Biomedical subjects
Publications and source records attributed to G Moscato.
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A 28 year old man with no history of atopy was referred to our hospital for possible work-related asthma. He had been employed in the production section of a pharmaceutical company for 2 yrs, and in the last 2 months he had complained of dyspnoea, wheezing, chest tightness, symptoms of rhinitis and a cutaneous rash when exposed to powdered antibiotics. Symptoms disappeared after being transferred to the packaging section. When the subject was admitted to our department he was asymptomatic. Basal lung function tests were in the normal range. Bronchial challenges with methacholine and with ultrasonically-nebulized distilled water were negative. Skin-prick test with piperacillin sodium gave a strong positive response at a very low concentration. Specific inhalation challenge with piperacillin sodium resulted in an immediate asthmatic reaction, and also reproduced rhinitis symptoms and the cutaneous rash. A control challenge with lactose, and the specific challenge test with cefuroxime sodium (another antibiotic to which the patient was exposed at the workplace) were negative. We conclude that piperacillin sodium is an agent that can cause occupational asthma.
The compliance of patients in educational programmes on asthma is sometimes lacking and this may be due in part to patients' scarce interest or refusal to expand their knowledge of the disease. In the present study, we aimed to evaluate the interest of a group of asthmatic patients in education on asthma and to point out the asthma-related topics considered particularly worth discussing. The study was conducted before starting the educational programme. Sixty adult patients with mild-to-moderate asthma were asked to complete a questionnaire, including a group of 14 questions aimed at evaluating the level of patients' interest in various asthma-related topics, one question regarding patients' willingness to attend a small-group educational course on asthma, and a further question asking patients to suggest topics of particular interest for discussion. For each of the first 14 questions, patients indicated their level of interest according to a score ranging 1-3. The sum of the scores obtained for each topic (partial score) and the sum of partial scores (total score) were calculated and classified into three classes of interest (I: low, II: medium; III: high), and the distribution of patients into the three classes was analysed (chi-squared test).(ABSTRACT TRUNCATED AT 250 WORDS)
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The role of peak expiratory flow (PEF) monitoring in the diagnosis of occupational asthma has recently been assessed by several studies, which agree that this procedure should always be used to confirm the relationship between symptoms and occupational exposure. Some specific issues should be satisfied: a minimum number of four PEF measurements in a day; several weeks of monitoring in and out of work; and the presence of specific patterns of PEF changes. The sensitivity and specificity of PEF monitoring to detect occupational asthma, in comparison with the specific challenge test in the laboratory (the "gold standard") have been shown to be fairly high, although many authors believe that PEF monitoring cannot substitute for the specific challenge test. Limitations include: the low sensitivity of PEF to detect mild changes in airway calibre with respect to forced expiratory volume in one second (FEV1); the blunting effect of pharmacological treatment; the episodic and irregular exposure to the sensitizer in the workplace; and the compliance and honesty of the subject. Further studies are required to select the best indices of daily and day-to-day variability to be used in the evaluation of PEF changes between work and out-of-work periods.
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We report the clinical findings and the results of inhalation challenge with toluene diisocyanate (TDI) and methacholine in 113 subjects with a history of exposure to TDI and work-related respiratory symptoms. Only some of the subjects (40.7%) had isocyanate asthma, diagnosed by a positive TDI inhalation challenge. Most reactors had a dual (30.4%) or a late (41.3%) response. The interval between the last occupational exposure and the specific challenge was significantly shorter in reactors, and among this group the number of immediate reactions to TDI decreased progressively with an increasing interval. The reactors had a significantly higher proportion of positive responses to methacholine and a significantly lower mean PD15 FEV-1 (provocative dose of methacholine which provoke a 15% decrease in forced expiratory volume in 1 second) (reactors: 557 micrograms, SEM 92.3; nonreactors: 1346 micrograms, SEM 128, P less than .01). Methacholine challenge could not identify subjects with isocyanate asthma.
