M.A. (Clinical Psychology) / The purpose of this study was to determine whether a behavioural intervention could reduce scratching behaviour in atopic dermatitis. The literature dealing with the psychological aspects, and existing approaches to the treatment of atopic dermatitis and related dermatoses was reviewed. It was hypothesized that if subjects with atopic dermatitis were able to reduce their scratching behaviour they would show a corresponding reduction in size of identified lesions. In order to test these hypotheses, SUbjects with atopic dermatitis participated in a self-control programme lasting between eight and ten weeks. Of the seven subj ects that originally started the programme, four completed it. SUbjects' self-monitoring details reflected changes in scratching behaviour, and a specially designed grid was used to measure changes in lesion size. Inspection of the data showed that two SUbjects eliminated their scratching behaviour and lesions entirely; the other two showed marked reduction. The results of this study indicate that self-control procedures could be usefully applied as adjuncts to the conventional dermatological management of atopic dermatitis.

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Memoria para optar al Título Profesional de Médico Veterinario / La dermatitis atópica canina es una enfermedad de la piel, genética, inflamatoria, alérgica y prurítica. El signo clínico principal es el prurito marcado, el cual produce en el paciente una serie de signos secundarios en respuesta a éste. Este círculo conduce al paciente a presentar lesiones por autotraumatismo; las cuales conllevan a complicaciones secundarias como la dermatitis por Malassezia. En la literatura se describe la probabilidad de su presencia en pacientes atópicos, debiendo aplicar las medidas de manejo pertinentes. Este estudio tiene por objetivo general el estimar la asociación de dermatitis atópica canina y la presencia de Malassezia pachydermatis en pacientes caninos. En los objetivos específicos se busca establecer la presencia de Malassezia pachydermatis en pacientes atópicos y en individuos sanos; describir el número de levaduras observadas al examen microscópico directo con la gravedad de los signos y describir la presencia o ausencia de colonias al cultivo con la gravedad de los signos. Se realizó la prueba de X² a los pacientes con dermatitis atópica canina y al grupo control (animales sanos), para resultado del examen microscópico directo, la que dio como resultado la asociación de la dermatitis atópica canina y la presencia de Malassezia pachydermatis en pacientes caninos. Se aplicó la prueba exacta de Fisher a los resultados de cultivo de hongos en pacientes atópicos y en el grupo control, que arrojó la asociación de las variables. Se trabajó con un N=27, tanto para el grupo de atópicos y para el grupo de animales sanos. Al citológico, en un 52% de los pacientes del grupo en estudio se observó levaduras (40X). En el 22% de los pacientes se observó una a tres levaduras por campo. En el 11% se observó cuatro a diez levaduras por campo. Un 11% también registró más de diez levaduras por campo. En el cultivo de hongos, un 26% de los pacientes tuvo crecimiento de colonias y en el 74% restante no hubo crecimiento. En el grupo control, en el 89% de los pacientes no hubo observación de levaduras; en el 11% de los pacientes restantes se observó una cantidad leve. En el grupo control, no hubo desarrollo de colonias de Malassezia

Memoria para optar al Título Profesional de Médico Veterinario / La dermatitis atópica (DA) canina se define como una enfermedad a la piel con predisposición genética, inflamatoria y pruriginosa, con ciertas características clínicas propias de la enfermedad. Múltiples son los protocolos para tratar la enfermedad, siendo uno de ellos los inhibidores de la calcineurina como son la ciclosporina y el tacrolimus. En este estudio aleatorio doble-ciego, se evaluó la eficacia del tratamiento con tacrolimus 0,1% (base pomada) en comparación a un placebo (base pomada sin principio activo), para el tratamiento de DA localizada. Nueve perros diagnosticados con DA y con más de una lesión localizada ingresaron al estudio. En cada paciente se trataron dos lesiones, una con tacrolimus 