An in vitro allergen radioimmunoassay in which allergens are coupled to an immunosorbent. The coupled allergens bind the IgE in the sera of patients which in turn binds radioisotope-labeled anti-IMMUNOGLOBULIN E antibodies.
Epicutaneous or intradermal application of a sensitizer for demonstration of either delayed or immediate hypersensitivity. Used in diagnosis of hypersensitivity or as a test for cellular immunity.
An immunoglobulin associated with MAST CELLS. Overexpression has been associated with allergic hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).
Phthalic acid anhydrides. Can be substituted on any carbon atom. Used extensively in industry and as a reagent in the acylation of amino- and hydroxyl groups.
Hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigen-antibody reaction and causes smooth muscle contraction and increased vascular permeability.
Immunologically mediated adverse reactions to medicinal substances used legally or illegally.
Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen.
Antigen-type substances that produce immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).
Diseases caused by factors involved in one's employment.
A form of bronchial disorder with three distinct components: airway hyper-responsiveness (RESPIRATORY HYPERSENSITIVITY), airway INFLAMMATION, and intermittent AIRWAY OBSTRUCTION. It is characterized by spasmodic contraction of airway smooth muscle, WHEEZING, and dyspnea (DYSPNEA, PAROXYSMAL).
Gastrointestinal disturbances, skin eruptions, or shock due to allergic reactions to allergens in food.
The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation.

Latex glove allergy among hospital employees: a study in the north-west of England. (1/122)

The frequency of use and duration of wearing latex gloves among hospital employees has increased due to concerns about AIDS and hepatitis. In many countries there is increased consciousness about latex sensitization. In the UK, the Medical Device Agency has been monitoring latex allergy for a number of years but has not found any conclusive evidence of any significant problem. We report following a detailed questionnaire study in two hospitals in the north-west of England. A total of 1,827 members of staff were questioned about latex allergy at work. One hundred and twenty-four (7%) of these hospital employees had experienced symptoms strongly suggestive of latex allergy. Of this group, 56 had a-RAST test (IgE specific to latex), which was positive in seven (12.5%). There was a history of atopy in 31%, and a family history of atopy in 17% of the individuals. As a result of the study it was found that 17% (21 of the affected individuals) had already changed their working practice by using latex-free gloves. We were able to increase awareness of latex allergy within the hospitals. Both individuals and health care organizations need to be aware of the problem and hospital organizations should encourage staff to seek guidance to address the problem and, if necessary, to take appropriate measures to improve working practices. Practical guidelines are given with regard to identifying the problem and glove use for hospital staff.  (+info)

Repeated hand urticaria due to contact with fishfood. (2/122)

BACKGROUND: The etiology of urticaria is often difficult to determine. However, in case of repeated circumstance-connected urticaria, the reason may be easily clarifyable. CASE: A 51-year-old healthy woman repeatedly experienced occupational hand urticaria when handling fish food. An unexpected reason for the urticaria was found in that the fishfood contained histamine as a "contaminant". CONCLUSIONS: In fishfood batches, biological degradation can produce histamine and possibly other toxic substances that can lead to occupational health problems.  (+info)

Allergic bronchopulmonary aspergillosis due to Aspergillus niger without bronchial asthma. (3/122)

A 65-year-old woman was admitted to our hospital with a dry cough and pulmonary infiltrates. Chest radiograph and CT revealed mucoid impaction and consolidations. Peripheral blood eosinophilia and elevated serum IgE were observed. Aspergillus niger was cultured repeatedly from her sputum, but A. fumigatus was not detected. Immediate skin test and specific IgE (RAST) to Aspergillus antigen were positive. Precipitating antibodies were confirmed against A. niger antigen, but not against A. fumigatus antigen. She had no asthmatic symptoms, and showed no bronchial hyperreactivity to methacholine. Thus, this case was diagnosed as allergic bronchopulmonary aspergillosis (ABPA) without bronchial asthma due to A. niger, an organism rarely found in ABPA. The administration of prednisone improved the symptoms and corrected the abnormal laboratory findings.  (+info)

Selective cloning of allergens from the skin colonizing yeast Malassezia furfur by phage surface display technology. (4/122)

