Chlamydia pneumoniae and possible relationship to asthma. Serum immunoglobulins and histamine release in patients and controls

Chlamydia pneumoniae (C.pn.) is claimed to be of importance for the development of bronchial asthma in previously healthy individuals. This is a new and speculative theory. Earlier studies have mainly focused on C.pn. and exacerbation of asthma. If this new theory were true, one would expect titres of C.pn.-specific IgG to be higher or more common in patients compared with controls. It would also seem probable that pathobiological mechanisms as found in connection with other microorganisms could be demonstrated, i.e. presence of C.pn.-specific IgE and the capability of C.pn. to induce or enhance histamine release from basophil leukocytes. We therefore examined C.pn.-specific IgE, IgG and IgM in sera from 22 adults with bronchial asthma and 25 healthy controls. IgE was verified by passive sensitization of basophils from umbilical cord blood. The prevalence of IgE was approx. 69% and IgG approx. 23% in both groups. IgG-titres were between 1:16 and 1:64 in both groups. No IgM was found. Further, C.pn. could neither induce nor enhance histamine release from basophil leukocytes of patients or controls. We conclude that patients with bronchial asthma and healthy controls do not differ in relation to 1) C.pn.-specific IgE in sera, 2) the capability of C.pn. to induce or enhance histamine release from basophil leukocytes, since no such effect was found, or 3) previous C.pn. infection judged by the presence of specific IgG antibodies. Our results cannot support the theory that C.pn. is a cause of adult-onset asthma.     

Evaluation of the Brusini glaucoma staging system for follow-up in glaucoma

There is evidence that bronchial responsiveness to allergen is quantitatively correlated with bronchial responsiveness to nonspecific stimuli in subjects with allergic asthma. This association has been questioned in occupational asthma due to low molecular weight substances. It was the aim of this study to assess the quantitative association of bronchial responsiveness to methacholine (MCH) and platinum salts (Pt), in the form of hexachloroplatinic acid, in workers with occupational asthma due to Pt salts. Fifty-seven subjects with exposure to Pt, work-related asthma, and a positive bronchial challenge with Pt underwent skin prick test with Pt and bronchial challenge with MCH. Using the provocation concentration causing a > or = 50% fall in specific airway conductance (PC50sGaw(Pt)) as a dependent variable, anamnestic data (period from first symptoms to removal, period between removal from exposure and diagnosis, and smoking), season of the investigation, skin prick tests with environmental allergens, total immunoglobulin E (IgE), skin reactivity to Pt (Pt concentration causing a 2 mm wheal), and PC50sGaw(MCH) were included as independent variables for regression analysis. Fifty-two subjects (91%) showed a PC50sGaw(MCH) < 8 mg.mL-1 (geometric mean for all subjects 1.6 mg.mL-1). Responsiveness to Pt varied widely between subjects (geometric mean of PC50sGaw(Pt) 9 x 10(-5) mol.L-1, range 2 x 10(-7) to 10(-2) mol.L-1). There was no univariate correlation between bronchial responsiveness to MCH and Pt, but there was a correlation between skin reactivity to Pt and PC50sGaw(Pt) (r = 0.6). This association could not be improved by considering PC50sGaw(MCH), the period from first symptoms to removal, or the period between removal from exposure and diagnosis. The parameters that showed the highest (negative) associations with PC50sGaw(Pt) were skin reactivity to Pt and the period between removal from exposure and diagnosis (r = 0.65). We conclude that there is a moderate association between bronchial responsiveness to platinum salts and skin reactivity to platinum salts. However, there is no association between methacholine responsiveness and bronchial responsiveness to allergen in occupational asthma due to platinum salts.     

