Severe Atopy Research Articles

Autosomal recessive phosphoglucomutase 3 (PGM3) mutations link glycosylation defects to atopy, immune deficiency, autoimmunity, and neurocognitive impairment

Identifying genetic syndromes that lead to significant atopic disease can open new pathways for investigation and intervention in allergy. We sought to define a genetic syndrome of severe atopy, increased serum IgE levels, immune deficiency, autoimmunity, and motor and neurocognitive impairment. Eight patients from 2 families with similar syndromic features were studied. Thorough clinical evaluations, including brain magnetic resonance imaging and sensory evoked potentials, were performed. Peripheral lymphocyte flow cytometry, antibody responses, and T-cell cytokine production were measured. Whole-exome sequencing was performed to identify disease-causing mutations. Immunoblotting, quantitative RT-PCR, enzymatic assays, nucleotide sugar, and sugar phosphate analyses, along with matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry of glycans, were used to determine the molecular consequences of the mutations. Marked atopy and autoimmunity were associated with increased T(H)2 and T(H)17 cytokine production by CD4(+) T cells. Bacterial and viral infection susceptibility were noted along with T-cell lymphopenia, particularly of CD8(+) T cells, and reduced memory B-cell numbers. Apparent brain hypomyelination resulted in markedly delayed evoked potentials and likely contributed to neurologic abnormalities. Disease segregated with novel autosomal recessive mutations in a single gene, phosphoglucomutase 3 (PGM3). Although PGM3 protein expression was variably diminished, impaired function was demonstrated by decreased enzyme activity and reduced uridine diphosphate-N-acetyl-D-glucosamine, along with decreased O- and N-linked protein glycosylation in patients' cells. These results define a new congenital disorder of glycosylation. Autosomal recessive hypomorphic PGM3 mutations underlie a disorder of severe atopy, immune deficiency, autoimmunity, intellectual disability, and hypomyelination.

Mendelian Inheritance Of Elevated Tryptase Associated With Atopy and Connective Tissue Abnormalities

Mendelian diseases of atopy are rare, but have revealed important insights and novel pathways in the pathophysiology of allergic disease. A large cohort of patients and their families were referred for evaluation of suspected mast cell disorders, severe atopy, and/or eosinophilic inflammation. Comprehensive clinical evaluations were performed and fractionated serum tryptase levels were obtained. Bone marrow biopsies were performed as clinically indicated, and mast cell number was quantified in the marrow. In vitro basophil activation was assayed and patients were subjected to cutaneous vibratory challenge. Nine families were identified with inherited elevations in basal serum tryptase (mean, 21.9 ng/mL) following an autosomal dominant pattern. Episodic flushing, abdominal pain, gastrointestinal distress and/or urticaria were seen in 26/32 individuals with elevated tryptase. Atopic disease, anaphylaxis, connective tissue abnormalities, chronic musculoskeletal pain, eosinophilic esophagitis, autonomic dysregulation and neuropsychiatric illness were additional common features. Upon cutaneous vibratory challenge, all tested individuals (n = 16) rapidly developed pruritis and expansive erythema. Bone marrow biopsies were performed in 5 index patients revealing an increase in mast cell number without pathologic changes or evidence of clonality. Basophil activation was also significantly reduced in vitro, among all affected individuals assayed (n = 10). This is the first clinical description of a dominantly inherited atopic syndrome characterized by elevated basal serum tryptase, allergic disease, connective tissue abnormalities, and diminished in vitro basophil activation.

Recurrent Skin and Lung Infections in Autosomal Dominant Hyper IgE Syndrome with Transactivation Domain STAT3 Mutation.

