Allergy testing of multiple patients with a common syringe.
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Biomedical subjects
Publications and source records attributed to J C Selner.
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We detected a significant amount of SO2 released from commercially used bronchodilators, including isoproterenol (Isuprel; Breon Laboratories, Inc., New York, N. Y.), metaproterenol (Alupent; Boehringer Ingelheim, Ridgefield, Conn., or Metaprel; Dorsey Laboratories, Lincoln, Neb.), isoetharine (Bronkosol; Breon Laboratories, Inc., New York, N. Y.), and racemic epinephrine (Micronefrin; Bird Corp., Palm Springs, Calif.). During standard nebulization of these agents, SO2 concentration varied from 0.1 to 6.0 ppm. These levels are known to be bronchoconstrictive in asthmatic patients. We believe clinicians should be aware of this observation when sulfite-containing bronchodilators are used.
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Clinical measurements and serum prostaglandin concentrations were monitored in three normal subjects, three asthmatic controls and five asthmatic patients with aspirin (ASA) idiosyncrasy before and after oral challenge with small doses of aspirin. Additionally, in the latter group, the effects of ASA were compared with those of piroxicam, a new nonsteroidal anti-inflammatory agent. Challenge with either agent caused bronchospasm in patients with aspirin idiosyncrasy, but was more severe after piroxicam. Nasal stuffiness and/or rhinorrhea preceded or accompanied the changes in pulmonary function with both agents. Serum prostaglandin concentrations, which reflect synthesis by platelets during the clotting of blood, revealed significant decreases in PGE1, PGE2, and PGF2 alpha and thromboxane B2 within two to four hours after drug administration in all subjects with or without ASA idiosyncrasy. The change in serum PG concentration was presented when bronchospasm developed in patients with ASA idiosyncrasy, but persisted for a longer time, reflecting the irreversible effect of these agents on the cyclo-oxygenase enzyme in platelets. The results demonstrate that administration of minute doses of ASA and other nonsteroidal anti-inflammatory drugs alters prostaglandin synthesis in normal and asthmatic subjects with or without ASA idiosyncrasy. Alteration in arachidonate metabolism may be responsible for the induction of bronchospasm, and cautious use of cyclo-oxygenase inhibitors in patients with known or suspected ASA idiosyncrasy is indicated.
A program evaluation was conducted on a sample of 40 families with asthmatic children who were managed in private practice and participated in a self-help education-exercise program in Denver. Baseline measures were collected for the six-month period before the program, and follow-up measures were collected for the six-month period following completion of the eight-week program. The results indicated that a significant number of children experienced less debilitation after completing the program and also had less need of medical services. The interpersonal relations between the child and the parents were judged to have improved in a significant number of families, and a significant number of mothers reported that they experienced less emotional distress in getting a significant number of parents to quit smoking. Additional evaluations are recommended with a sample of asthmatic children who are more severely debilitated and more difficult to manage.
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A self-help education-exercise program for asthmatic children and their parents was evaluated in Denver, Colorado. The objective of the program was to instill better self-care practices in the child which are expected to reduce utilization and cost of medical services and reduce the amount of interference in the child's normal activities. The program was designed to educate the family about the nature of asthma and its treatment, the importance of self-responsibility for the child, and the psychosocial aspects which may affect both the child and the parents in a family with an asthmatic child. The program also included specific lessons pertaining to self-care practices including general health exercises on land and in water, relaxation training, and diaphragmatic breathing. The results of subjective evaluations of the parents indicated that the program was successful in achieving its goals to: Reduce the number of severe attacks, reduce medication usage, improve compliance, reduce days of school missed, increase exercise activity, and control wheezing by the steps taught in the course. While the results are suggestive, a further, controlled evaluation of the program is recommended.
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Cyclic AMP was measured in leukocytes of normal and asthmatic subjects before and after one week of treatment with equal amounts of ephedrine. During the control and placebo periods, the measurements of cyclic AMP in leukocytes of asthmatic subjects were similar to those of normal individuals. After one week of treatment with ephedrine, both groups exhibited suppression of the leukocyte cyclic AMP response to adrenergic stimulation in vitro: however, the suppression of response was significantly greater in asthmatic subjects (p less than .u1). Subcutaneous administration of epinephrine was followed by further suppression of the leukocyte cyclic AMP response to in vitro stimulation which was similar in both groups during all treatment periods. The results indicate that in vivo exposure to adrenergic medications is followed by desensitization of the leukocyte responses to subsequent adrenergic stimulation in vitro. After administration of small doses of medication, the severity and/or duration of desensitization is significantly greater in asthmatic leukocytes.
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Beclomethasone dipropionate nasal spray is widely used in the treatment of seasonal allergic rhinitis; however, the time of onset of action has not been determined. This study assessed the onset of action, level of relief, and efficacy of beclomethasone nasal spray in patients with seasonal allergic rhinitis. In a double-blind, randomized, placebo-controlled, parallel-group, multicenter, 7-day study, symptomatic patients were administered two inhalations of beclomethasone dipropionate (n = 80) or placebo (n = 81) into each nostril twice daily. Patients assessed the onset of action and level of relief at 6, 24, and 48 hours and at days 3 and 7. Investigators evaluated symptoms at days 0, 3, and 7 and response to therapy at days 3 and 7. The difference in the cumulative number of patients reporting relief of symptoms was statistically significant in favor of beclomethasone dipropionate by hour 24 (P = 0.05). Patients in the beclomethasone dipropionate group experienced a greater level of relief than patients receiving placebo at hour 24, and improvement increased over the 7-day study compared with a decrease in relief in the placebo group. Beclomethasone dipropionate was significantly more effective than placebo in reducing symptoms (P < or = 0.02), and patients in the beclomethasone dipropionate group showed a more favorable response to treatment than did patients in the placebo group (P < 0.01). Adverse events were minor in both groups. Beclomethasone dipropionate nasal spray produced significant onset of relief of symptoms the first day of treatment; improvement was sustained and increased over the course of the study.