Scorpion stings in Spain. Popular therapies, proverbs and pharmacopoeias]

There is evidence that bronchial responsiveness to allergen is quantitatively correlated with bronchial responsiveness to nonspecific stimuli in subjects with allergic asthma. This association has been questioned in occupational asthma due to low molecular weight substances. It was the aim of this study to assess the quantitative association of bronchial responsiveness to methacholine (MCh) and platinum salts (Pt), in the form of hexachloroplatinic acid, in workers with occupational asthma due to platinum salts. Fifty seven subjects with exposure to Pt, work-related asthma, and a positive bronchial challenge with Pt, underwent skin prick tests with Pt and bronchial challenge with MCh. Using the provocation concentration causing a > or = 50% fall in specific airway conductance (PC50sGaw(Pt)) as dependent variable, anamnestic data (period from first symptoms to removal, period between removal from exposure and diagnosis, and smoking), season of the investigation, skin prick tests with environmental allergens, total immunoglobulin E (IgE), skin reactivity to Pt (Pt concentration causing a 2 mm wheal), and PC50sGaw(MCh) were included as independent variables for regression analysis. Fifty two subjects (91%) showed a PC50sGaw(MCh) < 8 mg.mL-1 (geometric mean for all subjects 1.6 mg.mL-1). Responsiveness to Pt varied widely between subjects (geometric mean of PC50sGaw 9 x 10-5 mol.L-1, range 2 x 10-7 to 10-2 mol.L-1). There was no univariate correlation between bronchial responsiveness to MCh and Pt, but there was a correlation between skin reactivity to Pt and PC50sGaw(Pt) (r = 0.6). This association could not be improved by considering PC50sGaw(MCh), the period from first symptoms to removal, or the period between removal from exposure and diagnosis. The parameters that showed the highest (negative) associations with PC50sGaw(Pt) were skin reactivity to Pt and the period between removal from exposure and diagnosis (r = 0.65). We conclude that there is a moderate association between bronchial responsiveness to platinum salts and skin reactivity to platinum salts. However, there is no association between methacholine responsiveness and bronchial responsiveness to allergen in occupational asthma due to platinum salts.     

Mental illness in the biological and adoptive families of adopted individuals who have become schizophrenic

Early asthmatic responses (EAR) of similar severity were produced by allergen inhalation challenges in nine asthmatic subjects. The severity of the airways allergic reaction was estimated by measuring the skin test weal size produced by the same dilution of allergen which caused the EAR. The non-specific bronchial reactivity was assessed by inhalation of incresing concentrations of histamine acid phosphate. Possible relationships between the severtiy of the airways allergic reaction, the level of non-specific bronchial hyper-reactivity and the pattern of asthmatic response were examined. There was a marked inverse correlation between the required severity of the airways allergic reaction and the non-specific bronchial reactivity (log10) of the individual (r = -0-96, P less than 0-001). The EAR was followed by a late asthmatic response (LAR) in five subjects. There was no evident correlation between the magnitude of the EAR and that of the LAR. In addition, no correlation was obtained between the pattern of response interms of EAR or LAR and the severity of the allergic reaction, or the level of non-specific bronchial reactivity. These results indicate that the allergic reaction and the non-specific bronchial reactivity are interrelated in the production of allergen-induced asthma. Thus a mild allergic reaction will induce and EAR in patients with markedly increased non-specific bronchial reactivity, whereas a severe allergic reaction is required to produce an EAR in those with only slightly increased non-specific reactivity. The lack of correlation between the occurrence of the LAR and the intensity of the airways allergic reaction, the non-specific bronchial reactivity and the intensity of the EAR indicates that other factors are involved in the development of LAR.     

Patterns in children''s fruit and vegetable consumption by meal and day of the week

Seasonal bronchial asthma causally connected with the exposure to pollen allergens is a chronic, eosinophilic mucosal inflammation of airway. This inflammation is the basis for the development of nonspecific bronchial hyperreactivity which is the most typical but mutable feature of asthma. Bronchial hyperreactivity often determines asthma intensity and the need of asthma treatment. The nonspecific bronchial hyperreactivity over two consecutive years was evaluated in 11 patients (2 women and 9 men) with seasonal bronchial asthma, sensitized to grass, remaining under the conditions of natural allergen exposure and out of this period. Bronchial reactivity to histamine was measured by Cockcroft's at all method. So called histamine threshold (PC20H) in mg/ml was assessed. The values of ventilatory parameters (FVC, FEV1) and asthma symptom scores were also measured. It was showed that nonspecific bronchial hyperreactivity significantly increased in subjects with seasonal bronchial asthma during natural pollen exposure. PC20H in two studies performed during this period decreased 3 and 6 times when compared to preseasonal values. The majority part of patients (80%) has the increased bronchial reactivity to histamine also beyond the of grass season when clinical symptoms of asthma and rhinitis are not observed. This postseasonal hyperreactivity could be the effect of the chronic inflammation process persisted from the period of natural allergen exposure. Continuous subthreshold, which means asymptomatic exposure to perennial allergens to which most of patients are sensitized, could be another reason of this hyperreastivity. The possibility of exposure to the activity of seasonal allergens the whole year in persons with asthma can not omitted, as the presence of pollens in the sample of the house dust in patient's flat is observed during the yield of pollen season. Nonspecific bronchial hyperreactivity in individual patients is fluctuated, which probably is not dependent on the intensity of natural allergen exposure.     