Inhaled furosemide has been shown to prevent bronchoconstriction induced by inhalation of ultrasonic nebulization of distilled water (UNDW) in bronchial asthma. To evaluate whether inhaled furosemide also prevents the increase in serum neutrophil chemotactic activity (NCA) observed during UNDW bronchoconstriction, we measured NCA during UNDW challenge without (control) and immediately after inhalation of furosemide (40 mg) or placebo (saline) in 10 asthmatics responsive to UNDW, in a randomized, double-blind study. NCA was assessed by measuring the maximal distance reached by neutrophils in a filter when challenged with the subject serum in a Boyden chamber ("leading front"). UNDW inhalation produced a significant increase in NCA in each subject. Gel filtration chromatography on S400 column indicated that the NCA released were 600 to 700 kD. Saline had no effect on bronchoconstriction nor on NCA increase induced by UNDW in nine patients. Furosemide did not change baseline FEV1, but it prevented bronchoconstriction and NCA increase in nine patients. In the whole group the maximal decrease in FEV1 after UNDW was -31.1%, SEM 4.7 after saline and -7.5%, SEM 5.2 after furosemide, p less than 0.001, the maximal increase in NCA after UNDW was +52.9%, SEM 9.2 after saline and +3.8%, SEM 3.1 after furosemide, p = 0.001. These results indicate that inhaled furosemide prevents both the bronchoconstriction and the NCA increase induced by UNDW inhalation in most asthmatic patients. This finding adds support to the suggestion that furosemide acts on mast cells.
In the present work two commercially available immunoassays for allergen-specific IgG4 detection were compared, IgG4 FAST Test and ALLERBLOCK-MS IgG4 EIA Kit. For this purpose 30 serum samples were tested for IgG4 antibodies (Abs) specific to Dermatophagoides pteronyssinus (Dp) by the two immunoassays. Eleven serum samples were collected from normal subjects, 6 from Dp-atopic patients never treated by specific immunotherapy (ITS) and 13 from Dp-atopic patients previously treated by ITS. Pearson's linear correlation analysis showed a significant correlation of results from the two immunoassays. However, a better discrimination of Dp-specific IgG4 values between ITS-treated and untreated patients or normal subjects was obtained by FAST than ALLERBLOCK-MS method; moreover, the former showed a better intra-assay coefficient of variation than the latter.
To verify the efficacy and the tolerability of local immunotherapy (LI) by inhalation of a powder extract of house dust mite (HDM), in comparison with parenteral immunotherapy (PI) by injection, 10 patients with asthma due to HDM were studied in a blind fashion. 5 patients (Group A) underwent LI and subcutaneous injections of placebo, 5 patients (Group B) underwent PI and inhalation of lactose for 6 months. In both groups each inhalation was preceded by premedication with disodium cromoglycate (DSCG) (40 mg). In Group A a significant decrease in symptoms score and in peak expiratory flow (PEF)-derived parameters was observed already after 3 months of treatment, and 2 patients lost the late component of the bronchial response to the challenge with HDM. No significant variation was found in bronchial responsiveness to methacholine and ultrasonically nebulized distilled water (UNDW) and in immunologic humoral and cellular parameters in peripheral blood after treatment in either group. No local important adverse reactions were observed in Group A and no systemic side effects were observed in either group. We conclude that LI is as effective as PI, but more rapid in its action, in the treatment of asthma due to HDM. Moreover, LI is locally well tolerated, providing DSCG is inhaled before each therapeutic inhalation, and does not induce systemic side effects.
To investigate whether salbutamol and sodium cromoglycate (SCG) inhibit airway response and the associated mediator release induced by ultrasonic nebulation of distilled water (UNDW, "fog"), we measured the serum neutrophil chemotactic activity (NCA) during bronchial challenge with "fog" with and without premedication with placebo, salbutamol, or SCG in 10 subjects with asthma, in four sets of studies. To assess changes in airway caliber, we measured FEV1. To assess changes in NCA, we measured the maximal distance reached by neutrophils in a filter when neutrophils were challenged with the subject's serum in a Boyden chamber. Treatment with placebo did not change baseline FEV1 or serum NCA; however, FEV1 decreased and serum NCA increased (p less than 0.05) after inhalation of "fog". Treatment with SCG did not affect either FEV1 and baseline serum NCA. After inhalation of "fog", no significant bronchoconstriction nor NCA increase was observed in eight of 10 patients with maximal mean percent decrease in FEV1 of -4.26, SEM 0.99, and maximal mean percent increase in NCA of +8.6, SEM 5.28. In the two patients who developed a bronchoconstriction after challenge with SCG pretreatment, an associated significant increase in NCA was observed but did not affect baseline NCA. After inhalation of "fog", no significant decrease in FEV1 (maximal mean percent decrease FEV1, -6.71, SEM 0.17) nor significant increase in serum NCA (maximal mean percent increase NCA, +3.6, SEM 7.1) was observed in nine of 10 patients. After salbutamol, only one patient developed a bronchoconstrictive response to "fog" associated with a significant increase in serum NCA. These results suggest that both SCG and salbutamol may prevent the bronchoconstriction induced by "fog" by inhibiting mediator release.
