, MD; Chief Editor: William D James, MD more... 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 4
- 5. Keratoconjunctivitis, Atopic Diaper Rash Pediatric Atopic Dermatitis Lifetime Exposure to Cigarette Smoking and t COL29A1 Gene Not Tied to Atopic Dermatitis Atopic Dermatitis in Adults 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 5
- 7. Dos hipótesis para explicar la El desarrollo de las lesiones inflamatorias Dermatitis Imbalance Th1/ Th2 aumento Th17 IgE elevada ( mecanismo alérgico) Problema de la barrera - piel…In fact, filaggrin mutations are associated with early-onset AD and with airway disease in the setting of AD.[16] 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 7
- 8. Es más importante saberQ Que clase de persona tiene esta enfermedad Que clase de enfermedad tiene esta persona. Paradigma Educativo Del Paciente Educado….agente al ….. Manejo de la Enfermedad 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 8
- 9. Prevención › Primaria ( no fumar , pecho) › Secundaria ( tratamiento temprano eczema, rinitis, eliminar cucarachas. › Terciaria ( control alergénico, leche de vaca, no aspirina )….. › http://www.worldallergy.org/professional/who_paa2003.pdf Alergia Enfermedades Alérgicas Atopia Diatesis Atópica 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 9
- 10. 10 -15 % Población Infantil 1er año de Vida ( 50% ). 1-5 años ( 30% 50% desarrolla Asma 50% desarrolla Asma Alergia Alimenticia 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 10
- 11. Precede: Rinitis,Asma Test cutaneos +++ IgE elevada Inflamación Prurito Crónico (Credit: DR P MARAZZI / ISP) Eczema on face and head 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 11
- 12. The Allergic March Ulrich Wahn, PhD MD Virchow-Kl. Humboldt-Universitat 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 12
- 13. Alergia a los Alimentos Dermatitis -Eczema Rinitis Rinoconjunctivitis Asma Triade Atópica 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 13
- 14. Copyright ©2002 BMJ Publishing Group Ltd. Barnetson, R. S. C et al. BMJ 2002;324:1376-1379 No Caption FoundEl eczema puede ser primera manifestación de Atopia 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 14
- 15. No alimento sólido por 4 meses. Breast-feeding for 6 months WHO dietary guidelines recommend 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 15
- 16. EHF. …Formulas lacteas hidrolizadas extensas. Marcas: Ver charla ….Wich infant formula…. Med book de JHS… 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 16
- 17. Feed Protein Source Fat Source Indications Nutramigen (Mead Johnson) Hydrolysed Casein LCT Malabsorption of whole protein with/without disaccharide intolerance Pregestimil (Mead Johnson) Hydrolysed Casein 55% MCT As above plus fat malabsorption Pepti Junior (Cow & Gate) Hydrolysed Whey 50% MCT As above plus fat malabsorption Pepti (Cow & Gate) Hydrolysed Whey LCT CHO – 40% lactose Cows Milk intolerance Nan H.A. (Nestle) Partially hydrolysed whey LCT Atopic allergy prophylaxis Neocate (SHS) Free amino acids LCT Severe malabsorption/ multiple allergy 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 17
- 18. En Nicaragua , no tenemos esas leches No las importan por el alto costo… Bueno mejor prevenir que remediar…. Siga dando el pecho… 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 18
- 20. Indice de Predicción ….Martinez Herramienta fundamental para intervención precoz . Ig E cordón Umbilical Lactancia Materna No fumar 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 20
- 21. No huevo No leche de vaca No usar leches de Soya Primeros años: Mani , nueces, mariscos. Uso de Probióticos ….Isolauri….. Ver charla… En Nicaragua Yogurt de Parmalat después del primer año de vida…. Usar leches hidrolizadas… ( Cochrane review ) ver… notas Allergy prevention in children Position Statement: ASCIA Position Statement: Summary of Allergy Prevention in Children, as published in the Medical Journal of Australia 2005; 182 (9): 464- 467 http://www.mja.com.au/public/issues/182_09_ 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 21
- 22. Reference: Sporik, R., Hill, D.J., Hosking, C.S. (2000). http://www.ncbi.nlm.nih.gov/sites/entrez 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 22
- 23. DOIA PeDOIA Dermis Atlas http://www.dermis.net/dermisroot/es/272 Atopia ( Familia ) IgE cordón Alergía alimenticia Dermatitis atópica Marcha Atópica 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 23
- 24. Crosta lactea Milia Areas alrededor boca, fosas nasales, ojos Diagnóstico Precoz Patologías asociadas Rinitis Conjuntivitis Asma Triade de la Mamá Nicaragüense.. Mi hijo Tiene : Moqueras, ojeras y Tos… 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 24
- 25. Evitar aeroalergenos Gato Acaros Polvo…. Cucarachas … Inner city study.. Buscar Signología Atópica Recordar el control biológico 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 25
- 26. • Resfriados # 3 • Eczema de Pañal • Rinitis • Sibilancias Factores de Riesgo Martinez,, taussig 95,2002, 2007 Buscar Signología Atópica 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 26
- 27. No conocemos la incidencia en Nicaragua…. Australia …..alta UK 1: 100…. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 27
- 28. Historia familiar atopia , Asma ( papá, mamá). Diagnóstico de dermatitis atópica Diagnóstico de rinitis alérgica Eosinofilia más de 4% Tres episodios de sibilancias el año anterior Sibilancias sin estar resfriado Otros posibles factores JHS… Eosinofilia muco nasal…. Diagnóstico de Eczema…. En el trópico coproparasitológico 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 28
- 29. Exposure to environmental tobacco smoke increasesthe risk of respiratory illness in children but data are inconclusive regarding the risk of IgE-sensitisation. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 29
- 30. Ulrich Wahn, PhD MD Virchow-Kl. Humboldt-Universitat 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 30
- 31. Notificar de las alergias del niño Llevar documentación escrita…. No intercambiar comida No aspirina No enlatados…. Seguir guías…. Ver doc pie de página Manejo de epinefrina… 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 31
- 32. Historia.... Iritantes químicos Irritantes físicos. Examen Físico Criterios Diagnósticos Hanifin, Rajka....80 UK working party..96 Paciente trabajo en busca signología atópica http://www.portalesmedicos.com/blogs/DrJuanHerre Cuestionarios operacionales …. Casas amistosas para Atópicos….Dr. Juan Herrera Salazar 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 32
- 33. eMedecine Atopic Dermatitis Bernice R Krafchik, MBChB, FRCPC, Updated: Mar 18, 2011 Barrera de protección…consecuencias inmunológicas ( Th1, Th2 The filaggrin gene (FLG) Anomalías en la producción de ceramide. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 33
- 34. Hiperreactividad de la piel ( esta reacciona a factores ambientales inocuos a la mayoría de las personas ) La piel funciona como barrera protectora. Aumento de la pérdida de agua trans epidérmica: Reducción ceramides: moléculas hidrofílicas presentes en el estrato corneo, barrera menos eficiente. Aumento de la absorción de antígenos 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 34
- 35. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 35
- 36. Este sitio ofrece uno de los Atlas de dermatologia más completos . Lo encontraremos en varios idiomas A cooperation between the Dept. of Clinical Social Medicine (Univ. of Heidelberg) and the Dept. of Dermatology (Univ. of Erlangen) http://www.dermis.net/derm 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 36
- 37. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 37
- 38. Until Hanifin and Rajka[7] developed diagnostic criteria for the diagnosis of atopic dermatitis in 1980, no standardized methods were available to make the diagnosis. Ver pàgina en excel: Criterios UK Hanifin JM, Rajka G 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 38
- 39. Coloque 144 imagenes encontradas en miniatura,…. Hagan click en la imagen que quieran discutir con su paciente … Link a la descripción y el diagnóstico diferencial …. Ora et lavora… 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 39
- 40. Mascherone ( máscara ) Palor perioral Prurigo Diatésico de Besnier Neurodermitis diseminata Neurodermitis constitutionalis Eczema endógeno Síndrome Hiper IgE 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 40
