Occupational skin diseases (OSDs) often have considerable medical and occupational consequences. Previous data on prognostic factors have been derived from studies with fairly small sample sizes.
To determine the medical and occupational outcome in 1048 patients diagnosed with OSD at the Finnish Institute of Occupational Health and to identify the prognostic risk factors for the continuation of OSD.
Patients examined in 1994-2001 filled out a follow-up questionnaire 6 months after the diagnosis. Data on atopy, contact allergies, and occupation were analysed.
Six months after the diagnosis the skin disease had healed in 27% of the patients. The OSD had cleared up in 17% of those with no changes at work, and in 34% of those who had changed their job/occupation. The best clearing had occurred in the patients with contact urticaria (35%), whereas the healing of allergic (27%) and irritant (23%) contact dermatitis was similar. The risk factors for continuing occupational contact dermatitis (OCD) were no changes in work, age > 45 years, food-related occupations, respiratory atopy, and male sex.
The healing of OSD was associated with discontinuation of the causative exposure. A change in work and the presence of easily avoidable work-related allergies were associated with a good prognosis.
99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: immune therapies of type 1 diabetes: new opportunities based on the hygiene hypothesis.
Insulin-dependent (type 1) diabetes is a prototypic organ-specific autoimmune disease resulting from the selective destruction of insulin-secreting beta cells within pancreatic islets of Langerhans by an immune-mediated inflammation involving autoreactive CD4(+) and CD8(+) T lymphocytes which infiltrate pancreatic islets. Current treatment is substitutive, i.e. chronic use of exogenous insulin which, in spite of significant advances, is still associated with major constraints (multiple daily injections, risks of hypoglycaemia) and lack of effectiveness over the long term in preventing severe degenerative complications. Finding a cure for autoimmune diabetes by establishing effective immune-based therapies is a real medical health challenge, as the disease incidence increases steadily in industrialized countries. As the disease affects mainly children and young adults, any candidate immune therapy must therefore be safe and avoid a sustained depression of immune responses with the attendant problems of recurrent infection and drug toxicity. Thus, inducing or restoring immune tolerance to target autoantigens, controlling the pathogenic response while preserving the host reactivity to exogenous/unrelated antigens, appears to be the ideal approach. Our objective is to review the major progress accomplished over the last 20 years towards that aim. In addition, we would like to present another interesting possibility to access new preventive strategies based on the 'hygiene hypothesis', which proposes a causal link between the increasing incidence of autoimmune diseases, including diabetes, and the decrease of the infectious burden. The underlying rationale is to identify microbial-derived compounds mediating the protective activity of infections which could be developed therapeutically.
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Cites: J Immunol. 2000 Jun 1;164(11):5683-810820244
The -112G>A polymorphism of the secretoglobin 3A2 (SCGB3A2) gene encoding uteroglobin-related protein 1 (UGRP1) increases risk for the development of Graves' disease in subsets of patients with elevated levels of immunoglobulin E.
Department of Molecular Diagnostics, National Research Center GosNIIgenetika, 1st Dorozhny Proezd 1, 117545, Moscow, Russia. dimitry.chistiakov@lycos.com
The human secretoglobin 3A2 (SCGB3A2) gene encoding secretory uteroglobin-related protein 1 (UGRP1) resides on the chromosome region 5q31-33 that harbors a susceptibility locus to several autoimmune and inflammatory diseases, including asthma and Graves' disease (GD). Recently, association between the marker rs1368408 (-112G?>A), located in the promoter region of the SCGB3A2 gene, and susceptibility to GD was found in Chinese and UK Caucasians. The study aim was to evaluate whether this polymorphism confers GD susceptibility in a large population cohort comprising 1,474 Russian GD patients and 1,619 controls. The marker rs1368408 was studied using a TaqMan allele discrimination assay. Serum levels of UGRP1 and immunoglobulin E (IgE) were assessed using enzyme-linked immunosorbent assay (ELISA) analyses. Association between the allele A of SCGB3A2 and a higher risk of GD (odds ratio [OR] = 1.33, P = 2.9 × 10(-5)) was shown. Both affected and non-affected carriers of the higher risk genotype A/A had significantly decreased levels of serum UGRP1 compared to the subjects homozygous for G/G (93 ± 37 pg/ml vs. 132 ± 45 pg/ml, P = 0.0011 for GD patients; 77 ± 28 pg/ml vs. 119 ± 33 pg/ml, P = 0.0019 for controls). Serum IgE levels were significantly higher in non-affected subjects homozygous for A/A compared to control individuals homozygous for G/G (153 ± 46 IU/ml vs. 122 ± 40 IU/ml, P = 0.0095). Our data suggest that the carriage of the SCGB3A2 -112A/A variant increases the risk for GD in subsets of patients with elevated levels of IgE, a hallmark of allergic asthma. Therefore, the SCGB3A2 -112G?>A polymorphism may be considered as a likely marker linking susceptibility to allergy/asthma and GD on chromosome 5q31-33.
The detection of anergy or relative anergy by delayed hypersensitivity skin tests was predictive of infection and related mortality in 354 surgical patients. Cancer or advanced age alone did not account for the increased morbidity and mortality seen in this study. Altered delayed hypersensitivity response is a reflection of abnormalities in cell-mediated immunity and possibly humoral or phagocytic defects, or both. Skin testing is of value to the clinical surgeon both in identifying the population at risk and in monitoring the immune response to therapy in the seriously ill patient. Failure to improve skin-test response may indicate underlying infection or malnutrition, which, if untreated, results in a high mortality.