The yeast Malassezia furfur, also known as Pityrosporum orbiculare (ovale), is part of the normal microflora of the human skin but has also been associated with different skin diseases including atopic dermatitis. More than 50% of atopic dermatitis patients have positive skin test and specific IgE to M. furfur extracts; however, the pathophysiologic role of these IgE-mediated reactions in the development of the disease remains unknown. The yeast is able to produce a wide panel of IgE-binding proteins, variably recognized by sera of individual patients. In order to assess the contribution of individual components to the disease, highly pure allergen preparations are required. We have cloned M. furfur allergens from a cDNA library displayed on the phage surface, sequenced the inserts and produced recombinant proteins in Escherichia coli. Phage displaying IgE-binding proteins were selectively enriched from the library using IgE from a M. furfur-sensitized atopic dermatitis patient as a ligand. We were able to identify five different inserts coding for IgE-binding polypeptides. Three of the sequenced cDNA encode incomplete gene products with molecular masses of 21.3 kDa (MF 7), 14.4 kDa (MF 8), and 9.7 kDa (MF 9), respectively, having no sequence similarity to known proteins. The other two cDNA encode allergens of 18.2 kDa (Mal f 5) and 17.2 kDa (Mal f 6). Mal f 5 shows significant homology to M. furfur allergens Mal f 2, Mal f 3 and an Aspergillus fumigatus allergen Asp f 3. Mal f 6 has significant homology with cyclophilin. All of the recombinant polypeptides were capable of binding serum IgE from atopic dermatitis patients in immunoblotting experiments. The availability of pure recombinant M. furfur allergens will allow the careful investigation of the role of IgE-binding proteins in atopic dermatitis.  (+info)

Allergy to laboratory animals in children of parents occupationally exposed to mice, rats and hamsters. (5/122)

Sensitization to laboratory animals (LA) has a high prevalence among laboratory workers. It is unknown whether transportation of LA allergens can be a risk factor for sensitization of subjects outside the laboratory environment. The aim of the study was to investigate the prevalence of sensitization to LA among children whose parents were and were not occupationally exposed to LA. The first group consisted of 50 children (age 12.3+/-4.3 yrs) whose parents were occupationally exposed to mice, rats and hamsters. The second group consisted of 40 children (age (mean+/-SD) 10.8+/-3.0 yrs) whose parents were not occupationally exposed to LA. Children having LA at home were eliminated from the study. All children responded to a questionnaire, underwent spirometry and were also tested with skin prick tests with the use of common allergens and prick tests with hair extracts from mouse, hamster and rat. Total immunoglobulin (Ig)E levels and the presence of specific IgE against LA were also estimated. Children of parents occupationally exposed to LA presented significantly more positive skin prick tests against allergens from the hair of laboratory animals compared to children of nonexposed parents. Five children from the first group were also found to have specific IgE against LA, with three of these five children complaining of rhinitis and cough while visiting their parents' workplace. It is concluded that the observed increased sensitization to laboratory animals among children of occupationally exposed parents could be the result of poor hygienic conditions at their parents' workplace. Hence, parents' job seems to be an additional risk factor of sensitization and should be taken into consideration when recording an allergic history.  (+info)

Risk of enzyme allergy in the detergent industry. (6/122)

OBJECTIVES: To assess the prevalence of enzyme sensitisation in the detergent industry. METHODS: A cross sectional study was conducted in a detergent factory. Sensitisation to enzymes was examined by skin prick and radioallergosorbent (RAST) tests. 76 Workers were tested; 40 in manufacturing, packing, and maintenance, and 36 non-exposed people in management and sales departments. The workers were interviewed for work related respiratory and skin symptoms. Total dust concentrations were measured by a gravimetric method, and the concentration of protease in air by a catalytic method. RESULTS: Nine workers (22%) were sensitised to enzymes in the exposed group of 40, whereas none were sensitised in the non-exposed group. All the sensitised people had symptoms at work; all had rhinitis and one had asthma. Protease concentrations were generally < 20 ng/m3, but occasional peak values up to 80 ng/m3 were detected in the packing and maintenance tasks, and high values of > 1 microgram/m3 in the mixing area. CONCLUSION: Despite the use of encapsulated enzyme preparations, high enzyme concentrations in workplace air are possible, resulting in a higher risk of sensitisation than expected.  (+info)

Natural rubber latex aeroallergen exposure in rubber plantation workers and glove manufacturers in Thailand and health care workers in a UK hospital. (7/122)