- 41. 144 imagenes encontradas todas en miniatura,…. Hagan click en la imagen que quieran discutir con su paciente … descripción y el diagnóstico diferencial …. Ora et lavora… 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 41
- 42. Signo Hertoghe Palmae hiperlinearis 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 42
- 43. Escamas …………………… xerosis 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 43
- 44. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 44
- 45. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 45
- 46. Cluster de la Ictiosis Piel seca Keratosis pilaris Palmae hiperlinearis Prominencia Folicular Ictiosis vulgar 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 46
- 47. Dirty Neck 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 47
- 48. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 48
- 49. Piel seca Liquenificación Lichen Simplex Chronicus 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 49
- 50. Perleche 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 50
- 51. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 51
- 52. 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 52
- 53. Blefaritis Asociado a Eczema Atópico 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 53
- 54. Eritrema Periorbitario Allergic shinners 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 54
- 55. Distorsión arquitectura Palpebral Simblefarón Ectropión Entropión Triquiasis 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 55
- 56. • Síntomas • Picazón • Quemazón • Fotofobia • Lagrimeo • Signos – Eczema palpebral – Hiperemia – Neovascularización Cornea – Keratopatia Punctata – Ulcera cornea – Keratocono – Catarata 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 56
- 57. • Neovascularización de la cornea edema,moco,ulceración 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 57
- 58. Atopic Dermatitis Author: Brian S Kim, MD; Chief Editor: William 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 58
- 59. Contact Dermatitis, Allergic Contact Dermatitis, Irritant Immunodeficiency Lichen Simplex Chronicus Mollusca contagiosa with dermatitis Mycosis fungoides Nummular Dermatitis Psoriasis, Plaque Relative zinc deficiency Scabies Seborrheic Dermatitis Tinea Corporis 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 59
- 60. tratamiento… Medicamentos… Bibliografía y fotos de emedecine… 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 60
- 61. http://emedicine.medscape.com/article/10 Encontrara 4 fotos muy ilustrativas… Gracias por la paciencia… 02/09/13Marcha atopicaTel 2278-1169, 2270-3359, 8946-5022, 8882-5513 61
- 62. Desde Nicaragua Dr. Juan Herrera Salazar….
Editor's Notes
- Pathophysiology: Good evidence indicates that genetic factors are important in the development of atopic dermatitis, but the pathophysiology is still poorly understood. Two main hypotheses have been proposed regarding the development of the inflammatory lesions. The first suggests an immune dysfunction resulting in IgE sensitization and a secondary epithelial-barrier disturbance. The second proposes a defect in epithelial cells leading to the defective barrier problem, with the immunological aspects being epiphenomena. In healthy individuals, balance exists between 2 important subdivisions of T cells (ie, T H 1, T H 2). The immune hypothesis invokes an imbalance in the T lymphocytes, with T H 2 cells predominating; this results in cytokine production of interleukins 4, 5, 12, and 13 and granulocyte macrophage colony-stimulating factor, causing an increase in IgE and lowered interferon gamma levels. Later, in persons with chronic atopic dermatitis, the T H 1-type cells predominate. Other cell types are also involved in the process, including eosinophils, Langerhans cells, keratinocytes, and B cells. [2] The second hypothesis involves defective barrier function in the stratum corneum of Atopic dermatitis patients, leading to the entry of antigens that result in the production of inflammatory cytokines. Some authors question whether the antigens can also be absorbed from the gut (eg, from food) and the lungs (eg, from house dust mites). Xerosis is known to be an associated sign in many atopic dermatitis patients. Evidence has shown multiple loss-of-function mutations in the filaggrin gene ( FLG ) on band 1q21.3 in patients with atopic dermatitis in Europe and other filaggrin mutations in Japanese patients. This gene is mutated in persons with ichthyosis vulgaris ; it is associated with early-onset atopic dermatitis and with airway disease in the setting of atopic dermatitis. These changes are only found in 30% of European patients, begging the question of whether other genetic variants may also be responsiblefor some of the findings in the pathogenesis of atopic dermatitis. In atopic dermatitis, transepidermal water loss is increased. Defective lamellar bodies may be caused by abnormalities of ceramide production. Whether the inflammation causes primary or secondary epidermal barrier breakdown is not known, but with the knowledge that filaggrin is involved in epithelial disruption, it is now thought that this finding leads to increased transepidermal penetration of environmental allergens, increasing inflammation and sensitivity. [3, 4]
- Vamos a partir del paradigma educativo… debemos hacer que nuestros pacientes conozcan su enfermedad… podemos sólo asi llevarlos a modificar su conducta… debemos como médicos adoptar una filosofía de la educación, … debemos lograr darles un sentido , que sepan que existe una dimensión ética de la salud, ( educar al familia ) que ellos son agentes que pueden intervenir para modificar su enfermedad… Empowerment dicen los americanos … Formación capacitante diriamos en iberoamérica, dar a las familias las herramientas para lograr la autoeficacia. Con los pacientes debemos lograr acuerdos para beneficiar su salud….esto es un proceso Concordare… llegar a mutuos acuerdos.. El principio de benificialidad orientará nuestro comportamiento ético. La ética Nicomaquea ( Aristóteles ) se fundamenta en la ética de la virtud y puede ser un marco de referencia apropiado para la ética médica, y necesaria para la problemática bioética médica y especial.
- En la reunión de expertos de la OMS y la WAO se publicó el doc en el Link….. Guía importante …. Dar el documento a los pacientes.
- Curso WAO 2009: Answer: Family history, taken by an experienced clinician, is the most helpful identifier of children at increased risk of the development of allergy and asthma THIS IS CORRECT - Well done: For practical purposes a family history taken by an experienced clinician is helpful in identifying children at an increased risk for developing allergic manifestations and asthma. If both parents have allergic asthma, allergic rhinitis and allergic conjunctivitis, or atopic eczema/atopic dermatitis, the child has a four-fold risk of developing allergies compared with a child whose parents do not have allergies. If only one parent has allergic disease, the risk is about two-fold. Early signs of an allergic disease, especially atopic eczema/atopic dermatitis, and presence of IgE antibodies specific to inhalant allergens, are important risk factors for later respiratory allergy. For further information on the risks of developing atopic disease, access the references below: Prevention of Allergy and Allergic Asthma The Allergic March
- Allergy testing in children: why, who, when and how? WAO Course….. A. Høst , S. Andrae , S. Charkin , C. Diaz-Vázquez , S. Dreborg , P. A. Eigenmann , F. Friedrichs , P. Grinsted , G. Lack , G. Meylan , P. Miglioranzi , A. Muraro , A. Nieto , B. Niggemann , C. Pascual , M-G. Pouech , F. Rancé , E. Rietschel , M. Wickman Statement of The Section on Pediatrics, European Academy of Allergy and Clinical Immunology
- Curso Enero WAO: Well done: WHO dietary guidelines recommend exclusively. Studies suggest that exclusive breastfeeding and avoidance of solid foods for at least 4 months appears effective for allergy prevention.
- Curso Enero WAO: Well done: WHO dietary guidelines recommend exclusively. Studies suggest that exclusive breastfeeding and avoidance of solid foods for at least 4 months appears effective for allergy prevention.
