Serum sickness from streptokinase.
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Humans↗
Biomedical subjects
R Patterson
Publications and source records attributed to R Patterson.
Idiopathic anaphylaxis: classification, evaluation, and treatment of 123 patients.
The manifestations, evaluation, treatment, and course of 123 patients with idiopathic anaphylaxis (IA) are described for a total of 374 patient years of our management. Observation of this group of patients resulted in the description and classification of IA as one or more episodes of generalized IA with multiple systemic manifestations or IA with life-threatening angioedema of the tongue or larynx. Therapy is based on the frequency of episodes. Acute therapy is appropriate for infrequent episodes, but prophylactic therapy is indicated for frequent episodes. In patients with frequent episodes, remissions can be induced and maintained with prednisone. Prolonged remissions may occur after prednisone is stopped. There have been no deaths from IA in patients managed by our service. By definition, there is no identifiable antigen responsible for episodes of IA, and there is no underlying disease in these patients. A mast cell basophil-activation mechanism is suggested. IA may represent the most severe form of a spectrum of diseases that include idiopathic urticaria and angioedema.
Adolescent↗
Antibody response to trimellityl hemoglobin in trimellitic anhydride-induced lung injury.
Sprague-Dawley rats were exposed to trimellitic anhydride by inhalation, and the antibody response to trimellityl (TM)-conjugated hemoglobin (HB) and TM rat serum albumin (RSA) was compared. Groups of rats were exposed to trimellitic anhydride by inhalation 6 hours per day for 2, 6, or 10 days at 100 micrograms/m3 and compared to a control group exposed to filtered air. The IgG antibody response to TM-HB in both serum and bronchoalveolar lavage (BAL) fluid was measured with ELISA. IgG antibody levels to TM-HB rose significantly throughout the exposure. A positive correlation was found between IgG to TM-HB in serum and BAL fluid. In addition, this response in both serum and BAL fluid correlated with the IgG antibody response to TM-RSA. Cross-inhibition studies indicated the existence of shared antigenic determinants on TM-RSA and TM-HB. The IgG antibody to both antigens was specific for new antigenic determinants and not for the TM hapten.
Animals↗
Diagnosis and treatment of drug allergy.
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Animals↗
Woodman's disease: hypersensitivity pneumonitis from cutting live trees.
A 28-year-old man developed multiple episodes of fever, cough, shortness of breath, and leukocytosis several hours after cutting live oak and maple trees. Fungal cultures of wood chips from oak and maple trees were positive for Penicillium (three species), Paecilomyces sp., Aspergillus niger, Aspergillus sp., and Rhizopus sp. Gel-immunodiffusion studies demonstrated serum precipitins to extracts of oak chips, Penicillium sp., and Paecilomyces sp., and suggested that Penicillium sp. and Paecilomyces sp. shared cross-reactive antigens that were the significant antigens in the oak chips. ELISA studies demonstrated elevated serum levels of IgG to an oak chip extract, inhibition of that ELISA by preincubation of serum with Penicillium sp., and absence of elevated IgG levels to an extract of freshly cut oak wood that had been stripped of bark to minimize mold contamination. The case analysis indicates that the patient likely had hypersensitivity pneumonitis on exposure to Penicillium sp., when he was cutting trees, and identifies cutting live trees as another occupational exposure that may cause hypersensitivity pneumonitis.
Adult↗
The laboratory evaluation of IgE antibody to metabisulfites in patients skin test positive to metabisulfites.
An immediate-type hypersensitivity reaction has been proposed as one possible mechanism in which metabisulfites (MBSs) cause reactions. As demonstrated with certain occupational chemicals, we proposed that MBS might conjugate with human proteins, such as human serum albumin, and then cause an immunologic response. Because we had identified no reactions to MBS at the Northwestern Allergy Service, we used sera from four patients reported elsewhere as having positive skin tests and positive oral challenges to sulfites. We attempted to demonstrate, both in vitro by ELISA and in vivo by passive cutaneous transfer to monkey, evidence for IgE-mediated hypersensitivity to MBSs. Our results demonstrated that there is evidence of IgE antibody by passive transfer for one patient studied, but no evidence of IgE antibody by ELISA to an MBS-albumin conjugate in any of the four patients. This study illustrates the complexities involved in the evaluation and mechanism of MBS-induced disease and the caution with which results must be interpreted.
