Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient (E.M.) with marked eosinophilia and hyperimmunoglobulin E (IgE) has been followed for 4 years. Peripheral blood eosinophilia reached levels in excess of 18,000 cells/mm3 and serum IgE concentration increased to more than 210,000 units/ml (about 0.48 mg IgE/ml). The IgE has both lambda and kappa light chains and is therefore considered polyclonal. The patient has an increase in peripheral blood lymphocytes which stain for surface IgE. Transfer of the patient's plasma (plasmsEM) to a rhesus monkey did not induce peripheral boood eosinophilia. The half life of IgEEM in a rhesus monkey was 2.2 days, which is similar to the half life of myeloma IgE in human subjects. The condition was not associated with defined morbidity except for mild persistent pruritus. Various studies revealed no evidence for atopic parasitic, immune deficiency or neoplastic disease.
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PMID:Massive polyclonal hyperimmunoglobulinemia E, eosinophilia and increased IgE-bearing lymphocytes. 4 11

The preparation of food in restaurant kitchens carries a high risk of occupational dermatoses. Analysis of 33 cases revealed four different etiological types. Simple irritant dermatitis was rare (2 cases), plain contact dermatitis was more common (6 cases). Fifteen patients had relevant patch tests and scratch tests; ten had positive scratch tests only to explain the cause of their dermatitis. The last type was termed protein contact dermatitis. The major type IV allergens incriminated were metals, onion and garlic. The major proteinaceous allergens indicated by history and test results were fish and shell-fish. Open patch tests with the incriminated foods may cause erythema or oedema on normal skin after 20 minutes. Previously eczematous, now normal looking, skin often responds with a crop of dyshidrotic vesicles preceded by erythema and itching 30 minutes after the application of an open test. Examination for specific IgE is not always positive in such cases. Inhalant allergy was rare. The results indicate that food handlers are sensitized by the protein they touch, and then react to later contact with the proteins. Protein contact dermatitis is similarly common among veterinary surgeons, while the importance in other occupational groups remains to be studied.
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PMID:Occupational protein contact dermatitis in food handlers. 14 23

Occupational contact dermatitis caused by obstetric work and/or contact with cows is common among veterinary surgeons. We examined serum from nine veterinary surgeons of whom seven gave a history of itching and flare of eczema after obstetric work and/or contact with cows. By means of crossed radioimmunoelectrophoresis the occurrence of specific IgE against cow hair and dander was demonstrated. The IgE did not differ qualitatively or quantitatively from IgE in serum from patients with allergic asthma from cows. Four veterinary surgeons with flare-up of eczema during obstetric aid to cows did not have assignable s-IgE against bovine amnion or allantoic fluids.
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PMID:Type I allergy from cows in veterinary surgeons. 15 86

A survey was made on workers handling powdered drugs in a pharmaceutical factory. In this factory, two kinds of anti-inflammatory enzyme (bromelain and trypsin), one anti-inflammatory agent (flufenamic acid), one antispasmodic (flopropion) and two kinds of antibiotics (ampicillin and cephalexin) are mainly produced. Twenty four workers were examined by interviews and checked by Cornell Medical Index, and 18 of them complained of respiratory symptoms. These 18 workers were physically examined by skin scratch tests, pulmonary function tests and serum immunological tests. Among 24 workers, 9 handled powdered drugs (A group), 5 handled the same in the past and had already been transferred to other sections for their symptoms (B group), 3 engaged in the process of capsul-filling (C group) and 7 handled several times occasionally during one year (D group). Their average months spent in handling powdered drugs were, in the case of anti-inflammatory enzyme, A group 53.2, B group 66.2, and in the case of antibiotics, 5 workers in A group 24.0, 2 workers in B group 7.0, 3 workers in C group 25.7. Twenty workers complained of symptoms which were mainly irritation of mucosa including the respiratory system and itching of the skin while they were working, and accelerated nasal discharge, urticaria and asthma after working. Group A and group B were higher than group D in the rate of respiratory complaints in C.M.I. (p less than 0.001). Fourteen workers pointed out anti-inflammatory enzyme as a cause of main symptoms, 7 workers flufenamic acid, 3 workers flopropion, 4 workers antibiotics. Three workers who had past history of asthma or articular rheumatism had been transferred to other sections. Of 18 workers who were physically examined, 11 workers showed positive reactions to skin scratch tests with handling drugs. On 8 workers of them, some kinds of drugs which were pointed out as drugs causing main symptoms reacted positively. Numbers of workers with increased immunoglobin values were, IgE 3, IgM 2, IgA 4, IgM 2. Two workers showed decreased FVC and FEV (1.0 sec.) values in pulmonary function tests. The causes of the occupational allergic reaction in this factory are guessed as follows: 1) control of powdered materials was incomplete in the process of production, 2) various kinds of sensitizing drugs were handled by the same workers.
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PMID:[Some experiments on the allergic reaction among workers in a pharmaceutical factory (author's transl)]. 16 Apr 71

IgE antibodies can produce a late inflammatory response 6--12 h after allergen challenge which is characterized by diffuse edema, erythema, pruritus, tenderness and heat. That IgE is involved in inducing the late reaction was shown by the abolition of both immediate and late responses by passive transfer tests: (1) by heating atopic serum at 56 degrees C for 4 h; (2) by removing IgE from the atopic serum by a solid phase anti-IgE immunoabsorbent, and (3) by competitively inhibiting the binding of IgE antibodies to cells by an IgE myeloma protein. Also, both responses were induced by affinity chromatography-purified IgE antibody followed by antigenic challenge. Very similar lesions could be induced by intradermal injection of Compound 48/80. The late phase is characterized by edema and a mixed cellular infiltration, predominantly lymphocytic but also containing eosinophils, neutrophils and basophils. Direct immunofluorescent staining did not show deposition of immunoglobulins or complement components, except IgM in two of 15 and C3 in one of 15 patients, respectively.
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PMID:Late cutaneous reactions due to IgE antibodies. 33 13