- Nutramigen used in alllergy, Pregestimil for malabsorption and surgical patients (both lactose free) ESPACi recommmendation – use of extensively hydroysed formula for the prevention of allergy in high risk infants American Academy Pediatrics – formula should be tolerated by 90% of infants with CMPA with 95% confidence High risk is usually defined as infants with at least 1 first degree relative with documented atopic disease. Whey based formulations are more palatable Nan HA not for the treatment of CMPA
- Curso Enero WAO: Breastfeeding for at least 6 months and avoiding exposure to environmental tobacco smoke THIS IS CORRECT - WHO dietary guidelines recommend exclusively breast-feeding for 6 months. Studies suggest that exclusive breastfeeding and avoidance of solid foods for at least 4 months appears effective for allergy prevention. Environmental tobacco smoke causes wheezing in infants and aggravates asthma. All children benefit through avoidance of tobacco smoke. For further information on the risks of developing atopic disease, access the references below: Prevention of Allergy and Allergic Asthma The Allergic March Exposure to Environmental Tobacco Smoke and Sensitization in Children Abstract Background: Exposure to environmental tobacco smoke increases the risk of respiratory illness in children but data are inconclusive regarding the risk of IgE-sensitisation. Objective: To elucidate whether exposure to smoking pre- and/or postnatally is related to IgE-sensitisation in children at 4 years of age. Methods: As part of a prospective birth cohort study (BAMSE) a total of 4,089 families with children answered questionnaires when the child was 2 months, 1, 2 and 4 years on environmental factors and symptoms of allergic disease. Blood collected at age 4 years from 2,614 children was analysed for IgE antibodies to common inhalant and food allergens. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression with adjustments for potential confounders. Results: There was no evident association between maternal smoking during pregnancy and risk of IgE-sensitisation. In contrast, a dose-response effect was found for exposure to environmental tobacco smoke (ETS) from parental smoking during the first few months of life and IgE-sensitisation. There was an increased risk for sensitisation to inhalant and/or food allergens, ORadj= 1.28, (95% CI 1.01 to 1.62), among children exposed to ETS at 2 months of age. The risk appeared particularly elevated for indoor inhalant allergens, such as cat (ORadj 1.96; 95% CI 1.28 to 2.99), and for food allergens (ORadj 1.46; 95% CI 1.11 to 1.93). The IgE sensitising effect of ETS seemed to be confined to infants of parents without allergic diseases and to ETS exposure during early infancy. Conclusions: Our data indicate that exposure in early infancy to ETS increases the risk of IgE-sensitisation to indoor inhalant and food allergens. Keywords: Children, ETS, Parental smoking, Prevention, Sensitisation
- Summary When babies are not exclusively breastfed, use of hydrolysed infant formula instead of ordinary cow's milk formula may reduce allergies in babies and children, although further studies are needed to confirm this. Infant formulas have been designed to try to lower the chances of developing allergy or food intolerance. These include hydrolysed cow's and soy milk formulas. Hydrolysed formulas break down the milk proteins into smaller, potentially less allergy producing proteins. The review of trials found that there is no evidence to support feeding with a hydrolysed formula to prevent allergy in preference to exclusive breastfeeding. In infants at high risk for allergy who are unable to be completely breastfed, there is limited evidence that feeding with a hydrolysed formula compared to a cow's milk formula reduces allergies in babies and children, including cow's milk allergy. Concerns regarding quality of the evidence and consistency of the results indicates further studies are needed. This is a Cochrane review abstract and plain language summary, prepared and maintained by The Cochrane Collaboration, currently published in The Cochrane Database of Systematic Reviews 2008 Issue 3, Copyright © 2008 The Cochrane Collaboration. Published by John Wiley and Sons, Ltd.. The full text of the review is available in The Cochrane Library (ISSN 1464-780X). This record should be cited as: Osborn DA, Sinn J. Formulas containing hydrolysed protein for prevention of allergy and food intolerance in infants. Cochrane Database of Systematic Reviews 2006, Issue 4. Art. No.: CD003664. DOI: 10.1002/14651858.CD003664.pub3. This version first published online: October 20. 2003 Date of last substantive update: July 27. 2006
- Specificity of allergen skin testing in predicting positive open food challenges to milk, egg and peanut in children. Clin Exp Allergy, [Online]. 30(11), [Accessed Friday 18 th January 2008], pp. 1495-8, Available from World Wide Web: <>
- Ese link nos da 144 imágenes tengalas listas para que muestre a la madre una como la de sus hijos y se persuada del diagnostico correcto….. En nuestro pais hay mucho sarcoptes scabaie…. Y en medicina general se usa benzoato de bencilo….. Y estas lesiones se sobre infectan ,…. Impetigo…. Bueno en en tropico no podemos olvidar las formas numulares …granulomatosas de estas manifestaciones parasitarias…
- Ver libro de cuentos en el blog Juan Herrera Salazar….. Programas educativos
- Exposure to these aeroallergens should be reduced as much as is possible. THIS IS CORRECT - Well Done: Well Done: The evidence that avoidance of "indoor allergens" can help in the management of perennial rhinitis, asthma and atopic dermatitis is derived from two kinds of studies: First, where the patients are moved to a sanatorium or "allergen free unit" and second, where avoidance measures are taken in the patient's home. Studies of the first type have been uniformly successful, whether they involved moving to an alpine village or a hospital room. By contrast, there has been a wide range of results with avoidance studies at home and many such studies have not been successful often due to an adequate reduction of allergen exposure: This and other reasons for negative studies are discussed in this review . However, a recent study investigated 937 inner-city children with atopic asthma (aged 5 to 11 years) in seven major U.S. cities. This study was a randomized, controlled trial that lasted one year and included education and individualized, home-based, comprehensive environmental intervention, including impermeable bedding covers. The result showed a significantly decreased exposure to indoor allergens (including cockroach and dust-mite allergens) and significantly reduced asthma-associated morbidity.