Bronchial reactivity to prostaglandins F2alpha, E2, and histamine in different types of asthma

Bronchial reactivity to prostaglandins F2alpha (PGF2alpha), E2 (PGE2) and histamine has been studied in 27 patients with aspirin-sensitive asthma and in 28 asthmatics without this sensitivity. Of the latter group, 13 patients had atopic, 9 infectious, and 6 mixed type of asthma. Atopic patients were characterized by vivid reactivity to low doses of both PGF2alpha and histamine. In patients with infectious asthma significantly higher doses of both PGF2alpha and histamine were necessary to induce bronchoconstriction as compared to atopics. Aspirin-sensitive patients responded quickly with bronchial spasm to similar doses of histamine as atopics, but tolerated significantly higher doses of PGF2alpha. There was no difference in reactivity to PGF2alpha between patients with aspirin sensitivity and those with infectious asthma. 5 and 10 min after administration of 60 microgram PGE2 significantly better improvement in ventilation occurred in aspirin-sensitive patients than in those of either atopic or infectious groups. The results obtained point to differences in bronchial reactivity to prostaglandins and histamine depending on type of asthma and severity of its symptoms.     

Outcome of wheeze in childhood: the influence of atopy

We have previously demonstrated that the adult outcome of childhood asthma differs from that of wheeze occurring only in the presence of infection. This paper examines the role of atopy in relation to outcome. We investigated the atopic status, current symptoms and bronchial reactivity to methacholine of 235 subjects aged 34-40 yrs, originally classified at age 10-15 yrs as having asthma (asthma group), wheeze only in the presence of infection (wheezy group), or no respiratory symptoms (comparison group). Subjects from the original asthma group were more likely to be atopic as defined by skin test reactivity, total serum immunoglobulin E (IgE) measurement or specific IgE radio allergosorbent test (RAST) measurement than those from the wheezy group. The wheezy group differed significantly from the reference group only in RAST results, when other variables were taken into account. In a logistic regression model, the important independent predictors for adult wheezing symptoms were original group, atopy and current smoking. Methacholine responsiveness was independently associated with original group (the asthma group were more likely to respond positively), atopy and female gender. The results suggest that atopy is an important predictor for wheeze and bronchial hyperreactivity in middle age. However, the difference in outcome for children who had asthma compared to those who had wheeze only in the presence of infection cannot be explained by atopy alone.     

Bronchial reactivity, lung function, and serum immunoglobulin E in smoking-discordant monozygotic twins

Smokers with chronic bronchitis and/or chronic obstructive pulmonary disease (COPD) have been reported to have an increased bronchial reactivity (BR). It has been discussed whether increased BR is a risk factor for the development of COPD in smokers. We studied 10 monozygotic twin pairs who were discordant for tobacco smoking by means of histamine provocation tests, lung function tests, and serum samples for total IgE. The smokers had a mild obstructive ventilatory impairment, with FEV1 significantly lower than that of the partner both when it was determined from the flow-volume loops (3.2 +/- 1.0 L for smokers and 3.4 +/- 0.8 L for nonsmokers) and by the Vitalograph spirometer (3.5 +/- 1.0 L for smokers and 3.8 +/- 0.8 L for nonsmokers). Forced midexpiratory flow (FEF25-75%) and forced expiratory flow at 75 to 85% of vital capacity (FEF75-85%) were both significantly lower in the smokers (p < 0.05). The alveolar plateau phase N2-delta test and lung clearing index in the multibreath nitrogen washout test were both significantly affected in the smokers (p < 0.05 and p < 0.01, respectively). We found no significant difference in histamine reactivity between smokers and nonsmokers and no correlation between differences in reactivity and differences in lung function within pairs. Total serum IgE was significantly higher in the smokers than in their nonsmoking siblings. These data suggest that obstructive ventilatory impairment and raised serum IgE are earlier and more constant manifestations of tobacco smoking than increased bronchial reactivity. Thus, bronchial hyperreactivity does not seem to be a major risk factor for the development of early airways obstruction in smokers.     