Background. Hyper IgE is a rare systemic disease characterized by the clinical triad of high serum levels of IgE (>2000 IU/mL), eczema, and recurrent staphylococcal skin and lung infections. The presentation of hyper IgE syndrome is highly variable, which makes it easy to confuse the diagnosis with that of severe atopy or other rare immunodeficiency disorders. Case Report. A 23-year-old Hispanic presented with history of frequent respiratory and gastrointestinal infections as a child and multiple episodes of skin and lung infections (abscess) with Staphylococcus aureus throughout his adult life. He had multiple eczematous lesions and folliculitis over his entire body, oral/esophageal candidiasis, and retention of his primary teeth. The IgE was elevated (>5000 IU/mL). Genetic mutation analysis revealed a mutation affecting the transactivation domain of the STAT3 gene. Conclusion. The hallmark of hyper IgE syndrome is serum IgE of >2000 IU/mL. Hyper IgE syndrome is a genetic disorder that is either autosomal dominant or recessive. A definite diagnosis can be made with genetic mutation analysis, and in this case, it revealed a very rare finding of the transactivation domain STAT3 mutation. Hyper IgE syndrome is a challenge for clinicians in establishing a diagnosis in suspected cases.

Sleep and allergic disease: A summary of the literature and future directions for research

Atopic diseases, such as asthma and allergic rhinitis, are common conditions that can influence sleep and subsequent daytime functioning. Children and patients with allergic conditions from ethnic minority groups might be particularly vulnerable to poor sleep and compromised daytime functioning because of the prevalence of these illnesses in these groups and the high level of morbidity. Research over the past 10 years has shed light on the pathophysiologic mechanisms (eg, inflammatory mediators) involved in many atopic diseases that can underlie sleep disruptions as a consequence of the presence of nocturnal symptoms. Associations between nocturnal symptoms and sleep and poorer quality of life as a result of missed sleep have been demonstrated across studies. Patients with severe illness and poor control appear to bear the most burden in terms of sleep impairment. Sleep-disordered breathing is also more common in patients with allergic diseases. Upper and lower airway resistance can increase the risk for sleep-disordered breathing events. In patients with allergic rhinitis, nasal congestion is a risk factor for apnea and snoring. Finally, consistent and appropriate use of medications can minimize nocturnal asthma or allergic symptoms that might disrupt sleep. Despite these advances, there is much room for improvement in this area. Asummary of the sleep and allergic disease literature is reviewed, with methodological, conceptual, and clinical suggestions presented for future research.

The HLA‐G and IL‐17A Expression in Nasal Polyposis

Objective: The HLA-G molecules are nonclassic class I antigens with anti-inflammatory and tolerogenic properties, while interleukin-17A (IL-17A) is a key inflammatory cytokine in many disorders. Considering that, the aims of this study were: 1) to evaluate the HLA-G molecule, and 2) to evaluate IL-17A expression in patients presenting with nasal polyposis. Method: Samples of patients presenting with nasal polyposis (n = 20) were subjected to immunohistochemistry technique. All patients were grouped into atopic and nonatopic patients according to skin prick test and IgE dosage. All statistical analyses were performed using the GraphPad Prism 5.0. The level of statistical significance was accepted at P < .05. Results: Our preliminary results showed the HLA-G and IL-17A expression in nasal polyposis. Immunohistochemical staining demonstrated a higher expression of HLA-G molecule in samples of nonatopic patients when compared with atopic patients ( P = .04). The IL-17A expression was also observed in both atopic and nonatopic patients; however, the numbers of IL-17A positive cells were greater in nasal polyps of atopic patients than in those of nonatopic patients. Conclusion: These preliminary results indicated that HLA-G and IL-17A may play an important role in the pathology of nasal polyposis. Considering the anti-inflammatory properties of HLA-G and inflammatory activities of IL-17A, we suggest that HLA-G could decreased the susceptibility to disease, while IL-17 should be associated with more severe atopy.