- Martinez F. Definition, risk factors and early natural history. Am J Resp Crit Care Med 1995; 151: s1-244. 2.-Savcdev HP, Vasanti B, Satyanarayana L, Puri PK. Simple predictors to differentiate acute asthma froma ARI in children: implications for refining case management in the ARI Control Programme. Indian Pediatrc 1994; 31: 1251-9 3.-Martinez FD. What we have learned from the Tucson Children´s Respiratory Study? Paediatr Respir Rev 2002; 193-7 4.-Van Asperen PP, Mukhi A. Role of atopy in the natural history of wheeze and bronchial hyperresponsiveness in childhood. Pediatrc Allergy Immunol 1994; 178-83 5.-Phelan PD, Robertson CF, Olinsky A. The Melbourne Asthma Study 1964-1999. J Allergy Clin Immunol 2002; 109: 189-194 6.-Seidler A, Schauld M, Raum E, Schwartz FW. Predictors of follow-up course of asthma complaints in early childhood – results od a follow-up study. Klin Padiatr 1998; 210: 24-9. 6.-National Asthma Education and Prevention Program. Expert Panel Report: Gudelines for the Diagnosis and Management of Asthma. Update on Selected Topics-2002. J Allergy Clin Immunol 2002; 110: s141-s219 7.-Castro-Rodríguez JA, Holberg JC, Wright AL , Martinez FD. A clinical index to define risk of asthma in young children with recurrent wheezing. Am J Respir Crit Care Med 2000; 162: 1403-1406 8.-Wahn U. What drives the allergic march?. Allergy 2000; 55: 591-599 9.-Hofer MF. Atopic dermatitis: the first allergic step in children Rev Med Suisse Romande 2000 Mar;120(3):263-7. 10.-Hattevig G y cols. Appearance of IgE antibodies to ingested and inhaled allergens during the first 12 years of life in atopic and non-atopic children. Pediatr Allergy Immunol 1993;4:182-86. 11.-Kulig M y cols. Long-lasting sensitization to food during the first two years precedes allergic airway disease. Pediatr Allergy Immunol 1998;9:61-67 12.-Sherrill D.L. y cols Total IgE and its association with asthma symptoms and allergic sensitization among children. J Allergy Clin Immunol 1999;104:28-36. 13.-Tariq S.M. y cols. The prevalence of and risk factors for atopy in early chilhood: A whole population birth cohort study. J Allergy Clin Immunol 1998;101:587-93 14.-Nickel R. y cols. Sensitization to hen’s egg at the age of twelve months is predictive for allergic sensitization to common indoor and outdoor allergens at the age of three years. J Allergy Clin Immnunol 1997;99:613-17. 15.-Bruno G y cols. Natural history of IgE antibodies in children at risk for atopy. Ann Allergy Asthma Immunol 1995;74:431-36 Dermatitis atópica 1.-Rajka G: Dermatitis atópica. En Rook Aj, Maibach HI eds. Recents advances in dermatology-6. Churchill Livinstone, Edinburgh, 1983. 2.-European Task Force on Atopic Dermatitis. Severity scoring of atopic dermatitis. Dermatology 1993; 186: 23-31. Pruebas de alergia 1.-Ten R, Klein J, Frigas E. Allergy skin testing. Mayo Clin Proc 1995: 70: 783-784. 2.-Bousquet J. In vivo methods for study of allergy; skin tests, techniques and interpretation. En Middlenton, Reed, Ellis, Adkinson & Yunginger (eds). Allergy: Principles and practice. St Louis: The CV Mosby Co; 1988: 419-36. 3.-Allergen standardization and skin test. Position Paper. The European Academy of Allergy and Clinical Immunology. Allergy 1993; 48 (suppl14): 44-82 4.-Lilja G, Oman H, Johansson SG. Development of atopic disease during childhood and its prediction by Phadiatop Paediatric. Clin Exp Allergy 1996 Sep;26(9):1073-9 5.-Sigurs N y cols. Sensitization in childhood atopic disease identified by Phadebas RAST, serum IgE and Phadiatop. Pediatr Allergy Immunol 1990;1:74-78. 6.-Lilja G, Kusoffsky E, Johansson SG, Oman H . Screening of atopic allergy in 5-year-old children--a comparison of the diagnostic properties of Phadiatop Paediatric and Phadiatop. Allergy 1995 Apr;50(4):316-21. 7.-Morell J, Mora I, Diaz C, Roldan B. Diagnóstico de los factores etiopatogénicos en el asma. En Cano A, Diaz CA, Monton JL editores. Asma en el niño y adolescente. Aspectos fundamentales para el pediatra de atención primaria. Madrid. ExLibris Ediciones, 2001. P 43-71 8.-NHZTA Group. Validity of clinical history and laboratiry tests in the diagnosis of asthma. A critical appraisal of the literature-2001. The Clearinghouse for the Health Outcomes and Health Technology Assesment. Disponible en http://nhzta.chmeds.ac.nz/ . fecha de consulta 14-enero-2003. 9.-Larraud L, Lasierra M. Metodos de diagnóstico en alergia (II): técnicas in vitro. En Martin Mateos Ed. Tratado de Alergologia Pediatrica.Madrid. Ergon, 2002. 89-125 10.-Dieguez MA. Estado actual de las técnicas de diagnóstico in vitro. Diaz CA, Garcia M editores. Curso Practico de Asma Infantil. Madrid. Ergon, 1997 32-38 11.-Kam KL, Hsieh KH Comparison of three in vitro assays for serum IgE with skin testing in asthmatic children. Ann Allergy 1994 Oct;73(4):329-36 13.-Plebani M, Borghesan F, Faggian D Clinical efficiency of in vitro and in vivo tests for allergic diseases. Ann Allergy Asthma Immunol 1995 Jan;74(1):23-8 14.-García-Noriega Fernández M. Pruebas cutáneas (prick test). En Diaz CA, Garcia M editores. Curso práctico sobre asma infantil: Ergón; 1997: 31-5. 15.-Dolen WK. Skin testing and immunoassays for allergen-specific IgE:a workshop report. An Allergy Asthma Immunol 1999; 82: 407-12
- he prevalence of food induced anaphylaxis varies with the dietary habits of a region. THIS IS CORRECT - Well Done: While the frequency of food induced anaphylaxis is becoming increasingly common in westernised countries, it is thought to be less common in non-westernised countries. The highest prevalence of anaphylaxis is in Australia and in the United Kingdom where the estimated prevalence is as high as one in one hundred people.
- Recordar la importancia de la giardia intestinalis….se asocia a urticaria crónica….
- Thorax . Published Online First: 18 December 2007. doi:10.1136/thx.2007.079053 Copyright © 2007 BMJ Publishing Group Ltd & British Thoracic Society This Article Full Text (Rapid PDF) All Versions of this Article: thx.2007.079053v1 63/2/172 most recent Alert me when this article is cited Alert me if a correction is posted Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lannerö, E. Articles by Nordvall, L. Search for Related Content PubMed PubMed Citation Articles by Lannerö, E. Articles by Nordvall, L. Papers Exposure to environmental tobacco smoke and sensitisation in children Eva Lannerö 1* , Magnus Wickerman 1 , Marianne van Hage 2 , Anna Bergström 1 , Göran Pershagen 1 and Lennart Nordvall 3 1 Institute of Environmental Medicine, KI, Sweden 2 Clinical and Allergy Unit, Department of medicine, KI, Sweden 3 Department of Women's and Children's Health, Uppsala University, Sweden * To whom correspondence should be addressed. E-mail: [email_address] . Abstract Background: Exposure to environmental tobacco smoke increases the risk of respiratory illness in children but data are inconclusive regarding the risk of IgE-sensitisation. Objective: To elucidate whether exposure to smoking pre- and/or postnatally is related to IgE-sensitisation in children at 4 years of age. Methods: As part of a prospective birth cohort study (BAMSE) a total of 4,089 families with children answered questionnaires when the child was 2 months, 1, 2 and 4 years on environmental factors and symptoms of allergic disease. Blood collected at age 4 years from 2,614 children was analysed for IgE antibodies to common inhalant and food allergens. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression with adjustments for potential confounders. Results: There was no evident association between maternal smoking during pregnancy and risk of IgE-sensitisation. In contrast, a dose-response effect was found for exposure to environmental tobacco smoke (ETS) from parental smoking during the first few months of life and IgE-sensitisation. There was an increased risk for sensitisation to inhalant and/or food allergens, ORadj= 1.28, (95% CI 1.01 to 1.62), among children exposed to ETS at 2 months of age. The risk appeared particularly elevated for indoor inhalant allergens, such as cat (ORadj 1.96; 95% CI 1.28 to 2.99), and for food allergens (ORadj 1.46; 95% CI 1.11 to 1.93). The IgE sensitising effect of ETS seemed to be confined to infants of parents without allergic diseases and to ETS exposure during early infancy. Conclusions: Our data indicate that exposure in early infancy to ETS increases the risk of IgE-sensitisation to indoor inhalant and food allergens. Keywords: Children, ETS, Parental smoking, Prevention, Sensitisation
- La explicación de este tema es una tarea díficil….. Trato de situarme para comunicar con mi paciente desde una propuesta de estilo de vida antroposófico, en cierto modo orgánico… No usar muchos desinfectantes…. No uso de Lysol y similares en spray, usar con mucho cuidado los antibióticos , sólo cuando deba prescribirlos por una indicación verdadera….. Ver amoníacos cuaternarios, hipocloritos , otros irritantes, no fumar… Explicar lo de las mascotas requiere mucho equilibrio…. Esto es un arte… avancemos en el aprendizaje del arte de la comunicación, por ahora los exhorto a aprender …si descubro tips, se los comunicaré..
