Bronchial asthma induced by an antithyroid drug.

We report the case of a 67-year-old woman who suffered from a severe asthma exacerbation as a consequence of an antithyroid drug treatment prescribed for her multinodular, hyperfunctioning goiter. Asthma symptoms were associated with a very significant increase in the number of eosinophils, detected in both blood and induced sputum.

Effects of specific immunotherapy in allergic rhinitic individuals with bronchial hyperresponsiveness.

Allergic rhinitis can be associated with bronchial hyperresponsiveness (BHR), and carries an increased risk for the development of asthma. The aim of this study was to evaluate the ability of specific immunotherapy (SIT) to reduce the progression of allergic rhinitis to asthma and prevent the associated increase in BHR. Forty-four subjects monosensitized to Dermatophagoides pteronyssinus, with perennial rhinitis and BHR to methacholine, were randomly assigned to receive SIT or placebo in a double-blind study conducted over a period of 2 yr. After 1 yr of treatment, a 2.88-fold increase in the provocative dose of methacholine producing a 20% decrease in FEV(1) (PD(20)FEV(1)) was recorded in the SIT-treated group (95% confidence interval [CI]: 3.98- to 2.09-fold; p < 0.001), with a further increase to fourfold at the end of Year 2 (95% CI: 2.9- to 5.7-fold; p < 0.001). At the end of the study, the methacholine PD(20)FEV(1) was within the normal range in 50% of treated subjects (p < 0.0001), and was significantly higher in this group than in the group receiving placebo (p < 0.0001). In contrast, no changes in methacholine PD(20)FEV(1) were found in the placebo group throughout the study. Although 9% of subjects given placebo developed asthma, none of those treated with SIT did. This study suggests that SIT, when administered to carefully selected, monosensitized patients with perennial allergic rhinitis, reduces airway responsiveness in subjects with rhinitis, and may be an appropriate prophylactic treatment for rhinitic patients with hyperreactive airways.

Short-term cardiovascular effects of salmeterol.

The occurrence of cardiovascular side effects is sometimes associated with the utilization of beta-adrenoceptor agonists. The most important causes of these undesirable pharmacologic actions are as follows: (1) direct stimulation of cardiac beta-adrenoceptors; (2) reflex activation of adrenergic mechanisms due to peripheral vasodilation; (3) hypokalemia; and (4) hypoxemia. The aim of this study was to evaluate the potential short-term, cardiovascular side effects of salmeterol, a long-acting and highly selective beta2-adrenoceptor agonist. Eight volunteer healthy subjects and eight patients with reversible airway obstruction and without cardiovascular alterations were treated with 50 microg of salmeterol twice a day for 3 days and then with 100 microg of salmeterol twice a day for a further 3-day period. The 24-h ECG (Holter) monitoring and measurement of arterial BP, performed on the admission day and on the third and the sixth day of pharmacologic treatment, showed that salmeterol did not produce any significant change in mean heart rate, number of supraventricular and ventricular premature complexes, and BP. Furthermore, no ECG abnormality related to myocardial ischemia was recorded during 24-h Holter monitoring. These data suggest that salmeterol, administered in regular and high doses for a short period, does not cause significant cardiovascular effects in both normal subjects and patients with reversible airway obstruction.