Tilarin in combination with astemizole.

This multicentre double-blind, placebo controlled study had a practical objective, based on the expectation that many patients with seasonal allergic rhinitis will be prescribed oral antihistamine monotherapy by their primary care physician, whereas allergy specialists are more likely to prescribe combination therapy including antiinflammatories. The specific question was, "Will the addition of nedocromil sodium 1% nasal spray to astemizole tablets improve control of symptoms of seasonal allergic rhinitis induced by ragweed pollen, as compared to astemizole therapy alone?'. Following a one-week baseline, planned to coincide with the start of the local ragweed pollen season, patients (aged 12-64) were randomly assigned to four weeks' double-blind test treatment with either nedocromil sodium 1% nasal spray four times daily (QID) + astemizole (n = 146) or placebo nasal spray + astemizole (n = 148) or double-dummy (nasal spray + capsules) placebo (n = 71). Patient diary cards were kept throughout the five weeks, and clinic visits were made before and after baseline and after one and four weeks' treatment. During the 10-day peak pollen period, the diary card rhinitis symptom summary score (0-4 severity scale) was significantly reduced in patients receiving either astemizole alone (p < 0.001) or the combination therapy (p < 0.001) as compared with placebo. Direct comparison of the active treatments further showed that symptoms were significantly less severe (p < 0.01) with the combined therapy than with astemizole alone, and this despite significantly greater reliance on permitted rescue medications (p < 0.05 for pseudoephedrine usage) in the astemizole group. Clinical assessments of rhinitis made during the peak pollen visit, after the first week of test treatment, were also significantly (p < 0.05 - p < 0.01) in favour of combined therapy with nedocromil sodium 1% nasal spray + astemizole rather than astemizole alone, and at the same time this preference was confirmed by physician (p = 0.011) and patient (p = 0.003) opinions of symptom control. In conclusion, this antiinflammatory + antihistamine treatment proved superior to antihistamine alone for effective management of allergic rhinitis. The combined therapy worked quickly and was well-tolerated, with no serious adverse events or untoward effects on blood or urine variables.

A multicenter trial of nedocromil sodium, 1% nasal solution, compared with cromolyn sodium and placebo in ragweed seasonal allergic rhinitis.

This study was a double-blind, parallel-group study to evaluate a new medication, nedocromil sodium, 1%, in comparison with placebo and cromolyn sodium, 4%, for treatment of ragweed seasonal allergic rhinitis. Two hundred thirty-three patients (aged 12 to 65 years) from eight centers were randomized to treatment, one spray per nostril, four times daily, with nedocromil sodium, cromolyn sodium, or matched placebo (80, 76, and 77 patients, respectively). All patients had at least a 2-year history of ragweed seasonal allergic rhinitis. Treatment was for 8 weeks during the ragweed season, and daily pollen counts were used to identify the peak 3-week period. Clinic examinations were made before and after the 1-week baseline and after 1, 3, 5, and 8 weeks of treatment. Rhinitis symptoms were recorded each day by the patients. Nedocromil sodium was more effective than placebo (p less than 0.05) in relieving symptoms as recorded by the patients. Cromolyn sodium was also more effective than placebo, but the difference was not usually significant. Similarly, the active treatments were both better than placebo for clinical parameters measured at visits and for global opinions of treatment, and more rescue therapy was used by the placebo-treated group. There was no significant difference between the two active treatments, but the trend throughout was in favor of nedocromil sodium. Our findings demonstrated nedocromil sodium to be at least as effective as an established therapy (cromolyn sodium) in reducing symptoms of rhinitis during the peak ragweed pollen season.

Bronchial challenge with formaldehyde gas: lack of bronchoconstriction in 13 patients suspected of having formaldehyde-induced asthma.

We studied 13 selected patients with symptoms suggestive of asthma who suspected exposure to formaldehyde as a cause. These patients had a history of exposure to formaldehyde gas which either coincided with the onset of or aggravated their symptoms of asthma. The levels of exposure at their homes or at work ranged from 0.1 to 1.2 parts per million (ppm) of formaldehyde gas. The patients were tested with bronchial challenges of 0.1-, 1-, and 3-ppm concentrations of formaldehyde gas and randomly interspersed room-air placebos. The formaldehyde gas or placebo was delivered via a Dynacalibrator . The period of exposure to formaldehyde gas or placebo with each challenge was 20 minutes. Pulmonary function was measured before and for 24 hours after each bronchial challenge. No patient had a significantly greater decrease in the forced expiratory volume in 1 second after exposure to formaldehyde than after exposure to air. In no case were we able to substantiate that exposure to formaldehyde gas (3 ppm or less) was indeed causing or aggravating the asthmatic symptoms.

Identification by immunofluorescence of eosinophil granule major basic protein in lung tissues of patients with bronchial asthma.

To clarify the role of the eosinophil in asthma, tests were done to find out whether eosinophil granule major basic protein (MBP) is present at sites of epithelial damage in cases of asthma; this protein is toxic to respiratory epithelium and its levels are raised in the sputa of patients with asthma. The test used was an indirect immunofluorescence test, and the specimens tested were formalin-fixed, paraffin-embedded lung tissue obtained post mortem from patients with asthma and from control patients who had died of other diseases. The antiserum used was specific for MBP because it stained only eosinophils in the peripheral blood and because its activity was removed by absorption with MBP. Both controls and asthmatic patients had MBP in the cells, but patients dying of status asthmaticus also had extracellular MBP in mucus plugs, on damaged epithelial surfaces, and in necrotic areas below the basement membrane. Patients who had died of other diseases associated with severe asthma also had extracellular MBP in mucus plugs and on damaged epithelial surfaces. The results suggest that MBP in the eosinophil granule is released into respiratory tissue of patients with severe asthma and that it is associated with tissue damage.

Asthma induced by dust from urea-formaldehyde foam insulating material.

A patient developed severe asthma following insulation of her house with urea-formaldehyde foam. Bronchial challenge with the buoyant dust of the foam caused an asthmatic attack; inhalation of formaldehyde, 3 ppm, did not.