- t is essential that guidelines for managing children and students with food allergies, such a those developed by the Food Allergy and Anaphylaxis Network (FAAN) or other national organisations are followed carefully. THIS IS CORRECT - Well Done: Responsibilities lie with the sufferer when he/she is old enough and with the family and the Daycare center/school. Child/Student's Responsibility when of appropriate age: Should not trade food with others. Should not eat anything with unknown ingredients or known to contain any allergen. Should be proactive in the care and management of their food allergies and reactions based on their developmental level. Should notify an adult immediately if they eat something they believe may contain the food to which they are allergic. Family's Responsibility: Notify the Daycare center of the child's allergies. Work with the Daycare/school team to develop a plan that accommodates the child's needs throughout the Daycare/school including in the play area, in the cafeteria and in after-care programs. Provide written medical documentation, instructions, and medications as directed by a physician. Include a photo of the child on the written documentation. Provide properly labelled medications and replace medications after use or upon expiration. Educate the child in the self-management of their food allergy including: Safe and unsafe foods. Strategies for avoiding exposure to unsafe food.s Symptoms of allergic reactions. How and when to tell an adult they may be having an allergy-related problem. How to read food labels (age appropriate). Daycare center/school's Responsibility: Review the health records submitted by parents and physicians. Include food-allergic children in all Daycare activities. Children should not be excluded from activities solely based on their food allergy. Identify a core team of, but not limited to, nurse, teacher, principal, Daycare/school food service and nutrition manager/director to work with parents and the student (age appropriate) to establish a prevention plan. Changes to the prevention plan to promote food allergy management should be made with core team participation. Assure that all staff who interact with the child/student on a regular basis understand food allergy, can recognize symptoms, know what to do in an emergency, and work with other Daycare/school staff to eliminate the use of food allergens in the allergic hild/student's meals, educational tools, arts and crafts projects, or incentives. For further information, access the references below: Prevention of Allergy and Allergic Asthma Food allergy and Anaphylaxis Network - School Guidelines For Managing Students with Food Allergies
- He elaborado un cuestionario operacional para ver que tan amistosas son las casas de los pacientes atópicos…. Exploren el Link y usen el cuestionario…. Este cuestionario no es una heramienta de investigación sirve para ayudar a las familias a cambiar sus hábitos….. Ellas van a reconocer un mal hábito…. Ej. fumar …. Trabajaremos para cambiar el hábito , cambiarlo por uno amistoso…no fumar…. Uds. pueden usar las unidades que propuse para dar un valor númerico o simplemente construir una escala analógica par evaluar el progreso.
- Pathophysiology Good evidence indicates that genetic factors are important in the development of atopic dermatitis (AD), but the pathophysiology is still poorly understood. Two main hypotheses have been proposed regarding the development of the inflammatory lesions. The first suggests an immune dysfunction resulting in IgE sensitization and a secondary epithelial-barrier disturbance. The second proposes a defect in epithelial cells leading to the defective barrier problem, with the immunological aspects being epiphenomena. In healthy individuals, balance exists between 2 important subdivisions of T cells (ie, T H 1, T H 2). The immune hypothesis invokes an imbalance in the T lymphocytes, with T H 2 cells predominating; this results in cytokine production of interleukins 4, 5, 12, and 13 and granulocyte macrophage colony-stimulating factor, causing an increase in IgE and lowered interferon gamma levels. Later, in persons with chronic AD, the T H 1-type cells predominate. Other cell types are also involved in the process, including eosinophils, Langerhans cells, keratinocytes, and B cells. 2 The second hypothesis involves defective barrier function in the stratum corneum of AD patients, leading to the entry of antigens that result in the production of inflammatory cytokines. Some authors question whether the antigens can also be absorbed from the gut (eg, from food) and the lungs (eg, from house dust mites). Xerosis is known to be an associated sign in many AD patients. Evidence has shown multiple loss-of-function mutations in the filaggrin gene ( FLG ) on band 1q21.3 in patients with AD in Europe and other filaggrin mutations in Japanese patients. This gene is mutated in persons with ichthyosis vulgaris ; it is associated with early-onset AD and with airway disease in the setting of AD. These changes are only found in 30% of European patients, begging the question of whether other genetic variants may also be responsible for some of the findings in the pathogenesis of AD. In AD, transepidermal water loss is increased. Defective lamellar bodies may be caused by abnormalities of ceramide production. Whether the inflammation causes primary or secondary epidermal barrier breakdown is not known, but with the knowledge that filaggrin is involved in epithelial disruption, it is now thought that this finding leads to increased transepidermal penetration of environmental allergens, increasing inflammation and sensitivity. 3, 4
- Por eso nosotros recetamos esas cremas liquidas restauradoras…. Explicar a la madre …. La piel no la podemos cambiar….es el hábito ( habitus ) del niño…pero si podemos hidratar abundantemente.
- Figure 1. Clinical, Histologic, and Immunohistochemical Aspects of Atopic Dermatitis. Panel A shows initial lesions of early-onset atopic dermatitis involving the cheek and scalp in an infant at 4 months of age. Panel B shows classic head and neck manifestations of atopic dermatitis in an adult. Panel C shows typical chronic, lichenified flexural lesions in an adult. The arrow in Panel D (hematoxylin and eosin), which shows the typical histologic aspects of acute lesions, indicates a spongiotic area within the epidermis. The asterisk indicates the prominent perivascular infiltrate. Panel E (hematoxylin and eosin) shows a chronic lesion with thickening of the epidermis. The asterisk indicates the prominent perivascular infiltrate.
- Figure 1. Clinical, Histologic, and Immunohistochemical Aspects of Atopic Dermatitis. Panel A shows initial lesions of early-onset atopic dermatitis involving the cheek and scalp in an infant at 4 months of age. Panel B shows classic head and neck manifestations of atopic dermatitis in an adult. Panel C shows typical chronic, lichenified flexural lesions in an adult. The arrow in Panel D (hematoxylin and eosin), which shows the typical histologic aspects of acute lesions, indicates a spongiotic area within the epidermis. The asterisk indicates the prominent perivascular infiltrate. Panel E (hematoxylin and eosin) shows a chronic lesion with thickening of the epidermis. The asterisk indicates the prominent perivascular infiltrate.
- Hanifin JM, Rajka G. Diagnostic features of atopic dermatitis. Acta Derm Venereol (Stockh) . 1980;92 (suppl):44-7.