0,1% y la otra con el placebo por un periodo de cuatro semanas, dos veces al día. Se evaluaron las lesiones al inicio, a los 14 y 28 días, midiendo el grado de eritema, liquenificación, excoriación y alopecia autoinducida, con valores de cero a tres puntos, llegando a tener un posible total de 12 puntos por lesión. Después de las cuatro semanas de tratamiento la disminución significativa de las valoraciones de las lesiones fue tanto para el tacrolimus 0,1% (p= 0,00035) como para el placebo (p= 0,048). En los controles realizados los días 14 y 28 no se obtuvieron diferencias significativas entre las valoraciones de las lesiones de los tratamientos realizados. El porcentaje de lesiones que alcanzó el 50% de mejoría fue de un 66%, tanto para el tratamiento realizado con el tacrolimus 0,1% y como para el tratamiento con el placebo. A través de la Prueba de Fisher se concluyó que la mejoría de las lesiones no estaba asociada al tratamiento entregado (p=0,0012). Ninguno de los perros presentó reacciones adversas a la droga en los sitios de aplicación. Los resultados de este estudio sugieren que el tacrolimus 0,1% no presenta una eficacia significativa en comparación con el placebo para el tratamiento de lesiones localizadas de DA

Atopic dermatitis, AD (synonym eczema) is a chronic inflammatory skin disease. It affects between 10 to 20% of children and 1 to 3% of adults worldwide. It is an important cause of morbidity and is estimated to cost £465 million per annum to the UK. AD is part of a family of Th-2 driven diseases and is often the first of these atopic diseases to manifest. The development of AD is often followed by asthma and allergic rhinitis later in life (a phenomenon known as the ‘atopic march’). Up to 50% of moderate to severe AD cases have been associated with genetic mutations affecting the epidermal barrier protein filaggrin. Filaggrin aggregates keratin filaments during terminal keratinocyte differentiation, allowing normal epidermal stratification. The role of filaggrin in maintaining a functional skin barrier is further supported by a clinical study conducted by ourselves. This is the first clinical study on a European cohort (58 participants) which showed that FLG mutations were associated with experimentally demonstrable defects of skin barrier function (increased baseline transepidermal water loss), more so following exposure to a chemical irritant. However, the majority of patients with AD, especially the milder cases, do not have FLG mutations. Some of the wild-type patients in our study were noticed to have accumulation of the large filaggrin proprotein and a lack of filaggrin monomers, indicating defective proteolysis of profilaggrin into the functional monomers. Our study also found disproportionately raised protease inhibitory activities amongst the AD participants. This inappropriately raised protease inhibition may interfere with profilaggrin proteolysis, leading to the development of AD in some wild-type patients. Having demonstrated that deficiency of filaggrin monomers is associated with a defective skin barrier, we focused on the function of filaggrin in the skin and attempted to improve the skin barrier function. In addition to keratin aggregation, filaggrin constitutes the natural moisturizing factors in the epidermis following its natural breakdown into amino acids. We note that filaggrin is disproportionately rich in amino acid histidine, implying that this amino acid may have a particular significance in maintaining a functional epidermal barrier. Using an in-house skin-equivalent model, we have shown that by increasing the histidine content in the cell culture media, we could increase the expression of filaggrin monomers and reduce the penetration of a fluorescent dye into the skin-equivalents. The latter indicates improved barrier function. Finally, we conducted a pilot human study which showed that histidine, when applied to mechanically damaged skin in AD and healthy participants, was associated with a faster recovery of the skin barrier function. These studies suggest that histidine is of therapeutic benefits in AD. A histidine-based treatment may be developed as an alternative to current anti-inflammatory and immunosuppressive agents used to treat AD.

