Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0393754 (HSA)
 2,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A worker developed two episodes of severe asthma 90 min after cutting a polyurethane plate made of diphenylmethane diisocyanate (MDI) using a rapidly turning carbide blade. Intradermal skin testing with MDI-human serum albumin (MDI-HSA) and p-tolyl isocyanate-HSA (p-TMI-HSA) were positive at 0.002 mg/ml. Control subjects showed no reaction at 2 mg/ml. Bronchial provocations of the worker with MDI-HSA and p-TMI-HSA, made 1 year after the occupational asthmatic episode, were negative at 10 mg/ml. Bronchial reactivity to methacholine decreased toward normal during a 2-year follow-up. RAST using MDI-HSA or p-TMI-HSA were strongly positive when compared with binding by sera from atopic controls which contained the same amount of total IgE. RAST titres decreased during a 1-year follow-up. In the MDI-HSA RAST, inhibition studies indicated specificity of antibodies for MDI-HSA. In the p-TMI-HSA RAST, p-TMI-HSA was a very effective inhibitor whereas MDI-HSA was not. These results indicated the formation of at least two distinct groups of IgE antibodies: those reactive with MDI, and those reactive with p-TMI determinants. Guinea pigs immunized with MDI formed antibodies with specificities similar to those of the patient. We conclude that the worker had occupational asthma accompanied by the formation of specific IgE antibodies of the specificities. The causal relationship of the antibodies to the occupational asthma remains uncertain.
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PMID:Diphenylmethane diisocyanate (MDI)-induced asthma: evaluation of the immunologic responses and application of an animal model of isocyanate sensitivity. 646 57

In a four-year clinical, immunologic, and environmental study of trimellitic anhydride (TMA) exposure in a single plant, 20 workers exposed to TMA powder were evaluated in 1979 and a total of 32 workers were evaluated from 1979 to 1983. Two distinct groups emerged before and after workplace control improvements were made in 1979. Seventeen of the original 20 workers were available for longitudinal study through 1983. Annual clinical evaluations and serum radioimmunoassays for total antibody binding and specific IgE binding to 125I TM-HSA (human serum albumin) were performed on all 32 workers. In 1979, six workers had antibody against TM-HSA, three had the late respiratory systemic syndrome, and two had TMA-induced allergic rhinitis or allergic rhinitis and asthma. One worker had antibody against TM-HSA without illness. Fifteen additional workers were evaluated longitudinally after institution of several workplace control measures. Four of these 15 workers had TMA exposure prior to environmental improvement and joined the study in 1982. The remaining 11 workers joined the study in 1982 and had at least two years of TMA exposure in the modified workplace. None of these 11 workers developed a TMA-induced immunologic syndrome or significant total or specific IgE antibody binding to 125I TM-HSA.
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PMID:Four-year evaluation of workers exposed to trimellitic anhydride. A brief report. 648 2

Serum and tear levels of IgE were compared in patients with contact lens papillary conjunctivitis (CLPC), vernal keratoconjunctivitis (VC), healthy contact lens wearers (CLW), and healthy controls without lenses. The mean of serum IgE was elevated only in the VC group. Tear IgE levels were significantly higher for CLPC and VC than for CLW and healthy controls. Tear IgG levels were also increased in CLPC patients. With serum albumin (HSA) as a marker for leakage of proteins from the circulation to the tear fluid, the data indicated, that tear IgG was blood-borne whereas tear IgE was essentially a product of local synthesis. In one of the 10 CLPC patients, high titers of IgE type antibodies to housedust mites and cat epithelium were demonstrated in both serum and tears. We conclude that CLPC is usually an IgE mediated reaction to the lens material or to contaminations of allergenic material that sticks to the lenses.
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PMID:An immunological study of papillary conjunctivitis due to contact lenses. 648 48