Non-specific airway hyperresponsiveness in mono-sensitive Sicilian patients with allergic rhinitis. Its relationship to total serum IgE levels and blood eosinophils during and out of the pollen season

BACKGROUND: Initial attempts to evaluate the association between allergic rhinitis and non-specific bronchial responsiveness has produced conflicting results. In fact, some studies showed a strong correlation and other failed to find an association. However, little is known about the effect of natural specific allergen exposure on the bronchial reactivity of mono-sensitive patients with rhinitis in the southern Mediterranean area, in relation to skin reactivity to allergens, total serum IgE levels and blood eosinophils. OBJECTIVES: The significance of the association between allergic rhinitis, and abnormal airway responsiveness with regard to the pathogenesis of asthma is unclear. For this reason, we have studied non-specific bronchial hyperreactivity, in patients with seasonal allergic rhinitis, with reference to the responsible allergen. The aim of the study was to correlate the responsiveness to bronchoprovocation with methacholine in subjects a with allergic rhinitis during and out of the pollen season with total serum IgE and blood eosinophils. METHODS: Fourty-nine non-smoking patients with clinical diagnosis of allergic rhinitis and mono-sensitive skin-prick tests to pollen allergens were enrolled in the study. Twenty patients suffered from seasonal rhinitis to Parietaria pollen, 15 patients to Gramineae pollen and 14 patients to Olea pollen. In all patients lung function measurements (assessed as response to methacholine), total serum IgE and blood eosinophil counts were measured during and out of the pollen season. RESULTS: During pollen season, 16 out of 49 rhinitis patients demonstrated values of bronchial responsiveness measured as response to inhaled methacholine in the asthmatic range whereas out of the pollen season only eight patients were in the asthmatic range. By analysing the results with reference to the responsible allergen, during the pollen season 15 out of 16 patients were Parietaria-sensitive and out of the pollen season seven out of eight patients. Finally, in Parietaria-sensitive rhinitis bronchial responsiveness significantly correlated, during and out of the pollen season, with total serum IgE and with blood eosinophil counts. CONCLUSIONS: Our results are consistent with the hypothesis that Parietaria is more important than Olea and Gramineae as a risk for developing non-specific bronchial hyperresponsiveness. On the whole, present observations provide further evidence that there is an interrelationship of allergen kind, total serum IgE, eosinophil and bronchial hyperresponsiveness suggesting that they may play a role in the development of bronchial asthma in rhinitis patients.     

Serum eosinophil cationic protein in infants during first wheezing episode

We measured serum ECP levels in infants during first wheezing episode. Serum ECP in these infants are significantly higher than in control infants, although much higher in children with asthma. Serum ECP in these infants with high serum IgE and/or positive RAST score are higher than in infants with normal serum IgE and negative RAST score. In children with bronchial asthma serum ECP is correlated with peripheral eosinophil counts, but in infants during first wheezing episode serum ECP is often elevated not associated with increased peripheral eosinophil counts. These suggest that activated eosinophils could be responsible for bronchoconstriction in wheezing patients with atopic diathesis even in very early phase and that these eosinophilic inflammations could contribute to formation of increased airway reactivity and bronchial asthma.     

Relationship between serum IgE and airway responsiveness in adults with asthma

BACKGROUND: General population studies have shown a relationship between total serum IgE levels and airway responsiveness, but this association has not been documented in patients with asthma. OBJECTIVE: The study assesses the cross-sectional relationship between IgE levels and airway responsiveness in 208 subjects who had had emergency department treatment for asthma at least 2 years earlier. METHODS: All participants completed a standardized respiratory questionnaire and underwent spirometry, allergy skin testing, and a dose-response methacholine challenge test. RESULTS: After adjusting for age and gender, the percentage of patients with asthma and airway responsiveness (provocative concentration causing a 20% fall in forced expiratory volume in 1 second [PC20] < or = 8 mg/ml) increased from 52% in the lower quintile of IgE to 72% in the upper quintile (p < 0.01). After adjusting for age, gender, baseline percent predicted forced expiratory volume in 1 second, and smoking, the association between IgE (both in quintiles and continuous) and PC20 appeared consistent and statistically significant (p < 0.01). This association was stronger in patients who were not given inhaled steroid (odds ratio for twice the concentration of IgE, 1.42; 95% confidence interval, 1.09 and 1.84), than in patients treated with inhaled steroid (odds ratio, 1.10; 95% confidence interval, 0.82 and 1.50). Eosinophilia and skin reactivity were associated with PC20 although to a lesser extent. CONCLUSION: These findings strengthen the role played by IgE in facilitating the development of bronchial responsiveness in patients with asthma.     