The cause of urticaria and angioedema often is difficult to ascertain. In most cases the conditions are transient, but a chronic idiopathic form does occur and may be intractable. Acute urticaria and angioedema usually result from an IgE-mediated mechanism; success in treatment depends on recognition of the underlying factor. Chronic urticaria may ultimately necessitate use of corticosteroids. Hereditary angioedema is easily differentiated from idiopathic angioedema by the family history and absence of pruritus.
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PMID:Urticaria and angioedema. Common clinical problems. 42 57

The therapeutic effect of transfer factor (TF) from healthy donors was investigated in two children with extensive intractable atopic dermatitis, recurrent pyogenic skin infections, hyperimmunoglobulinaemia E, defective neutrophil chemotaxis and depressed cell-mediated immunity. Striking clinical improvement was noted in both patients with disappearance of skin infections, pruritus and eczema. No new lesions have occurred 13 months after the completion of therapy in the first patient but a few new atopic lesions have reappeared after 8 months in the second. Both patients are off steroids and antibiotics. Transfer factor administration did not influence the T cell rosette number or the lymphocyte blastic transformation response, but it did cause conversion of the skin-test reactivity in both patients and correction of polymorphonuclear chemotaxis in one of them. Non clinical side-effects were noted but marked and persistent rise of serum IgE was observed in both patients. Our data suggest that patients with hyper-IgE syndrome may be benefited by TF therapy and they lend further support to the notion that T lymphocyte deficiency may be the basis of the eczema in this syndrome.
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PMID:Transfer factor therapy in hyperimmunoglobulinaemia E syndrome. 48 48

A man who was suffering from recurrent staphylococcal infection had antecedent symptoms of severe pruritus. Laboratory investigations showed leukocytosis with eosinophilia, hyperimmunoglobulinemia of all fractions, but particularly of IgE, and a deficiency of cell-mediated immunity on in vivo testing. Phagocytosis and bactericidal activity of polymorphonuclear leukocytes were normal, but a cellular and serum-associated defect in leukocytotaxia was present. Ultrastructural changes were observed in polymorphonuclear leukocytes. Association of impaired leukocytotaxia and elevated levels of IgE is not uncommon. Recurrent bacterial infections in the patient described are probably related to defective chemotaxis.
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PMID:Defective leukocytotaxia and recurrent staphylococcal infecion: deficiency of leukocytotaxia and abnormal granulocytes associated with increase serum IgE levels in an adult with recurrent staphylococcal infection. 68 54

IgE antibodies are usually thought to induce only immediate skin reactions. We have shown that the intradermal injection of a number of different allergens can produce a prolonged inflammatory reaction after the immediate wheal and flare in most sensitive subjects. This late inflammatory response occurs 6-12 h after challenge and is characterized by diffuse edema, erythema, pruritus, and heat. Both immediate and late responses can also be seen after passive sensitization of skin sites in nonatopic subjects. That IgE is involved in inducing the reaction was shown by the abolition of both immediate and late responses by passive transfer tests in the following experiments: (a) heating atopic serum at 56degreesC for 4 h, (b) removing IgE from the atopic serum by a solid phase anti-IgE immunoabsorbent, and (c) competitively inhibiting the binding of IgE antibodies to cells by an IgE myeloma protein. In addition, both responses were induced by affinity chromatography-purified IgE antibody, followed by antigenic challenge. Very similar lesions could also be induced by intradermal injection of Compound 48/80, thus suggesting a central role in the reaction for the mast cell or basophil. Histologically, the late phase is characterized by edema and a mixed cellular infiltration, predominantly lymphocytic but also containing eosinophils, neutrophils and basophils. Direct immunofluorescent staining did not show deposition of immunoglobulins or complement components, except IgM in 2 of 15 and C3 in 1 of 15 patients. This finding indicates that the late phase does not depend on the deposition of immune complexes. The results of the study suggest that IgE-allergen interaction on the surfaces of mast cells or on infiltrating basophils causes both immediate and late cutaneous responses.
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PMID:The late phase of the immediate wheal and flare skin reaction. Its dependence upon IgE antibodies. 78 99

A 25-year-old white female returned from West Africa with a two-year history of epidosic swelling, pruritus, and pain in a wrist, associated with peripheral eosinophilia. Serologic and immediate skin tests with Dirofilaria immitis antigen were positive, and blood smears transiently showed microfilariae of Acanthocheilonema perstans after the patient had been treated with diethylcarbamazine. Before treatment, both the serum concentration of IgE and the eosinophil content of arylsulfatase, an enzyme that selectively inactivates slow-reacting substance of anaphylaxis, were elevated; the patient's peripheral leukocytes released histamine and eosinophil chemotactic factor of anaphylaxis when challenged with D. immitis antigen. After one course of diethylcarbamazine, the clinical manifestations and abnormal in vitro immunologic results resolved. Host response to A. perstans infection appears to involve both IgE-mediated hypersensitivity and alterations in an eosinophil enzyme.
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PMID:Studies of immediate hypersensitivity in a patient with Acanthocheilonema perstans filarial infection. 107 19


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