It has shown recently that Evening Primrose Oil (Efamol) produces a significant clinical improvement in atopic eczema. Efamol contains gamma-linolenic acid which is a precursor to PGE1 a more consistent bronchodilator than PGE2. We have conducted a double blind placebo controlled study in atopic asthmatics given Efamol for an eight week period looking at the control of asthma, including histamine challenge tests. We have found no effect on the asthma or challenge tests although Efamol produced an alteration in fatty acid profile. The patients showed an abnormal fatty acid profile. We speculate that such fatty acid abnormalities could be important in the aetiology of asthma.
Fourteen asthmatics volunteered to stop smoking. Seven managed to stop for only 24 h and seven for 1 week. There was a significant increase in peak flow and specific airways conductance as early as the first 24 h of abstention, while after 7 days of abstention there was a further increase in peak flow and specific airways conductance and a reduction in bronchial responsiveness to histamine. Two subjects felt that their symptoms were worse while abstaining and one of these showed an increase in bronchial responsiveness. After abstention for 1 week, four of the seven subjects recorded an improvement in symptoms. Asthmatics who smoke should be encouraged to stop. Despite an improvement in symptoms and objective measurements, asthmatics may find it difficult to stop smoking and will need considerable help and encouragement if they are to succeed.
Nineteen stable asthmatic patients were given killed influenza virus intramuscularly. In 9 patients who developed a fourfold or greater rise in haemagglutination antibodies, an increase in airway sensitivity to histamine was demonstrated 48 h later. There was no significant change in histamine sensitivity in those patients who failed to develop a fourfold rise in haemagglutination antibodies. The increased histamine sensitivity was not associated with a deterioration in asthma symptoms, peak expiratory flow, nor an increase in bronchodilator requirements.
ABSTRACT The maximal expiratory flow/static transpulmonary pressure relationship and the maximal expiratory flow response to breathing oxyhelium were used to distinguish between loss of elastic recoil and narrowing of small airways in 36 lifelong non-smoking non-bronchitic South Wales coalminers. On average the miners showed significantly (p < 0·05) reduced lung elastic recoil when compared with 10 healthy similarly aged non-miners. The mean forced expiratory volume in one second and the forced expiratory flow response to oxyhelium at 50% of the vital capacity were significantly (p < 0·05) lower in 12 miners with radiographic categories 2 or 3 when compared with 24 similarly aged miners with radiographic categories 0 or 1. The miners with categories 2 or 3 coalworkers9 simple pneumoconiosis (CWP) had worked underground for 10 years longer, and their mean residual volume, residual volume/total lung capacity ratio, volume of isoflow and critical transmural pressure were significantly higher (p < 0·05). The results indicate that in the prodromal and early stages of simple CWP (categories 0 and 1), the dominant pathophysiological abnormality is loss of elastic recoil suggesting the presence of “focal emphysema.” As simple CWP progresses to categories 2 and 3, the loss of recoil is maintained, and the small airways become narrower. These findings are consistent with the hypothesis that progression of simple CWP is associated with the development of both centrilobular emphysema and intrinsic narrowing of small airways.
Bronchial hyper-responsiveness is a particular feature of asthma, but also occurs in normal subjects after a viral upper respiratory tract infection or ozone inhalation. Such stimuli would be expected to result in the release of chemical mediators of inflammation. In this study, the effects of one of these, prostaglandin F2 alpha (PGF2 alpha), on the response of normal subjects to inhaled histamine has been investigated. Nine normal volunteers took 10 inhalations of increasing concentrations of PGF2 alpha at 15-minute intervals from a Wright's nebuliser under standard conditions until a change in sGaw could be detected. The next lowest serial dilution of PGF2 alpha was subsequently inhaled by each subject every 15 min for 90 min to ensure the absence of a cumulative effect. Inhalation dose-response curves to histamine diphosphate were constructed on two separate occasions using the same standardised technique. Doses were administered every 15 min and sGaw determined five minutes after each. On one occasion each dose of histamine was immediately preceded by the non-active test dose of PGF2 alpha and on the second by saline as placebo. The study was performed double-blind and in random order. After pretreatment with PGF2 alpha the histamine dose-response curve was significantly shifted to the left in a parallel fashion (p less than 0.001). There was a significant decrease in the doses of histamine required to cause a 20% fall in sGaw (p less than 0.0015) but no significant change in the slopes of the dose-response regression lines, indicating that bronchial muscle sensitivity rather than reactivity had been predominantly affected.