Testing bronchial hyper-responsiveness: provocation or peak expiratory flow variability?

BACKGROUND: Assessing bronchial hyper-responsiveness (BHR) is a main diagnostic criterion of asthma. Provocation testing is not readily available in general practice, but peak expiratory flow (PEF) is. Several guidelines promote the use of PEF variability as a diagnostic tool for BHR. This study tested the agreement between histamine challenge testing and PEF variability, and the consequences for diagnosing asthma. AIM: To investigate the possibility of assessing BHR by PEF variability, using a histamine provocation test as a reference. METHOD: Subjects with signs of symptoms indicating asthma (persistent or recurrent respiratory symptoms or signs of reversible bronchial obstruction) (n = 323) were studied. They had been identified in a population screening for asthma. A histamine provocation test and PEF variability were assessed over a three-week period. Asthma was defined as signs or symptoms together with a reversible airflow obstruction or BHR to the histamine challenge test. BHR was defined as a PC20 histamine of < or = 8 mg/ml or a PEF variability of > or = 15%. Overall correlation between PC20 and PEF variability was calculated using Spearman's rho. Furthermore, a decision tree was constructed to clarify the role of BHR in diagnosing asthma. RESULTS: Thirty-two patients had a reversibility in forced expiratory volume in 1 second (FEV1) of > or = 9% predicted, 131 patients showed a PC20 of < or = 8 and 11 patients had a PEF variability of > or = 15%. Overall correlation was poor at only -0.27 (P < 0.0001). One hundred and fourteen of the 131 patients diagnosed as having asthma when the histamine challenge test was used were not diagnosed by PEF variability. CONCLUSION: PEF variability cannot replace bronchial provocation testing in assessing BHR. This indicates that PEF variability and bronchial provocation do not measure the same aspects of BHR. If BHR testing is required in diagnosing asthma, a bronchial provocation test has to be used in general practice as well.     

Allergic bronchopulmonary aspergillosis in a patient with no symptoms of asthma until after bronchial lavage

An asymptomatic 56-year-old man was admitted to our hospital because of an abnormal shadow on a chest X-ray film. Allergic bronchopulmonary aspergillosis was diagnosed on the basis of five findings: eosinophilia, immediate skin reactivity to Aspergillus antigen, the presence of precipitating antibodies against Aspergillus antigen, a high concentration of IgE in serum, and central bronchiectasis. He had no symptoms of asthma at the time of diagnosis, but did a few days after he underwent bronchial lavage. We speculate that the asthma attack was related to the bronchial Lavage as follows: First, drainage of mucus plugs by bronchial lavage may have exposed the bronchial epithelium, which had already been sensitized, to aspergillus antigens. Second, the scattered antigen may have dose-dependently stimulated the bronchi. Third, the infection may have increased bronchial responsiveness to the antigen. Symptoms of bronchial asthma are not necessary for the diagnosis of allergic bronchopulmonary aspergillosis.     

