Search PubMed⌕ Search

Biomedical subjects

D D Stevenson

Publications and source records attributed to D D Stevenson.

72 records · Page 4Linked to original sources
PubMed1976

Plasma histamine changes during provoked bronchospasm in asthmatic patients.

Seven patients with bronchial asthma underwent bronchial inhalation challenge with aerosolized allergen extracts and methacholine. Simultaneously, venous blood samples were collected and histamine was measured. Each patient was challenged on successive days with an allergen extract to which he had no skin-sensitizing antibody (skin test-negative allergen), followed by methacholine and skin test-positive allergen. Bronchospasm was not induced by inhalation of skin test-negative allergens but was observed in all patients after methacholine and in the majority of patients after skin test-positive allergens. No changes in plasma histamine were detected after challenges with methacholine and skin test-negative allergens. After challenge with skin test-positive allergens, significant rises in plasma histamine were detected in 5 of 7 patients. Plasma histamine was elevated within the first 5 min after inhalation of aerosolized allergen, and elevations persisted as long as 30 min. These studies showing that histamine increases significantly in the plasma during allergen-induced asthma in man suggest that histamine should be considered as at least one of the mediators of bronchospasm in allergic asthma. Bronchospasm induced by the cholinergic drug methacholine, unlike allergen-induced bronchospasm, is not associated with changes in plasma histamine.

Administration, Intranasal↗
PubMed1976

Oral aspirin challenges in asthmatic patients: a study of plasma histamine.

Under carefully controlled conditions, seven aspirin-intolerant asthmatic patients were challenged with oral aspirin and experienced respiratory tract reactions with a decline in forced expiratory volume in 1 sec (FEV1) ranging from 26 to 64%. Venous blood samples, which were collected during the challenges, showed a rise in plasma histamine in all seven patients. The increase in plasma histamine occurred at the onset of their respiratory reactions and those patients with the most severe asthmatic responses were found to have the highest and most prolonged levels of plasma histamine. The aspirin-intolerant asthmatic patients were able to ingest Maalox or sodium salicylate without untoward effects, decline in FEV1 values or changes in plasma histamine levels. Ten non-asthmatic individuals and eight out of ten asthmatic control patients were able to ingest aspirin without any reactions or changes in their plasma histamine levels. However, two asthmatic control individuals, with severe asthma requiring treatment with moderate dosages of corticosteroids, were found to have elevated pre-challenge plasma histamine levels which increased during their ASA challenges despite the absence of respiratory reactions or changes in FEV1 values. It is possible that these two individuals were unsuspected aspirin-intolerant asthmatics. These studies demonstrate that asthmatic reactions to acetylsalicylates are associated with release of histamine into plasma in the subgroup of asthmatic patients with the aspirin-intolerance syndrome. Such a finding suggests that histamine may be one of the mediators of bronchospasm in aspirin-induced asthma.

Administration, Oral↗
PubMed1975

Transtracheal aspiration studies in asthmatic patients in relapse with "infective" asthma and in subjects without respiratory disease.

Exacerbations of bronchial asthma that cannot be accounted for by allergic reactions have sometimes been called "infective" asthma. The validity of this designation was tested by study of transtracheal aspirates (TTA) obtained from 27 asthmatic patients in relapse who had findings suggestive of respiratory infection and 12 subjects without respiratory disease. Aspirates were cultured for aerobic and anaerobic bacteria, Mycobacteria, fungi, Mycoplasma, and viruses. A comparable variety of bacterial and fungal growth in small numbers was obtained from a majority of both groups. Microbial growth did not correlate with the presence of symptoms or signs compatible with infection. Aspirates from asthmatics with chronic bronchitis, immediate hypersensitivity to aeroallergens, or aspirin intolerance yielded no greater growth than did aspirates from asthmatics without these characteristics. In only one asthmatic was there suggestion that overt infection of the lower respiratory tract contributed to exacerbation of asthma. These results do not lend support to the empiric use of antibiotics in the management of unexplained asthmatic relapse.

Adolescent↗
PubMed1975

Provoking factors in bronchial asthma.

Asthmatic patients were identified as having asthma on the basis of lung function studies (76%), objective physical findings of asthma (11%), or a strong history of asthma (13%). Each of the 234 patients so identified was assigned to an asthma subgroup determined by careful clinical assessment of the major provoking factor or factors for his asthmatic episodes; minor provoking factors were also identified. Only 20% of the patients had asthmatic episodes provoked by a single factor. Most asthmatics had at least one major and one or more minor provoking factor(s). Reagin-mediated mechanisms constituted the major provoking factor in 25% of patients and were a minor provoking factor in an additional 20% of the patients. Thus, in only 45% of the patients, were reaginic mechanisms responsible for some part of their asthmatic episodes.