Memoria para optar al Título Profesional de Médico Veterinario / La dermatitis atópica canina ha sido definida como una enfermedad alérgica prurítica, inflamatoria y predispuesta genéticamente que se cree afecta a un 10-15% de la población canina. La inmunoterapia es, según la OMS, el único tratamiento que puede alterar el curso de las enfermedades alérgicas y ha sido definida como la práctica de administrar gradualmente cantidades crecientes de un extracto alergénico a un sujeto alérgico para aminorar los síntomas asociados con exposición subsiguiente al alergeno causante. En Medicina Veterinaria, varios estudios han reportado la eficacia de la inmunoterapia. Sin embargo, con raras excepciones, estos estudios han sido diseñados como experimentos abiertos y no controlados. Los objetivos de este estudio fueron averiguar la proporción de perros atópicos positivos a Dermatophagoides farinae en una prueba de intradermorreacción, describir la población en estudio en cuanto a raza, sexo y edad, describir los cambios clínicos en perros atópicos bajo tratamiento con inmunoterapia alergeno específica para D. farinae y describir los cambios en el resultado de una segunda prueba de intradermorreacción después de la inmunoterapia. Se realizó una prueba de intradermorreacción a treinta perros atópicos. Quince de los perros positivos a D. farinae fueron ingresados al estudio y colocados al azar en dos grupos. Un grupo (n = 10) fue tratado con inmunoterapia para D. farinae durante 6 meses, y el otro grupo (n = 5) no fue tratado. Los perros fueron evaluados mensualmente para los signos clínicos de prurito, eritema, hiperpigmentación, tinción salival, pioderma, alopecia, liquenificación, otitis, seborrea, queilitis, conjuntivitis y mal olor. Después del tratamiento, se repitió la prueba de intradermorreacción para D. farinae. El 75% de los perros fueron positivos a D. farinae. El 26,66% de los perros ingresados al estudio fueron mestizos, el 80% fueron hembras y el promedio de edad fue de 4,6 años. Hubo diferencia significativa entre ambos grupos para los signos de prurito, eritema y tinción salival, pero no la hubo para hiperpigmentación, pioderma, alopecia, liquenificación, otitis, seborrea, queilitis, conjuntivitis y mal olor. No hubo diferencia significativa entre los grupos para la disminución del tamaño de la pápula de D. farinae en la segunda prueba de intradermorreacción

Wong Kin Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 151-166). / Abstracts in English and Chinese. / Chapter (I) --- ABSTRACT (IN ENGLISH) --- p.i / Chapter (II) --- Abstract (in Chinese) --- p.iv / Chapter (III) --- ACKNOWLEDGEMENTS --- p.vii / Chapter (IV) --- PERSONAL CONTRIBUTION TO THE WORK --- p.ix / Chapter (V) --- PUBLICATIONS --- p.x / Chapter (VI) --- TABLE OF CONTENTS --- p.xi / Chapter (VII) --- List of Abbreviations --- p.xvi / Chapter (VIII) --- LIST OF FIGURES --- p.xx / Chapter (IX) --- LIST OF TABLES --- p.xxii / Chapter Section 1: --- GENERAL INTRODUCTION / Chapter CHAPTER 1 --- General Introduction of Atopic Dermatitis --- p.1-8 / Chapter 1.1. --- Definition of Atopic Dermatitis --- p.1 / Chapter 1.2. --- Epidemiology and Classification --- p.3 / Chapter 1.3. --- Factors Provoking Flares of AD / Chapter 1.3.1. --- Genetics --- p.5 / Chapter 1.3.2. --- "Allergens-Food Allergens, Aeroallergens and Autoallergens" --- p.6 / Chapter 1.3.3. --- Microbial Colonization: Staphylococcus Aureus (S. aureus) --- p.7 / Chapter CHAPTER 2 --- Measurements of AD Severity and Quality of Life Impairment --- p.9-14 / Chapter 2.1. --- Scoring of Atopic Dermatitis severity and the SCORing Atopic Dermatitis (SCORAD) Index --- p.9 / Chapter 2.2. --- Quality of life