Vitamin D Insufficiency and Severe Asthma Exacerbations in Puerto Rican Children

Vitamin D insufficiency (a serum 25(OH)D <30 ng/ml) has been associated with severe asthma exacerbations, but this could be explained by underlying racial ancestry or disease severity. Little is known about vitamin D and asthma in Puerto Ricans. To examine whether vitamin D insufficiency is associated with severe asthma exacerbations in Puerto Rican children, independently of racial ancestry, atopy, and time outdoors. A cross-sectional study was conducted of 560 children ages 6-14 years with (n = 287) and without (n = 273) asthma in San Juan, Puerto Rico. We measured plasma vitamin D and estimated the percentage of African racial ancestry among participants using genome-wide genotypic data. We tested whether vitamin D insufficiency is associated with severe asthma exacerbations, lung function, or atopy (greater than or equal to one positive IgE to allergens) using logistic or linear regression. Multivariate models were adjusted for African ancestry, time outdoors, atopy, and other covariates. Vitamin D insufficiency was common in children with (44%) and without (47%) asthma. In multivariate analyses, vitamin D insufficiency was associated with higher odds of greater than or equal to one severe asthma exacerbation in the prior year (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.5-4.9; P = 0.001) and atopy, and a lower FEV(1)/FVC in cases. After stratification by atopy, the magnitude of the association between vitamin D insufficiency and severe exacerbations was greater in nonatopic (OR, 6.2; 95% CI, 2-21.6; P = 0.002) than in atopic (OR, 2; 95% CI, 1-4.1; P = 0.04) cases. Vitamin D insufficiency is associated with severe asthma exacerbations in Puerto Rican children, independently of racial ancestry, atopy, or markers of disease severity or control.

The Predictors of Elderly Asthma Control

The GINA guideline emphasizes the importance of achieving controlled state of asthma. We conducted this study to evaluate asthma control state in the elderly and predict factors related with poor control. A retrospective observational study evaluating 108 elderly asthmatics was done from October 2010 to March 2011. Subjects were classified into two: group I consisted of 38 patients with ACT≤19, group II included 70 patients with ACT>20. Spirometry, sputum eosinophil count and questionnaire survey (ACT and AQOL) were performed. Medication possession ratio(MPR) was calculated to evaluate compliance. The prevalence of severe asthma, aspirin intolerance, occupational asthma and atopy were 21.3%, 13.0%, 4.6% and 47.2%. The prevalence of co-morbid conditions was found in more than 50% of the patients in which allergic rhinitis was the most common followed by cardiovascular disease and degenerative arthritis. The 35.2% of patients were in poorly controlled state with significantly lower AQOL score and higher admission rate (p< 0.05 respectively). The prevalence of history with old pulmonary tuberculosis(TB) and admission for asthma showed significant differences between group I and II (31.6% vs 12.9%, 21.1% vs 7.1%, p <0.05 for both). Multivariate logistic regression analysis showed that history of TB was a significant predictor for poorly-controlled state (OR 4.61, CI 1.08-19.63, p value =0.039). The history of TB may contribute to the poorly-controlled state in elderly.

Resposta cutânea a alérgenos ambientais em indivíduos atendidos em serviço de pneumologia, Maringá, Estado do Paraná, Brasil

Respiratory allergies, especially rhinitis and asthma, are becoming increasingly common. Given that in northwestern Parana there is little data on the subject, our objective was to verify the causative agents of respiratory allergies and their complications in patients treated at a private pulmonology service in the municipality of Maringa, Parana. The study was observational, retrospective, lasting from January 2004 to December 2005. Patients were evaluated clinically, and the Prick TestR was performed. The age, positive test, major allergen reagents, presence or absence of atopy, rhinitis or asthma were noted for each individual. Of 396 individuals, 236 (59.3%) were positive for one or more allergens, whereas 80 (20.2%) were positive for three antigens and 85 (21.5%) to four or more. The reactivity of individuals was more frequent for house dust (207), Dermatophagoides pteronyssimus (184), Dermatophagoides farinae (158) and Blomia tropicalis (95). House dust, D. pteronyssimus and D. farinae occurred mainly in subjects with moderate to severe atopy. Over 70% of individuals from six to 20 years of age had atopy. Considering the high level of atopy in patients seen by the pulmonology service in Maringa, it is essential to undertake environment programs, along with monitoring and medical treatment of atopic individuals.

Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze

Severe viral respiratory illnesses and atopy are risk factors for childhood wheezing and asthma. The aim of this study was to explore associations between severe respiratory infections and atopy in early childhood with wheeze and asthma persisting into later childhood. 147 children at high atopic risk were followed from birth to age 10 yrs. Data on all respiratory infections occurring in infancy were collected prospectively and viral aetiology ascertained. Atopy was measured by skin prick tests at 6 months, and 2 and 5 yrs. History of wheeze and doctor-diagnosed eczema and asthma was collected regularly until 10 yrs of age. At 10 yrs, 60% of the cohort was atopic, 25.9% had current eczema, 18.4% current asthma and 20.4% persistent wheeze. 35.8% experienced at least one lower respiratory infection (LRI) associated with fever and/or wheeze in first year of life. Children who had wheezy or, in particular, febrile LRI in infancy and were atopic by 2 yrs, were significantly more likely to have persistent wheeze (RR 3.51, 95% CI 1.83-6.70; p<0.001) and current asthma (RR 4.92, 95% CI 2.59-9.36; p<0.001) at 10 yrs. Severe viral respiratory infections in infancy and early atopy are risk factors for persistent wheeze and asthma. The strongest marker of the asthmatogenic potential of early life infections was concurrent fever. The occurrence of fever during respiratory illnesses is an important marker of risk for wheeze and asthma later in childhood, suggesting it should be measured in prospective studies of asthma aetiology.

Letter concerning “Enzyme replacement therapy in a patient with Fabry disease and the development of IgE antibodies against agalsidase beta but not agalsidase alpha”, by Tanaka et al.

Dear editor, Recently, Tanaka and co-workers published a report in the Journal of Inherited Metabolic Disorders on the treatment of a young male with Fabry disease who developed an immunoglobulin E (IgE) response toward one of the two available enzyme preparations (agalsidase beta) but not to the other (agalsidase alpha) (Tanaka et al. 2010). As has been shown by several groups, the emergence of IgG antibodies toward the infused enzyme alpha galactosidase occurs frequently in male Fabry disease patients (Linthorst et al. 2004; Whitfield et al. 2005; Ohashi et al. 2007), irrespective of the enzyme preparation used. In these studies, cross-reactivity was shown: in anti-agalsidase IgG-positive patients, these antibodies were always equally reactive toward either agalsidase alpha or beta, again irrespective of the enzyme preparation given to the patient. The presence of anti-agalsidase IgG results in less urinary GL-3 clearance and is associated with infusion-associated events (Linthorst et al. 2004, 2006). The study by Tanaka et al. is interesting for two reasons: First, the patient had a known severe atopy, and this led the authors to decide to monitor anti-agalsidase IgG and IgE levels routinely between infusions. Following the first infusion of agalsidase beta of 1 mg/kg, a positive anti-agalsidase beta IgE result was obtained. The authors do not mention the anti-agalsidase IgG status. The emergence of anti-agalsidase IgE after the first infusion is remarkably early, as most anti-agalsidase (IgG) antibodies will be detectable between infusions four and 12 (e.g., months 2–6). The patient’s atopy may have contributed to the early immunization toward agalsidase beta. Second, this is the first case in which no cross-reactivity is reported for antibodies between agalsidase beta and alpha. Unfortunately no anti-agalsidase IgE titers are mentioned, and it is not known how the authors determined anti-agalsidase IgE. Was the same assay employed using the two different enzymes to capture (and determine) the actual presence of anti-agalsidase IgE? Did the authors use an in-house assay, or was the antibody status measured by the respective manufacturers of agalsidase alpha and beta? As a service to the medical community, both producers of agalsidase alpha (Replagal, Shire Inc.) and beta (Fabrazyme, Genzyme Corp.) measure anti-agalsidase IgG and IgE in plasma from patients treated with their products. Substantial differences on the presence (or absence) of anti-agalsidase IgG in the assays employed by the two companies have become apparent. This observation resulted in an initiative to develop a uniform method to measure, quantify, and report antibody status (Schellekens 2008). This initiative is sponsored by the two involved companies and is joined by several academic laboratories. Its results are eagerly awaited. Such a uniform assay will aid greatly the ability to discern possible differences in antibody response toward the two products. The possibility that some anti-agalsidase IgG or IgE antibodies may not be cross-reactive offers hope for those who develop such antibodies and subsequently may develop severe infusion reactions or reduced efficacy. However, it is imperative that the findings of Tanaka et al. be substantiated in a uniform assay expressing agalsidase alpha and beta. Only then can a true comparison be made.