Adolescent↗
PubMedDate not supplied

Administration of radiographic contrast media in high-risk patients.

Patients with a prior history of an anaphylactoid reaction (AR) to radiographic contrast media (RCM) have an increased risk of an AR during subsequent RCM studies. Based on previous studies in high-risk patients using prednisone or diphenhydramine to reduce the incidence of AR, high-risk patients were treated with a combined prednisone and diphenhydramine protocol in an effort to develop an effective, practical approach to this problem. All patients with convincing histories of AR to RCM with an essential need for a repeat RCM study received 50 mg of prednisone orally every 6 hours for 3 doses ending 1 hour before the RCM study, and 50 mg of diphenhydramine intramuscularly 1 hour prior to the procedure. Resuscitation equipment was readily available. One hundred forty-seven repeat procedures using RCM were carried out in 142 high-risk patients. No serious AR occurred. Two patients had generalized urticaria that resolved in 1 hour. The overall reaction rate in these pretreated high-risk patients was 6.8%, suggesting that this prednisone-diphenhydramine program may be the preferred prophylactic regimen when repeat RCM studies are necessary.

Anaphylaxis↗
PubMedDate not supplied

Approach to the patient with a history of adverse reactions to aspirin or NSAIDs: diagnosis and treatment.

Aspirin and nonsteroidal antiinflammatory drugs can induce several different reactions. It is incumbant upon the astute physician to recognize the differences between these reactions, the clinical settings in which they occur, and the management of each type of reaction. In this article, I have attempted to clarify and simplify, as much as possible, the approach I take in addressing the problems of adverse reactions to these drugs. In addition, the problems of cross-reactions are explained in terms of COX-1 and 2 isoenzymes. Aspirin desensitization and treatment with daily ASA are also addressed.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Aspirin desensitization.

Aspirin desensitization can be carried out in all aspirin sensitive patients in whom the reaction is confined to the respiratory tract. Because only a few patients with urticarial reactions to ASA have been studied and the results are inconsistent, desensitization of urticaria patients cannot be recommended at this time. In asthmatic patients with aspirin sensitivity, who undergo ASA desensitization, continuous treatment with ASA or NSAIDs is realistic. Such treatment maintains the desensitized state indefinitely while allowing the beneficial anti-inflammatory effects of these drugs to participate in the treatment of various diseases, including arthritis, thromboembolic diseases, and probably inflammation in the respiratory tract.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Oral challenges to detect aspirin and sulfite sensitivity in asthma.

Oral challenge with aspirin, or potential cross-reacting substances, is an effective method for establishing the presence of these sensitivities in asthmatic subjects. However, in patients with concomitant active irritable airways, testing is inaccurate and potentially dangerous. Strategies for dealing with these problems and other details important in conducting oral challenges are outlined. Sulfite challenges are conducted in a different manner and there has not been cross-sensitivity established between sulfite sensitive and aspirin sensitive asthmatics. However, many of the same problems created by heightened airway activity interfere with the accuracy of sulfite challenges. A special obstacle in interpreting the results of sulfite challenges is the issue of specificity. Oral challenges with solutions of sulfite improve sensitivity of the challenge procedure. But only low dose sulfite solutions (50 mg/ml or less) and capsules of sulfite salts are specific provoking substances for sulfite sensitivity.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Commentary: the American experience with aspirin desensitization for aspirin-sensitive rhinosinusitis and asthma.

The experience in the United States with aspirin sensitivity associated with rhinosinusitis and asthma is generally in agreement with the European perspective offered by Drs. Szczeklik and Kowalski, though our approach to challenging these patients is slightly different. Most aspirin-sensitive patients no not have a family history of aspirin sensitivity. Aspirin sensitivity is found in one third of patients having nasal polyps, rhinosinusitis, and asthma, the remaining two thirds of these patients having no adverse response to aspirin ingestion. In 85% of asthmatics who give a history of aspirin-induced bronchospasm, oral aspirin challenges are positive. Thus, a small group of patients have inappropriately assigned aspirin-sensitive asthmatic (ASA) as the cause of a prior asthmatic attack that in reality had been induced by an independent provoking factor.

Aspirin↗