Serum samples obtained from seven hemodialysis patients with immediate-type allergic reactions, from six hemodialysis patients without reactions, and from three nonatopic control subjects were analyzed for IgE against human serum albumin exposed to ethylene oxide (ETO-HSA). ETO is used to sterilize medical equipment like dialyzers that cannot withstand heat sterilization. IgE to ETO-HSA, measured by a polystyrene tube technique was found in six of seven dialysis reactor patients but in only one of six nonreactor patients (p less than 0.05 two-tailed Fisher's exact test). No control sera from three nonatopic individuals had antibody. The reactor patients had 2.0 +/- 8.0 ng (SD) of ETO-HSA bound per milliliter of serum, whereas nonreactor patients had 0.2 +/- 8.0 ng per milliliter bound (p less than 0.05 one-tailed Student's t test on log transformed values). We suggest that there is an association between the presence of IgE to ETO-HSA and immediate-type allergic reactions to dialysis in this group of patients.
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PMID:IgE against ethylene oxide-altered human serum albumin in patients who have had acute dialysis reactions. 649 Nov

To assess the immunological cross-reactivity of the monobactam antibiotic aztreonam (AZ), rabbits were immunized with protein conjugates of benzylpenicillin, cephalothin (CEPH), and AZ. The resulting antibenzylpenicilloyl (BPO) and anti-CEPH rabbit antibodies showed negligible cross-reactivity with AZ conjugated to human serum albumin (AZ-HSA), whereas anti-AZ showed negligible cross-reactivity with BPO-HSA and CEPH-HSA. Unlike benzylpenicillin and CEPH, unconjugated AZ was as effective as AZ conjugated to epsilon aminocaproic acid (AZ-EACA) in inhibiting the binding of homologous antibody. Studies with various analogs of AZ confirmed that immunoglobulin G (IgG) anti-AZ was entirely side-chain specific. The inhibition of the binding of human IgE anti-penicilloyl to BPO-HSA was studied in the presence of AZ-EACA, BPO-formyl lysine, and CEPH-EACA. Whereas CEPH-EACA displayed 3% cross-reactivity with BPO-lysine, AZ-EACA showed little or no cross-reactivity (much less than 0.9%). To assess the immunogenicity of AZ in humans, IgE and IgG antibodies were measured in sera from 36 healthy male volunteers receiving 0.5 or 1 g intravenously or intramuscularly every 8 h for 7 days. None of the subjects had detectable preexisting IgE reactive with AZ or demonstrated an IgE response to antibiotic administration. Four subjects gave evidence for naturally occurring IgG cross-reactive with AZ, but only one subject demonstrated a rise in IgG levels after exposure to AZ. This anti-AZ IgG did not cross-react with BPO or CEPH conjugates of bovine thyroglobulin and was completely side-chain specific. These studies suggest that AZ displays very low immunological cross-reactivity with other beta-lactam antibiotics and may be only weakly immunogenic in humans.
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PMID:Immunology of the monobactam aztreonam. 653 98

Eighteen workers exposed to trimellitic anhydride (TMA) powder were evaluated in 1979. Twelve of these workers were available for longitudinal study until 1982. Annual clinical evaluations and serum radioimmunoassays for total antibody binding and specific IgE binding to 125I-TM-HSA were performed. In 1979, five workers had antibody against TM-HSA. Of these, three workers were diagnosed with the late respiratory systemic syndrome (LRSS) and one worker with TMA-induced allergic rhinitis. The LRSS workers had significantly elevated total antibody binding of 125I-TM-HSA and the worker with rhinitis had significantly elevated specific IgE binding of 125I-TM-HSA per milliliter of serum. Although TMA handling was intermittent throughout the year, average airborne dust concentrations from 1974 to 1978 at job stations of the two heaviest TMA-exposed occupations, operator and assistant operator, were 2.1 and 0.82 mg/m3, respectively. After local exhaust ventilation had been improved, average airborne dust concentrations of TMA at the two latter job stations fell to levels of 0.03 and 0.01 mg/m3, respectively, in 1982. The decrease in TMA exposure coincided with a gradual fall in total antibody binding of 125I-TM-HSA per milliliter in 1982 and symptomatic improvement in the three individuals with the LRSS. The continuous low-level exposure of the worker with TMA rhinitis was sufficient to elicit a rise in specific IgE against TM-HSA from 1.1 ng of 125I-TM-HSA bound per milliliter in 1979 to 2.12 in 1982.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationship of airborne trimellitic anhydride concentrations to trimellitic anhydride--induced symptoms and immune responses. 664 75