OBJECTIVES: To estimate personal airborne natural rubber latex (NRL) concentrations for three occupational exposure groups; rubber plantation workers and NRL glove manufacturers in Thailand and health care workers in the UK. To utilise these data to classify the populations into appropriate exposure groups for the exposure-response analysis in the epidemiological study on latex allergy. METHODS: Two rubber plantations (110 workers), three NRL glove manufacturing factories (583 workers) in Thailand and one UK hospital (490 workers) were selected for the study. A preliminary workplace survey was carried out at each workplace in order to assign job titles subjectively in to high, moderate or low exposure groups for the purpose of sample selection. Between 5 and 20% of workers from each group for the three populations were then selected randomly for personal measurement of latex airborne allergens. Personal sampling was conducted using a 25 mm PTFE filter loaded in to an IOM sampling head at 2 l. min(-1). NRL aeroallergens were measured by an inhibition assay with NRL-specific IgE antibodies from NRL-sensitised people. RESULTS: A total of twenty-two personal samples were collected from plantation workers, sixty-one samples from the glove manufacturer employees and twenty seven from health care workers. The highest geometric mean (GM) NRL aeroallergen concentration was found in the glove manufacturing factories (7.3 microg m(-3)), followed by the rubber plantations (2.4 microg m(-3)) and the UK hospital (0.46 microg m(-3)). Amongst the NRL glove factories, the NRL aeroallergen concentrations were highest for those conducting the following tasks; glove stripping, glove inspections and packing of powdered gloves. The GM NRL aeroallergen for these tasks were in the range of 12.9 to 17.8 microg m(-3). CONCLUSIONS: In the process from tapping and manufacture of latex gloves through to their use the highest exposure to NRL aeroallergens is likely to occur in the manufacturing factories. Exposure to aeroallergens for the plantation workers was considered to be moderate and that of health care workers to be low.  (+info)

Differentiated dendritic cells expressing nuclear RelB are predominantly located in rheumatoid synovial tissue perivascular mononuclear cell aggregates. (8/122)

OBJECTIVE: Differentiated dendritic cells (DC) and other antigen-presenting cells are characterized by the nuclear location of RelB, a member of the nuclear factor kappaB/Rel family. To characterize and enumerate differentiated DC in rheumatoid arthritis (RA) peripheral blood (PB), synovial fluid (SF), and synovial tissue (ST), the expression and location of RelB were examined. METHODS: RelB protein expression and cellular location were determined in RA PB, SF, and ST by flow cytometry and immunohistochemical analysis of purified cells or formalin-fixed tissue. DNA-binding activity of RelB was determined by electrophoretic mobility shift-Western immunoblotting assays. RESULTS: Circulating RA PBDC resembled normal immature PBDC in that they did not express intracellular RelB protein. In RA ST serial sections, cells containing nuclear RelB (nRelB) were enriched in perivascular regions. A mean +/- SD of 84 +/- 10% of these cells were DC. The remaining nRelB+,HLA-DR+ cells comprised B cells and macrophages. Only 3% of sorted SFDC contained nRelB. However, RelB present in the nucleus of these SFDC was capable of binding DNA, and therefore capable of transcriptional activity. CONCLUSION: Circulating DC precursors differentiate and express RelB after entry into rheumatoid ST. Differentiated DC can thus be identified by immunohistochemistry in formalin-fixed ST. Signals for DC maturation may differ between RA ST and SF, resulting in nuclear location of RelB predominantly in ST. This is likely to have functional consequences for the DC in these sites.  (+info)

A Radioallergosorbent Test (RAST) is a type of blood test used in the diagnosis of allergies. It measures the presence and levels of specific antibodies, called immunoglobulin E (IgE), produced by the immune system in response to certain allergens. In this test, a small amount of blood is taken from the patient and then mixed with various allergens. If the patient has developed IgE antibodies against any of these allergens, they will bind to them, forming an antigen-antibody complex.

The mixture is then passed over a solid phase, such as a paper or plastic surface, which has been coated with allergen-specific antibodies. These antibodies will capture the antigen-antibody complexes formed in the previous step. A radioactive label is attached to a different type of antibody (called anti-IgE), which then binds to the IgE antibodies captured on the solid phase. The amount of radioactivity detected is proportional to the quantity of IgE antibodies present, providing an indication of the patient's sensitivity to that specific allergen.

While RAST tests have been largely replaced by more modern and sensitive techniques, such as fluorescence enzyme immunoassays (FEIA), they still provide valuable information in diagnosing allergies and guiding treatment plans.