Animals↗
Prospective immunologic and clinical study of a population exposed to hexamethylene diisocyanate.
We have prospectively evaluated 150 workers exposed to hexamethylene diisocyanate (HDI) and its trimer (THDI) during an 18-month period. The evaluation consisted of periodic serum antibody studies and a questionnaire that was designed to attempt to identify symptoms compatible with work-related syndromes of allergic rhinitis, allergic conjunctivitis, hypersensitivity pneumonitis, asthma, or irritant reactions. The study population was divided into seven groups on the basis of job classification. The groups differed in exposure levels but were similar in terms of age, sex, smoking history, and duration of work with isocyanates. IgE and IgG against HDI and THDI conjugated to human serum albumin (HSA) (HDI-HSA and THDI-HSA) were determined by ELISA. There were no instances of immunologically induced disease among the 21% of workers in this sample with antibody; however, there is insufficient evidence at this time to make judgments about the relationship between antibody and clinical disease. The antibody was generally low-level IgG that may be a sensitive indicator to detect exposure to certain reactive chemicals. The level of antibody was not different among job classes or between smokers and nonsmokers. Moreover, there was no correlation between antibody level and exposure duration in these workers whose exposure levels are all well below National Institute for Occupational Safety and Health recommendations. Further evaluation will extend these observations.
Antibodies↗
Minimal complications in a surgical population with severe asthma receiving prophylactic corticosteroids.
Sixty-eight patients with asthma followed by the Northwestern Allergy Service underwent a total of 92 surgical procedures from July 1973 to December 1986. In 41 of 92 procedures outpatient prednisone was administered, and in 92 procedures a pretreatment regimen of 100 mg hydrocortisone parenterally every 8 hours beginning the night before surgery was administered. Postoperatively, the overall incidence of pulmonary complications (either pulmonary infection or asthma) was 9.7%. Three patients developed pneumonia, demonstrated by an infiltrate on chest x-ray examination, and two patients developed wheezing requiring epinephrine, giving a complication rate of 5.4%. In addition, four patients developed mild wheezing postoperatively. Statistical analyses to compare the overall infection rate in this asthmatic population with that in two other surgical populations showed no statistical differences. There were no deaths and no patient developed any wound complication or adrenocortical insufficiency. These results indicate that patients with asthma in optimal respiratory condition who have received preoperative clinical evaluation and a hydrocortisone pretreatment regimen can undergo surgery with minimal complications.
Asthma↗
Allergic bronchopulmonary aspergillosis and the evaluation of the patient with asthma.
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Aspergillosis, Allergic Bronchopulmonary↗
Sensitivity and reliability of force tracking and joint-movement tracking scores in healthy subjects.
The purpose of this study was to examine the sensitivity and reliability of two tracking tests designed to measure control of handgrip force and finger movement. In one test, the subject exerts careful control of handgrip force on a dynamometer, which is interfaced with a computer, and attempts to guide a cursor as accurately as possible along a stationary target track displayed on the computer screen. In the second test, the subject attempts to trace a different target track by precise flexion-extension movement of the metacarpophalangeal joint of the index finger to which an electrogoniometer is attached. For both tests, the computer quantifies the subject's performance with an accuracy index. Fourteen healthy subjects participated in the force tracking test (FTT), which involved three pretest tracking trials, a 20-minute inactivity period, and three posttest trials. Thirteen different healthy subjects participated in the joint-movement tracking test (JMTT) using the same testing format. One-tailed, paired t tests of the pretest-posttest tracking scores showed significant (p less than .01) improvement in tracking accuracy for both the FTT and the JMTT. Additionally, intraclass correlation coefficients for both the pretest and the posttest trials showed acceptable reliability in the FTT and the JMTT. We concluded, for healthy subjects, that 1) these tracking tests are sensitive to small changes in force control and joint-movement control, and 2) the tracking scores are reliable. We believe that these tests could be very useful in documenting objectively the effects of treatment applied to the hand.
Adult↗
Effect of inhaled leukotriene D4 on human airways.
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Adult↗
Evidence for in vitro regulation of IgE receptors on the human basophil membrane by their removal and reexpression: effects of Ca2+, Mg2+, some metabolic inhibitors and fetal calf serum.