- Nota : es siempre imortante consultar al oftalmólogo….. Cuidado las complicaciones….. En todo caso debe evaluar….. Ver roximas diapositivas… Keratoconjunctivitis atópica…
- Complicaciones ver el recuadro… consultar siempre oftalmólogo….. Muy importante ver siguiente diapositiva…
- Desde mi primera evaluación , discuto con el oftalmólogo los hallazgos …. Estos son exclusivos del manejo especializado , es importante enseñar al paciente el manejo evitativo… ver en la próxima charla aspectos prácticos del manejo…. El uso del jabón , shampoo , evitar sprays para el cabello y otros cosméticos……
- Desde mi primera evaluación , discuto con el oftalmólogo los hallazgos …. Estos son exclusivos del manejo especializado , es importante enseñar al paciente el manejo evitativo… ver en la próxima charla aspectos prácticos del manejo…. El uso del jabón , shampoo , evitar sprays para el cabello y otros cosméticos……
- Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in early infancy (an adult-onset variant is recognized); it is characterized by pruritus, eczematous lesions, xerosis (dry skin), and lichenification (thickening of the skin and an increase in skin markings). Atopic dermatitis may be associated with other atopic (immunoglobulin E [IgE]) diseases (eg, asthma, allergic rhinitis, urticaria, acute allergic reactions to foods). [1] Atopic dermatitis has enormous morbidity, and the incidence and prevalence appear to be increasing. Other conditions with different etiologies and prognoses are often grouped under the umbrella of a diagnosis of atopic dermatitis. Pathophysiology Good evidence indicates that genetic factors are important in the development of atopic dermatitis, but the pathophysiology is still poorly understood. Two main hypotheses have been proposed regarding the development of the inflammatory lesions. The first suggests an immune dysfunction resulting in IgE sensitization and a secondary epithelial-barrier disturbance. The second proposes a defect in epithelial cells leading to the defective barrier problem, with the immunological aspects being epiphenomena. In healthy individuals, balance exists between 2 important subdivisions of T cells (ie, T H 1, T H 2). The immune hypothesis invokes an imbalance in the T lymphocytes, with T H 2 cells predominating; this results in cytokine production of interleukins 4, 5, 12, and 13 and granulocyte macrophage colony-stimulating factor, causing an increase in IgE and lowered interferon gamma levels. Later, in persons with chronic atopic dermatitis, the T H 1-type cells predominate. Other cell types are also involved in the process, including eosinophils, Langerhans cells, keratinocytes, and B cells. [2] The second hypothesis involves defective barrier function in the stratum corneum of Atopic dermatitis patients, leading to the entry of antigens that result in the production of inflammatory cytokines. Some authors question whether the antigens can also be absorbed from the gut (eg, from food) and the lungs (eg, from house dust mites). Xerosis is known to be an associated sign in many atopic dermatitis patients. Evidence has shown multiple loss-of-function mutations in the filaggrin gene ( FLG ) on band 1q21.3 in patients with atopic dermatitis in Europe and other filaggrin mutations in Japanese patients. This gene is mutated in persons with ichthyosis vulgaris ; it is associated with early-onset atopic dermatitis and with airway disease in the setting of atopic dermatitis. These changes are only found in 30% of European patients, begging the question of whether other genetic variants may also be responsiblefor some of the findings in the pathogenesis of atopic dermatitis. In atopic dermatitis, transepidermal water loss is increased. Defective lamellar bodies may be caused by abnormalities of ceramide production. Whether the inflammation causes primary or secondary epidermal barrier breakdown is not known, but with the knowledge that filaggrin is involved in epithelial disruption, it is now thought that this finding leads to increased transepidermal penetration of environmental allergens, increasing inflammation and sensitivity. [3, 4] Epidemiology Frequency United States The prevalence rate for atopic dermatitis is 10-12% in children and 0.9% in adults. More recent information examining physician visits for atopic dermatitis in the United States from 1997-2004 estimates a large increase in office visits for atopic dermatitis occurred. In addition, blacks and Asians visit more frequently for atopic dermatitis than whites. Note that this increase involves all disease under the umbrella of atopic dermatitis and it has not been possible to allocate which type has increased so rapidly. [5] International The prevalence rate of atopic dermatitis is rising, and atopic dermatitis affects 15-30% of children and 2-10% of adults. This figure estimates the prevalence in developed countries. In China and Iran, the prevalence rate is approximately 2-3%. The frequency is increased in patients who immigrate to developed countries from underdeveloped countries. [6] Mortality/Morbidity Incessant itch and work loss in adult life is a great financial burden. A number of studies have reported that the financial burden to families and government is similar to that of asthma, arthritis, and diabetes mellitus. In children, the disease causes enormous psychological burden to families and loss of school days. Mortality due to atopic dermatitis is unusual. Kaposi varicelliform eruption (eczema herpeticum) is a well-recognized complication of atopic dermatitis.It usually occurs with a primary herpes simplex infection, but it may also be seen with recurrent infection. Vesicular lesions usually begin in areas of eczema and spread rapidly to involve all eczematous areas and healthy skin. Lesions may become secondarily infected. Timely treatment with acyclovir ensures a relative lack of severe morbidity or mortality. Another cause of Kaposi varicelliform eruption is vaccination with vaccinia for the prevention of small pox, but because this is no longer mandatory, patients with atopic dermatitis do not develop the sequelae of eczema vaccinatum that has been seen in the past. It was usually contracted by the patient from the vaccination of themselves or their close relatives. This condition had a high mortality rate (up to 25%). In the current climate of threats of bioterrorism, vaccination may once again become necessary, and physicians should be aware of eczema vaccinatum in this setting. Note that chickenpox vaccine does not carry the same risk as herpes simplex and vaccinia. Bacterial infection with Staphylococcus aureus or Streptococcus pyogenesis is not infrequent in the setting of atopic dermatitis . The skin of patients with atopic dermatitis is colonized by S aureus. Colonization does not imply clinical infection, and physicians should only treat patients with clinical infection. The emergence of methicillin-resistant S aureus (MRSA) may prove to be a problem in the future in these patients. Eczematous and bullous lesions on the palms and soles are often infected with beta-hemolytic group A Streptococcus. Urticaria and acute anaphylactic reactions to food occur with increased frequency in patients with atopic dermatitis. The food groups most commonly implicated include peanuts, eggs, milk, soya, fish, and seafood. In studies in peanut-allergic children, the vast majority were atopic. Latex allergy is more common in patients with atopic dermatitis than in the general population. Of atopic dermatitis patients, 30% develop asthma and 35% have nasal allergies. Race Atopic dermatitis affects persons of all races. Immigrants from developing countries living in developed countries have a higher incidence of atopic dermatitis than the indigenous population, and the incidence is rapidly rising in developed countries Sex The male-to-female ratio for atopic dermatitis is 1:1.4. Age In 85% of cases, atopic dermatitis occurs in the first year of life; in 95% of cases, it occurs before age 5 years. The incidence of atopic dermatitis is highest in early infancy and childhood. The disease may have periods of complete remission, particularly in adolescence, and may then recur in early adult life. In the adult population, the rate of atopic dermatitis frequency is 0.9%, but onset may be delayed until adulthood. History Incessant pruritus is the only symptom of atopic dermatitis, children often scratch themselves uncontrollably. Although pruritus may be present in the first few weeks of life, parents become more aware of the itch as the itch-scratch cycle matures when the patient is aged approximately 3 months. The disease typically has an intermittent course with flares and remissions occurring, often for unexplained reasons. Physical Primary findings of atopic dermatitis include xerosis, lichenification, and eczematous lesions. Excoriations and crusting are common. The eczematous changes and its morphology are seen in different locations depending on the age of the patient. InfancyAtopic dermatitis is usually noticed soon after birth. Xerosis occurs early and often involves the whole body; the diaper area is usually spared. The earliest lesions affect the creases (antecubital and popliteal fossae), with erythema and exudation. Over the following few weeks, lesions usually localize to the cheeks, the forehead and scalp, and the