Measurement --- p.10 / Chapter 2.3. --- The Children's Dermatology Life Quality Index --- p.11 / Chapter CHAPTER 3 --- Management of AD --- p.15-19 / Chapter 3.1. --- Current Management of AD and Their Drawbacks --- p.15 / Chapter 3.2. --- Traditional Chinese Herbal Medicne (TCHM) / Chapter 3.2.1. --- General Principle of TCHM --- p.17 / Chapter 3.2.2. --- Side Effects of Using TCHM --- p.18 / Chapter 3.2.3. --- Literature Reviews of TCHM Use in Treating AD --- p.18 / Chapter CHAPTER 4 --- The Pentaherbs Formula for AD Treatment --- p.20-26 / Chapter 4.1. --- Pilot study: Pentaherbs Capsule as Treatment Option of AD Children --- p.20 / Chapter 4.2. --- Literature Review: Nature of Five Herbs / Chapter 4.2.1. --- PHF as Treatment Option of AD under TCHM Concepts --- p.22 / Chapter 4.2.2. --- PHF as Treatment Option of AD from Modern Research Literature --- p.22 / Chapter CHAPTER 5 --- Pathobiology of Atopic Dermatitis --- p.27-40 / Chapter 5.1. --- Nature of Complexity of Pathogenesis --- p.27 / Chapter 5.2. --- Skin barrier-impairment of epidermal barrier --- p.28 / Chapter 5.3. --- Biphasic T cell response in skin of AD --- p.29 / Chapter 5.4. --- Nature of Immunoglobulin-E and its Role in Atopic Dermatitis --- p.32 / Chapter 5.5. --- Innate Immunity Defect in AD --- p.33 / Chapter 5.6. --- Role of Superantigen in Pathogenesis of AD --- p.35 / Chapter 5.7. --- "Cytokines, Chemokines and Inflammatory Mediators in Pathogenesis of Atopic Dermatitis" / Chapter 5.7.1. --- Proinflammatory Cytokines --- p.37 / Chapter 5.7.2. --- Th1/Th2 Cytokines --- p.37 / Chapter 5.7.3. --- Chemokines --- p.38 / Chapter 5.7.4. --- Pruritus Mediators --- p.39 / Chapter Section 2: --- CLINICAL TRIAL OF PENTAHERBS / Chapter CHAPTER 1 --- Objective --- p.41 / Chapter CHAPTER 2 --- Materials and Methods (RCT) --- p.42-51 / Chapter 2.1. --- Materials / Chapter 2.1.1. --- SCORAD worksheet --- p.42 / Chapter 2.1.2. --- CDLQI questionnaire --- p.42 / Chapter 2.1.3. --- Allergic Rhinitis Score (ARS) --- p.43 / Chapter 2.1.4. --- ELISA Assay Kits --- p.43 / Chapter 2.1.5. --- EDTA blood collestion tubes --- p.43 / Chapter 2.2. --- Methods / Chapter 2.2.1. --- Design --- p.45 / Chapter 2.2.2. --- Intervention --- p.45 / Chapter 2.2.3. --- Treatment / Chapter 2.2.3.1 --- The Pentaherbs Formula --- p.45 / Chapter 2.2.3.2 --- Randomization --- p.48 / Chapter 2.2.3.3 --- Concomitant Treatment in Study Period --- p.48 / Chapter 2.2.4. --- Participants --- p.49 / Chapter 2.2.5. --- Outcome Measures --- p.50 / Chapter 2.2.6. --- Statistical Analysis --- p.50 / Chapter CHAPTER 3 --- Results (RCT) --- p.52-67 / Chapter 3.1. --- Demographics --- p.52 / Chapter 3.2. --- Drug Compliance --- p.55 / Chapter 3.3. --- Efficacy / Chapter 3.3.1. --- SCORAD Score --- p.56 / Chapter 3.3.2. --- Quality of Life Score --- p.56 / Chapter 3.3.3. --- Duration and Amount of CS Usage --- p.59 / Chapter 3.3.4. --- Amount of Antihistamine Usage --- p.61 / Chapter 3.3.5. --- Allergic Rhinitis Score --- p.61 / Chapter 3.3.6. --- Blood chemistry and Haematology --- p.63 / Chapter 3.3.7. --- Plasma TARC and BDNF level --- p.63 / Chapter 3.4. --- Tolerability --- p.65 / Chapter Section 3: --- IN VITRO STUDY OF PENTAHERBS / Chapter CHAPTER 1 --- Objectives and Study Design --- p.68 / Chapter CHAPTER 2 --- Materials and Methods (In vitro Study) --- p.69-86 / Chapter 2.1. --- Materials for in vitro study / Chapter 2.1.1. --- Preparation of the Water Extracts of PHF Capsules --- p.69 / Chapter 2.1.2. --- Endotoxin Assay --- p.69 / Chapter 2.1.3. --- Cell isolation and culture ofPBMC / Chapter 2.1.3.1 . --- Cell Isolation from Human Peripheral Blood --- p.70 / Chapter 2.1.3.2. --- Culture of