Biomedical subjects
Publications and source records attributed to H M Hollingsworth.
Seasonal allergic rhinoconjunctivitis can be incapacitating, but an extensive therapeutic arsenal is available. The author describes the advantages and disadvantages of various oral, intranasal, and ophthalmic medications and discusses when they should be prescribed and how they may be combined. Options for circumventing side effects, satisfying patient preferences, and controlling even severe symptoms are reviewed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Acute respiratory failure in pregnancy is an important cause of maternal and fetal morbidity and mortality. Causes include: ARDS, venous air embolism, beta-adrenergic tocolytic therapy, asthma, thromboembolic disease, pneumothorax, and pneumomediastinum. The most common predisposing diseases for ARDS complicating pregnancy are sepsis, pneumonia, aspiration of gastric contents, and amniotic fluid embolism. Knowledge of normal maternal-fetal physiology and determinants of fetal oxygen delivery (uterine blood flow, placental transfer, fetal circulation) can help sustain normal fetal development, usually without compromising maternal care. The increased microvascular permeability seen in ARDS is likely mediated by neutrophils, proinflammatory mediators (e.g., tumor necrosis factor, interleukin-1, arachidonic acid metabolites) and activation of the complement cascade. Treatment of respiratory failure in pregnancy is largely supportive, including mechanical ventilation, hemodynamic support, nutrition, and prophylaxis against thromboembolism. No specific therapy has as yet been proven effective for ARDS, other than treating the underlying cause. Respiratory failure from status asthmaticus is treated with vigorous bronchodilator therapy, high-dose glucocorticosteroids, magnesium sulfate, and careful ventilator management. Occasionally, more experimental therapies (e.g., isoproterenol infusion, halothane anesthesia) are indicated. Certain strategies can help prevent respiratory failure from aspiration of gastric contents, beta-adrenergic tocolytic therapy, and thromboembolic disease.
To determine whether thyrotoxicosis has an effect on the asthmatic state in subjects with mild asthma, airway responsiveness, lung function, and exercise capacity were measured in a randomized double-blind placebo-controlled trial before and after liothyronine (triiodothyronine, T3)-induced thyrotoxicosis. Baseline evaluation of 15 subjects with mild asthma included clinical evaluation, thyroid and routine pulmonary function tests, airway responsiveness assessment by methacholine inhalation challenge, and a symptom-limited maximal exercise test. For all subjects, the initial testing revealed that the dose of methacholine which provoked a 20% fall in forced expiratory volume in 1s (PD20) was in a range consistent with symptomatic asthma. There was no significant change in pulmonary function tests, airway reactivity (PD20), or exercise capacity in either the placebo or the T3-treated groups. Thyroid function tests confirmed mild sustained thyrotoxicosis in the T3-treated groups. We conclude that mild T3-induced thyrotoxicosis of 4-wk duration had no effect on lung function, airway responsiveness, or exercise capacity in subjects with mild asthma.
Wheezes are defined as high-pitched, continuous, adventitious lung sounds. They are produced by oscillation of opposing airway walls whose lumen is narrowed. Although asthma is the most common cause of wheezing, a wide variety of disease processes may result in wheezing due to airway obstruction. This obstruction may be caused by airway edema, smooth muscle constriction, increased secretions, vascular congestion, mass lesions, scarring, or foreign bodies. Stridor is a special kind of wheeze described as a loud musical sound of constant pitch, which is heard in patients with tracheal or laryngeal obstruction. The full differential diagnosis of airway obstruction should be carefully considered in any patient with wheezing or stridor.
A patient with bronchogenic carcinoma developed acute thrombophlebitis below the knee followed by pulmonary embolism. Sequential nuclear venograms, perfusion lung scans, bilateral impedance plethysmography, and the patient's clinical course indicated that the below-knee thrombus had embolized in its entirety, causing clinically significant disease. This case demonstrates that below-knee thrombi are not always benign and, in certain circumstances, merit anticoagulation.
In order to determine if mast cell mediators are released during aspirin challenge in aspirin-sensitive asthmatics, we measured neutrophil chemotactic activity, which has been shown to be an indicator of mast cell degranulation. Four aspirin-sensitive asthmatic subjects were given doses of aspirin (60 to 325 mg) previously determined to cause a 20 to 30% fall in forced expiratory volume in one second (FEV1); pulmonary function was followed by serial spirograms and body plethysmography. Serum was obtained before and at 30, 60, 90, 120, 180, and 240 min after challenge, corresponding to the times of pulmonary function measurements. Neutrophil chemotactic activity was measured using a modified Boyden chamber assay. Maximal bronchoconstriction occurred 60 to 120 min after aspirin ingestion. An increase in neutrophil chemotactic activity of 300 to 600% over baseline was detected in all subjects. In 3 subjects, neutrophil chemotactic activity release paralleled bronchoconstriction, and in 1 subject, it followed onset of bronchoconstriction. Physicochemical analysis showed that the neutrophil chemotactic activity eluted in the void volume of a Sephadex G-200 column (greater than or equal to 250,000 daltons) and from Sephadex QAE anion exchange chromatography in a region corresponding to 0.2 to 0.3 M NaCl. Its isoelectric point was in the pH range 6.5 to 7.5. These characteristics are compatible with neutrophil chemotactic factor of mast cell origin. Pretreatment with sodium cromolyn (40 mg) completely eliminated neutrophil chemotactic factor release, but only partially suppressed the fall in FEV1 in 2 subjects and had no effect on FEV1 fall in a third.(ABSTRACT TRUNCATED AT 250 WORDS)