Longitudinal determinants of bronchial responsiveness to inhaled histamine

BACKGROUND AND STUDY OBJECTIVE: The point prevalence of bronchial hyperresponsiveness (BHR) is imperfectly associated with current asthma, possibly due to changes over time in bronchial responsiveness (BR). To evaluate cross-sectional and longitudinal determinants of BR, a population sample comprising 408 children and adolescents, aged 7 to 17 years at enrollment, was examined twice, 6 years apart. METHODS: Case history was obtained by interview and questionnaire. BR to inhaled histamine, pulmonary function, and skin prick test reactivity were measured using standard techniques. RESULTS: The point prevalence of BHR (the concentration of histamine causing a 20% decline in FEV1 <8 mg/mL) declined from childhood to early adulthood (25% and 6%, respectively; p<0.001); and similarly a decline in histamine dose-response slope was observed. At both surveys, prechallenge FEV1 percent predicted, asthma, and atopy, especially atopy to house dust mite (HDM), were important determinants for the degree of BR. After adjustment for prechallenge FEV1 percent predicted, no male-female difference was observed in degree of BR. Lower FEV1 percent predicted (p=0.003), asthma (p<0.001), higher degree of BR (p=0.003), and atopy to HDM (p=0.007) at enrollment predicted a higher degree of BR at the second survey (degree of BR at second survey adjusted for prechallenge FEV1). Furthermore, new asthma (p<0.001) and/or atopy to HDM (p=0.003) were associated with higher BR at the second survey. Confining the analysis to nonasthmatics showed that subjects with new or persistent atopy to HDM had significantly increased BR compared with nonatopic subjects; and, moreover, prechallenge FEV1 percent predicted was significantly correlated with BR. CONCLUSIONS: BR declines from childhood to early adulthood, possibly reflecting the increase in airway caliber. The level of FEV1 and atopy, especially to HDM, are important determinants for changes over time in level of BR, also in nonasthmatic subjects.     

The effect of nedocromil sodium on the clinical course, ventilatory parameters and nonspecific bronchial hyperreactivity in patients with nonatopic bronchial asthma treated with beclomethasone dipropionate

The efficacy of nedocromil sodium (NED) (8mg twice daily) in controlling the clinical symptoms of asthma (score symptoms), the pulmonary parameters (FEV1, FVC) and bronchial hyperreactivity to histamine was assessed. The study was performed in double-blind, cross-over and placebo-controlled way in 16 patients suffering from nonatopic, stable, moderate asthma treated with beclomethasone dipropionate (from 400 micrograms to 800 micrograms). NED and placebo were administered in a randomized way with 8-week wash-out period. Bronchial reactivity to histamine, was measured as the amount of histamine causing a 20% fall in FEV1 (PC20H in mg/ml). Treatment with NED did not change asthma symptom scores, FVC and FEV1. Decreased usage of beta 2-agonist was observed. NED did not influence bronchial hyperreactivity to histamine (xg PC20H was respectively 0.09 and 0.11 mg/ml after placebo and 0.06 and 0.08 after NED). The authors conclude that studies with NED in nonatopic asthmatics should be continued, but the dosage of the drug ought to be bigger and the time of treatment ought to be longer.     

Carbamoyl phosphate synthetase: a tunnel runs through it

BACKGROUND: Sensitivity to specific allergens and increased sensitivity to common spasmogens are characteristic features of allergic asthma and are also features demonstrated by tissues passively sensitized with serum from atopic donors, displaying high levels of IgE. It is evident that the specific response to allergen is related to circulating levels of allergen-specific IgE, but it is unclear whether the histamine hypersensitivity is also related to this immunoglobulin. OBJECTIVE: The objective was to deplete IgE in the serum of a donor with high levels of total and allergen-specific IgE and compare specific-allergen sensitivity and sensitivity to histamine in tissues passively sensitized with either the whole serum or the IgE-depleted serum. METHODS: Serum from a Dermatophagoides farinae-sensitive asthmatic (total IgE = 1047 U/mL, D. farinae-specific IgE > 17.5 U/mL) was subjected to an immunomagnetic separation technique to reduce the levels of IgE (total and specific) to below 10 U/mL. Bronchial tissue from six non-atopic donors was then passively sensitized overnight with either the whole serum or IgE-depleted serum and D. farinae and histamine sensitivity were evaluated the next day using standard organ bath techniques. RESULTS: Passive sensitization with the whole serum resulted in the development of sensitivity to D. farinae and increased sensitivity to histamine (750+/-169 mg contraction to 10 U/mL D. farinae, histamine pEC50 5.64+/-0.16 and max. 813+/-109 mg in sensitized vs 37+/-34 mg contraction to 10 U/mL D. farinae histamine pEC50 5.05+/-0.23 and max. 490+/-84 in non-sensitized tissues, P>0.05). Incubation with IgE-depleted serum still produced histamine hypersensitivity (histamine pEC50 5.57+/-0.16 and max. 737+/-70 mg P>0.05), but no significant response to allergen was detected (20+/-13 mg contraction to 10 U/mL D. farinae). CONCLUSION: These results demonstrate, that increased reactivity to histamine and airway contraction to allergen induced by passive sensitization, occur through independent mechanisms and that, unlike allergen-sensitivity, histamine hypersensitivity is caused by a serum factor other than IgE.     