Clinical and immunologic evaluations were performed on workers who manufacture trimellitic anhydride (TMA), a chemical used widely in the plastics industry. Serum samples of 29 workers exposed to TMA dust and fumes were assayed for total IgE, as well as specific IgE and total antibody binding to radiolabeled trimellityl human serum albumin (TM-HSA). Fifteen workers were determined to have significant specific IgE to TM-HSA (greater than or equal to 1 ng of 125I-TM-HSA bound per milliliter). Of these 15 individuals, seven workers had immediate asthma and rhinitis and positive cutaneous prick tests and eight were nonasthmatic and skin test negative. Mean peak total serum IgE was significantly higher in the prick test positive group (p less than 0.02) and higher than in 12 exposed asymptomatic IgE antibody-negative workers (p less than 0.001). Total serum IgE followed rises and falls in TM-HSA--Specific IgE binding, correlating to the onset of allergic symptoms in all seven workers. Total antibody binding of 125I-TM-HSA, as determined by the ammonium sulfate precipitation technique, was higher in the skin test-negative group of eight (mean 12,062 ng per milliliter 125I-TM-HSA bound) than in the seven symptomatic skin test-positive workers (mean 2930, p less than 0.004). Determinations of total antibody divided by specific IgE (both in nanograms of 125I-TM-HSA bound per milliliter) or blocking ratios clearly discriminated the seven skin test-positive workers with TMA-induced asthma (range 10 to 666) from the eight skin test-negative workers (range 1580 to 16,000).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationship of total serum IgE and blocking antibody in trimellitic anhydride--induced occupational asthma. 664 76

Vernal keratoconjunctivitis (VC) is an inflammatory disorder of the outer eye, probably of allergic etiology. The present study was performed on patients with a typical clinical appearance of VC and examined periodically for serum and tear IgE and albumin (HSA). The geometric mean of serum and tear IgE was 219 and 18 IU/ml, respectively, for the patients, but about 100 and less than 1 IU/ml for serum and tears of healthy controls and of parents of VC patients. A positive correlation between variations in tear IgE and tear HSA was observed, indicating that tear IgE levels have a significant influence on the intensity of the inflammatory process.
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PMID:Vernal keratoconjunctivitis: the significance of immunoglobulin E levels in tears and serum. 671 62

We describe seven women with asthma induced by occupational exposure to an acid anhydride, tetrachlorophthalic anhydride (TCPA), an epoxy resin hardening agent. Inhalation tests with TCPA at atmospheric concentrations of less than one tenth of a manufacturer's recommended exposure limit provoked asthmatic reactions in the four women tested. None had evidence of pretest bronchial hyperreactivity. Immediate skin prick test reactions were elicited in the seven subjects by a conjugate of TCPA with human serum albumin (TCPA-HSA) but not in others tested. Specific IgE antibody levels to TCPA-HSA, measured by radioallergosorbent test scores, were significantly elevated in the seven, but not in TCPA-exposed and unexposed comparison groups. These results imply that occupational asthma caused by TCPA is an allergic reaction mediated by specific IgE antibody.
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PMID:Tetrachlorophthalic anhydride asthma: evidence for specific IgE antibody. 682 91

T lymphocytes in the mesenteric lymph nodes of rats infected with Nippostrongylus brasiliensis spontaneously released a soluble factor that selectively potentiated the IgE-forming cell response of antigen-primed cells to homologous antigen. The factor could enhance the IgE response of DNP-OA-primed cells to DNP-HSA and T cell-replacing factor. In contrast, the treatment of OA-primed T cells with the factor failed to enhance either the IgE or IgG response of the mixture of DNP-KLH primed cells and OA-primed T cells to DNP-OA. The results collectively suggested that the target cells of the IgE-potentiating factor are B cells. Indeed, IgE potentiating factor was absorbed by B cells rather than T cells or thymocytes. Evidence was obtained that IgE-potentiating factor could be absorbed by IgE-bearing B cells or IgE-coupled Sepharose, indicating that the factor had affinity for IgE. It appeared that the potentiating factor bound to IgE-bearing B cells and selectively enhanced the differentiation of IgE-B cells to IgE-forming cells. It was also found that the major source of the factor was Fc epsilon R-bearing T cells.
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PMID:Regulatory role of IgE-binding factors from rat T lymphocytes. I. Mechanism of enhancement of IgE response by IgE-potentiating factor. 696 48


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