extensors of the lower legs; however, they may occur in any location on the body, usually sparing the diaper area. Lesions are ill-defined, erythematous, scaly, and crusted (eczematous) patches and plaques. Lichenification is seldom seen in infancy. A typical presentation is shown in the image below.Typical atopic dermatitis on the face of an infant. ChildhoodXerosis is often generalized. The skin is flaky and rough. Lichenification is characteristic of childhood atopic dermatitis. It signifies repeated rubbing of the skin and is seen mostly over the folds, bony protuberances, and forehead. Lesions are eczematous and exudative. Pallor of the face is common; erythema and scaling occur around the eyes. Dennie-Morgan folds (ie, increased folds below the eye) are often seen. Flexural creases, particularly the antecubital and popliteal fossae, and buttock-thigh creases are often affected. See the image below.Flexural involvement in childhood atopic dermatitis. Excoriations and crusting are common. The crusting with atopic dermatitis should not be confused with infection because both may manifest oozing and crusting. AdulthoodLesions become more diffuse with an underlying background of erythema. The face is commonly involved and is dry and scaly. Xerosis is prominent. Lichenification may be present. A brown macular ring around the neck is typical but not always present. It represents localized deposition of amyloid. See the image below.Dirty neck sign in chronic atopic dermatitis. Until Hanifin and Rajka [7] developed diagnostic criteria for the diagnosis of atopic dermatitis in 1980, no standardized methods were available to make the diagnosis. Since then, numerous other experts have developed different criteria suitable for their own environment, and varying with age. The original criteria of Hanifin and Rajka have been modified many times. Efforts to develop practical clinical criteria have not been successful, and those available are not suitable for all geographic areas and age groups. The lack of a good chemical marker for diagnosing the disease is an enormous obstacle to the study of atopic dermatitis. The following is a constellation of criteria commonly used for the diagnosis of atopic dermatitis: Pruritus Eczematous changes that vary with age Chronic and relapsing course Early age of onset Atopy (IgE reactivity) Xerosis Personal history of asthma or hay fever or a history of atopic diseases in a first-degree relative in patients younger than 4 years Onset younger than age 2 years (not used if child is aged < 4 y) A firm diagnosis of atopic dermatitis depends on excluding conditions such as scabies, allergic contact dermatitis, seborrheic dermatitis (SD), cutaneous lymphoma, ichthyosis, psoriasis, immunodeficiency, and other primary disease entities. Causes Genetics [8, 9] : A family history of atopic dermatitis is common. Genome-wide scans have highlighted several atopic dermatitis–related loci on 3q21, 1q21, 16q, 17q25, 20p, and 3p26. Several candidate genes have been identified (5q31-33); they all encode cytokines involved in the regulation of IgE synthesis. Infection: The skin of patients with atopic dermatitis is colonized by S aureus . Clinical infection with S aureus often causes a flare of atopic dermatitis, and S aureus has been proposed as a cause of atopic dermatitis by acting as a superantigen. Hygiene: The hygiene hypothesis is touted as a cause for the increase in atopic dermatitis. This attributes the rise in atopic dermatitis to reduced exposure to various childhood infections and bacterial endotoxins. [10, 11] Climate: Atopic dermatitis flares occur in extremes of climate. Heat is poorly tolerated, as is extreme cold. A dry atmosphere increases xerosis. Sun exposure improves lesions, but sweating increases pruritus. These external factors act as irritants or allergens, ultimately setting up an inflammatory cascade. Food antigens: The role of food antigens in the pathogenesis of atopic dermatitis is controversial, both in the prevention of atopic dermatitis and by the withdrawal of foods in persons with established atopic dermatitis. Most reported studies have methodologic flaws. Because of the controversy regarding the role of food in atopic dermatitis, most physicians do not withdraw food from the diet. Nevertheless, acute food reactions (urticaria and anaphylaxis) are commonly encountered in children with atopic dermatitis. Probiotics [12] : The role of probiotics in the diet of patients with atopic dermatitis remains controversial Aeroallergens: A role for aeroallergens and house dust mites has been proposed, but this awaits further corroboration.
- Laboratory Studies No chemical marker for the diagnosis of atopic dermatitis is known. Laboratory testing is seldom necessary. A swab of infected skin may help with the isolation of a specific organism and antibiotic sensitivity. Allergy and radioallergosorbent testing is of little value. A platelet count for thrombocytopenia helps exclude Wiskott-Aldrich syndrome , and testing to rule out other immunodeficiencies may be helpful. Scraping to exclude tinea corporis is occasionally helpful. Histologic Findings Biopsy shows an acute, subacute, or chronic dermatitis, but no specific findings are demonstrated. Medical Care Patients with atopic dermatitis do not usually require emergency therapy, but they may visit the emergency department for treatment of acute flares caused by eczema herpeticum and bacterial infections. For further information on treatment, see the NICE Guidelines Issued for Treating Atopic Eczema in Children . [14] Moisturization in atopic dermatitisDepending on the climate, patients usually benefit from 5-minute, lukewarm baths followed by the application of a moisturizer such as white petrolatum. Frequent baths with the addition of emulsifying oils (1 capful added to lukewarm bath water) for 5-10 minutes hydrate the skin. The oil keeps the water on the skin and prevents evaporation to the outside environment. In infants, 3 times a day is not a great burden; in adults, once or twice a day is usually all that can be achieved. Leave the body wet after bathing. Advise patients to apply an emollient such as petrolatum or Aquaphor all over the body while wet, to seal in moisture and allow water to be absorbed through the stratum corneum. The ointment spreads well on wet skin. The active ingredient should be applied before the emollient. Newer emollients such as Atopiclair and Mimyx have been advocated as having superior results, but they are expensive and need further evaluation. Topical steroids in atopic dermatitisTopical steroids are currently the mainstay of treatment. In association with moisturization, responses have been excellent. Ointment bases are preferred, particularly in dry environments. Initial therapy consists of hydrocortisone 1% powder in an ointment base applied 3 times daily to lesions on the face and in the folds. A midstrength steroid ointment (triamcinolone or betamethasone valerate) is applied 2-3 times daily to lesions on the trunk until the eczematous lesions clear. Steroids are discontinued when lesions disappear and are resumed when new patches arise. Flares may be associated with seasonal changes, stress, activity, staphylococcal infection, or contact allergy. Contact allergy is rare but accounts for increasing numbers of flares. These are seen mostly with hydrocortisone. The results of a study from the Netherlands by Haeck et al suggest that the use of topical corticosteroids for atopic dermatitis on the eyelids and periorbital region is safe with the respect to induction of glaucoma or cataracts. [15] Immunomodulators in atopic dermatitisTacrolimus (topical FK506) is an immunomodulator that acts as a calcineurin inhibitor. Studies have shown excellent results compared with placebo and hydrocortisone 1%. Little absorption occurs. A stinging sensation may occur following application, but this can be minimized by applying the medication only when the skin is dry. The burning usually disappears within 2-3 days. Tacrolimus is available in 2 strengths, 0.1% for adults and 0.03% for children, although some authorities routinely use the 0.1% preparation in children. Tacrolimus is an ointment and is indicated for moderate-to-severe atopic dermatitis. It is indicated for children older than 2 years. Pimecrolimus 1% is also an immunomodulator and calcineurin inhibitor. It is more effective than placebo. Pimecrolimus is produced in a cream base for use twice a day; it is indicated for mild atopic dermatitis in persons older than 2 years and is particularly useful on the face. A 2006 black box warning has been issued in the United States based on research that has shown an increase in malignancy in association with the calcineurin inhibitors. While these claims are being investigated further, the medication should likely only be used as indicated (ie, for atopic dermatitis in persons older than 2 y and only when first-line therapy has failed). These agents are much more expensive than corticosteroids and should only be used as second-line therapy. Other treatments, effective and ineffective, in atopic dermatitisProbiotics have been explored as a therapeutic option for the treatment of atopic dermatitis. The rationale for their use is that bacterial products may induce an immune response of the T H 1 series instead of T H 2 and could therefore