Skin tests are medical diagnostic procedures that involve the application of a small amount of a substance to the skin, usually through a scratch, prick, or injection, to determine if the body has an allergic reaction to it. The most common type of skin test is the patch test, which involves applying a patch containing a small amount of the suspected allergen to the skin and observing the area for signs of a reaction, such as redness, swelling, or itching, over a period of several days. Another type of skin test is the intradermal test, in which a small amount of the substance is injected just beneath the surface of the skin. Skin tests are used to help diagnose allergies, including those to pollen, mold, pets, and foods, as well as to identify sensitivities to medications, chemicals, and other substances.

Immunoglobulin E (IgE) is a type of antibody that plays a key role in the immune response to parasitic infections and allergies. It is produced by B cells in response to stimulation by antigens, such as pollen, pet dander, or certain foods. Once produced, IgE binds to receptors on the surface of mast cells and basophils, which are immune cells found in tissues and blood respectively. When an individual with IgE antibodies encounters the allergen again, the cross-linking of IgE molecules bound to the FcεRI receptor triggers the release of mediators such as histamine, leukotrienes, prostaglandins, and various cytokines from these cells. These mediators cause the symptoms of an allergic reaction, such as itching, swelling, and redness. IgE also plays a role in protecting against certain parasitic infections by activating eosinophils, which can kill the parasites.

In summary, Immunoglobulin E (IgE) is a type of antibody that plays a crucial role in the immune response to allergens and parasitic infections, it binds to receptors on the surface of mast cells and basophils, when an individual with IgE antibodies encounters the allergen again, it triggers the release of mediators from these cells causing the symptoms of an allergic reaction.

I'm sorry for any confusion, but "Phthalic Anhydrides" is not a medical term. It is a chemical compound with the formula C6H4(CO)2O. Phthalic anhydride is a white crystalline powder used in the industrial synthesis of plasticizers, resins, and dyes.

If you have any questions about medical terminology or concepts, please don't hesitate to ask!

Hypersensitivity, Immediate: Also known as Type I hypersensitivity, it is an exaggerated and abnormal immune response that occurs within minutes to a few hours after exposure to a second dose of an allergen (a substance that triggers an allergic reaction). This type of hypersensitivity is mediated by immunoglobulin E (IgE) antibodies, which are produced by the immune system in response to the first exposure to the allergen. Upon subsequent exposures, these IgE antibodies bind to mast cells and basophils, leading to their degranulation and the release of mediators such as histamine, leukotrienes, and prostaglandins. These mediators cause a variety of symptoms, including itching, swelling, redness, and pain at the site of exposure, as well as systemic symptoms such as difficulty breathing, wheezing, and hypotension (low blood pressure). Examples of immediate hypersensitivity reactions include allergic asthma, hay fever, anaphylaxis, and some forms of food allergy.

Drug hypersensitivity is an abnormal immune response to a medication or its metabolites. It is a type of adverse drug reaction that occurs in susceptible individuals, characterized by the activation of the immune system leading to inflammation and tissue damage. This reaction can range from mild symptoms such as skin rashes, hives, and itching to more severe reactions like anaphylaxis, which can be life-threatening.

Drug hypersensitivity reactions can be classified into two main types: immediate (or IgE-mediated) and delayed (or non-IgE-mediated). Immediate reactions occur within minutes to a few hours after taking the medication and are mediated by the release of histamine and other inflammatory mediators from mast cells and basophils. Delayed reactions, on the other hand, can take several days to develop and are caused by T-cell activation and subsequent cytokine release.

Common drugs that can cause hypersensitivity reactions include antibiotics (such as penicillins and sulfonamides), nonsteroidal anti-inflammatory drugs (NSAIDs), monoclonal antibodies, and chemotherapeutic agents. It is important to note that previous exposure to a medication does not always guarantee the development of hypersensitivity reactions, as they can also occur after the first administration in some cases.

The diagnosis of drug hypersensitivity involves a thorough medical history, physical examination, and sometimes skin or laboratory tests. Treatment typically includes avoiding the offending medication and managing symptoms with antihistamines, corticosteroids, or other medications as needed. In severe cases, emergency medical care may be required to treat anaphylaxis or other life-threatening reactions.

Hypersensitivity is an exaggerated or inappropriate immune response to a substance that is generally harmless to most people. It's also known as an allergic reaction. This abnormal response can be caused by various types of immunological mechanisms, including antibody-mediated reactions (types I, II, and III) and cell-mediated reactions (type IV). The severity of the hypersensitivity reaction can range from mild discomfort to life-threatening conditions. Common examples of hypersensitivity reactions include allergic rhinitis, asthma, atopic dermatitis, food allergies, and anaphylaxis.