Loss of Corneodesmosin Leads to Severe Skin Barrier Defect, Pruritus, and Atopy: Unraveling the Peeling Skin Disease

Generalized peeling skin disease is an autosomal-recessive ichthyosiform erythroderma characterized by lifelong patchy peeling of the skin. After genome-wide linkage analysis, we have identified a homozygous nonsense mutation in CDSN in a large consanguineous family with generalized peeling skin, pruritus, and food allergies, which leads to a complete loss of corneodesmosin. In contrast to hypotrichosis simplex, which can be associated with specific dominant CDSN mutations, peeling skin disease is characterized by a complete loss of CDSN expression. The skin phenotype is consistent with a recent murine Cdsn knockout model. Using three-dimensional human skin models, we demonstrate that lack of corneodesmosin causes an epidermal barrier defect supposed to account for the predisposition to atopic diseases, and we confirm the role of corneodesmosin as a decisive epidermal adhesion molecule. Therefore, peeling skin disease will represent a new model disorder for atopic diseases, similarly to Netherton syndrome and ichthyosis vulgaris in the recent past.

The role of lipopolysaccharide in the development of atopy in humans

Atopy is a highly prevalent condition and remains the single biggest risk factor for asthma. Although atopy has a heritable component, the time frame of the increase in the prevalence indicates that it is not due to genetic factors alone. The relationship between allergen exposure and sensitization is complex. Lipopolysaccharide (LPS) and its bioactive moiety endotoxin are common to all gram-negative bacteria, and have been used as a surrogate of microbial load. Endotoxin can be readily measured in dust collected from homes. Some studies have demonstrated a clear inverse dose-response relationship between exposure to endotoxin and the risk of atopy but this finding has not been reproduced in all studies. Our innate immune system recognizes LPS readily via the LPS signal transduction pathway, which has the trimolecular complex of CD14/TLR4/MD2 at the core. A common single-nucleotide polymorphism in the promoter region of CD14 rs2569190 C to T (CD14/-260 or CD14/-159) has been associated with elevated sCD14. Although early studies suggested that this variant was associated with more severe atopy, this finding was not uniformly replicated. It has now been demonstrated in four independent populations that high exposure to endotoxin in the domestic environment is protective against the development of atopy, but only among carriers of the C allele, that is, the environmental exposure is only relevant when taken in the context of the genotype. Furthermore, this interaction is biologically plausible. We propose that neither the environmental exposure nor the genotype in isolation is sufficient to cause complex diseases like asthma and atopy, but disease results from the one acting in the context of the other, of which CD14 and endotoxin is one example contributing to the risk for atopy.

Genetic, clinical, and laboratory markers for DOCK8 immunodeficiency syndrome.

DOCK8 immunodeficiency syndrome (DIDS) is a combined immunodeficiency characterized by recurrent viral infections, severe atopy, and early onset malignancy. Genetic studies revealed large, unique deletions in patients from different families and ethnic backgrounds. Clinical markers of DIDS include atopic dermatitis, allergies, cutaneous viral infections, recurrent respiratory tract infections, and malignancy. Immune assessments showed T cell lymphopenia, hyper-IgE, hypo-IgM, and eosinophilia. The impaired lymphocyte functions in DIDS patients appear central for disease pathogenesis.