Styrene is an aromatic compound widely used in the production of plastic polymers and rubbers. Studies of the effect of styrene on the respiratory tract are scarce. We describe three cases of occupational asthma and one case of occupational rhinitis due to styrene, which have been recently observed in our center. There is evidence that styrene can be a primary cause of occupational asthma and rhinitis. The mechanisms of action are unknown. Our findings suggest the need for preventive strategies for styrene exposed workers.
Two cases of occupational asthma due to styrene are described. The subjects complained of cough, breathlessness, and symptoms of asthma when coming into contact with styrene; in patient 1 the respiratory reaction was followed by a late cutaneous rash. The symptoms disappeared when the subjects were away from work on weekends or holidays. In both cases, inhalation challenge with styrene produced an immediate bronchospastic reaction which was followed by a late cutaneous rash in patient 1. Prior administration of disodium cromoglycate (40 mg from a spinhaler) prevented the respiratory reactions completely, but failed to prevent the late skin response in case 1. Styrene removal was followed by complete disappearance of the symptoms. We conclude that styrene can be a primary cause of occupational asthma.
To investigate whether exercise- and ultrasonic "fog"-induced asthma are due to the same mechanism, i.e. mediator release induced by osmotic changes, we measured the serum neutrophil chemotactic activity before and after exercise and inhalation of "fog" in 15 asthmatic subjects. To assess changes in airway caliber we measured specific airway conductance (SGaw); to assess changes in neutrophil chemotactic activity we measured the maximum distance reached by neutrophils in a filter when challenged with the subject's serum in a Boyden chamber. In 10 subjects, SGaw decreased by more than 35% and neutrophil chemotactic activity increased significantly (P less than 0.05) both after exercise and "fog", whereas in five subjects no change occurred either after exercise or "fog". We conclude that both exercise- and "fog"-induced asthma are associated with increased serum neutrophil chemotactic activity, and that both stimuli may cause asthma by osmotically triggering mediator release from mast cells.
Each subject answered a questionnaire, and was submitted to respiratory function tests, bronchial challenge with methacholine and ultrasonic "fog", specific challenge with fumes and powder of PA, measuring nasal and bronchial resistances at the same time by means of a plethysmograph. Serum specific IgE against PA were assessed by the method E.L.I.S.A. Inhalation of "fog" induced a positive nasal response (i.e. nasal resistance increase greater than 70% from baseline) in 73.7% of the subjects, whereas only 3 subjects had a positive bronchial response; specific challenge with PA induced a positive nasal response in 75% out of the subjects, whereas a positive bronchial response was observed in only one subject. 22.7% of the subjects had bronchial hyperreactivity to methacholine. In none of the subjects specific IgE against PA were detectable. We conclude that PA acts as an aspecific irritative agent of airways, particularly of nasal airways.
To test a method for assessing non-specific nasal hyperreactivity, we submitted 23 allergic rhinitis sufferers, 12 normal subjects, 2 patients with asthma and 3 patients with asthma and rhinitis to bronchial challenge with ultrasonic fog (UNDW), recording nasal resistance (NR) and specific bronchial conductance (sGaw) simultaneously by means of a plethysmograph. A significant post-challenge NR increase was observed in 19 of the 23 rhinitis patients, in every patient with asthma and rhinitis, but in only 2 of the 12 normals and in none of the patients with asthma. There was no disturbing increase of nasal secretion. A significant post-challenge sGaw decrease was observed in all the asthmatics and in the patients with asthma and rhinitis, but only in 1 of the 12 normals and in 3 of the 23 rhinitis patients. We conclude that bronchial UNDW could be a suitable method for assessing both nasal and bronchial hyperreactivity.
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Recent reports in the literature suggest that disorders in the regulation of calcium ion concentration in airway smooth muscle may be at the basis of bronchial hyperreactivity. In order to evaluate whether nifedipine, a calcium channel blocking drug, could alter the bronchial reactivity to methacholine, nine patients suffering from occupational asthma were submitted to bronchial challenge with methacholine with and without premedication with nifedipine, 20 mg sublingually. The bronchial responses were followed by measuring FEV1 by means of a bell spirometer. The provocation dose of methacholine capable to induce a 15% decrease of FEV1, (PD15FEV1) was considered the bronchial threshold dose for each subject. Average PD15FEV1 increased from 310.6 micrograms (SD = 191.7) in the test without premedication with nifedipine to 1,012.3 micrograms (SD = 640.0) in the test with premedication (P less than .01). Subjectively, all the patients showed better tolerance to the bronchoconstriction during the test with nifedipine. Our data indicate that nifedipine decreases bronchial reactivity to methacholine.