An allergen is a substance that can cause an allergic reaction in some people. These substances are typically harmless to most people, but for those with allergies, the immune system mistakenly identifies them as threats and overreacts, leading to the release of histamines and other chemicals that cause symptoms such as itching, sneezing, runny nose, rashes, hives, and difficulty breathing. Common allergens include pollen, dust mites, mold spores, pet dander, insect venom, and certain foods or medications. When a person comes into contact with an allergen, they may experience symptoms that range from mild to severe, depending on the individual's sensitivity to the substance and the amount of exposure.

Occupational diseases are health conditions or illnesses that occur as a result of exposure to hazards in the workplace. These hazards can include physical, chemical, and biological agents, as well as ergonomic factors and work-related psychosocial stressors. Examples of occupational diseases include respiratory illnesses caused by inhaling dust or fumes, hearing loss due to excessive noise exposure, and musculoskeletal disorders caused by repetitive movements or poor ergonomics. The development of an occupational disease is typically related to the nature of the work being performed and the conditions in which it is carried out. It's important to note that these diseases can be prevented or minimized through proper risk assessment, implementation of control measures, and adherence to safety regulations.

Asthma is a chronic respiratory disease characterized by inflammation and narrowing of the airways, leading to symptoms such as wheezing, coughing, shortness of breath, and chest tightness. The airway obstruction in asthma is usually reversible, either spontaneously or with treatment.

The underlying cause of asthma involves a combination of genetic and environmental factors that result in hypersensitivity of the airways to certain triggers, such as allergens, irritants, viruses, exercise, and emotional stress. When these triggers are encountered, the airways constrict due to smooth muscle spasm, swell due to inflammation, and produce excess mucus, leading to the characteristic symptoms of asthma.

Asthma is typically managed with a combination of medications that include bronchodilators to relax the airway muscles, corticosteroids to reduce inflammation, and leukotriene modifiers or mast cell stabilizers to prevent allergic reactions. Avoiding triggers and monitoring symptoms are also important components of asthma management.

There are several types of asthma, including allergic asthma, non-allergic asthma, exercise-induced asthma, occupational asthma, and nocturnal asthma, each with its own set of triggers and treatment approaches. Proper diagnosis and management of asthma can help prevent exacerbations, improve quality of life, and reduce the risk of long-term complications.

Food hypersensitivity is an umbrella term that encompasses both immunologic and non-immunologic adverse reactions to food. It is also known as "food allergy" or "food intolerance." Food hypersensitivity occurs when the body's immune system or digestive system reacts negatively to a particular food or food component.

Immunologic food hypersensitivity, commonly referred to as a food allergy, involves an immune response mediated by immunoglobulin E (IgE) antibodies. Upon ingestion of the offending food, IgE antibodies bind to the food antigens and trigger the release of histamine and other chemical mediators from mast cells and basophils, leading to symptoms such as hives, swelling, itching, difficulty breathing, or anaphylaxis.

Non-immunologic food hypersensitivity, on the other hand, does not involve the immune system. Instead, it is caused by various mechanisms, including enzyme deficiencies, pharmacological reactions, and metabolic disorders. Examples of non-immunologic food hypersensitivities include lactose intolerance, gluten sensitivity, and histamine intolerance.

It's important to note that the term "food hypersensitivity" is often used interchangeably with "food allergy," but it has a broader definition that includes both immunologic and non-immunologic reactions.

Occupational exposure refers to the contact of an individual with potentially harmful chemical, physical, or biological agents as a result of their job or occupation. This can include exposure to hazardous substances such as chemicals, heavy metals, or dusts; physical agents such as noise, radiation, or ergonomic stressors; and biological agents such as viruses, bacteria, or fungi.

Occupational exposure can occur through various routes, including inhalation, skin contact, ingestion, or injection. Prolonged or repeated exposure to these hazards can increase the risk of developing acute or chronic health conditions, such as respiratory diseases, skin disorders, neurological damage, or cancer.

Employers have a legal and ethical responsibility to minimize occupational exposures through the implementation of appropriate control measures, including engineering controls, administrative controls, personal protective equipment, and training programs. Regular monitoring and surveillance of workers' health can also help identify and prevent potential health hazards in the workplace.

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