Genetic, Clinical, and Laboratory Markers for DOCK8 Immunodeficiency Syndrome

DOCK8 immunodeficiency syndrome (DIDS) is a combined immunodeficiency characterized by recurrent viral infections, severe atopy, and early onset malignancy. Genetic studies revealed large, unique deletions in patients from different families and ethnic backgrounds. Clinical markers of DIDS include atopic dermatitis, allergies, cutaneous viral infections, recurrent respiratory tract infections, and malignancy. Immune assessments showed T cell lymphopenia, hyper-IgE, hypo-IgM, and eosinophilia. The impaired lymphocyte functions in DIDS patients appear central for disease pathogenesis.

ORIGINAL ARTICLE: Pre‐Eclampsia, Placental Abruption and Increased Risk of Atopic Sensitization in Male Adolescent Offspring

Problem The aim of this study was to investigate maternal pre‐eclampsia (PE), placental abruption (PA) and atopy among offspring.Method of study Obstetric data was recorded from 378 women who were included into the Caesarean delivery birth cohort during 1990–1992. When their children were 15–17 years old skin prick tests (SPTs) and inhalant allergen‐specific (IAS) immunoglobulin E (IgE) were determined among offspring.Results Adolescents whose mothers had either PE or PA at the time of delivery had more atopy and especially more severe atopy as measured by the incidence of SPTs positive for ≥5 allergens (RR: 4.28, 95% CI: 1.54–11.92; P &lt; 0.005) and elevated IAS IgE levels (≥1.0 kU/L) (RR: 4.27, 95% CI: 1.08–16.99; P &lt; 0.039). This increased risk was particularly observed in male adolescents.Conclusion Maternal PE and PA were associated with an increased risk of severe atopy, especially in male adolescent offspring.

Asthma attributable to atopy: does it depend on the allergen supply?

The use of the population attributable fraction (PAF) of asthma owing to atopy has not been widely used in epidemiological studies on childhood asthma, especially to compare regions of the same country. The present study includes 1039 children from Cartagena, Spain (Mediterranean coast) and 663 from Madrid (centre of Spanish plateau) using the ISAAC phase II methodology (questionnaire and prick test to the most common allergens). While there were no differences in asthma symptoms between school children (aged 10-11 yr) from Madrid and Cartagena, atopy to any allergen was significantly higher in those from Madrid (40.9% vs. 29.3%, respectively, p < 0.0001). However, children from Madrid were mainly positive to pollen allergy whereas those from Cartagena were positive for mite allergy. PAF of all the different asthma symptoms owing to atopy (any positive skin test) and PAF of current wheezing owing to a more severe atopy (three positive wheals) were higher in children from Cartagena than those from Madrid (45.5% vs. 28.6% and 14.2% vs. 6.2%, respectively). Per cent of previous year wheezing attributable to atopy to specific allergens varied among those cities and was higher for D. pteronissinus, D. farinae, cat, and olive tree in children from Cartagena, and--conversely--higher for mixed grasses, mixed trees and Alternaria in those from Madrid. All of these differences remained significant even after adjusting for risk factors. PAF for asthma owing to atopy could be very different within the same country, probably depending on the allergen supply which may depend on environmental factors such as the climate.

Sensitization to Ascaris lumbricoides and severity of childhood asthma in Costa Rica