Specific IgE to isocyanates: a useful diagnostic role in occupational asthma

BACKGROUND: Isocyanates are the most frequent cause of occupational asthma in industrialized countries. OBJECTIVE: We sought to investigate the utility of specific IgE measurement in the diagnosis of isocyanate-induced asthma. METHODS: Fifty-eight of 101 patients referred for investigation were diagnosed as having isocyanate-induced occupational asthma by means of history, serial peak flow records, and bronchial provocation tests. Specific IgE antibodies to toluene diisocyanate:human serum albumin (HSA), diphenylmethane diisocyanate:HSA, and hexamethylene diisocyanate: HSA were measured in all patients by Phadebas RAST. RESULTS: Twenty patients had a RAST ratio of 2 or greater to at least one isocyanate. Thirteen (28%) of the 46 patients with a positive provocation test response had a RAST ratio of 2 or greater, and nine (20%) had a RAST ratio of 3 or greater. Raising the RAST cut-off from 2 or greater to 3 or greater reduced its sensitivity but increased the specificity of the test to 100%. RAST measurement was most likely to be positive within 30 days of exposure. Serial measurements suggested that the half-life of the IgE antibodies was approximately 6 months. Evidence of cross-reactivity between isocyanate RAST responses was found in eight subjects. CONCLUSION: Specific IgE to isocyanates is a more specific than sensitive index of occupational asthma. With a RAST score of 3 or greater, it is wholly specific and therefore diagnostic of isocyanate-induced asthma. The sensitivity of specific IgE measurement is highest when blood is taken less than 30 days from last exposure, which is consistent with the observed half-life.     

Clinical and experimental studies on preventing and treating anaphylactic asthma with Zusanli point immunotherapy

We have studied on preventing and treating anaphylactic asthma with Zusanli (S36) point immunotherapy (ZPIT). Sixty-nine patients were observed. The results showed that the clinical curative effect of ZPIT was not only much higher than that of conventional desensitization therapy, but also the patients' total IgE level was reduced, anti-acarid IgE was lowered, SIgA level was raised, the absolute eosinophilic granulocyte level dropped and pulmonary function recovered. Animal experiment results showed that the ZPIT could more effectively suppress the guinea pigs' anaphylactic asthma allergized by albumin and more obviously resist the guinea pigs' bronchial spasm induced by histamine and acetylcholine than the conventional desensitization therapy and injected normal saline. The immunomodulating action of the ZPIT are elucidated from clinical study and animal experiment in the paper.     

Occupational asthma caused by fish inhalation

Occupational asthma (OA) due to fish inhalation, confirmed by specific bronchial challenge (SBC), has not been described as yet in medical literature, as far as we know. We describe two patients whose asthma was induced by occupational exposure to fish and confirmed by serial measurements of PEFR and SBC. Two fish-processing workers reported asthma symptoms related to their workplace. They were skin tested with fish extracts and their sera assayed for IgE antibodies to various fish species. Nonspecific bronchial reactivity was assessed by methacholine challenge. The occupational relationship was confirmed by PEFR monitoring in working and off-work periods. SBC with fish extracts was carried out to confirm the diagnosis of OA. Skin tests with raw and cooked plaice, salmon, hake, and tuna in patient 1 and anchovy, sardine, trout, salmon, Atlantic pomfret, and sole in patient 2 were positive. Specific IgE serum antibodies were found to salmon in patient 1 and to trout, anchovy, and salmon in patient 2. PEFR measurements differed significantly (P < 0.001) between work and off-work periods for both patients. A bronchial challenge with methacholine was positive in patient 1. SBC with raw hake, salmon, plaice, and tuna extracts in patient 1 and raw salmon extract in patient 2 were all positive with an immediate response. SBC with Dermatophagoides pteronyssinus extract was entirely negative in both patients. In three asthmatic, non-fish-allergic controls, SBC with tuna, hake, salmon, and plaice were all negative. These results suggest that fish inhalation can elicit IgE-mediated occupational asthma.