Peripheral Blood Mononuclear Cells --- p.70 / Chapter 2.1.4. --- Trypan Blue Exclusion Assay --- p.72 / Chapter 2.1.5. --- [3H]-Thymidine incorporation Assay --- p.72 / Chapter 2.1.6. --- Supernatant Collection and ELISA --- p.72 / Chapter 2.1.7. --- RNA Extraction and RT-PCR / Chapter 2.1.7.1. --- Reagents for RNA Extraction --- p.73 / Chapter 2.1.7.2. --- Reagents for Reverse Transcription --- p.73 / Chapter 2.1.7.3. --- Reagents for Polymerase Chain Reaction --- p.74 / Chapter 2.1.7.4. --- Reagents for Gel Electrophoresis --- p.74 / Chapter 2.2. --- Methods / Chapter 2.2.1. --- Isolation and Culture PBMC / Chapter 2.2.1.1. --- Isolation of PBMC --- p.76 / Chapter 2.2.1.2. --- Culture of Isolated PBMC --- p.76 / Chapter 2.2.1.3. --- PHA/SEB Treatment --- p.77 / Chapter 2.2.2. --- Preparation of PHF Water Extracts and Endotoxin Level / Chapter 2.2.2.1. --- Hot Water Extraction --- p.78 / Chapter 2.2.2.2. --- Limulus Amebocyte Lysate Assay --- p.78 / Chapter 2.2.3. --- Study on the Cytotoxic and Mitogenic Effects of PHF on PBMC / Chapter 2.2.3.1. --- Trypan Blue Exclusion Assay --- p.80 / Chapter 2.2.3.2. --- [3H]-Thymidine Incorporation Assay --- p.80 / Chapter 2.2.4. --- Study on the Effect of PHF on PBMC Inflammatory Mediator Production / Chapter 2.2.4.1. --- Determination of Inflammatory Mediator Expression Levels by ELISA --- p.82 / Chapter 2.2.4.2. --- Semi-quantification of Inflammatory Mediator mRNA Levels by RT-PCR --- p.83 / Chapter 2.2.5. --- Statistical Analysis --- p.86 / Chapter CHAPTER 3 --- Results(In vitro) --- p.87-114 / Chapter 3.1. --- preparation of PHF Water Extracts and Endotxin Level --- p.87 / Chapter 3.2. --- Cytotoxicity Effect of PHF on PBMC --- p.88 / Chapter 3.3. --- Mitogenicity Effect of PHF on PBMC --- p.93 / Chapter 3.4. --- Effects of PHF on Expression of Inflammatory Mediators from PBMC Following Mitogen (PHA) Stimulation / Chapter 3.4.1. --- Effects of PHF on mRNA Expression of Inflammatory Mediators from PHA-stimulated PBMC --- p.98 / Chapter 3.4.2. --- Effects of PHF on Secretion of Inflammatory Mediators from PHA-stimulated PBMC --- p.101 / Chapter 3.5 --- Effects of PHF on Expression of Inflammatory Mediators from SEB-stimulated PBMC / Chapter 3.5.1. --- Effects of PHF on mRNA Expression of Inflammatory --- p.106 / Chapter 3.5.2. --- Effescts of PHF on secretion of inflammatory Mediatorsfrom SEM-Stimulated PBMC --- p.109 / Chapter 3.6. --- Summarization of Effects of PHF on Expression of Inflammatory Mediators from PHA- and SEB-stimulated PBMC / Chapter 3.6.1. --- Mitogen (PHA) Stimulation --- p.114 / Chapter 3.6.2. --- Superantigen (SEB) Stimulation --- p.114 / Chapter Section 4: --- DISCUSSIONS / Chapter CHAPTER 1 --- Discussions on RCT of PHF --- p.115-122 / Chapter 1.1. --- Clinical Efficacy and Tolerability of PHF for Treatment of Children AD: a RCT study / Chapter 1.2. --- Efficacy of PHF for Treatment of Children with AD --- p.117 / Chapter 1.3. --- Safety and Tolerability of PHF Use for Treatment of Children with AD --- p.119 / Chapter 1.4. --- Rounding up --- p.121 / Chapter CHAPTER 2 --- Discussions on In vitro Immunomodulatory Activities of PHF --- p.123-130 / Chapter 2.1. --- General Effects of PHF on PBMC --- p.123 / Chapter 2.2. --- Effects of PHF on Inflammatory Mediators Expression in PBMC --- p.124 / Chapter CHAPTER 3 --- Limitations of the Present Study --- p.131-132 / Chapter Section 5: --- CONCLUSIONS AND FUTURE PROSPECTS / Chapter CHAPTER 1 --- Conclusions --- p.133 / Chapter CHAPTER 2 --- Future Prospects --- p.134-135 / Chapter Section 6: --- APPENDICES / Appendix1 --- p.137 / Appendix2 --- p.142 / Appendix3 --- p.149 / Chapter Section 7: --- BIBLIOGRAPHY --- p.151-166