In the course of the "1998 Health and Social Survey", questions were included to verify the prevalence of chronic respiratory diseases and also of wheezing. The objectives of this study were 1) to verify the prevalence of wheezing and its validity as an indicator of chronic respiratory diseases in Québec; and 2) to examine the relationship between chronic respiratory diseases and some of their potential determinants. A total of 30,386 individuals participated in the study. For all ages, the prevalence of wheezing was 5.4%. It was associated with asthma, allergies, chronic bronchitis and emphysema. A low familial income and tobacco smoking were associated with wheezing, asthma, chronic bronchitis and emphysema. Passive smoking was associated with wheezing whereas the presence of carpets was associated with wheezing and asthma. Between 32 and 48% of families with an asthmatic or an allergic member modified their dwelling to alleviate respiratory problems. The prevalence of wheezing documented here was lower than in anglosaxon countries. This result could be explained by a cultural factor (the French translation or the perception of wheezing). This study emphasizes the role of reducing tobacco smoking in the prevention of chronic respiratory diseases.
Faculty of Pharmacy & Pharmaceutical Sciences, HIV, Northern Alberta HIV Program and Regional Pharmacy Services, Capital Health Region, Edmonton, Alberta, Canada. hughes@ualberta.ca
OBJECTIVE: To review the clinical features, risk factors, diagnosis, and management of abacavir hypersensitivity reaction (HSR). DATA SOURCES: A MEDLINE (1950-October 2007) and EMBASE (1980-October 2007) search using key words abacavir, HIV, human immunodeficiency virus, hypersensitivity reaction, HLA-B(*)5701, and patch tests was conducted. Conference abstracts and article bibliographies were reviewed to identify relevant studies. STUDY SELECTION AND DATA EXTRACTION: Studies that investigated the clinical and immunogenetic risk factors for abacavir hypersensitivity and the benefit of genetic screening, as well as articles that focused on the clinical presentation, assessment, and management of abacavir HSR, were considered for this review. DATA SYNTHESIS: Abacavir hypersensitivity is an immune-mediated reaction that typically occurs within the first 6 weeks of therapy. Signs and symptoms of abacavir HSR are nonspecific, which makes the diagnosis challenging, particularly in medically complex patients. Patch testing may improve the diagnosis and confirmation of abacavir HSR, but it remains experimental. Clinical management is aimed at supportive therapy and discontinuation of abacavir. Rechallenge with abacavir is contraindicated due to the risk of precipitating a life-threatening reaction. Appropriate patient education and a clear communication plan are essential for the safe use of this medication. Identification of patients at risk of developing abacavir hypersensitivity through routine genetic screening for human leukocyte antigen (HLA) HLA-B(*)5701 represents a significant advance in the field of pharmacogenomics, with an apparent 100% negative predictive value when used to screen for abacavir HSR. Preliminary data suggest that pharmacogenetic testing for HLA-B(*)5701 is cost effective. However, until routine testing is available, pharmacovigilance is necessary for the safe and effective use of abacavir. CONCLUSIONS: Serious adverse events associated with the use of abacavir can be avoided by appropriate recognition and management of the HSR. Screening patients for HLA-B(*)5701 prior to initiation of abacavir represents a tool to further decrease the risk of HSRs as well as unnecessary discontinuation of this drug.
In the summer forest there are allergens and irritating substances that cause respiratory or cutaneous symptoms. Birch and alder pollen allergy is common in Finland. Pollens of other trees cause sensitization only sporadically. Spores of molds and mushrooms cause allergic reactions, but the means to study spore allergy are inadequate. Even edible mushrooms may cause allergic abdominal discomforts, and trehalose intolerance is supposed to be present in a small percentage of the population. Lichen allergens may bring about IgE-mediated reactions, contact allergy and photoallergic reactions.
BACKGROUND: An inverse association between tuberculin responses and atopy has been observed in Japanese children, indicating that BCG immunisation, subclinical exposure to Mycobacterium tuberculosis without clinical disease, or host characteristics may influence the T helper (Th) lymphocyte balance with decreased atopy as a result. This study was undertaken to determine whether tuberculin reactivity is inversely related to atopy in young adults vaccinated with BCG at the age of 14. METHODS: Men and women aged 20-44 years were tested using the adrenaline-Pirquet test with Norwegian produced synthetic medium tuberculin (n = 891). In addition, their serum total and specific IgE antibodies against mite, cat, timothy grass, mould and birch were measured. RESULTS: Of the 574 subjects with complete examinations, 64% had a positive adrenaline-Pirquet tuberculin test (> or =4 mm) and 27% exhibited IgE antibodies (> or =0.35 kU/l) to one or more of the five specific allergens. The geometric mean of total serum IgE in the population was 30.2 kU/l. Tuberculin reactivity and log IgE were not correlated (r = 0.043, p = 0.30). The mean tuberculin reactivity was 4.6 mm, 4.9 mm, and 5.0 mm in the lower, middle and upper tertile of IgE distribution (61 kU/l). The prevalence of atopy, as assessed by either the presence of any of the five specific IgE antibodies or by each specific IgE antibody separately, did not differ between subjects with a positive and those with a negative tuberculin test. These results persisted after adjustment for age, sex, and smoking status in multivariate logistic regression analyses. CONCLUSIONS: In this young adult population, BCG vaccinated at the age of 14, no significant relationship between a positive tuberculin reaction and atopy was observed. If a true relationship had been found, our study suggests that it may be limited to populations immunised in early childhood when a substantial modulation of the immune system can occur.