Human basophils free of receptor-bound IgE and suspended in RPMI-1640 + 0.2% EDTA or in a buffered salt solution lacking Ca2+ and Mg2+ bound optimal quantities of 125I IgE. In media containing Ca2+ and Mg2+ such as RPMI-1640 alone or a buffered physiologic salt solution binding was reduced significantly in the first 60 min and remained essentially unchanged in the next 120 min. Scatchard analysis showed the reduction to be due both to loss of number and affinity of receptors. The presence of both 2-deoxy-d-glucose and 2,4-dinitrophenol usually prevented the reduction of binding in RPMI-1640. Suspension of cells in RPMI-1640 supplemented with fetal calf serum (FCS) demonstrated reduction in binding at 60 min characteristic of divalent-cation-containing media but this was followed by a rise in binding to approximately control levels in the next 120 min. This pattern of binding occurred in about 70% of the experiments. In most of the remaining experiments there was no difference from control binding in that there was no early decrease and no late rise in binding. This variability was not leukocyte-donor-dependent. When cells were preloaded with 125I IgE and incubated in RPMI-1640 dissociation of IgE was more rapid than in media free of Ca2+ and Mg2+. The results suggest that membrane-bound IgE receptors on basophils may be shed by an energy and Ca2+ and Mg2+ requiring process and reexpressed dependent on a factor or factors present in FCS.
2,4-Dinitrophenol↗
Irritant symptoms and immunologic responses to multiple chemicals: importance of clinical and immunologic correlations.
An evaluation of workers in a plant was conducted because of multiple complaints of ocular, nasal, skin and chest symptoms. Antibody activity against 4 different chemicals was identified: an aliphatic diisocyanate, 4-vinylcyclohexene dioxide, trimellitic anhydride (TMA) and an unknown chemical present in a plasticizing ester known as n-octyl-n-decyl-trimellitate. The source of TMA which resulted in immunization in the plant is unknown. The presence or absence of antibodies did not correlate with the presence or absence of symptoms and it was concluded that no occupational allergic disease was present in these workers. Antibody studies alone do not make a diagnosis of occupational allergic disease and clinical correlation is required. Immunoassays may be useful in identifying exposures to immunizing chemicals in the workplace for potential clinical correlation or for exposure monitoring in the workplace.
Air Pollutants, Occupational↗
Effect of a leukotriene D4 (LTD4) antagonist on LTD4 and ascaris antigen-induced airway responses in rhesus monkeys.
An acute airway response to aerosolized leukotriene D4 (LTD4) qualitatively simulates an IgE-mediated ascaris antigen-induced airway response. The LTD4 airway response is completely inhibited by the LTD4 antagonist, ICI 198615, in normal monkeys. This LTD4 antagonist was then evaluated to determine whether it could inhibit the IgE-mediated ascaris antigen response using the threshold antigen dose-response system or the single antigen dose-response system. In 6 ascaris airway-reactive monkeys, the LTD4 antagonist demonstrated partial inhibition in 2 animals by either the threshold dose system in 1 animal or the single dose system in another animal. In the remaining animals there was no inhibition of the antigen-induced response by the LTD4 antagonist.
Animals↗
A serial immunologic and histopathologic study of lung injury induced by trimellitic anhydride.
Trimellitic anhydride (TMA) can induce immunologic lung disease in exposed workers. We have developed a rat model of TMA lung injury characterized by lung hemorrhage and an immune response to trimellityl (TM) haptenized lung proteins. The model is similar to the pulmonary disease-anemia syndrome (PDA) seen in workers exposed to TMA fumes. Sprague-Dawley rats, 15 per exposure period, inhaled micronized TMA powder, 100 micrograms/m3, 6 h/day, for 2,6, or 10 days and were sacrificed. At each time period, total, IgG, IgA, and IgM antibody to TM-rat serum albumin (TM-RSA) were measured by radiolabeled antigen binding and enzyme-linked immunosorbent assay (ELISA) in serum and bronchoalveolar lavage fluid (BAL). Hemorrhagic lung foci, weight, and displacement volume were determined, and lungs were examined by light and electron microscopy. There was no lung injury or antibody response at 2 days. There was minimal lung injury at 6 days with low levels of antibody in BAL and serum. At 10 days, there was a marked increase in hemorrhagic foci and in BAL and serum antibody levels. BAL antibody levels at 6 and 10 days had higher correlations with measures of lung injury than corresponding serum levels. There was minimal ultrastructural change at 6 days. By Day 10, there was marked intraalveolar hemorrhage, alveolar septal inflammatory nodules, abundant alveolar macrophages, and evidence of endothelial and epithelial cell injury. These results indicate that the immune response to inhaled TMA occurs parallel with the development of lung lesions, and antibody levels in BAL and serum are highly correlated with lung injury.