Little is known about sensitization (defined as a positive IgE) to helminths and disease severity in patients with asthma. To examine the relationship between sensitization (defined as a positive IgE) to Ascaris lumbricoides and measures of asthma morbidity and severity in a Costa Rican population with low prevalence of parasitic infection but high prevalence of parasitic exposure. Cross-sectional study of 439 children (ages 6 to 14 years) with asthma. Linear regression and logistic regression were used for the multivariate statistical analysis. After adjustment for parental education and other covariates, sensitization to Ascaris lumbricoides was associated with having at least 1 positive skin test to allergens (odds ratio, 5.15; 95% CI, 2.36-11.21; P < .001), increased total serum IgE and eosinophils in peripheral blood, reductions in FEV(1) and FEV(1)/forced vital capacity, increased airway responsiveness and bronchodilator responsiveness, and hospitalizations for asthma in the previous year (odds ratio, 3.08; 95% CI, 1.23-7.68; P = .02). Sensitization to Ascaris lumbricoides is associated with increased severity and morbidity of asthma among children in Costa Rica. This association is likely mediated by an increased degree of atopy among children with asthma who are sensitized to Ascaris. In areas with a low prevalence of helminthiasis such as Costa Rica, Ascaris sensitization may be an important marker of severe atopy and disease morbidity in children with asthma.

Atopic Disease and Herpes Simplex Eye Disease: A Population-Based Case-Control Study

To determine whether atopy is associated with herpes simplex virus (HSV) ocular disease. Retrospective, population-based, case-control study. Large, regional health maintenance organization (Northern California Kaiser Permanente). 1,042,351 people over a one-year period. Electronic database search for HSV ocular disease and subsequent chart review determined study eligibility. Two age-matched control groups (one population-based and one clinic-based) were randomly chosen. Medical record review determined the presence of atopy. Severe atopic disease was defined by diagnostic code or illness requiring an emergency room visit, hospitalization, or treatment with a systemic corticosteroid. Presence of HSV eye disease, presence of atopy, and characterization of atopy severity. HSV eye disease was found in 172 patients. HSV cases had a greater prevalence of atopy (34%, 58/172) than the clinic-based (25%, 43/172) or the population-based controls (21%, 36/172, odds ratio (OR) 1.5, 95% confidence interval (CI) 0.9 to 2.6 and OR 1.9, 95%, CI 1.1 to 3.3, respectively). The association of HSV ocular disease with severe atopy was even greater, with a history of severe atopic disease in 13% (22/172) of patients with HSV ocular disease as compared with 6% (11/172) of patients in the clinic control group and 3% (5/172) of patients in the population control group (OR 2.0, 95% CI 0.7 to 5.9 and OR 4.8, 95% CI 1.6 to 19.2, respectively). Patients with HSV ocular disease are more likely to have a history of atopic disease, especially severe atopic disease, than age-matched controls.

Persistent warts in an adolescent with severe atopy

Persistent warts in an adolescent with severe atopy

Atopy in Patients with Bronchiectasis: More than Coincidence

Bronchiectasis is common in developing countries, but its precise underlying mechanism can be detected in only about 40% of the cases. The studies reporting the frequency of atopy and its relation to radiological findings and lung function in bronchiectasis are limited in number, and the results are controversial. The present study was designed to investigate the relationship between atopy and bronchiectasis by means of high resolution computed tomography (HRCT) and pulmonary function tests. Skin prick test, HRCT and pulmonary function tests, including spirometric values of forced expiratory volume in one second (FEV1), FEV1/FVC (forced vital capacity) ratio were performed in 121 bronchiectatic patients of unknown etiology and in 68 healthy controls. Atopy and HRCT scores for the severity of atopy and extent of bronchiectasis respectively were determined for each patient. The rate of atopy (48.8% vs 11.8%) and mean atopy score (14.3 +/- 10.1 mm vs 5.5 +/- 2.1 mm) were significantly higher in patients with bronchiectasis than those in controls. Atopic patients had significantly worse spirometric values and more extended bronchiectasis than non-atopics. There is a significant correlation between atopy and HRCT scores (r = 0.54, p < 0.001), indicating that the more severe atopy is the more extended bronchiectasis. In conclusion, we suggest that the rate of atopy is higher in bronchiectatic patients than that in healthy controls. Bronchiectatic patients with atopy have lower spirometric values and higher HRCT scores. Atopy might be considered as a deteriorating and/or a causative or contributing factor for development of bronchiectasis.