inhibit the development of allergic IgE antibody production. Some report limited benefit in preventive and therapeutic roles. [16] This research has yet to be proven. UV-A, UV-B, a combination of both, psoralen plus UV-A (PUVA), or UV-B1 (narrow-band UV-B) therapy may be used. Long-term adverse effects of skin malignancies in fair-skinned individuals should be weighed against the benefits. In patients with eczema herpeticum, acyclovir is effective. In patients with severe disease, and particularly in adults, phototherapy, methotrexate (MTX), azathioprine, cyclosporine, and mycophenolate mofetil [17] have been used with success. Both hydroxyzine and diphenhydramine hydrochloride provide a certain degree of relief from itching but are not effective without other treatments. Ketotifen (a calcium channel blocker) may be effective. Oil of evening primrose was believed to be effective, but in a randomized controlled study, it showed no benefit in children and little improvement in adults. Unsuccessful therapy with everolimus, a rapamycin-derived macrolide, has been reported in 2 patients with severe atopic dermatitis. Combination therapy with either prednisone or cyclosporine A was not effective. [18] However, reports of the ineffectiveness of everolimus have be questioned. [19] Results with many other medications, such as thymopentin, gamma interferon, and Chinese herbs, have been disappointing. Many medications are not practical to use, and they can be expensive. Some Chinese herbal preparations contain prescription medications, including prednisone, and have been associated with cardiac and liver problems. Antibiotics are used for the treatment of clinical infection caused by S aureus or flares of disease. They have no effect on stable disease in the absence of infection. Laboratory evidence of S aureus colonization is not evidence of clinical infection because staphylococcal organisms commonly colonize the skin of patients with atopic dermatitis. A randomized, investigator-blinded, placebo-controlled trial including 31 patients showed that intranasal mupirocin ointment and diluted bleach (sodium hypochlorite) baths improved atopic dermatitis symptoms in patients with clinical signs of secondary bacterial infection. [20] Nonmedical efforts in atopic dermatitisClothing should be soft next to the skin. Cotton is comfortable and can be layered in the winter. Cool temperatures, particularly at night, are helpful because sweating causes irritation and itch. A humidifier (cool mist) prevents excess drying and should be used in both winter, when the heating dries the atmosphere, and in the summer, when air conditioning absorbs the moisture from the air. Clothes should be washed in a mild detergent with no bleach or fabric softener. Food avoidance is discussed in Diet, below, and in Causes. Consultations Consulting an allergist may be necessary, particularly if the patient develops asthma and/or hay fever or an acute reaction to a food. Diet Avoid foods that provoke acute allergic reactions (hives, anaphylaxis). Most frequently, allergic reactions occur to peanuts (peanut butter), eggs, seafood, milk, soya, and chocolate. Additionally, advise patients to apply a barrier of petroleum jelly around the mouth prior to eating to prevent irritation from tomatoes, oranges, and other irritating foods. Activity Advise patients to avoid activities that cause excessive sweating. Also, swimming in an outdoor pool (or wading pool for babies) in summer provides therapeutic benefit by exposing the person to the sun but avoiding the heat. Medication Summary The basis of treatment for atopic dermatitis is to provide moisturization for dryness, allay pruritus, and manage inflammation of the eczematous lesions. Anti-inflammatory agents Class Summary Provide relief of inflammation of eczematous lesions. Ointment base provides moisturization. White petrolatum is useful to avoid potential sensitization to preservatives in water-based moisturizers. View full drug information Hydrocortisone ointment 1% (Cortaid) Mild topical corticosteroid mixed in petrolatum. Has mineralocorticoid and glucocorticoid effects and anti-inflammatory activity. Use 1% ointment 2-3 times daily. View full drug information Betamethasone topical (Beta-Val) Medium-strength topical corticosteroid for body areas. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells. Use 0.05-0.1% ointment in adults and 0.05% ointment in pediatrics. Antihistamines Class Summary Provide symptomatic relief of pruritus. View full drug information Hydroxyzine hydrochloride (Atarax) Antihistamine with antipruritic, anxiolytic, and mild sedative effects. Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS. Syr available as 10 mg/5 mL. View full drug information Diphenhydramine (Benadryl) Antihistamine used for pruritus and allergic reactions. Immunomodulators Class Summary For treatment of patients with severe disease in whom conventional therapy is ineffective. In more severe cases and particularly in adults, consider using both MTX and cyclosporine. The latter is more efficacious, but lesions recur when it is stopped. View full drug information Cyclosporine (Neoral, Sandimmune) Demonstrated to be helpful in a variety of skin disorders, especially psoriasis. Acts by inhibiting T-cell production of cytokines and ILs. Like tacrolimus and pimecrolimus (ascomycin), cyclosporine binds to macrophilin and then inhibits calcineurin, a calcium-dependent enzyme, which, in turn, inhibits phosphorylation of nuclear factor of activated T cells and inhibits transcription of cytokines, particularly IL-4. Discontinue treatment if no response within 6 wk. View full drug information Methotrexate (Folex PFS, Rheumatrex) Antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction. Satisfactory response seen 3-6 wk following administration. Adjust dose gradually to attain satisfactory response. View full drug information Tacrolimus (Protopic) ointment 0.03% or 0.1% Immunomodulator that suppresses humoral immunity (T-lymphocyte) activity. Used for refractory disease. Antiviral agents Class Summary For management of herpetic infections and to treat atopic dermatitis in patients who develop chickenpox. View full drug information Acyclovir (Zovirax) Inhibits activity of both HSV-1 and HSV-2. Has affinity for viral thymidine kinase and, once phosphorylated, causes DNA-chain termination when acted on by DNA polymerase. Patients experience less pain and faster resolution of cutaneous lesions when used within 48 h of rash onset. May prevent recurrent outbreaks. Early initiation of therapy is imperative. Zoster dose is 4 times higher than that for herpes simplex. Duration of therapy varies. Antibiotics Class Summary Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. For the treatment of clinical infection by S aureus, cloxacillin or cephalexin is used. In streptococcal infections, cephalexin is preferred. If not effective, penicillin and clindamycin in combination are effective. Consider staphylococcal infection in every flare of atopic dermatitis. View full drug information Cephalexin (Keflex) First-generation cephalosporin arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora; used for skin infections or prophylaxis in minor procedures. Available susp include mauve granules (125 mg/5 mL) and peach granules (250 mg/5 mL). View full drug information Cloxacillin (Cloxapen, Tegopen) For treatment of infections caused by penicillinase-producing staphylococci. May be used to initiate therapy when a staphylococcal infection is suspected. View full drug information Penicillin VK (Beepen-VK, Betapen-VK, Veetids) Inhibits biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached, and most effective during stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects. View full drug information Clindamycin (Cleocin) Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Further Outpatient Care Monitor atopic dermatitis patients frequently. Reinforce therapeutic regimens with patients. Inpatient & Outpatient Medications Medications are used as described in Medication. Deterrence/Prevention Moisturization is important on an ongoing basis and may prevent flares. Complications If topical corticosteroids are used inappropriately or if superpotent steroids are used in teenagers during rapid growth, striae may occur. Skin thinning can result if steroids are used inappropriately in older patients. Whether verrucae vulgaris and mollusca contagiosa are more frequent is difficult to assess, but they are more widespread and difficult to eliminate. Tachyphylaxis to topical steroids occurs if they are not used on a stop-start basis. Prognosis Most patients improve; this can occur at any age. While the frequency of atopic dermatitis is as high as 20% in childhood, [21] it is 0.9% in adults. One third of patients develop allergic rhinitis. One third of patients develop asthma. Patient Education Frequently reinforce treatment and maintenance regimens with patients. Advise patients to contact the National Eczema Association for Science and Education at 4460 Redwood Hwy, Suite 16-D, San Rafael, CA 94903-1953. Inform patients that treatment does not produce cure but good control can be achieved Show videos to patients that show how to apply medication and that discuss the role of moisturization. For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Eczema.