Animals↗
Mechanism of platelet activating factor-induced bronchoconstriction in humans.
The inhalation of platelet activating factor (PAF) produces bronchoconstriction in normal and asthmatic subjects. To identify the mechanism by which PAF-induced bronchoconstriction occurs in humans, bronchoprovocation testing was performed in 7 subjects (3 normal, 4 with mild asthma) after pretreatment with phosphate-buffered saline (PBS), atropine, chlorpheniramine, or indomethacin. We determined the nebulizer concentration of PAF which reduced specific airway conductance (SGaw) 35% (PC35 SGaw) and the slope of the PAF dose-response curve. Atropine produced baseline bronchodilatation (SGaw increased 50%), while chlorpheniramine and indomethacin had no effect on baseline pulmonary function. Atropine increased airway responsiveness to PAF: the PC35 SGaw decreased 40% (p less than 0.05) and the slope of the PAF dose-response curve increased 86% (p less than 0.05). In contrast, chlorpheniramine inhibited the airway response to PAF: the PC35 SGaw increased 87% (p less than 0.05), while the slope of the PAF dose-response curve decreased an insignificant 37%. Indomethacin did not affect either measurement. Chlorpheniramine also prevented the PAF-induced facial flushing and feeling of warmth; atropine and indomethacin did not. These results suggest that PAF-induced bronchoconstriction in humans is mediated at least in part by histamine release, not by cholinergic or cyclooxygenase-dependent mechanisms. Other indirect effects, such as the release of sulfidopeptide leukotrienes, or a direct effect on airway smooth muscle may also contribute to PAF-induced bronchoconstriction. Why atropine heightened the airway response to PAF is unclear.
Adolescent↗
Localized neuroblastoma treated by surgery: a Pediatric Oncology Group Study.
A prospective study was designed to evaluate the outcome of patients with localized resectable neuroblastoma without regional lymph node involvement when no therapy beyond surgical resection was administered. One hundred one patients observed for 3 to 60 months had a 2-year disease-free survival of 89% (SE = 5%). Of the nine patients experiencing relapse, only three have died. There were no apparent distinguishing characteristics of the nine failures. Due to the favorable prognosis of the subset of neuroblastoma patients, prognostic factor analysis had very limited power and lacked clinical importance. Complete gross removal of the localized tumors is adequate therapy to ensure the survival of the majority of these patients.
Child↗
Induction of antigen-specific bronchial reactivity to trimellityl-human serum albumin by passive transfer of serum from humans to rhesus monkeys.
A rhesus monkey model was developed to demonstrate the pathogenetic role of IgE to chemical hapten-protein conjugates in causing human occupational asthma from reactive chemicals. Serum from a worker with trimellitic anhydride (TMA) asthma that contained high titers of IgE, IgG, IgM, and IgA to trimellityl-human serum albumin (TM-HSA) was aerosolized into the lungs of two monkeys to afford passive airway sensitization. After the monkeys were challenged with aerosolized TM-HSA, pulmonary functions demonstrated acute airway responses similar to that of Ascaris antigen-induced, IgE-mediated bronchospasm in Ascaris-sensitive monkeys. The monkeys had no airway reactivity when challenged with TM-HSA 1 week after the first positive TM-HSA response elicited with passive sensitization. Passive cutaneous reactivity to TM-HSA was also elicited by the donor serum, but heat-treated donor serum failed to confer cutaneous or bronchial reactivity. These results indicate that airway reactivity in this passive-transfer monkey model of TMA asthma is an antigen-specific response mediated by heat-labile serum factors, presumably IgE to TM-HSA, and does not occur by irritant mechanisms. This experimental model could become a valuable system for evaluating the role of IgE to hapten-protein conjugates in the immunopathogenesis of asthma caused by other reactive chemicals capable of acting as haptens. We postulate that immunologic and clinical features should be consistent with asthma caused by such reactive chemicals and mediated by such mechanisms.
Animals↗